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Cardiology
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Version 5.3
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System is Active Corrected, Updated, Lighter
PLAB 1 Keys is for PLAB-1 and UKMLA-AKT (Based on the New MLA Content-Map)

With the Most Recent Recalls and the UK Guidelines

ATTENTION: This file will be updated online on our website frequently!
(example: Version 2.2 is more recent than Version 2.1, and so on)

Key Acute Coronary Syndrome (ACS)

1

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◙ Acute Coronary Syndrome includes:

√ ST elevation myocardial infarction (STEMI).
√ Non-ST elevation myocardial infarction (NSTEMI).
√ Unstable angina.

◙ Symptoms and signs

The classic and most common feature of ACS is chest pain.

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√ Typically, central/left-sided/ substernal/ epigastric.

√ May radiate to the jaw, the left arm, the shoulder.
√ Often described as ‘heavy’ or constricting, ‘like an elephant on my chest’

- It should be noted however in real clinical practice that patients present with
a wide variety of types of chest pain and patients/doctors may confuse
ischaemic pain for other causes such as dyspepsia.

- Certain patients e.g. diabetics/elderly may not experience any chest pain
→ Silent MI

◙ Other possible symptoms in ACS include:

Dyspnoea ▐ sweating ▐ nausea and vomiting ▐ may appear pale and clammy

◙ Risk Factors of Ischemic Heart Disease:

Unmodifiable risk factors Modifiable risk factors

Increasing age Smoking
Male gender Diabetes mellitus
Family history Hypertension
Hypercholesterolaemia
Obesity
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◙ Investigations

√ ECG
√ cardiac markers e.g. troponin
ECG in ST-elevation MI
→ elevated ST segment in certain leads gives a clue about the site and type
of the STEMI as follows:

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Example:

ECG features of Left main coronary artery occlusion [LMCA]:

√ Wide spread ST depression.
√ ST elevation in aVR.

Do → Emergency coronary angiography.

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Management of ST elevation MI (STEMI):

◙ In Acute Settings → MONA

(IV Morphine, O2, Nitrates, Aspirin 300 mg)

• If the patient presents within 12 hours of the onset of the symptoms

→ Primary PCI (Percutaneous Coronary Intervention) ‘’The gold standard’’

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In this procedure (PCI), the blocked arteries are opened up using a balloon
(angioplasty) following which a stent may be deployed to prevent the artery
occluding again in the future. This is done via a catheter inserted into either the
radial or femoral artery

• If Not, or PCI is unavailable

→ Thrombolysis (Alteplase is preferred over Streptokinase).

• (Chronic) Long-term Management of MI:

1) Aspirin for life.
2) Ticagrelor or Prasugrel for 12 months ‘’or: Clopidogrel”.
3) Beta Blockers (for 12 months) “e.g. atenolol, bisoprolol ® concor, zebeta”.
4) ACE inhibitors (for life) “e.g. captopril, enalapril, ramipril”
[If intolerant to ACEi such as dry cough, use ARBs instead e.g. losartan,
valsartan, irbesartan]
5) Statins (for life) “e.g. Atorvastatin 80 mg PO OD”.

So, Long-term MI Rx = 5 Drugs: Aspirin, Clopidogrel, BB, ACEi, Statins

AABC+S → Aspirin, ACE inhibitors, Beta-blockers, Clopidogrel + Statins

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Management of NSTEMI & Unstable Angina:

(based on the recent UK guidelines)

Important:
For all patients where the diagnosis of NSTEMI or Unstable Angina is
made → Aspirin 300 mg (+) LMWH e.g. Enoxaparin, Dalteparin “or
Fondaparinux” need to be given as soon as possible.

√ Aspirin 300 mg.

√ Nitrates or morphine to relieve chest pain if required.
√ Antithrombin: LMWH e.g. Enoxaparin, Dalteparin “or Fondaparinux” should
be offered to patients who are not at a high risk of bleeding and who are not
having angiography within the next 24 hours.
If angiography is likely within 24 hours or a patient’s creatinine is > 265
µmol/l, unfractionated heparin should be given.
[Note: Fondaparinux and LMWH are given Subcutaneously, whereas
Unfractionated Heparin is given Intravenously].

√ Second antiplatelet: e.g. Clopidogrel, Prasugrel.

√ Intravenous glycoprotein Iib/IIIa receptor antagonists (eptifibatide or

tirofiban) should be given to patients who have an intermediate or higher risk
of adverse cardiovascular events (predicted 6-month mortality above 3.0%),
and who are scheduled to undergo angiography within 96 hours of hospital
admission.
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√ Coronary angiography should be considered within 96 hours of first

admission to hospital to patients who have a predicted 6-month mortality
above 3.0%. It should also be performed as soon as possible in patients who
are clinically unstable.

Examples of recent exams’ questions:

[Example 1]
A patient presents with (acute chest pain radiating to jaw and shoulder
+ other features suggesting ischemic heart disease…) However, without
ST elevation on ECG. What to Do Next?

→ Measure Cardiac Enzymes, especially (Troponin)

√ If Troponin is high → NON-STEMI = Non-ST elevation MI

√ Immediate management
→ Give Subcutaneous LMWH OR Fondaparinux + Aspirin 300 mg

Notes:

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LMWH = Low Molecular Weight Heparin

Examples → Dalteparin, Enoxaparin

Fondaparinux (trade name Arixtra) is an anticoagulant medication chemically

related to low molecular weight heparin.

[Example 2]
A 60 YO man with Hx of smoking, HTN and DM presents to his GP
complaining of 25 minutes of left side dull aching chest pain radiating to his
jaw. He was given Aspirin 300 mg by his GP and then sent to medical services
in a local hospital. He is no longer in pain. The ECG is normal. The troponin is
elevated 202 ng/L (Normal: < 5 ng/L). What is the next step in management?

A) Alteplase.
B) Subcutaneous fondaparinux.
C) IV Glyceryl trinitrate (GTN).
D) IV Morphine.

Since the ECG is normal, alteplase is wrong.

Since ECG is normal and Troponin is high → Non-STEMI

→ Anti-coagulation (LMWH e.g. Dalteparin, Enoxaparin or Fondaparinux).

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[Example 3]
A 62 YO man with Hx of smoking and HTN presents complaining of 25
minutes of left side constricting chest pain radiating to his left shoulder. He
was given Aspirin 300 mg and trinitrates for the pain. ECG was then done
and showed ST elevation in leads V1-V4. What is the most appropriate next
step in management?

→ PCI “Percutaneous Coronary Intervention”.

If not among the choices, pick → Alteplase “Thrombolysis”

[Example 4]
A 59 YO hypertensive patient presents to the A&E complaining of dull
central chest pain for around 4 hours. His vitals are as follows:
HR: 99, BP: 155/95, RR: 21, O2 sat on room air: 97%
Chest X-ray is normal. Troponin level is pending.
He was given IV morphine for his chest pain.
The ECG is as follows:

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What is the most appropriate next step in management?

Chest pain + T wave inversion suggests → myocardial ischemia.

In this case, 2 drugs should be given immediately:

√ Aspirin 300 mg.
√ LMWH or Fondaparinux.
Pick the one that is given in the choices.

“low-risk patients can be treated conservatively. However, if subsequent

ischemia develops → coronary angiography with PCI”.

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What if the ECG shows features of left main coronary artery occlusion (Wide
spread ST depression + ST elevation in aVR)?
→ Emergency coronary angiography.

[Example 5]
A 61 YO patient presents to the A&E complaining of dull central chest pain
for around 4 hours. His vitals are as follows:
HR: 75, BP: 135/85, RR: 21, O2 sat. on room air: 97% He was given IV
morphine for his chest pain. The ECG is as follows:

What is the most appropriate next step in management?

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This ECG shows the typical features of Left main coronary artery occlusion:
• Widespread ST depression, and
• ST elevation in aVR.

Do → Emergency coronary angiography.

Key Cardiac Tamponade

2

Accumulation of pericardial fluid under pressure

• Beck’s Triad:

Hypotension ▐ Muffled Heart Sounds ▐ High JVP (Distended neck veins).

• Others: Dyspnea, Pulsus Paradoxus, Tachycardia.

• Cardiac Tamponade can develop as a complication of MI

After MI → Acute pericarditis → Pericardial effusion → Cardiac Tamponade

• Trauma is the most important cause of cardiac tamponade.

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N.B. Chest X-ray that shows enlarged globular heart

→ Think of either Pericardial effusion (OR) Cardiac Tamponade.

• Dx: Echocardiogram is diagnostic

• Rx: Urgent pericardiocentesis.

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Cardiac Tamponade

Important!
If the patient is in hypovolemic shock (severely low BP) and the question
asks about the [INITIAL] treatment line and IV fluids is within the
option, pick it!
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Cardiac Tamponade:
Oxygenation and ventilation → 1 to 2 L IV fluid NS → bedside Pericardiocentesis.

Key Atrial Myxoma

3

o Benign tumours.

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o 75% in the left atrium.

o Tend to grow on the wall (inter-atrial septum).
o 10% are inherited → Familial myxoma

o Features:

◙ Obstruction of Mitral valve → Mid-diastolic murmur, Dyspnea, Syncope,

Congestive HF.
◙ Small pieces may break off and travel to arteries causing (ischemia) of
different parts of the body such as:
♦ Lung → Can cause PE (Pulmonary Embolism)
♦ Brain →Can cause Stroke
♦ Peripheries → Clubbing and Blue fingers.

◙ Atrial Fibrillation

o Dx → Echo → Pedunculated heterogenous mass typically attached to the

region of fossa ovalis (inter-atrial septum).
o Important note:

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If acute limb ischemia develops “sudden painful swollen limb with a loss of
pulse” → we could save the limb by performing an urgent catheter
embolectomy.

Key A patient was hit by a car into his chest and is brought to the emergency
4 department. His neck veins are distended, Heart sounds are faint,
hypotensive and tachycardic.

The likely Diagnosis → Cardiac Tamponade.

The most appropriate management → Pericardiocentesis

• Beck’s Triad:
Hypotension, Muffled Heart Sounds, High JVP (Distended neck veins).

Key Axis Deviation

5

o If QRS in lead I is up (+ve) and in lead II is down (negative) →

Left axis deviation

o If QRS in lead I is down (-ve) and in lead II is up (+ve) →

Right axis deviation

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These causes are important!

Causes of Left Axis Deviation Causes of Right Axis Deviation
Inferior MI Lateral MI
Left Ventricular Hypertrophy Right Ventricular Hypertrophy
Left Anterior Fascicular block (or Left Posterior Fascicular Block (or
hemiblock) hemiblock)
Obese Thin, Tall, Children
Wolff Parkinson White Syndrome Chronic Lung Disease
(delta wave)
Pulmonary Embolism

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• Causes of EXTREMER Right Axis Deviation (No man’s land) = (North

west axis):
o Congenital Heart Disease.
o Left Ventricular Aneurysm.

For PLAB 1, you need to know either it is left axis deviation (Lead I is up and
Lead II is down) or right axis deviation (Lead I is down and Lead II is up) and
the causes of each (in the table above).

Key Types of heart block

6

First degree heart block

• PR interval > 0.2 seconds (Only prolonged PR intervals).
(i.e., PR interval occupies more than 1 large square (or 5 small squares).

Second degree heart block

• type 1 (Mobitz I = Wenckebach)
→ Progressive prolongation of the PR interval until a dropped beat occurs.

• type 2 (Mobitz II)

→ PR interval is constant but the P wave is often not followed by a QRS
complex.

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Third degree (complete) heart block

• There is no association between P waves and QRS complexes.

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Management of AV Heart Block:

◙ 1st Degree Heart Block and Mobitz type 1 usually

→ do not require treatment (as long as the patient is Asymptomatic).

◙ Mobitz type 2 and Complete heart block (3rd degree heart block)
→ require permanent pacemaker

• Initially → Atropine (first choice for all symptomatic bradycardia).

• Then → Transcutaneous pacing. (Used to buy time until transvenous
pacing is done).
• Then → Transvenous pacing.
• Then → Permanent pacing (Pacemaker).

For your knowledge:

• 1 small square = 0.04 sec.
• 1 large square contains 5 small squares = 0.2 sec.

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Key
7

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• Agents used to control rate (Rate Control) in patients with

Atrial Fibrillation: (if the patient is stable and no hypotension)

o Beta-blockers (eg, atenolol, bisoprolol, metoprolol) → First line but

Contraindicated in Asthma.
o Calcium channel blockers [non-dihydropyridine CCB] (eg, diltiazem,
verapamil) → used in Asthmatic patient.
o Digoxin → (not considered first-line anymore as they are less effective at
controlling the heart rate during exercise. However, they are the preferred
choice if the patient has coexistent heart failure).

√ If haemodynamically unstable (eg, SBP ≤ 90) → Cardioversion (Shock).

√ If the patient with AF is unstable (eg, hypotension) and the AF has just
started and no cardioversion in the options, Pick → IV amiodarone. Imp √

Note:
• Atrial fibrillation is a common arrhythmia after surgery. So, if it develops
after surgery → Continue to observe and monitor vital signs.
• If it does not resolve on its own or if it worsens → Intervene (eg, bisoprolol).

• Atrial Flutter management → Cardioversion (Shock)

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Key Ventricular tachycardia

8

√ Ventricular tachycardia (VT) is broad-complex tachycardia originating from a

ventricular ectopic focus.
√ It can develop into ventricular fibrillation and therefore requires urgent
treatment.
√ P wave might be present or absent.

N.B:
• ECG showing broad complex tachycardia in a (still) conscious patient even
if semiconscious ± atrial activity and “haemodynamically STABLE”
→ Ventricular tachycardia → Give Amiodarone He is stable!

• ECG showing ventricular tachycardia in a haemodynamically unstable (e.g.

SBP ≤ 90) patient → DC cardioversion = shock. He is unstable but has a pulse.

• If the patient is Unconscious, Collapsed, or Not breathing + No Pulse!

→ Ventricular Fibrillation → Defibrillation = Asynchronized shock

[As the patient is still conscious and with a felt pulse, it is likely ventricular
tachycardia; not ventricular fibrillation. However, remember that
ventricular tachycardia is managed by amiodarone if the patient is stable
and by cardioversion if unstable]. If No pulse → Immediate Defibrillation.

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• Ventricular fibrillation is the most important shockable arrhythmia.

• Hypokalemia (↓ K+) is the most important cause of ventricular

tachycardia (VT) clinically.

Atrial Fibrillation Palpitation, Tachycardia, Dyspnea, Fibrillatory waves

on the ECG, Irregularly irregular rhythm
→ Give Beta-Blocker.
If Asthmatic → Give Calcium Channel Blocker.
If with hypotension → Cardioversion / IV amiodarone.

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Atrial Flutter ‘’Fluttering Feeling in the chest’’, Sawtooth waves on

the ECG → Synchronized ardioversion.

Ventricular Regular and Fast rhythm.

Tachycardia Ongoing lightheadness, Palpitations, Chest pain.
→ Give Amiodarone.

If unstable (SBP <90, ↓ consciousness)

→ Immediate synchronized Cardioversion.

If Pulseless VT → Immediate defibrillation.

Defibrillation = Unsynchronized cardioversion “high”

Ventricular Older adult, Sudden collapse, Not breathing,

Fibrillation Unconscious, No pulse
→ ‘’Immediate Defibrillation’’

Sinus Bradycardia Lightheadness, hypotension, vertigo, syncope,

dizziness.
N.B. Sinus bradycardia is normal in young athletes.
◙ The first drug of choice for Symptomatic
Bradycardia (Dizziness, feeling unwell) → Atropine
Sinus Tachycardia Physiological situation (exercise, stress, anger).

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Hx of infection.
WPWS Delta wave on the ECG

Narrow-complex ◙ Usually in young patients

Supraventricular ◙ Presents with Palpitations, Light-headedness,
tachycardia (SVT) Recurrent, Young
♠ Initial line
→ Valsalva manoeuvre, Carotid massage.

♠ Not improved?
→ Intravenous adenosine

Polymorphic ◙ Beat-to-beat variations with no uniform pattern of

(Broad-Complex) ventricular contractions.
Ventricular ◙ Broad QRS (except in resting status), Prolonged QT,
Tachycardia Fainting episodes, Patient might be a young athlete,
= Torsades De Recurrent.
Pointes (TDP) ◙ Treatment → IV Magnesium Sulphate.

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Key Management of Congestive Heart Failure

9

While loop diuretics (furosemide, bumetanide) and nitrates are important in

the management of acute or decompensated cardiac failure, they have no
effect on long-term survival.

◙ The following medications have all been shown to reduce

mortality in patients with left ventricular failure:

• ACE-inhibitors
• Beta-blockers
• Angiotensin receptor blockers (ARBs)
• Aldosterone antagonists (e.g. Eplerenone, Spironolactone)
• Hydralazine with nitrates

How to manage CHF? (Important)

• For all patient, for symptomatic relief and to reduce the volume overload
→ Diuretics (e.g., Furosemide ▐ Lasix ™) or (Bumetanide).

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• Start with either an ACE inhibitor or Beta blocker (one drug at a time).

• If the symptoms persist → Add the other one (ACEi or BB).

• If the symptoms still persist → Add Spironolactone

Side Notes:
√ Spironolactone is a potassium-sparing diuretic and an aldosterone antagonist.

√ (Important) If the patient of congestive heart failure is already on FUROSEMIDE,

Beta blocker, and ACEi and still has lower limb edema → This means that the
diuretic is not efficient (the furosemide) → Therefore, one of the following is
needed:
• Increase the dose of the furosemide.
• Switch the furosemide to either bumetanide or torsemide.
• Consider admission for IV loop diuretics.

V. Imp. Note: If the patient has Diabetes, we start with ACE inhibitors (e.g.
Ramipril) instead of Beta-Blockers.

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ACE inhibitors are reno-protective and thus beneficial for diabetic patients.

“Try to link ACEi with DM in your mind”!

• If HF + AF → Digoxin

N.B. One might ask “Won’t Furosemide + ACE inhibitors lead to

hyperkalemia?

The answer is → No!

• Thiazide and Loop Diuretics (e.g. Furosemide) → HypOkalemia.
• ACEi (e.g., Ramipril) and Spironolactone → HypeRkalemia.

Key The Summary of STEMI (ST-Elevation MI) Management

10

◙ In Acute Settings
→ MONA
(Morphine, O2, Nitrates, Aspirin 300 mg)
+ Heparin (either unfractionated or LMW such as enoxaparin/
fondaparinux)

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• If the patient presents within 12 hours of the onset of the symptoms

→ PCI (Percutaneous Coronary Intervention) ‘’The gold standard’’

• If Not, or PCI is unavailable → Thrombolysis (Alteplase).

◙ (Chronic) Long-term Management of MI

Aspirin for life, Ticagrelor or Prasugrel for 12 months ‘’Clopidogrel
previously’’, Beta Blockers (for 12 months), ACE inhibitors, Statins

So, Long-term MI Rx = 5 Drugs: Aspirin, Clopidogrel, BB, ACEi, Statins

AABC+S → Aspirin, ACE inhibitors, Beta-blockers, Clopidogrel + Statins

Key Patent Foramen Ovale

11

√ The foramen allows blood to pass from the right atrium to the left atrium.
√ The opening is supposed to close soon after birth, but sometimes it does
not. In about 1 out of 4 people, the opening never closes. If it does not close,
it is called a PFO.
√ In most of these individuals, the PFO causes no problems and remains
undetected throughout life.

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√ PFO has long been studied because of its role in paradoxical embolism (an
embolism that travels from the venous side to the arterial side). This may lead
to a stroke or transient ischemic attack.
√ Transesophageal echocardiography is considered the most accurate
investigation to demonstrate a patent foramen ovale.
√ A patent foramen ovale may also be an incidental finding.

The important point to remember is:

Trans-oesophageal Echocardiography (TOE) with bubble contrast is the gold
standard in diagnosing Patent Foramen Ovale (PFO).

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Key Important Complications of Myocardial Infarction (MI)

12

Cardiac arrest
• This most commonly occurs due to patients developing ventricular
fibrillation and is the most common cause of death following a MI.
• Patients are managed as per the ALS protocol with defibrillation.

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Chronic heart failure

If the patient survives the acute phase, their ventricular myocardium may
become dysfunctional resulting in chronic heart failure.
Management:
◙ For all patient for symptomatic relief and to reduce the volume overload →
Loop Diuretics (e.g., Furosemide)
◙ Start with either ACEi or BB. (One drug at a time)
(Remember that ACEi and ARBs is delt with as similar in effect).
◙ If the symptoms persist → Add the other one (ACEi or BB).
◙ If the symptoms still persist → Add Spironolactone (Aldosterone
Antagonist).

[Important: If a patient is already on an ACE inhibitor (eg, lisinopril) or is

already on ARBs (eg, losartan, candesartan) and he needed an additional
medication for his chronic heart failure, pick a beta-blocker eg, bisoprolol].
If he is already on an ACEi or ARBs + BB → go for spironolactone.

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Tachyarrhythmias
◙ Ventricular fibrillation, as mentioned above, is the most common cause of
death following a MI. Other arrhythmias can also occur e.g. ventricular
tachycardia.
◙ Management:
1) Check the patient’s pulse, if no pulse, commence the arrest protocol
immediately (and deliver immediate defibrillation)
2) Administer O2.

Pericarditis “important √”
◙ Occurs within 48 hours (i.e. 2 days) after MI.
◙ Features → Pleuritic chest pain that is worse on lying flat and during
inspiration ± Fever ± Pericardial rub.
◙ Pericardial effusion may develop leading to enlarged globular heart on chest
X-ray and is confirmed by echocardiogram.
◙ ECG → Widespread Saddle Shaped ST Elevation with upward concavity +
PR Depression.
◙ Management of Pericarditis (imp):
√ A full-dose NSAID should be used (eg, aspirin, 2-4 g/d; ibuprofen 1200-1800
mg/d; indomethacin 75-150 mg/d); treatment should last at least 7-14 days.
√ Colchicine (as an adjunct to NSAIDs to ↓ inflammation and recurrence).

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Dressler’s syndrome “important √”

◙ Similar to pericarditis in features but it tends to occur 2-6 weeks following a
myocardial infarction.
◙ The underlying pathophysiology is thought to be an autoimmune reaction
against antigenic proteins formed as the myocardium recovers.
◙ It is characterised by a combination of fever, pleuritic chest pain that
worsens on inspiration and lying flat, pericardial effusion and a raised ESR.
◙ It is treated with NSAIDs.
◙ ECG: Widespread Saddle Shaped ST Elevation ± PR Depression.

Left ventricular aneurysm

◙ The ischaemic damage sustained during a MI episode may weaken the
myocardium resulting in a thin muscular layer; thus, aneurysm formation.
◙ This usually occurs 4-6 weeks post MI.
◙ This is typically associated with persistent ST elevation and left ventricular
failure.
◙ A thrombus may form within the aneurysm increasing the risk of stroke.
Patients are therefore anticoagulated.
ECG → Persistent ST Elevation + Left Ventricular Failure.

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CXR → Enlarged heart with a bulge at the left heart border.

Echo → Paradoxical movement of the ventricular wall.

Ventricular septal defect (VSD)

◙ Rupture of the interventricular septum usually occurs in the first week after
a MI attack and is seen in around 1-2% of patients.
◙ Features: acute heart failure associated with a pan-systolic murmur best
heard at the left lower sternal border + Heart Failure (eg, bibasilar crackles) +
Shock (hypotension, tachycardia).
◙ An echocardiogram is diagnostic and will exclude acute mitral regurgitation
which presents in a similar fashion.
◙ Urgent surgical correction is needed.

Acute mitral regurgitation (MR): “important √” pansystolic murmur

◙ Occurs 2-15 days after the MI (Mostly inferior MI).
◙ Due to → Ischemia or rupture of the papillary muscles of the mitral valve.
◙ An early-to-mid systolic or Pansystolic murmur is typically heard at Apex.
◙ May present with Hypotension, Tachycardia, and Pulmonary edema.
If with Pulmonary Edema → SOB (Dyspnea), Bi-basal Crackles, Tachycardia.
◙ To diagnose MR → Echocardiogram.

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◙ Treatment → vasodilators, but often requires emergency surgical repair.

Acute Tricuspid regurgitation (MR):

Similar to mitral regurgitation but the pan-systolic murmur is heard over the
lower left sternal border.

Important Note:

◙ Pericarditis (Can occur as a Complication of MI, may develop shortly

after MI within 2 days) and Dressler’s syndrome (presents 2-6 weeks

after MI) both have the same features:
→ Pleuritic chest pain that worsens on lying flat and during
inspiration, and improves on upright sitting forward.
± Pericardial rub,
± Widespread Saddle shaped ST elevation on the ECG.

◙ They can also lead to Pericardial effusion (Enlarged globular heart on chest
X-ray) and if severe enough, Cardiac Tamponade can also develop (also
enlarged globular heart of the X-ray + Beck’s Triad: Hypotension, Muffled
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Heart Sounds, High JVP).

Key
13

Wide spread ST depression (+) ST elevation in aVR

→ Left main coronary artery [LMCA] occlusion
→ Emergency coronary angiography

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Key For Theoretical Exams:

14
◙ Any patient presents with STEMI:
→ Give MONA (Morphine, O2, Nitroglycerin, Aspirin) and then:
→ Send immediately for PCI (Percutaneous Coronary Intervention).
• If PCI is not obtainable → Alteplase. [i.e. thrombolysis].
• If PCI and Alteplase are not given, pick →Streptokinase. [i.e. thrombolysis].

◙ Any patient presents with NSTEMI or Unstable angina:

→ After giving morphine, 2 medications should be given immediately:
√ Oral Aspirin 300 mg (+)
√ SC Low molecular weight heparin “or” SC Fondaparinux.

• If left main coronary artery occlusion:

i.e. (widespread ST depression + ST elevation in aVR):
after giving morphine → Emergency coronary angiography.

Key ◙ The first drug of choice for Symptomatic Bradycardia

15
(Dizziness, feeling unwell) is
→ Atropine

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(Given 0.5 mg IV push and may be repeated up to a total dose of 3 mg).

What if he was given atropine but no response?
Next step would be → Temporary transcutaneous pacemaker.

◙ 2nd Line → Dopamine.

◙ 3rd Line → Epinephrine.

♠ N.B. If the question was “the next best step” (or) “the initial line”, the
Answer will be → O2 (ABCD).

Key Beck’s Triad:

16
√ Hypotension,
√ Muffled “faint = weak” Heart Sounds,
√ High Jugular Venous Pressure [JVP] (= Distended neck veins).

→ Cardiac Tamponade.

→ Echo for Dx and Pericardiocentesis for Rx

Key Infective Endocarditis (IE)

17
New Murmur + Fever → think of Infective Endocarditis (IE)
± Malaise, Rigors.

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The initial step → Blood Culture √ Then → Echo

Example:
6 weeks following MI, a 59-year-old patient presented with a 10-day history of
intermittent fever and a new-onset of a soft high-pitched murmur at the apex.
His ECG is normal.
Fever + New-onset murmur, Think → Endocarditis.

• Risk Factors:
◙ A previous episode of endocarditis → the strongest risk factor.
◙ Rheumatic valve disease.
◙ Prosthetic valves.
◙ Congenital heart defects.
◙ Intravenous drug users (IVDUs: typically causing tricuspid lesion).

• The Causative Organisms:

- Staph. Aureus is the commonest cause of IE in general.
- Staph. Epidermidis is the commonest cause after prosthetic valve surgery.
- Strept. Viridans (especially sterpt. Mitis and strept. Sanguinis) are the
commonest cause in people with poor dental hygiene or following a dental
procedure.

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• Features and Diagnosis → Modified Duke criteria

Infective endocarditis is diagnosed in any of the following situations:

• 2 major criteria, or
• 1 major and 3 minor criteria, or
• 5 minor criteria

Major criteria

1) Positive blood cultures

◙ Two positive blood cultures showing typical organisms consistent with
infective endocarditis, such as Streptococcus viridans and the HACEK group,
(Or)
◙ Persistent bacteraemia from two blood cultures taken > 12 hours apart or
three or more positive blood cultures where the pathogen is less specific such
as Staph aureus and Staph epidermidis.
Not to be confused, it is true that staph. Aureus is the commonest pathogen in
IE; however, it is not specific for IE as it causes many other inflammations.

2) Evidence of endocardial involvement (i.e. +ve Echo for IE)

◙ Positive echocardiogram (oscillating structures, abscess formation, new
valvular regurgitation or dehiscence of prosthetic valves). (Or)
◙ New valvular regurgitation

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Minor criteria
1. Predisposing heart condition or intravenous drug use.
2. Microbiological evidence that does not meet the major criteria.
3. Fever > 38°C.
4. Vascular phenomena → Major emboli, Splenomegaly, Clubbing, Splinter
haemorrhages, Janeway lesions, Petechiae or purpura.
5. Immunological phenomena → Glomerulonephritis, Osler’s nodes, Roth
spots.

N.B.
- Osler’s Nodes: painful, red nodules on the hands or feet that can persist for
hours to days.
- Janeway lesions: Non-tender, small, erythematous or hemorrhagic macular
or nodular lesions on the soles or palms. (they occur due to septic micro-
emboli that deposit the bacteria under the skin).

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Endocarditis: initial “Empirical” “Blind” therapy

• Native valve endocarditis →
- Amoxicillin + low-dose Gentamicin. (Or),
- Vancomycin + low-dose Gentamicin (If Penicillin allergic or MRSA
“Methicillin-Resistant Staph. Aureus” is suspected or Severe Sepsis).
• If Hx of prosthetic valve endocarditis→
Vancomycin + low-dose Gentamicin + Rifampicin

The most important note to remember is that in any patient

presenting with Fever + a new heart Murmur → suspect Infective
Endocarditis and order Blood Culture until proven otherwise.
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Example 1:
A man who had dental extraction a few days ago presents with petechia. His
vitals are stable except his body temperature which is 38.9. On examination
(O/E): He has petechiae, painful nodules on his palms, and a cardiac
murmur.
The likely Dx → Infective Endocarditis. (Fever + New Murmur).
The underlying cause of this condition → infection.
The next investigating step → blood culture (followed by Echo).

Example 2:
A man presents with Fever, confusion, petechiae. This is a picture of his soles

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What is the most appropriate investigation?

→ Blood Culture

These lesions are likely Janeway lesions (minor criteria of infective

endocarditis).
♦ Likely → Infective endocarditis

→ Do Blood culture then Echocardiogram

Key ◙ In a patient with Atrial Fibrillation → We use the CHA2DS2-VASc Score

18

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“To determine the need to anticoagulants”.

◙ Give Warfarin or DOAC (Direct-Acting Oral AntiCoagulants, such as

Apixaban, Rivaroxaban, Edoxaban, Dabigatran) To:
√ All patients with score ≥ 2.
√ Consider giving Warfarin or DOAC to Men who score ≥ 1.

Advantages of DOAC:
o No need for INR Monitoring,
o Faster Onset of Action (2-4 hours),
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o Reduces the risk of intracranial Hemorrhage.

Disadvantages of DOAC:
o No Antidote
o Require strict compliance by the patients.

Important Scoring Systems to Know

◙ The CHA2DS2-VASc score is used to determine the need to anticoagulants

in a patient who has atrial fibrillation. √ important

◙ The ABCD2 score (Prognostic) is used to identify the risk of future stroke in
patients who have had a suspected TIA in the following 7 days. √ Not advised
to be used now according to the recent 2019 CKS guidelines.

◙ The HAS-BLED score estimates the risk of major bleeding for patients on
anticoagulation for atrial fibrillation.

◙ The DRAGON score predicts the 3-month outcome in ischaemic stroke

patients receiving tissue plasminogen activator (tPA) e.g. alteplase.

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◙ The QRISK2 score is used to determine the risk of a cardiovascular event in

the next 10 years.

Key Pulmonary edema

19

Mechanism:
Often caused by congestive heart failure. When the heart is not able to pump
efficiently → blood may return into the veins → then to the lungs.
As the pressure in these blood vessels increases, fluid is pushed into the air
spaces (alveoli) in the lungs.

Features:
Desaturation (Low O2 Sat.),
Dyspnea (SOB),
Orthopnea (SOB worsens when lying down),
Auscultation → Crepitations “Crackles = rales”. Mostly bi-basal.
Tachycardia.

Investigations:
While chest X-ray usually shows features of pulmonary edema (The single
most appropriate Investigation), the underlying cause requires
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Echocardiogram to be identified (e.g. Congestive Heart Failure, Complication

of MI → Acute Mitral Regurgitation due to papillary rupture, Ventricular
aneurysm, …etc.)
Therefore, pay attention to the question words!
◙ The Most Appropriate Investigation → Chest X-Ray. “imp √”
◙ The Investigation Needed to Identify the Underlying Cause → Echo. “imp √”

Management:

MONA (But the last A -Aspirin- is replaced by F -Furosemide-):

→ Morphine, O2, Nitrates, Furosemide (Lasix).

1) Sit the patient up (Popup position) and give O2 (aim for O2 saturation of
≥ 95%, or ≥ 90% in COPD patients).
2) Spray 2 puffs of sublingual GTN (Glyceryl TriNitrates).
3) Give Furosemide (Lasix) 40 mg IV (Slowly).
4) Give Diamorphine (2.5-5 mg IV slowly) or Morphine (5-10 mg IV slowly)
to relieve pain, anxiety and distress.

N.B. A good difference between Pulmonary Edema and Pulmonary Embolism

is that Pulmonary Oedema can be diagnosed by Chest X-ray
while Pulmonary Embolism needs CTPA (CT Pulmonary Angiogram).

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This might be given as a hint in a question.

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Pulmonary Oedema → Kerley Lines (Expansion of the interstitial space by fluid)

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Pulmonary Oedema → Kerley Lines + Bat’s wing hilar shadow

Key Scenario
20
20 days after MI, a patient developed sudden Dyspnea. O/E →
Tachycardia, Desaturation (88% on Room Air), Hypotension and Bilateral
Chest Crackles.

◙ The likely Dx → Pulmonary Oedema.

◙ The appropriate Initial investigation → Chest X-Ray.
◙ The best investigation to identify the cause → Echocardiography.
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◙ Treatment → MONF (Morphine, O2, Glyceryl Trinitrates, FUROSEMIDE).

Pulmonary Oedema → Kerley Lines (Expansion of the interstitial space by fluid)

Important:
If pulmonary edema is cuased by existent hear failure, the patient needs to be
discharged on either ACE inhibitor or a beta blocker (one drug at a time).
If asthmatic → ACE inhibitor is preferred over BB as BB may worsen asthma.

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Key The Typical Presentation of Acute MI (75% of cases):

21

◙ Central Chest Pain or Epigastric pain or Substernal pain that is severe,

sudden, crushing, pressuring, squeezing, constricting or burning.
◙ Radiates to arms, shoulders, neck or jaw.
◙ ± Sweating (Diaphoresis), Nausea, Vomiting, Fatigue and/or Palpitations.
◙ SOB “Shortness of breath”.

Important DD: [Dissecting Aneurysm] Aortic dissection

Although Dissecting aortic Aneurysm may have more or less a similar
presentation to MI, to be chosen as an answer, there should be other
clinchers pointing towards dissecting aneurysm such as:
√ Unequal pulses in upper limbs.
√ Hx of Marfan Syndrome (tall, long slender limbs and fingers).
√ Hx of Ehlers-Danlos syndrome/ turner syndrome.
√ Severe tearing chest pain that radiates to the Back.
√ HTN is the most important risk factor.
√ The patient presents with Hypotension, SOB, tachycardia, sweating.

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Points on Aortic Dissection

• Aortic dissection is a rare but serious cause of chest pain.
• Pathophysiology → tear in the tunica intima of the wall of the aorta.
• Injury of the innermost layer of the aorta allows blood to flow between the
layers of the aortic wall, forcing the layers apart.
• In most cases, this is associated with a sudden onset of severe chest or back
pain, often described as “tearing” in character. Also, vomiting, sweating, and
lightheadedness may occur.
• Other symptoms may result from decreased blood supply to other organs,
such as stroke or mesenteric ischemia.
• Aortic dissection can quickly lead to death from not enough blood flow to
the heart or complete rupture of the aorta.
• The transoesophageal echocardiogram (TEE) is a good test in the diagnosis
of aortic dissection, with a sensitivity up to 98% and a specificity up to 97%. It
has become the preferred imaging modality for suspected aortic dissection.
• Other good investigations → CT scan with contras/ MRI.
• In emergency settings → US or CT scan.

• Stanford classification of Aortic Dissection:

type A: ascending aorta, 2/3 of cases
type B: descending aorta, distal to left subclavian origin, 1/3 of cases

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◙ Management od Aortic Dissection

• Type A → surgical management, but blood pressure should be controlled to

a target systolic of 100-120 mmHg whilst awaiting intervention.

• Type B → conservative management, bed rest, reduce blood pressure: IV

labetalol to prevent progression

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Key Left Bundle Branch Block (LBBB)

22
In the context of chest pain, new LBBB is significant as it is an indication for
thrombolysis / percutaneous coronary intervention (PCI).

LBBB features on ECG:

◙ Notched (M shaped) broad complex QRS: usually in Lead (I), aVL and V6 but
not always.
◙ Deep inverted (Negative) QRS: usually in lead (V1).
◙ Left Axis Deviation (Not always)

Important Note
→ A new onset LBBB is characteristic for Myocardial Infarction (MI)

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Key Ruptured Abdominal Aortic Aneurysm (AAA)

23

◙ The classical picture: a triad of:

Pain, Hypotension, pulsatile tender abdominal mass.

- Sudden onset severe abdominal ± Lower back ± Flank pain.

- Shock (Hypotension, Sweating, Fainting)
- Absent Lower Limb Pulse, mottled skin.

◙ It is a surgical emergency; therefore, immediate Ultrasound is the

most appropriate initial investigation.
◙ If no U/S in the options, go for CT scan abdomen.

◙ Screening for Abdominal Aortic Aneurysm (AAA) in the UK:

√ Men only.
√ Once only.
√ In 65th year.
√ by Ultrasound.

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Key Management of Chronic Heart Failure

24
In a patient with Heart Failure
[LL Edema, Dyspnea, Orthopnea, Ejection fraction less than 40%],
The management would be:

• For symptomatic relief and to reduce the volume overload, all patients
should receive → Diuretics (e.g. loop diuretics e.g. Furosemide)
• Start with either ACEi or BB. (one drug at a time)
• If the symptoms persist → Add the other one (ACEi or BB).
• If still symptomatic → Add spironolactone “potassium sparing diuretics”.

• V. Imp. Note: If the patient with Heart Failure has Diabetes, we start with
ACE inhibitors (e.g. Ramipril) instead of Beta-Blockers.

“Try to link ACEi with DM in your mind”!

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Even in hypertension “as you will see in the coming keys”, any patient despite
the age and ethnicity who has diabetes and HTN, start with ACE inhibitors as
step 1.

Key Coronary Artery Dominance

25

• The artery that supplies the Posterior Descending Artery (PDA) determines
the coronary dominance.
• In 85% of the population, the Right coronary artery (RCA) gives off the PDA
(Right Dominant).
• In 15% of the population, the left circumflex gives off the PDA (Left
Dominant).

◙ Hence, the artery that has artery dominance is the (RCA), as it gives off the
PDA in 85% of people.

Key Dressler’s syndrome

26
◙ It tends to occur around 2-6 weeks following a MI.

◙ The underlying pathophysiology is thought to be an autoimmune reaction

against antigenic proteins formed as the myocardium recovers.

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◙ It is characterised by a combination of fever, pleuritic pain worsens on

inspiration and on lying flat, pericardial effusion and a raised ESR.

◙ ECG → Widespread Saddle Shaped ST Elevation + PR Depression

◙ It is treated by NSAIDs.

◙ Its features are more or less similar to acute pericarditis. However,

pericarditis usually occurs only a few days after MI.

Key Hypokalemia
27

◙ Muscle weakness and cramps + U wave on the ECG

◙ One important reason for hypokalemia is Thiazide like Diuretics (e.g.
Bendroflumethiazide) and Loop diuretics (e.g. Furosemide) But not
Potassium-sparing diuretics (e.g. Spironolactone) which causes HypeRkalemia.

◙ Spironolactone, ACE inhibitors, ARBs → HypeRkalemia.

◙ Loop diuretics, Thiazide like diuretics → HypOkalemia.

◙ The ECG changes in HypUkalemia → U Wave

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U wave (hypokalemia) → an additional wave after (T-wave)

Management of hypokalemia
1) Oral or IV Potassium chloride (based on severity), e.g. if K+ <2.5 → IV.
2) Stop/ Treat the cause (e.g. stop furosemide, thiazide like diuretics).

HypOkalemia HypeRkalemia
• Loop Diuretics (e.g. Furosemide) • ACE inhibitors (e.g. enalapril).
• Thiazide-like diuretics • ARBs (e.g. losartan).
(e.g. bendroflumethiazide, indapamide) • Potassium-sparing diuretics
• Vomiting and Diarrhea (e.g. Spironolactone/ Eplerenone)
• Villous Adenoma • CKD/ Acute renal failure
• Renal tubular failure • Addison’s (1ry Adrenal Insufficiency).
• Cushing Syndrome • Congenital Adrenal Hyperplasia (CAH).
• Conn’s disease (1ry hyperaldosteronism)

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Remember:
√ Severe vomiting can cause hypokalemia.
√ Hypokalemia features include muscle weakness and cramping.

Key Paroxysmal Supraventricular Tachycardia

28
= (Narrow-Complex SVT)

◙ Usually in young patients

◙ Presents with Palpitations, Light-headedness, Recurrent, Young.

◙ Management: imp √

♠ Initial line
→ Valsalva manoeuvre, Carotid massage.

♠ Not improved?
→ Intravenous adenosine (6mg Rapid IV Bolus),
still not improved? → give additional 12mg adenosine,
still not improved? → give another 12mg adenosine.

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N.B. Adenosine is contraindicated in asthmatics

→ Verapamil (CCB) is the preferred option in SVT in a patient with Asthma.

♠ Still not improved? → Electrical DC “Cardioversion”

• Prevention of future episodes

→ ß-Blockers or Radio-frequency ablation.

IMPORTANT NOTE:
If the patient is hemodynamically unstable (eg, hypotension, chest pain,
shock, and or altered mental status)
Proceed immediately to → electrical synchronised cardioversion.

In summary:

→ Carotid Massage and Valsalva Manoeuvre

→ IV Adenosine 6 mg
→ IV Adenosine 12 mg
→ IV Adenosine 12 mg
→ Cardioversion (Shock). [ Important Note: Start with this step if chest pain,
hypotension, and or altered mentation ie, hemodynamic unstable patient].

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Polymorphic (Broad-Complex) Ventricular Tachycardia

= Torsades De Pointes (TDP)

◙ Beat-to-beat variations with no uniform pattern of ventricular contractions.

◙ Broad QRS (except in resting status), Prolonged QT, Fainting episodes,
Patient might be a young athlete, Recurrent.
◙ Treatment → IV Magnesium Sulphate.
N.B. Verapamil should NOT be used in VT.

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◙ Quick Important Note to Remember:

High doses of Citalopram, (a SSRI), can cause prolonged QT intervals, which
can lead to Torsade De Pointes.

Key For patients who present with STEMI, give MONA (Morphine, O2,
29 Nitroglycerin, Aspirin) and send immediately for PCI (Percutaneous
Coronary Intervention).

What if PCI is not given in the options?

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Pick → Alteplase “preferred” or Streptokinase (Tissue Plasminogen Activator)

i.e. Thrombolysis.

Key MI (Acute chest pain radiating to jaw, shoulder…) BUT without ST elevation
30 on ECG. What to Do Next?

→ Request Cardiac Enzymes, especially (Troponin)

If Troponin is high → NON-STEMI Elevation MI

→ Give LMWH OR Fondaparinux + Aspirin 300 mg

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Key 6 weeks after MI, a patient returns with SOB when walking long distance
31 and his ECG shows ST elevation in V1-V5 leads.

The likely cause → Left Ventricular Aneurysm.

(Persistent ST elevation post-MI → Think of: Left Ventricular Aneurysm)

Left ventricular aneurysm

◙ The ischaemic damage sustained during a MI episode may weaken the
myocardium resulting in a thin muscular layer; thus, aneurysm formation.
◙ This usually occurs 4-6 weeks post MI.
◙ This is typically associated with persistent ST elevation and left ventricular
failure.
◙ A thrombus may form within the aneurysm increasing the risk of stroke.
Patients are therefore anticoagulated.
ECG → Persistent ST Elevation + Left Ventricular Failure.
CXR → Enlarged heart with a bulge at the left heart border.
Echo → Paradoxical movement of the ventricular wall.

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Key Hypertension Management

32

Hypertension classification
Stage Criteria

Stage 1 Clinic BP ≥ 140/90 mmHg and subsequent ABPM daytime

hypertension average or HBPM average BP ≥ 135/85 mmHg

Stage 2 Clinic BP ≥ 160/100 mmHg and subsequent ABPM daytime or

hypertension HBPM average BP ≥ 150/95 mmHg

Stage 3 “Severe Clinic systolic BP ≥ 180 mmHg,

hypertension” or clinic diastolic BP ≥ 110 mmHg

Keys:
ABPM → Ambulatory Blood Pressure Monitoring.
HBPM → Home Blood Pressure Monitoring.
N.B. Clinic BP is usually higher than ABPM and HBPM because some people get
stressed or feared while at a clinic → a slight increase in BP.

Management of hypertension
Lifestyle advice should not be forgotten:
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• Low salt diet.

• Caffeine intake should be reduced.
• Stop smoking.
• Drink less alcohol.
• Eat a balanced diet rich in fruits and vegetables.
• Exercise more.
• Lose weight.

♠ When to Treat Stage 1 Hypertension?

• Treat if the patient’s age is < 80 years AND + any of the following:
Target organ damage, established cardiovascular disease, renal disease,
diabetes (DM) or a 10-year cardiovascular risk equivalent to ≥ 10%.

◙ Note: If a patient is completely free and has a stage 1 Hypertension

→ Lifestyle and Diet Modification + review (Follow up).

◙ Note: In a patient with stage 2 hypertension at a clinic (Clinic BP ≥

160/100)
→ Before commencing antihypertensive drugs, record either ABPM or HBPM.

◙ Note: For patients < 40 years and with stage 2 hypertension or higher

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→ Consider a specialist referral to exclude secondary causes of the HTN.

If ABPM or HBPM ≥ 150/95 mmHg (i.e., confirmed stage 2 or higher

hypertension) → Always treat.

The Steps of The Management of Hypertension

Step 1

• Patients < 55-years-old → start with ACE inhibitor (A) or ARBs.

• Patients ≥ 55-years-old or of Afro-Caribbean origin “of any age”
→ start with Calcium channel blocker.

In other words:
• White + < 55 YO → start with ACEi/ARBs as a step 1 management of HTN.
• White + > 55 YO → start with CCB as a step 1 management of HTN.
• Afro-Caribbean + any age → start with CCB as a step 1 management of HTN.

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Step 2 (still hypertensive after step 1)

• Both: ACE inhibitor + Calcium channel blocker (A + C)

Step 3 (still hypertensive after step 2)

• Add a Thiazide Diuretic (D)
So, 3 medications are taken → ACEi + CCB + Thiazide like Diuretic (A+C+D).

- Example of ACEi → Enalapril, Ramipril.

- Example of ARBs → Valsartan, Losartan, Candesartan.
- Example of CCB → Amlodipine, Felodipine.
- Examples of thiazide diuretics → chlorthalidone (12.5-25.0 mg once daily)
or indapamide (1.5 mg modified-release once daily or 2.5 mg once daily).
- Bendroflumethiazide is a thiazide like diuretic; however, it is no longer
recommended by NICE as an antihypertensive.

Step 4 (For resistant hypertension) (For Reading)

• consider further diuretic treatment.
◙ If potassium < 4.5 mmol/l → add spironolactone (Potassium Sparing) 25mg
OD.
◙ If potassium > 4.5 mmol/l → add a higher-dose thiazide-like diuretic.

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• If further diuretic therapy is not tolerated or is contraindicated or

ineffective, consider an alpha- or beta-blocker.

■ Patients who fail to respond to step 4 measures should be referred to a

specialist.
■ NICE recommend: If blood pressure remains uncontrolled with the optimal
or maximum tolerated doses of four drugs → seek expert advice.

Blood pressure targets

◙ For Diabetic patients with Hypertension:
If end-organ damage (e.g. renal disease, retinopathy) < 130/80 mmHg
otherwise < 140/80 mmHg.
◙ For Hypertensive patients without DM:
Clinic BP ABPM / HBPM
Age < 80 years 140/90 mmHg 135/85 mmHg
Age > 80 years 150/90 mmHg 145/85 mmHg

Hypertension + Diabetes (V. Imp)

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◙ Always treat hypertension in a DIABETIC patient with ACE inhibitor

regardless of the age as it is reno-protective “Unless if the eGFR is <30”.

◙ However, if this diabetic patient is Afro-Caribbean,

→ start with both ACE inhibitor + Calcium Channel Blocker as a first step.

◙ Before commencing ACE inhibitor for any patient → check eGFR.

If eGFR (Glomerular Filtration Rate) is low; <30 as in advanced Chronic Kidney
Disease → ACEi and ARBS should be avoided in this case.

Why ACE inhibitor is used for Diabetic Hypertensive patients?

- It is reno-protective (unless eGFR is low; <30; in advanced CKD).
- It has protection against diabetic retinopathy.
- It has +ve effect on glucose metabolism.

Key Postural Hypotension (Orthostatic Hypotension)

33
- A drop in systolic blood pressure of at least 20 mm Hg within three
minutes of standing.

- or a drop in diastolic blood pressure of at least 10 mm Hg within three

minutes of standing.

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- BP is measured on lying position, then on standing position.

- Dx: Monitor BP.

- Other useful and important test → Tilt table test.

A tilt table test is used to evaluate the cause of unexplained fainting. A health
care provider might recommend a tilt table test to evaluate repeated,
unexplained episodes of lightheadedness, dizziness or fainting. The test can help
determine if the cause is related to heart rate or blood pressure.

◙ Postural hypotension is common in elderly people especially those who

take multiple drugs (Polypharmacy) and those with hypertension.

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◙ Anti-hypertensive medications can cause postural hypotension as well

(eg, ACE inhibitors as Ramipril). → This could lead to recurrent falls.

◙ The Baroreflex mechanisms that control HR (Heart Rate) and VR

(Vascular resistance) decline with age, particularly in patients with
hypertension.

Q] An elderly man complains of difficult mobilisation. He often feels dizzy

upon trying to stand ± He has a Hx of Recurrent Falls. Management?
→ Blood pressure monitoring & Assess and review the patient’s Medications.

Q] An elderly man takes several medications for hypertension and heart

failure. He often feels dizzy upon trying to stand ± He has a Hx of Recurrent
Falls?
The likely cause of his postural hypotension → polypharmacy.
Management → Blood pressure monitoring.

Q] An elderly man feels dizzy when he stands and loses balance and falls. He
is on a number of medications: ramipril for hypertension, zopiclone
insomnia, cetirizine for allergy of hay fever, metformin for diabetes, and
lithium for bipolar disorder. He has postural hypotension (his diastolic BP
while standing is > 10 mmHg lower than his diastolic BP while sitting). Which
medication is the most likely reason for his recurrent falls?
→ ACE inhibitors (Ramipril) . They can cause postural hypotension → thus falls.
Anti-hypertensive medications as ACE inhibitors and Calcium channel blockers
can cause postural hypotension → dizziness on standing → Falls.
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Note: if there was no postural hypotension, we would suspect zopiclone

(Although rare, it can lead to falls by balance impairments).

Key Again, any patient of any age and any ethnic group presents with
34 Hypertension and he is a Diabetic patient
Start with → ACE inhibitor (e.g. Enalapril).

(Note, if the eGFR is 30 or below, ACEi and ARBS should be avoided).

Key Absent “P” wave on ECG + Irregularly Irregular Rhythm + Palpitation

35

Diagnosis? → Atrial Fibrillation.

Management?
√ First line → beta-blockers.
√ If asthmatic → Avoid beta-blockers and give calcium channel blockers.
√ If the patient has associated HF → give digoxin.
+

→ Calculate CHA2DS2-VASc Score (Key number 18) and accordingly:

→ Give (Warfarin) or (DOAC) or nothing according to the Cha2ds2vasc score.

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◙ Examples of DOAC “Direct-Acting Oral AntiCoagulants” -important √-

Apixaban, Rivaroxaban, Edoxaban, Dabigatran”.

√ If haemodynamically unstable (eg, SBP ≤ 90) → Cardioversion (Shock).

√ If the patient with AF is unstable (eg, hypotension) and the AF has just
started and no cardioversion in the options, Pick → IV amiodarone. Imp √

Key Fever + New Murmur → Infective Endocarditis “until proven otherwise”.

36

Be careful, the reason of IE is → Infection “infective” endocarditis.

- Staph. Aureus is the commonest cause of IE in general.

- Staph. Epidermidis is the commonest cause after prosthetic valve surgery.
- Strept. Viridans (especially sterpt. Mitis and strept. Sanguinis) are the
commonest cause in people with poor dental hygiene or following a dental
procedure.

Key Ventricular Ectopics

37

= Three-beat patterns = Ventricular Trigeminy.

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◙ A sense of a missed/skipped beat, unsustained palpitation ± Dyspnea and

Dizziness due to immature discharge of a ventricular ectopic focus which
produces → an early and broad QRS complex.
◙ Causes → Ischemic heart disease (MI), Cardiomyopathy, Stress, Alcohol,
Caffeine, Cocaine, Medications OR Naturally.

◙ Over half the population have silent, or asymptomatic ventricular ectopics

which are discovered incidentally on a routine ECG.

◙ If there is No underlying Heart disease (e.g. IHD, Cardiomyopathy)

→ Benign; no clinical significance.

◙ If these ventricular ectopics are due to IHD or Cardiomyopathy

→ May precipitate to more life-threatening arrhythmias like Ventricular
Fibrillation.

Key The Typical Presentation of Acute MI (75% of cases)

38

◙ Central Chest Pain or Epigastric or Substernal pain that is severe, sudden,

crushing, pressuring, squeezing or burning and radiates to arms, shoulders,
neck or jaw.
◙ ± Sweating (Diaphoresis), Nausea, Vomiting, Fatigue and/or Palpitations.

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◙ SOB “Shortness of breath”.

♠ Keep in mind that some patients may present with additional Atypical
feature such as Abdominal Pain, Jaw pain or Altered mental status.

Key Long term medications post-Myocardial Infarction = 5 Drugs

39
Aspirin, Clopidogrel, , ACEi,
AABCS → Aspirin, ACEi, BB, Clopidogrel, Statin (e.g. Atorvastatin)

Key A patient with chronic heart failure developed gout. A medication for his
40 gout is prescribed. A few days later, the patient came back to the hospital
complaining of worsening of his Heart Failure symptoms (SOB, Orthopnea).

- The likely cause of this patient’s gout

→ Thiazide like diuretics (e.g. bendroflumethiazide) or Loop Diuretics
(Both can cause hyperuricemia (Gout) and both can be used to treat volume
overload caused by Heart Failure)

- The likely cause of this patient’s worsening of SOB and Orthopnea

→ NSAIDs (e.g. Ibuprofen) that was prescribed to treat his gout.

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Important Notes
◙ Never give NSAIDs (e.g. Ibuprofen) nor selective COX-2 inhibitors (e.g.
Celecoxib) to the following patients: CKD, CHD, IHD
(Chronic Kidney Disease, Chronic Heart Failure, Ischemic Heart Disease).
◙ These drugs can worsen the HF (worsening the SOB and Orthopnea) and
also the renal function.

◙ Remember that NSAIDs inhibit the synthesis of prostaglandins

→ thus, decrease the eGFR, retain more salt and water (risk factor for HF).

◙ N.B. Thiazide like diuretics and Loop diuretics decrease the clearance of
Uric Acid → leading to Gout (Hyperuricemia)

◙ N.B. NSAIDs such as Ibuprofen are used for the treatment of Gout. If given
to a patient with chronic heart failure, they would worsen the HF symptoms
(Orthopnea and Dyspnea).

Key In-Hospital Cardiac Arrest algorithm

41

If No Signs of Life (i.e. No breathing, No detectable Pulse):

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1) Ring the emergency bell and call resuscitation team (Code Blue) first. Then →
2) Start CPR 30:2. Then →
3) Get defibrillator. Then →
4) ALS when the resuscitation team arrives.

Key In STEMI patient, what if PCI is not given in the options?

42
Pick → Alteplase “preferred” or Streptokinase (Tissue Plasminogen Activator)
= i.e. Thrombolysis.

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Key Diabetic patients may develop “Silent MI” i.e. painless MI. Thus, they may
43 die suddenly and silently without feeling any chest pain (They won’t feel
chest pain → They won’t seek medical help).
This is because they may not feel chest pain due to autonomic neuropathy.

Key A scenario to test your knowledge on a previous topic

44

An elderly male presents with Palpitations and Shortness of breath on

exertion. The ECG is as follows.
What is the likely diagnosis and management?

Answer:

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Key Remember:
45
◙ In Supraventricular tachycardia (Narrow QRS Complex, absent p waves)
→ We firstly perform Carotid Massage and Valsalva Manoeuvre.
If this fails → We give IV Adenosine.

IMPORTANT NOTE:
If the patient is hemodynamically unstable (eg, hypotension, chest pain,
shock, altered mental status)
Proceed immediately to → electrical synchronised cardioversion.

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◙ In polymorphic ventricular tachycardia (i.e. torsade’s de pointes)

→ IV magnesium sulfate.

Key Beck’s Triad in Cardiac Tamponade

46
Hypotension,
Muffled Heart Sounds,

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High JVP (Distended neck veins).

• Trauma (e.g. stab in the chest) is the most important cause for cardiac
tamponade.

• Dx: Echocardiography is diagnostic.

• Tx: Urgent pericardiocentesis.

Key Remember that:

47

◙ In Atrial Myxoma → Mitral valve obstruction → Mitral Stenosis

→ Early or Mid-diastolic murmur, Dyspnea, Syncope

◙ In Atrial Myxoma → Breakdown of small emboli from the mass that can
travel down the blood and cause ischemia in multiple sites, leading to
→ (e.g. Pulmonary Embolism, Stroke, Clubbing, Blue fingers)
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Therefore, in a patient with Hx of syncope, SOB, Pulmonary Embolism and

early-mid diastolic murmur → Think of Atrial Myxoma.

Key Points on Alcohol

48
UK guidelines recommend that a person should drink
- No more than 14 units a week,
- No more than 3 units a day,
- with at least 2 alcohol-free days a week.

Example:
If someone drinks 7 units of alcohol a week and smoke 20 cigarette a day,
we should refer him to
→ Smoking Cessation Clinic.
This is because his alcohol intake is insignificant as per NICE whereas his
smoking is significant.

Key A scenario to test your knowledge on a previous topic

49

4 days after MI, an elderly patient presents with Fatigue and Dyspnea. On
Auscultation → Pansystolic murmur at the apex and radiates to the axilla
was heard.

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→ The likely Dx → Mitral Regurgitation.

→ The likely Cause → Rupture of Papillary Muscles.

Acute mitral regurgitation (MR): “important √” pansystolic murmur

◙ Occurs 2-15 days after the MI (Mostly inferior MI).
◙ Due to → Ischemia or rupture of the papillary muscles of the mitral valve.
◙ An early-to-mid systolic or Pansystolic murmur is typically heard.
◙ May present with Hypotension, Tachycardia and Pulmonary edema.
◙ Dx → Echocardiogram.
◙ Treatment → vasodilator therapy but often requires emergency surgical
repair

Key A scenario to test your knowledge on a previous topic

50

2 days after MI, an elderly patient presents with fever and chest pain. ECG
shows ST elevation with upward concavity.

→ Acute Pericarditis.

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Post-MI Pericarditis “important √”

◙ Occurs within 2-3 Days after MI.
◙ Features → Pleuritic chest pain that is worse on lying flat and during
inspiration ± Fever ± pericardial rub
◙ Pericardial effusion may develop leading to enlarged globular heart on chest
X-ray and is confirmed by echocardiogram.
◙ ECG → Widespread Saddle Shaped ST Elevation with upward concavity +
PR Depression.
◙ Management of Pericarditis (imp):
√ A full-dose NSAID should be used (eg, aspirin, 2-4 g/d; ibuprofen 1200-1800
mg/d; indomethacin 75-150 mg/d); treatment should last at least 7-14 days.
√ Colchicine (as an adjunct to NSAIDs to ↓ inflammation and recurrence).

Key For Acute Myocardial Infarction patients, the analgesic that can be
51 used while in the ambulance is still → IV Morphine.

◙ Remember the initial management for acute MI → (MONA):

Morphine, Oxygen, Nitrates, Aspirin.

MI Analgesia while in an ambulance (Pre-Hospital)

1) Glyceryl Trinitrate (GTN) sublingual or spray.

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2) ± Opioids (INTRAVASCULAR): 2.5-5 mg Diamorphine or 5-10 mg Morphine.

- N.B. Around 1/3 of the patients with MI have nitrate-resistant chest pain;
therefore, morphine is given additionally to relieve chest pain.

- Why IV and not IM?

√ IM absorption is unreliable +
√ If the patient receives thrombolysis later on, the site of IM injection might
bleed.

Key Ventricular Old adult, Sudden collapse, Not breathing,

52 Fibrillation Unconscious → Shock ‘’defibrillation’’

Broad Complex Tachycardia

◙ Tachyarrhythmia is one of the complications of MI.

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♠ An ECG showing broad complex tachycardia in a (still) conscious patient ±

atrial activity → Ventricular tachycardia → IV Amiodarone.

♠ If the patient is hemodynamically unstable; i.e. unconscious, collapsed, not

breathing → Ventricular Fibrillation →
1) Check the patient’s pulse, if no pulse, commence the arrest protocol
immediately.
2) Administer O2.
3) If the patient is hemodynamically unstable: Shock followed by IV
Amiodarone followed by further Shocks if needed.

◙ N.B. HypOkalemia is the most important cause of ventricular tachycardia

(VT) clinically.

Key Treatment of Cardiac Tamponade → Pericardiocentesis.

53

Key ◙ Tall Tented T-wave → HypeRkalemia.

54
◙ U-wave → HypOkalemia.

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Key A scenario to test your knowledge on a previous topic

55

45 Y/O African patient has BP 160/90 on three separate occasions.

What is the initial line of treatment?

→ Calcium Channel Blocker (CCB)

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(First Step Management of hypertension in African-Caribbean patients

is CCB regardless of the age).

• White + < 55 YO → start with ACEi/ARBs as a step 1 management of HTN.

• White + > 55 YO → start with CCB as a step 1 management of HTN.
• Afro-Caribbean + any age → start with CCB as a step 1 management of HTN.

• Any ethnicity + Any age + Diabetes

→ start with ACEi/ARBs as a step 1 management of HTN

Key Remember that

56
LBBB is associated with acute MI.

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Key Heart Murmurs

57

Defect Type of Where is it Symptoms

Murmur Best heard?
Aortic Ejection Systolic Right 2nd ICS just Dyspnea on
lateral to activity, Anginal
Stenosis sternum, radiates chest pain,
to Carotid artery syncope

Aortic Early Diastolic left lower sternal Symptoms of

Regurgitation border around Heart Failure
the 3rd to 4th
intercostal spaces
Pulmonary Ejection Systolic Left 2nd ICS just Systemic
Stenosis lateral to Cyanosis
sternum, radiates
to left shoulder
of infraclavicular
area
Pulmonary Early-Diastolic Left 2nd ICS just Symptoms of
Regurgitation lateral to Right-Sided Heart
sternum Failure
Mitral Stenosis Mid-Late Apex (left 5th ICS Symptoms of
Diastolic, with midclavicular Heart Failure
opening click line)

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Mitral Pan-Systolic Apex (left 5th ICS Symptoms of

Regurgitation MCL), radiates to congestive Heart
Axilla Failure; edema,
Ascites
Tricuspid Diastolic Rumble 4th-5th ICS over Fluttering
Stenosis the left sternal Discomfort in the
border. neck
Tricuspid Pan-Systolic 4th-5th ICS over Symptoms of
Regurgitation © Copyright the left sternal Right-Sided Heart
www.plab1keys.com border. Failure

Example:
A patient with a history of MI presents with Orthopnea (Cannot lie down
flat), Bibasilar crepitations, Pan-systolic murmur.

→ Mitral Regurgitation.
→ Request Echocardiogram.

Key A scenario to test your knowledge on a previous topic

58
A Young adult presents with frequent fainting attacks since childhood and
prolonged QT. There are sinus rhythm and normal P-R interval. No FHx of
arrhythmias or sudden death.

The likely Dx→ Polymorphic Ventricular Tachycardia (Torsades de pointes)

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Polymorphic (Broad-Complex) Ventricular Tachycardia

= Torsades De Pointes (TDP)

◙ Beat-to-beat variations with no uniform pattern of ventricular contractions.

◙ Broad QRS (except in resting status), Prolonged QT, Fainting episodes,
Patient might be a young athlete. Recurrent.
◙ Treatment → IV Magnesium Sulphate.
N.B. Verapamil should NOT be used in VT.

Key An elderly patient with a Hx of stroke presents with exertional dyspnea.

59
ECG shows Atrial Fibrillation. Chest X-ray shows Straight left heart border.

→ Mitral Stenosis.

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• The most common cause of mitral stenosis → rheumatic fever, rheumatic

fever and rheumatic fever.

Pathogenesis of Mitral Stenosis:

Mitral stenosis impedes left ventricular filling → increased left atrial pressure
(Which will lead to left atrial hypertrophy; therefore, CXR shows Straight left
side heart border) → Blood returns Back to lungs → Pulmonary Congestion →
Right Ventricular Failure (Hepatomegaly, Ascites, Oedema)

Features
• Mid-late diastolic murmur (best heard on expiration) ‘’low pitched’’
• Loud S1, opening snap
• Low volume pulse
• Malar flush
• Atrial fibrillation

Note:
◙ Left heart murmurs (Mitral and Aortic) are best heard during expiration
◙ Right heart murmurs (Tricuspid and Pulmonary) best heart in inspiration

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Careful!
Left and right refer to the site of the valve, not the area of auscultation

Features of severe MS
• The length of murmur increases
• The opening snap becomes closer to S2

Chest x-ray in MS

• Left atrial enlargement (often) → Straightening the left border of the heart.

ECG (may show):

- Signs of Right ventricular hypertrophy
- P mitrale (bifid P wave)
- AF

Echocardiography → (Thickening of Mitral valve leaflets)

Key First line treatment in AF (if no asthma) → ß-Blockers (e.g. Metoprolol)

60

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Key ◙ ↓ Ejection Fraction (+) ↓ Septal Wall Thickness →

61
Dilated Cardiomyopathy

◙ ↑ Ejection Fraction (+) ↑ Septal Wall Thickness →

Hypertrophic Cardiomyopathy.

Dilated Cardiomyopathy (DCM) Basics (For READING ONLY)

• Dilated heart leads to systolic (± diastolic) dysfunction
• All 4 chambers are affected but the Left Ventricle is more affected than the
Right Ventricle.
• Features include arrhythmias, emboli, mitral regurgitation
• Absence of congenital, valvular or ischaemic heart disease

◙ Causes often considered separate entities

• alcohol: may improve with thiamine
• postpartum
• hypertension

◙ Other causes

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• inherited
• previous MI
• infections e.g. Coxsackie B, HIV, diphtheria, parasitic
• endocrine e.g. Hyperthyroidism
• infiltrative e.g. Haemochromatosis, sarcoidosis
• neuromuscular e.g. Duchenne muscular dystrophy
• nutritional e.g. Kwashiorkor, pellagra, thiamine/selenium deficiency
• drugs e.g. Doxorubicin

◙ Inherited dilated cardiomyopathy

• around a third of patients with DCM are thought to have a genetic
predisposition
• a large number of heterogeneous defects have been identified
• the majority of defects are inherited in an autosomal dominant fashion
although other patterns of inheritance are seen

Key A Summary on Arrhythmias Management

62

◙ In Supraventricular tachycardia (Narrow-Complex) (SVT):

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♠ If the patient is haemodynamically stable → start with Valsalva manoeuvre

and Carotid massage to stimulate the vagal tone (Parasympathetic which
decreases the heart rate).
- If still ill? → Give Adenosine 6 mg IV bolus.
- If no response? → give another Adenosine double dose (12 mg).
- If still no response? → give another Adenosine double dose (12 mg).
- Unsuccessful yet? → Cardioversion.

♠ If the patient is haemodynamically Unstable → start with Cardioversion.

◙ In Polymorphic Ventricular Tachycardia (Broad-Complex)

= (Torsade De Pointe)
→ Give IV MgSO4 (Magnesium Sulphate)

◙ In AF:
- Start with ß-Blockers (e.g. Metoprolol).
- If Asthmatic patient → Calcium Channel Blockers.
- If Associated Heart Failure → Digoxin.

◙ In Ventricular Tachycardia →

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If stable patient → IV Amiodarone.

If unstable → Synchronized cardioversion (Shock).

Haemodynamically Unstable → e.g.

√ Hypotension (SBP < 90),
√ Loss of Consciousness,

Others:
√ HR > 150.
√ Severe dizziness or syncope.
√ Ongoing chest pain.
√ increasing SOB.

→ Synchronized DC Cardioversion.

[Any arrhythmia in an unstable patient → DC Cardioversion]

Key An elderly patient suddenly fell unconscious, he recovered completely

63 within a few minutes, he remembers the event very well, he did not trip, he
felt hot and flushed after the episodes but he did not feel dizzy or sweaty
before the fall.

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The best Investigation → 12-lead ECG

Analysis and Causes of Falls.

Causes are usually:

1) Cardiac cause (e.g. Arrhythmia).
2) Postural (Orthostatic) Hypotension.
3) Hypoglycemia.
4) Seizure.

◙ If the cause was hypoglycemia, he would have felt sweaty and dizzy before
the episode. Plus, he would not have recovered until Glucose is administered.

◙ If it was a seizure, the stem has to include an eyewitness to describe the

episode. Also, in seizure, there are usually post-ictal features such as
confusion and drowsiness. However, the patient in the above stem did not
feel any of these, he rather recovered completely.

◙ If it was Postural hypotension (Orthostatic hypotension), the fall usually

follow a standing from a sitting position. In addition, the patient would have
felt dizziness before the fall, Hx of difficult mobilisation, which are not
mentioned here.

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◙ Therefore, the likely cause here is arrhythmia (Cardiac cause), likely (Stokes
Adam attack). This is also supported by the fact that the patient felt hot and
flushed after recovery, which means that the blood has been, rapidly, pumped
back to the already dilated vessels. (Dilated due to hypoxia caused by the
irregular rhythm) → 12-lead ECG monitoring is required.

Stokes Adam attack [For Reading]:

Sudden collapse into unconsciousness due to a disorder of heart rhythm in
which there is a slow or absent pulse resulting in syncope (fainting) with or
without convulsions. In this condition, the normal heartbeat passing from the
upper chambers of the heart to the lower chambers is interrupted. This results
in a condition called a “heart block.” When a heart block occurs, the heart rate
usually slows considerably. This can cause inadequate blood flow to the brain
and result in fainting.

An elderly patient fell and collapsed “syncope”. He was transferred to the A&E
and now he is fully conscious. ECG shows irregular rhythm. What is the next
best investigation?

→ Echocardiogram.

◙ A Holter ECG (24-hour ECG) will not be beneficial as the ECG already shows
Irregular Rhythm; hence, there is no point of using it again.

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◙ Echo should be done to identify the underlying cause of this irregular

rhythm so the treatment can be decided accordingly.

Key Murmurs in Paediatrics

64
- Preterm baby with continuous or machinery murmur
→ PDA (Patent Ductus Arteriosus).

- Cyanotic baby with ejection systolic murmur

→ TOF (Tetralogy of Fallot).
Ejection systolic murmur here is due to pulmonary stenosis which is
one of the four major features of TOF.

- Progressive (Severe) Cyanosis + Poor feeding + Holosystolic

“pansystolic” murmur along the left sternal border
→ Tricuspid Atresia.

- Acyanotic + Pan-systolic murmur

→ VSD (Others: Poor feeding and poorly gaining weight)

Congenital Heart Disease

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It is important to remember that:

√ PDA, ASD, VSD → Acyanotic.
√ TOF, Tricuspid Atresia → Cyanotic.
√ Pansystolic murmur = MR or TA or VSD.

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Patent Ductus Arteriosus (PDA)

• A form of congenital heart defect

• generally classed as ‘acyanotic’. (√)
• connection between the pulmonary trunk and descending aorta
• more common in premature (Preterm) babies. (√)
• May close spontaneously

Features

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• left subclavicular thrill (sometimes rough systolic murmur along

the left sternal border)
• Continuous ‘machinery’ murmur (√)
• large volume, bounding, collapsing pulse
• wide pulse pressure

Diagnosis → Echocardiogram

Management

• Indomethacin / ibuprofen (NSAIDs) (ind=end=closes the

duct) (inhibits prostaglandin synthesis) closes the connection in the
majority of cases. (√)
• If associated with another congenital heart defect amenable to
surgery then prostaglandin E1 is useful to keep the duct
open until after surgical repair.

Indomethacin or ibuprofen → closes the duct.

Prostaglandin → keeps the duct open.

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Key 14 days old baby is Cyanosed, Desaturated with Ejection systolic murmur.
65

→ Tetralogy of Fallot.

The cause of ejection systolic murmur here is → pulmonary stenosis (one of

the four criteria of TOF).

Tetralogy of Fallot (TOF)

Tetralogy of Fallot (TOF) is the most common cause of Cyanotic congenital

heart disease

**however, at birth, transposition of the great arteries is the more common

lesion as patients with TOF generally present at around 1-2 months. **

It typically presents at around 1-2 months, although may not be picked up

until the baby is 6 months old

TOF is a result of anterior malalignment of the aorticopulmonary septum.

The four characteristic features are:

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1) Ventricular septal defect (VSD)

2) Right ventricular hypertrophy (RVH)
3) Right ventricular outflow tract obstruction “pulmonary
stenosis” (PS) → ejection systolic murmur
4) Overriding aorta

The severity of the right ventricular outflow tract obstruction determines the
degree of cyanosis and clinical severity.

Other features

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• cyanosis
• causes a right-to-left shunt
• ejection systolic murmur due to pulmonary stenosis (the VSD doesn’t
usually cause a murmur)
• a right-sided aortic arch is seen in 25% of patients
• chest x-ray shows a ‘boot-shaped’ heart.
• ECG shows right ventricular hypertrophy

Management

• Surgical repair is often undertaken in two parts.

• Cyanotic episodes may be helped by beta-blockers to reduce
infundibular spasm.

Key Familial Hypercholesterolemia

66

It is Autosomal Dominant

Q) When to highly suspect it?

1) If Cholesterol is > 7.5 (Normal: <5 mmol/L)
2) Family History of “MI” in a first degree relative before the age of 60 or 2nd
degree below 50.

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First degree relatives: Parents and siblings.

Second degree relatives: Grandparents, aunts, uncles

Key Ventricular Fibrillation

67

Key While in a hospital, an elderly patient was found unresponsive, no pulse and
68 no breathing (No signs of life). Management?

→ Ring the emergency bell and call the resuscitation team. First
→ Start CPR 30:2.
→ Get Defibrillator.
→ Commence ALS when the resuscitation team arrives.

(In this order. If the first one was not given in the options, pick the 2nd one)

Key Pan-Systolic murmur could be:

69

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◙ MR → Mitral Regurgitation.
◙ TR → Tricuspid Regurgitation.
◙ VSD → Ventricular Septal Defect.

VSD (Ventricular Septal Defect):

◙ If small hole → Asymptomatic ± Left sternal pan-systolic murmur with

systolic thrill.

◙ If large hole →
• Pan-systolic murmur along the left sternal border.
• Left sternal heave, and systolic thrill.
• Pulmonary HTN → Dyspnea, Fatigue.
• May develop a right-to-left shunt → Cyanosis

Key ◙ Myocardial Infarction (Weak dead part of the cardiac muscle) can cause
70
→ Congestive Heart Failure
→ Backflow of the blood to the lungs
→ Pulmonary Oedema

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→ Desaturation, Dyspnea, Orthopnea, Crepitations

→ Perform Chest X-Ray to Diagnose
→ Perform Echo to identify the Underlying cause of the Pulmonary Oedema

→ Treat with MONF ( Morphine , Oxygen , Nitrates , Furosemide )

Key On ECG, if there is no connection between P waves and QRS complexes

71

→ Complete heart Block (3rd degree heart block).

Key A 57 YO hypertensive patient is on Enalapril (ACE inhibitor) for

72 hypertension developed annoying dry cough. What is the most
appropriate action?

→ (Give ARBs e.g., Losartan instead -important-).

Other ARBs (Angiotensin II receptor blockers) that could be the valid

answer → Losartan, Valsartan, Candesartan.

√ One of the important and common side effects of ACE inhibitors is dry
cough. If developed, shift to ARBs.

√ Another side effect of ACEi to remember is → Hyperkalemia (↑ serum K+).

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Key Pansystolic murmur at the apex + Hx of Rheumatic fever

73

→ Mitral Regurgitation (MR).

Notes:
◙ MR can occur 2ry to MI (Rupture of papillary muscles).
◙ MR can occur 2ry to Rheumatic fever.

◙ MR may lead to → Right-sided (Congestive) heart failure (Ascites, LL oedema).

◙ MR may lead to → Pulmonary oedema

◙ Rheumatic fever can lead to either Mitral Regurgitation or Mitral Stenosis.

We can decide based on clinical features.

Mitral Mid-Late Diastolic At the Apex (left Symptoms of Heart

Stenosis murmur, with 5th ICS MCL) Failure
opening click
Mitral Pan-Systolic At the Apex (left Symptoms of
Regurgitation murmur 5th ICS MCL), congestive Heart
radiates to Axilla Failure; edema,
Ascites

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Key Scenario
74
A 60 Y/O patient with Hypertension, Previous MI and Asthma presents
complaining of recurrent falls. He is on Salbutamol inhaler as needed,
Aspirin, Corticosteroid inhaler (Beclomethasone), Indapamide, Enalapril and
Amlodipine.

The likely underlying cause of the recurrent falls

→ Postural Hypotension.

Why?
→ The patient is on multiple anti-hypertensive medications (CCB →
Amlodipine ▐ Thiazide-like diuretics → Indapamide ▐ ACEi → Enalapril).
These Blood Pressure Lowering agents are known to cause orthostatic
“Postural” hypotension.

Management?
→ Blood Pressure Monitoring + Review the patient’s medications.

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Key
75

Key An elderly patient fell and collapsed “syncope”. He was transferred to the A&E
76 and now he is fully conscious. ECG shows irregular rhythm. What is the next
best investigation?

→ Echocardiogram.

◙ A Holter ECG (24-hour ECG) will not be beneficial as the ECG already shows
Irregular Rhythm; hence, there is no point of using it again.
◙ Echo should be done to identify the underlying cause of this irregular
rhythm so the treatment can be decided accordingly.
◙ The most common Valvular heart disease that causes Syncopal attacks is →
Aortic Stenosis (ejection systolic murmur at the 2nd right ICS + Angina ± Dyspnea).
◙ Syncope during or shortly after exertion → Exercise ECG.

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This patient likely has AF causing TIA (syncope + irregular rhythm), and to
determine the cause of his Atrial fibrillation, do Echo.

◙ Causes of AF:
√ Endocardium → Endocarditis, Mitral valve disease.
√ Myocardium → Cardiomyopathy.
√ Pericardium → Constrictive pericarditis.
√ HF, HTN, MI.
√ Hyperthyroidism, excessive alcohol intake, chronic lung disease.

Aortic Ejection Right 2nd ICS just lateral to Dyspnea on activity,

Stenosis Systolic sternum, radiates to Carotid Anginal chest pain,
murmur artery syncope

Key A 6-week-old baby presents with the features of progressive cyanosis, poor
77 feeding and SOB since the age of two weeks. Holosystolic murmur is heard.

→ Tricuspid Atresia.

Key - Preterm, continuous murmur → PDA

78

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- Cyanotic baby with ejection systolic murmur (due to pulmonary stenosis)

→ TOF (Tetralogy of Fallot).
- Progressive (Severe) Cyanosis + Poor feeding + Holosystolic murmur along
the left sternal border → Tricuspid Atresia.
- Acyanotic, Pan-systolic murmur → VSD (Others: Poor feeding and poorly
gaining weight)

Key Before prescribing amiodarone

79

Request → Serum Electrolytes and Urea

Amiodarone
Amiodarone is a class III antiarrhythmic agent used in the treatment of atrial,
nodal and ventricular tachycardias. The main mechanism of action is by
blocking potassium channels which inhibits repolarisation and hence prolongs
the action potential.

Monitoring of patients taking amiodarone

• TFT (Thyroid), LFT (Liver), U&E (Serum electrolytes and Urea), CXR, ECG prior
to treatment
• TFT, LFT every 6 months
• ECG every 12 months

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Adverse effects of amiodarone use

• Thyroid dysfunction: both hypothyroidism and hyperthyroidism
• Corneal deposits
• Pulmonary fibrosis (The most serious)/pneumonitis
• Liver fibrosis/hepatitis
• Peripheral neuropathy, myopathy
• Photosensitivity
• ‘Slate-grey’ appearance (Grey skin)
• Thrombophlebitis and injection site reactions (So, usually given via central
veins)
• Bradycardia
• Prolonged QT interval

Key • A racing heart or palpitation is a common phenomenon in Alcoholics which

80 is not serious or harmful.

→ Reassurance.

Key Pulmonary Early- Left 2nd ICS just Symptoms of

81 Regurgitation Diastolic lateral to sternum Right-Sided Heart
Failure

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After surgical correction of Tetralogy of Fallot early in life, the

corrected pulmonary stenosis (one of the four criteria of TOF) can be
complicated into Pulmonary regurgitation (diastolic murmur at the left
upper sternal border) that can manifest many decades later.

A man who had cardiac surgery when he was a child presents with
diastolic murmur.

Suspect → pulmonary regurgitation (on top of the corrected pulmonary

stenosis as a child – due to TOF)

Key A patient who underwent surgery 2 days ago developed high fever, rigors,
82 night sweats and systolic murmur.

New murmur + Fever → Infective Endocarditis.

Investigation → Blood Culture then Echocardiogram.

Key Young Adult + Recurrent Palpitations + Light-headedness +

83 Tachycardia

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→ Think of SVT (Paroxysmal Supraventricular Tachycardia) = Narrow

Complex.

→ Valsalva manoeuvre and Carotid massage

→ IV Adenosine: 6 mg → 12 mg → 12 mg
→ Cardioversion

N.B. Adenosine is contraindicated in asthmatics

→ Verapamil (CCB) is the preferred option in SVT in a patient with Asthma.

Key ◙ 1st Degree Heart Block and Mobitz type 1 usually

84
→ do not require treatment (as long as the patient is Asymptomatic).

◙ Mobitz type 2 and Complete heart block (3rd degree heart block)
→ require permanent pacemaker.
• Initially → Atropine (first choice for all symptomatic bradycardia).
• Then → Transcutaneous pacing. (Used to buy time until transvenous
pacing is done).
• Then → Transvenous pacing.
• Then → Permanent pacing (Pacemaker).

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Key Aortic Stenosis

85
- The commonest valvular disease in the elderly (Over 65).
- Usually Asymptomatic apart of exercise intolerance (often mild).
- It can cause syncopal fainting.
- Ejection systolic murmur at the right 2nd ICS, louder on sitting upright and
during expiration, and radiates to carotid.
A scenario of an elderly presents with mild exercise intolerance or
is asymptomatic but visiting for the purpose of check-up is found to
have ejection systolic murmur.

→ Aortic Stenosis.

The most appropriate investigation → Echocardiogram.

Key Investigations following Syncope

86
Patients who have unannounced loss of postural tone leading to a period of
unconsciousness need to be investigated for 4 main causes:
1) Irregular rhythm (Cardiac syncopal events): Usually abrupt, with rapid
recovery and flushing → 12 Lead ECG.

2) Low blood pressure or postural drop → frequent falls, dizziness while

trying to stand from a sitting position, Hx of taking multiple medications

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→ Measure BP while lying and 3 minutes after standing

(i.e. Blood Pressure Monitoring).

3) Seizures → need eyewitness to confirm, as there is usually post-ictal

drowsiness or confusion.

4) Hypoglycemia → Hx of excessive alcohol intake, sweating, tachycardia,

hypotension, confusion before falling → Check blood glucose

N.B. A vasovagal attack is usually due to overwarm environment, or prolonged

standing period, or after visual stimuli e.g. seeing blood. The patients usually
feel dizzy and ‘’tunnel vision’’ before the attack.

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Another Clarification:

DDx of Sudden Falls.

• Drop attacks → Sudden falls without losing consciousness.

• Stokes Adam → Unconscious + Abnormal ECG.

• Hypoglycemia → Unconscious (or) ↓ level of consciousness + Sweating, do

not recover unless given glucose.

• Vasovagal attacks → Unconscious + Hx of prolonged standing, straining,

pooping, heavy weight lifting or after visual stimuli e.g. seeing blood. The patients
usually feel dizzy and ‘’tunnel vision’’ before the attack. Usually in a YOUNG
FEMALE (with NO chest pain, palpitation and with Normal ECG)

• Epilepsy → Unconscious ± Post-seizure confusion

Key Digoxin Toxicity

87

• GIT (Commonest): Nausea, Vomiting, Anorexia.

• Neurological: Hallucination, Confusion.

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• Visual: Yellow green vision, (Yellow haloes), blurred vision.

• Arrhythmias: Bradycardia, V tach, Premature contractions.

Management:
• Order Digoxin level
• Digibind [DigiFab] = (digoxin immune FAB).
• Correct Arrhythmia
• Monitor Potassium

Aspirin Toxicity
√ The earliest symptoms of acute aspirin poisoning may include
→ Ringing in the ears (tinnitus) and impaired hearing.
√ More clinically significant signs and symptoms may include rapid breathing
(hyperventilation), vomiting, dehydration, fever, double vision, and feeling
faint.

Key Thiazide-like diuretics

88

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◙ Thiazide-like diuretics work by inhibiting sodium reabsorption at the

beginning of the proximal part of the distal convoluted tubule (DCT) by
blocking the thiazide-sensitive Na+-Cl− symporter.
◙ The main use of bendroflumethiazide was in the management of
hypertension but recent NICE guidelines now recommend other thiazide-like
diuretics such as indapamide and chlortalidone.
◙ Remember that: Furosemide and Bumetanide (Loop diuretics) – inhibit the
Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle.

Common adverse effects

• Postural Hypotension. √
• HypOkalemia and HypOnatremia. √
• Gout (Hyperuricemia). √
• dehydration
• impaired glucose tolerance
• impotence
• Thiazide diuretics can cause hypercalcaemia and hypocalciuria

A patient with hypertension on treatment presents complaining of

recurrent falls especially when trying to get up.

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→ Postural hypotension likely due to thiazide being used for hypertension.

Key A patient who is hypotensive (90/70), but is still conscious and the pulse is
89 felt, his ECG shows a pattern between Ventricular tachycardia and
Ventricular fibrillation. What is the treatment?

As the patient is hemodynamically unstable (Hypotensive) → Cardioversion.

If there was No pulse (Hypotensive) → Defibrillation.

Remember:
Defibrillation = Asynchronized cardioversion
In 2 conditions:
√ Ventricular Fibrillation.
√ Pulseless Ventricular Tachycardia.

Key 2 weeks post MI, a patient was readmitted due to Hypotension, Tachycardia
90 and Pulmonary edema. What is the likely underlying cause?

→ Acute Mitral Regurgitation.

Acute mitral regurgitation (MR): “important √” pansystolic murmur

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◙ Occurs 2-15 days after the MI (Mostly inferior MI).

◙ Due to → Ischemia or rupture of the papillary muscles of the mitral valve.
◙ An early-to-mid systolic or Pansystolic murmur at cardiac apex is typically
heard.
◙ May present with Hypotension, Tachycardia and Pulmonary edema (SOB
and bibasilar crackles).
◙ Dx → Echocardiogram.
◙ Treatment → vasodilator therapy but often requires emergency surgical
repair

Key Stable Angina.

91

√ In the case of stable Angina, the pain is precipitated by predictable factors

such as exercise and emotional stress. This is because while exercising, the
Oxygen demand is more than the Oxygen supply.

√ Stable Angina is relieved by Rest and GTN “Glyceryl Trinitrates”.

Unstable Angina

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Occurs mostly at rest, unpredictable, random. It is an emergency.

Key ◙ A baby with Progressive (Severe) Cyanosis + Poor feeding + Holosystolic

92 murmur along the left sternal border → Tricuspid Atresia

◙ A baby who does not have cyanosis, presents with Poor feeding and poor
weight gaining + Holosystolic murmur along the left sternal border → VSD

Tricuspid Atresia → Cyanotic.

VSD → Acyanotic.

Key A patient known to have hypertension presents with Chest discomfort and
93 Nausea. His ECG is as follows:

The ECG shows → Tall Tented T-Waves → Hyperkalemia

(Likely 2ry to ACE inhibitors being used to control his Hypertension)
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Remember that:
◙ Spironolactone and ACE inhibitors and ARBs → HypeRkalemia.
◙ Loop diuretics, Thiazide diuretics → HypOkalemia.

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Key
94

U wave in → Hypokalemia “HypUkalemia”,

an additional wave after T wave.

Tall Tented T-wave [Peaked T-wave] in → Hyperkalemia

J wave (Osborn wave) in → Hypothermia

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Delta wave in → WPW syndrome (Wolff Parkinson White Syndrome)

Widespread Saddle Shaped ST Elevation with upward concavity

+ PR Depression in → Pericarditis.

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Key The table below summarises the most recent guidelines regarding
95 antiplatelets:

Diagnosis 1st line

Acute coronary Aspirin (lifelong) &
syndrome (medically
Ticagrelor or clopidogrel (12 months)
treated) “MI”
Percutaneous Aspirin (lifelong) & prasugrel or ticagrelor (12 months)
coronary
intervention (PCI)
TIA: Transient Aspirin 300 mg 2 weeks then Clopidogrel 75 mg
Ischemic Attack (lifelong)
Ischaemic stroke Aspirin 300 mg 2 weeks then Clopidogrel 75 mg
(lifelong)
Ischemic stroke + AF Aspirin 300 mg for 2 weeks then start
Anticoagulation (e.g. Warfarin or DOAC- apixaban,
rivaroxaban)
Peripheral arterial Clopidogrel (lifelong)
disease

Who should receive a statin?

• All people with established cardiovascular disease (stroke, TIA, ischaemic

heart disease, peripheral arterial disease).

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• following the 2014 update, NICE recommend anyone with a 10-year

cardiovascular risk ≥ 10% should receive statin.
• patients with type 2 diabetes mellitus should now be assessed using
QRISK2 like other patients are, to determine whether they should be
started on statins.
• patients with type 1 diabetes mellitus who were diagnosed more than 10
years ago OR are aged over 40 OR have established nephropathy.

Statins should be taken at night as this is when the majority of cholesterol

synthesis takes place. This is especially true for simvastatin which has a
shorter half-life than other statins.

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Key Atrial fibrillation in an unstable patient

96
→ Cardioversion
If not in the options → IV amiodarone (or IV flecainide) not oral!

If stable → BB, (or CCB if he is asthmatic), (or digoxin if associated heart

failure)

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Scenario,

A 70 YO female presents to the ED after a fall at home. She is confused, pale,

with irregularly irregular pulse and cold peripheries. Her BP is 80/50 and HR
is 150 bpm. ECG is done and shows narrow QRSs and absent P waves.

The next step in management is → Immediate DC Cardioversion

◘ The patient has AF (Irregularly irregular rhythm, Tachycardia, Absent P waves).

◘ Since she is unstable (Confusion, severe Hypotension) → cardioversion.

Key A man was hit by a car and sent to the ED. He is hypotensive with distended
97 neck veins and faint heart sounds. His blood pressure is 82/47 and HR is 120.

The most appropriate management → [Pericardiocentesis].

Cardiac Tamponade

Accumulation of pericardial fluid under pressure

• Beck’s Triad:

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Hypotension ▐ Muffled Heart Sounds ▐ High JVP (Distended neck veins).

• Dx: Echocardiogram is diagnostic
• Rx: Urgent pericardiocentesis.

Key Ventricular Old, Sudden collapse, confusion, severe

98
Fibrillation hypotension, Not breathing, Unconscious
→ Deliver immediate Shock ‘’defibrillation’’

Key Atrial fibrillation in an unstable patient → Immediate shock

99

If stable → BB, (or CCB if he is asthmatic), (or digoxin if associated heart

failure)

Scenario,

A 70 YO female presents to the ED after a fall at home. She is confused, pale,

with irregularly irregular pulse and cold peripheries. Her BP is 80/50 and HR is
150 bpm. ECG is done and shows narrow QRSs and absent P waves.
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The next step in management is → Immediate DC Cardioversion

◘ The patient has AF (Irregularly irregular rhythm, Tachycardia, Absent P waves).

◘ Since she is unstable (Confusion, severe Hypotension) → cardioversion.
If cardioversion is not given, pick → IV amiodarone.

Key MI (Acute chest pain radiating to jaw, shoulder…) BUT without ST

100 elevation on ECG. What to Do Next?

→ Order Cardiac Enzymes, especially (Troponin)

√ If Troponin is high → NON-STEMI Elevation MI

√ Immediate management → Give LMWH OR Fondaparinux √ recent exam

+ Aspirin 300 mg.

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Key A patient’s ECG shows SVT [Supraventricular Tachycardia].

101

→ Adenosine.

(Remember that Valsalva maneuverer and Carotid massage are tried initially and
IV Adenosine is then given).

IMPORTANT NOTE:
If the patient is hemodynamically unstable (eg, hypotension, chest pain,
shock, and or altered mental status)
Proceed immediately to → electrical synchronised cardioversion.

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Key Important Side Effects of Diuretics

102

Loop diuretic Thiazide-like Potassium-sparing

diuretics diuretics
e.g., Furosemide e.g., Bendroflumethiazide e.g., Spironolactone
bumetanide Indapamide eplerenone

Hyponatremia Hyponatremia Hyponatremia

Hypokalemia Hypokalemia HypeRkalemia
Gout (hyperuricemia) Gout (hyperuricemia) Gynecomastia
Postural Hypotension
Hyperglycemia
(impaired glucose tolerance)

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Key
103

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Key A man presents with Fever, confusion, petechiae. This is a picture of his soles
104

What is the most appropriate investigation?

→ Blood Culture

These lesions are likely Janeway lesions (minor criteria of infective

endocarditis).

♦ Likely → Infective endocarditis → Do Blood culture then Echocardiogram.

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Key The initial step for a patient with the following ECG:
105

initial line → give Calcium Chloride (or Calcium Gluconate) (or Calcium
carbonate)
(to prevent cardiac arrhythmia).

This is likely a case of Hyperkalemia (Tall Tented T waves are seen on the
ECG).

Note,
If severe hyperkalemia (> 6.5), and there is no hyperkalemic ECG changes, we
still give Calcium carbonate as a next step to protect the heart.

Key A patient is taking several drugs including Ace inhibitors + diuretics and
106 other drugs. Then, He developed Hyperkalemia.

The initial step → Withhold (stop) ACE inhibitors.

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Remember that ACE inhibitors can cause hyperkalemia. One of the initial steps
of the management is to stop the cause.

Key ◙ An elderly female with a history of Atrial Fibrillation presents to the A&E with
107 speech disturbance and asymmetric weakness of face and arm. These symptoms
started 3 hours ago. CT scan of the head shows no hemorrhage. The “long-term”
management of this patient would involve:

→ Rivaroxaban
(or any other DOAC e.g. Apixaban, Rivaroxaban, Edoxaban, Dabigatran)
“Now preferred over Warfarin”

This patient with TIA/ ischemic stroke will need to take Aspirin 300 mg for 2
weeks, then rivaroxaban (DOAC) and atorvastatin 80 mg for long-term
management. If he did not have AF, clopidogrel will be given instead of DOAC.

◙ In patients with Hx of ischemic stroke, the long-term medications:

√ with Atrial Fibrillation → DOAC (eg, apixaban) + Statins (eg, Atorvastatin).
√ Without Atrial Fibrillation → Clopidogrel + Statins (eg, Atorvastatin).
Important: What if a patient with a history of stroke is already on warfarin
and presents with a new onset atrial fibrillation?
Since he is already on an anticoagulant, he should continue on warfarin and
should not be switched to DOAC (eg, Edoxaban) unless his INR is increased.

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2ry Prevention (Long-term management) of Ischemic Stroke/ TIA:

[To prevent further stroke in the future].
√ Control Blood Pressure.
Remember, if he has DM, pick or add ACEi eg, ramipril.

√ Statins (for All patients regardless of their cholesterol baseline level).

√ Ani-platelets (or) Anti-coagulation: (Based on presence or absence of AF):

• If there is Atrial Fibrillation → Anticoagulants: Warfarin [or] DOAC

(Dabigatran/ Apixaban/ Rivaroxaban/ Edoxaban). DOAC is now preferred.
(Warfarin is almost obsolete nowadays. DOAC is recommended instead)

• If No Atrial Fibrillation → Antiplatelets: Clopidogrel 75 mg OD.

Important: What if a patient with a history of stroke is already on warfarin

and presents with a new onset atrial fibrillation?
Since he is already on an anticoagulant, he should continue on warfarin and
should not be switched to DOAC (eg, Edoxaban) unless his INR is increased.

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Key A patient has recovered form TIA. What score is helpful to determine the
108 risk of a stroke in the following week?

→ ABCD2 Score.

◙ The ABCD2 score (Prognostic) is used to identify the risk of future stroke in
patients who have had a suspected TIA in the following 7 days.

√ IMPORTANT: ABCD2 score is Not advised to be used now according to the

recent 2019 CKS guidelines. Therefore, it will not be a valid answer anymore.
Thus, this question is to not be considered. We have added it just in case!

♦ The CHA2DS2-VASc score is used to determine the need to anticoagulants in a

patient who has atrial fibrillation.

Key A Diabetic patient with heart failure on beta-blockers, ACE inhibitors, insulin
109 and furosemide was found to have hypokalemia. What is the likely cause?

→ Furosemide.
(Loop diuretics such as furosemide can cause hypokalemia).

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HypOkalemia HypeRkalemia

• Loop Diuretics (e.g. Furosemide) • ACE inhibitors.

• Thiazide-like diuretics • Potassium-sparing diuretics
(e.g. bendroflumethiazide, indapamide) (e.g. Spironolactone/ Eplerenone)
• Vomiting and Diarrhea • CKD “Chronic Kidney Disease”.
• Villous Adenoma • Addison’s (1ry Adrenal Insufficiency).
• Renal tubular failure • Congenital Adrenal Hyperplasia
• Cushing Syndrome (CAH).

• Conn’s disease (1ry hyperaldosteronism)

Key A patient with hypertension on treatment presents complaining of ankle

110 swelling/ edema. The likely cause of this ankle oedema is:
→ Amlodipine (a calcium channel Blocker).

√ This patient is likely taking CCB for his HTN.

√ CCB can cause ankle swelling as it causes vasodilatation.

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2 Important Side effects of Calcium Channel Blockers (e.g.

Diltiazem, Amlodipine) to be remembered:

◙ Ankle Swelling / oedema

◙ Gingival Hyperplasia

So, for one who takes CCB such as diltiazem, amlodipine, verapamil,
nifedipine, he might get swelling of his → Ankle + Gingiva.

Key Before prescribing amiodarone, what investigation should be ordered?

111
→ Serum Electrolytes and Urea.

(Do not mix thing up):

The 2 most important tests to be done before initiating lithium are:
(TFTs) Thyroid Function Tests, and:
(KFTs) Kidney Function Tests.

Key The following ECG is done for a 58 YO man who presents with palpitation.
112 He is otherwise healthy. What is the most appropriate line in Rx?

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→ Beta-blockers (eg, metoprolol, atenolol)

◙ Agents used to control rate (Rate Control) in patients with Atrial

Fibrillation (AF):

o Beta-blockers (eg, atenolol 50-100 mg PO OD, bisoprolol, metoprolol) →

First line but Contraindicated in Asthma.
o Calcium channel blockers [non-dihydropyridine = rate-limiting CCB] (eg,
diltiazem, verapamil) → if Asthmatic patient.

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o Digoxin → (not considered first-line anymore as they are less effective at

controlling the heart rate during exercise. However, they are the preferred
choice if the patient has coexistent heart failure).

√ If haemodynamically unstable (eg, SBP ≤ 90) → Cardioversion (Shock).

√ If the patient with AF is unstable (eg, hypotension) and the AF has just
started and no cardioversion in the options, Pick → IV amiodarone. Imp √

Key A patient presented with chest pain and breathlessness. Pulse rate is 35
113 b/m. ECG shows broad complexes with atrioventricular dissociation. Most
appropriate initial treatment?

A. Adenosine
B. carotid massage
C. atropine
D. verapamil
E. Amiodarone

◙ The first drug of choice for Symptomatic Bradycardia

(Dizziness, feeling unwell)
→ Atropine
(Given 0.5 mg IV push and may be repeated up to a total dose of 3 mg).

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Key A 76-year-old man was found outside by his carers this morning. He doesn’t
114 remember what happened but denies history of pain. Temperature 35.1, BP:
102/70mmHg, PR: 108bpm, mucous membrane is dry. No stiffness of any
limb, his heart sound is normal. His chest is grossly normal apart from some
scattered coarse crackle in his Left Lower lung zone. He was catheterized and
urinalysis showed Blood+++, Protein ++ and Ketone +, ECG showed peaked T
wave and broad complex Tachycardia. Which of the following is the
appropriate initial intravenous medication he should have?

A. Amiodarone
B. Calcium gluconate
C. Co- Amoxiclav
D. Insulin- Glucose infusion
E. Sodium Bicarbonate

Peaked T wave suggesting Hyperkalemia (2ry to kidney injury in this case).

→ IV calcium gluconate (or calcium chloride) to protect the heart should be
given initially.

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Key A question about a patient with unstable HR > 150, BP 80/60 and Having
115 broad complex tachycardia. Most appropriate management was asked?
→ DC Cardioversion.

Patient is unstable, SBP < 90 → (Cardioversion) Shock.

◘ Broad complex tachycardia + low BP (unstable) → Cardioversion

◘ Pulseless V. Tach or V. Fibrillation → Immediate Defibrillation.

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Key A 71-year-old man with 3 weeks history of fever, 1 month post inferior
116 myocardial infarct, chest pain with soft systolic murmur, inverted Q waves in
leads I, II & aVF. Temp- 37.5, BP- ?118/68

A. Pericarditis
B. Costochondritis
C. Pulmonary Embolism
D. Infective endocarditis
E. Papillary muscle rupture

New Murmur + Fever → think of Infective Endocarditis (IE)

± Malaise, Rigors, Fever
The initial step → Blood Culture. Then → Echo

Key Patient with Hx of MI presented after a few days with chest pain which
117 aggravates on inspiration and is relieved on bending forward. Most likely
Diagnosis?

A. Pericarditis
B. Pulmonary Embolism
C. Pleural Effusion

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◙ Pericarditis (A Complication of MI that can develop shortly after the MI

within 2 days) and Dressler’s syndrome (presents 2-6 weeks after MI) both
have t’e same features → Pleuritic chest pain that worsens on lying flat and
during inspiration, Pericardial rub, Widespread Saddle shaped ST elevation on
the ECG.
◙ They can also lead to Pericardial effusion (Enlarged globular heart on chest
X-ray) and if severe enough, Cardiac Tamponade can also develop (also
enlarged globular heart on the X-ray).

◙ Management of Pericarditis (imp):

√ A full-dose NSAID should be used (eg, aspirin, 2-4 g/d; ibuprofen 1200-1800
mg/d; indomethacin 75-150 mg/d); treatment should last at least 7-14 days.
√ Colchicine (as an adjunct to NSAIDs to ↓ inflammation and recurrence).

Key A 60 YO man with Hx of smoking, HTN and DM presents to his GP

118 complaining of 25 minutes left side dull aching chest pain radiating to his
jaw. He was given Aspirin 300 mg by his GP and then sent to medical services
in a local hospital. He is no longer in pain. The ECG is normal. The troIonin is
elevated 202 ng/L (Normal: < 5 ng/L). What is the next step in management?

E) Alteplase.
F) Subcutaneous fondaparinux.
G) IV Glyceryl trinitrate (GTN).

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H) IV Morphine.

Since the ECG is normal, alteplase is wrong.

Since ECG is normal and Troponin is high → Non-STEMI

→ Anti-coagulation (LMWH e.g. Dalteparin, Enoxaparin or Fondaparinux).

+ Oral Aspirin 300 mg.

Key Points on Alcohol and Heart Disease

119

√ Ankle swelling and orthopnea → features of Heart Failure.

√ Excessive alcoholism can lead to → Alcoholic Cardiomyopathy (Cardiac

Enlargement on Chest X-ray) → which can cause Atrial Fibrillation.

- The most common type of arrhythmia that develops in patients with

alcoholic cardiomyopathy is → Atrial Fibrillation.

√ Acute alcohol intake can lead to → AF or flutter ((Holiday heart Syndrome)).

√ AF presentation: Palpitation, Dyspnea, Dizziness or Syncope, Chest

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discomfort or pain, Stroke or TIC, Irregularly irregular pulse.

Key A 59 YO hypertensive patient presents to the A&E complaining of dull

120 central chest pain for around 4 hours. His vitals are as follows:
HR: 99, BP: 155/95, RR: 21, O2 sat on room air: 97%
Chest X-ray is normal. Troponin level was sent and still pending.
He was given IV morphine for his chest pain.
The ECG is as follows:

What is the most appropriate next step in management?

Chest pain + T wave inversion suggests → myocardial ischemia.

In this case, 2 drugs should be given immediately:

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√ Oral Aspirin 300 mg.

√ SC LMWH or Fondaparinux.
Pick the one that is given in the choices.

“low-risk patients can be treated conservatively. However, if subsequent

ischemia develops → coronary angiography with PCI”.

What if the ECG shows features of left main coronary artery occlusion (Wide
spread ST depression + ST elevation in aVR)?
→ Emergency coronary angiography.

Key A 61 YO patient presents to the A&E complaining of dull central chest pain
121 for around 4 hours. His vitals are as follows:
HR: 75, BP: 135/85, RR: 21, O2 sat. on room air: 97% He was given IV
morphine for his chest pain. The ECG is as follows:

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What is the most appropriate next step in management?

This ECG shows the typical features of Left main coronary artery occlusion:
• Widespread ST depression, and
• ST elevation in aVR.

Thus → Emergency coronary angiography.

To determine which artery is occluded so we can plan for interventional or

surgical procedures.

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Key Remember:
122

Long-term antiplatelet/anticoagulant drugs in:

√ Ischemic stroke (or TIA) → Aspirin for 2 weeks, then clopidogrel for life.
√ Ischemic stroke + AF → Aspirin for 2 weeks, then warfarin/DOAC for life.
If he was already on warfarin (anticoagulant) and develops atrial fibrillation
(AF), continue on warfarin and do not shift to DOAC unless his INR is poor.
√ MI → Aspirin for life, clopidogrel (or ticagrelor) for 12 months.

Key AF + Stable patient

123
→ BB (eg, metoprolol) or CCB (if asthmatic) or Digoxin (if with HF)

AF + Unstable patient (e.g. SBP ≤ 90, HR > 150, Loss of conscious)

→ Cardioversion

AF + Unstable patient but presents > 48 hours after beginning of symptoms

→ Do not cardiovert; but give rate control (e.g. BB) + LMWH
→ Then: assess for long-term intake of Warfarin or DOAC (e.g. apixaban,
rivaroxaban, dabigatran) upon discharge using CHA2Ds2-VASc score.

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Key A 60 YO asthmatic man presents to A&E complaining of chest discomfort and

124 difficulty in breathing over the past few hours. On chest auscultation, there
are widespread fine inspiratory crepitations. His vitals are as follows: HR
100, RR 28, BP 120/80, O2 saturation 90%.
Chest X-ray was performed (see the picture below). ECG: normal. Echo
showed left ventricular impairment.
The patient was given high flow O2, sublingual glyceryl trinitrates, and IV
furosemide (Lasix). His breathing improved significantly.
What is the most appropriate medication to be added?

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This patient has acute pulmonary edema 2ry to left ventricular failure.

Pulmonary edema:
Kerley B lines, bat’s wing hilar shadow, crepitations, SOB, low O2 sat.

Echo in the stem shows left ventricular impairment (HF).

HF can lead to → Pulmonary edema

Remember,
Management of HF:
• Furosemide (for symptomatic relief) “was already given here”.
• Start with either Beta-blocker or ACE inhibitor (one medication at a time).
• If still? Add the other medication.
• If still? Add spironolactone

Since this patient is Asthmatic, we would begin with ACE inhibitors (e.g.
lisinopril) instead of BB.
BB is better to be avoided in asthma as it can cause bronchospasm and thus
aggravates asthma.

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So, the answer is that this patient should be discharged on

→ ACE inhibitor (e.g. Lisinopril).

Key A 50 YO man with Hx of MI six months ago presents with a 3-day history of
125 fever, SOB and chest pain. He looks moderately ill. His temp, is 38.2 and his
BP is 140/77. On auscultation, a holosystolic murmur over the apex is heard.
His ECG shows Q waves in leads I and aVL. What is the most likely Dx?

√ Do not rush and pick papillary muscle rupture thinking it is mitral

regurgitation (evidenced by the holosystolic murmur over the apex)!
If MR, why there is fever?

√ Note that papillary muscle rupture usually occurs 2-15 days after MI, not 6
months!

√ Also, papillary muscle rupture is more common with inferior MI (II, III, aVR).

√ Q waves here → permanent markers of necrosis (indicate previous MI),

here, likely lateral MI (I, aVL, V5, V6).

So, what is the correct answer??

Remember :

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FEVER + NEW MURMUR → INFECTIVE ENDOCARDITIS!

Key An old patient with triple vessel disease presents with sudden onset chest
126 pain of 4 hours, shortness of breath, dizziness and sweating. His ECG shows
ST depression “ischemia” in several leads. His blood pressure is 140/80. The
patient is anaemic with haemoglobin level of 62 g/L. What is the most
appropriate management?

→ Dual antiplatelets (Aspirin + Clopidogrel)

+ Fondaparinux
+ Blood transfusion.

Notes:
√ Triple vessel disease means that 3 big vessels (the left anterior descending,
right coronary and circumflex arteries) have blockages from atherosclerotic
plaques.

√ This patient has ACS “acute coronary syndrome” secondary to anemia and
the pre-existing triple vessel disease.

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√ Aspirin (oral) and fondaparinux (SC LMWH) are given whenever there is
heart ischemia.

√ Blood Transfusion is indicated if:

♠ Hb < 80 g/L + Symptoms of Anemia. Or:
♠ HB < 70 g/L + With or Without Symptoms of Anemia.

Key Elderly + Episodes of Fainting + SOB + Systolic murmur at the right second
127 intercostal space
→ Aortic stenosis.

Do → Echocardiogram.

Key A patient with a classic presentation of MI (sudden onset central chest pain
128 radiating to neck and left shoulder, sweating, vomiting) but the ECG is
normal.
→ request troponin.

If troponin is elevated

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→ Myocardial infarction (Non-ST Elevation MI).

Key ◙ The best initial investigation for chest pain is → ECG.

129

◙ The most appropriate “initial” test for syncopal attacks that are not due to
hypoglycemia (no Hx of sweating, tachycardia, hunger, shakiness before the
syncope), and not due to epilepsy (No Hx of tongue biting, incontinence
during the syncope)
→ ECG
Measuring lying and standing blood pressure should also be done to R/O
postural hypertension
(Note that ambulatory blood pressure monitoring is used to diagnose
hypertension, not postural hypertension. Thus, not useful in syncopal attacks).

Key ◙ The QRISK3 score is used to determine the risk of a cardiovascular event in
130 the next 10 years.

◙ If QRISK3 is > 10% and the age is < or = 84 → the patient needs to start on
statins (atorvastatin) to reduce the risk of cardiovascular disease.

◙ If QRISK3 is 10%, this means that the patient has 10% chance of developing
cardiovascular disease over the next 10 years.

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Key ◙ Angina, Syncope, Dyspnea, Systolic murmur over the “right” sternal border
131
→ Aortic Stenosis.

◙ Dyspnea, Orthopnea, Diastolic murmur at the “apex”

→ Mitral stenosis.

Key ◙ SOB, Diastolic murmur, Chest X-ray showing straightening of the left atrial
132 appendage
Think→ Mitral stenosis.

(Remember, rheumatic fever is the commonest cause of mitral stenosis.

Rheumatic fever is commonly found in developing countries e.g. Syria,
Mozambique).

◙ Complications of MS:
As the left atrium enlarges → Atrial fibrillation → Venous thromboembolism
→ Cerebral infarction. “imp √”.

√ Note: left ventricular hypertrophy is a common complication of aortic

stenosis.

Key Broad complex tachycardia + Unstable patient (e.g. SBP < 90)
133
→ Synchronized Cardioversion.

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Key Long QT syndrome

134

Recurrent fainting episodes

+
Prolonged QT intervals on ECG
+
Hx of similar ECG during childhood

• Think → Congenital long QT syndrome (Congenital LQTS).

• The most common arrhythmia associated with Congenital LQTS is

→ Ventricular tachyarrhythmia.
There is risk of ventricular fibrillation. Thus, some patients use long-term beta
blocker treatment.

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Key
135

T wave inversion in leads (V1, V2, V3, V4)

Indicating → Myocardial Ischemia.

Key A 60 YO man on ramipril for his hypertension has serum potassium of

136 6.7 mmol/L (Normal: 3.5-5). His ECG shows sinus rhythm without
hyperkalemic changes. What is the next step in management?

Although there is no ECG changes of hyperkalemia “tall tented T waves”,

this patient has severe hyperkalemia (>6.5) and the initial step is to
protect the heart and prevent cardiac arrest by giving a medication that
antagonizes the cardiac membrane excitability as a temporary measure
such as calcium Gluconate 10% or calcium chloride or calcium carbonate.

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Key A 50 YO presents with a swollen left arm. It started suddenly a few hours
137 ago and it is painful. He has fever and breathlesness. O/E, loud S1 and mid-
diastolic murmur are heard. There is no left radial pulse felt. Echocardigram
is done and it reveals left atrial myxoma. What is the most appropriate
management?

→ Perform an urgent catheter Embolectomy.

• A piece of the atrial myxoma has broken off and caused left acute limb
ischemia (sudden swollen painful left arm with a loss of radial pulse).
• It has been only a few hours and the limb could be saved if embolectomy is
performed urgently.
• It is perfomed by a interventional radiologist who uses an angiogram in
theatre and introduce a catheter to aspirate the emboli “embolectomy”.
• Note that this is not a blood clot, but a piece of the benign tumor. Thus,
thrombolysis and anticoagulation would not be suitable.

Key Fatigue + Shortness of breath on exertion + Ankle oedema

138

Think → Heart failure.

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Next test → N-terminal (NT)-pro hormone BNP (NT-proBNP).

If raised → Echocardiogram.

• N-terminal (NT)-pro hormone BNP (NT-proBNP) is a non-active prohormone

that is released from the same molecule that produces BNP. Both BNP and NT-
proBNP are released in response to changes in pressure inside the heart. These
changes can be related to heart failure and other cardiac problems.

• Note: sometimes in heart failure, ECG may be normal.

Key A hypertension patient on ramipril. What shoulde be monitored?

139

→ Kidney function tests.

Key Dizziness + bradycardia + 3rd degree heart block

140

◘ Initial management → Atropine .

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◘ What if he was given atropine but no response?

Next step would be → Temporary transcutaneous pacemaker.

◘ Definitive management → Permanent pacemaker.

• Bradycardia is a condition typically defined wherein an individual has a

resting heart rate of under 60 beats per minute (BPM) in adults, although
some studies use a heart rate of less than 50 BPM. Bradycardia typically does
not cause symptoms until the rate drops below 50 BPM.

• All symptomatic bradycardia should initially be treated with atropine.

If no response → temporary pacemaker (in an emergency setting).

• Atropine is given 0.5 mg IV push and may be repeated up to a total dose of 3 mg.

Remember:
◙ 1st Degree Heart Block and Mobitz type 1 usually
→ do not require treatment (as long as the patient is Asymptomatic).

◙ Mobitz type 2 and Complete heart block (3rd degree heart block)
→ require permanent pacemaker.
• Initially → Atropine (first choice for all symptomatic bradycardia).

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• Then → Transcutaneous pacing. (Used to buy time until transvenous

pacing is done).
• Then → Transvenous pacing.
• Then → Permanent pacing (Pacemaker).

Key A 50 YO man presents for advice as his father dies of MI. He smokes 6
141 cigarettes a day, drinks 14 units of alcohol a week with 2 days free. He eats
an estimate of a teaspoon of salt a day. He eats fruits and vegetable. His
clinic BP is 138/87.
What is the best advice to reduce the risk of MI?

A) Refer to a cardiologist.
B) Refer to a smoking cessation clinic.
C) Refer to alcohol cessation services.
D) Advise to reduce salt.

√ His clinic BP is normal (<140/90).

√ Smoking is the major risk factor here.

√ His alcohol intake is within the recommended limit.

(no more than 14 units a week with at least 2 days free).

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√ His salt intake is within the recommended limit.

(Salt intake recommendation for adults in the UK is no more than 6 g per day
which is around 1 teaspoon).

Key If a patient has either systolic BP ≥ 140 and/or diastolic BP ≥ 90 in a clinic

142
→ Ambulatory blood pressure monitoring (ABPM) is needed before starting
lifestyle modifications and antihypertensive medications.

Key
143

• Dx → Anterior MI (note ST elevation in V1-V4).

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• The likely occluded artery → LAD “left anterior descending artery”.

Key (Important)
144 If the patient of congestive heart failure is already on FUROSEMIDE, Beta blocker,
and ACEi and still has lower limb edema → This means that the diuretic is not
efficient (the furosemide) → Therefore, one of the following is needed:
• Increase the dose of the furosemide.
• Switch the furosemide to either bumetanide or torsemide.
• Consider admission for IV loop diuretics.

Key A 67 YO man with hypertension for 7 years. He is on ramipril “ACEI”. However,

145 his BP now is not controlled. Knowing that he had used amlodipine “CCB” in the
past but stopped it because of ankle edema, what medication can be added?
• Choices are (Valsartan, Indapamide, Bisoprolol, Furosemide).

The right option is → Indapamide (which is a thiazide like diuretic0

He has started with CCB (step 1) and cannot use it because of ankle edema S/E.
Then stopped it and went for ACEi ramipril (step 2)
Now, (step 3) is a thiazide like diuretic e.g., indapamide.

Note that valsartan is ARBs. It is used instead of ACEi in some cases like those
who develop dry cough as a side effect of ACEi.
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Key √ Arrhythmia causing dizziness and palpitations sometimes but the ECG is normal
146 Do → Ambulatory 24-hour ECG. This is because the arrhythmia occurs in some
periods of the day and so the ordinary ECG may be normal. We need ambulatory
24-hour ECG to try to detect the arrhythmia.
Also known as an ambulatory ECG or EKG monitor, a Holter monitor records your
heart’s activity over 24 to 48 hours or up to 2 weeks while you maintain a diary of
your activity to help your doctor identify the cause of your symptoms.

√ If Stable angina (chest pain on exercise) is suspected

→ Exercise ECG “stress test”.

Key A 66 YO diabetic and hypertensive patient developed chest pain radiating to the
147 left arm 1 hour ago. His ECG is normal and his Troponin level is normal (below
12). He was given aspirin. What is the next step?

→ Admit and repeat troponin level after 3 hours of the symptom’s onset.

• The patient has arrived to the hospital after one hour of the beginning of the
chest pain. So, the troponin level was taken only one hour after the chest pain.

• Elevated troponin can be detected within 3 to 4 hours after the onset of

myocardial injury. Serum levels can remain increased for 7 to 10 days for troponin I
and 10 to 14 days for troponin T.

• Therefore, a second troponin level is needed after 3 hours of the onset of the
chest pain. Taking into consideration that he is Old + DM + HTN (All RFs for MI).
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◙ Rules:
If arrived < 3 hours of the chest pain onset:
√ troponin is < 12 → repeat after 3 hours of chest pain onset.
√ troponin is > 30 → correlate with ECG and Hx → treat as ACS.

If arrived > 3 hours of the chest pain onset:

√ troponin is < 12 → ACS is unlikely → suspect stable angina and refer to
cardiology outpatient or rapid access chest pain clinic.
√ troponin is > 30 → correlate with ECG and Hx → treat as ACS.

Key Pericarditis
148
Sharp chest pain + Age 20-55 YO + ECG shows Widespread ST elevation
+ Recent Hx of upper viral respiratory tract infection
Think → Acute pericarditis.
Rx → NSAIDS (eg, Ibuprofen) + Colchicine.

◙ Other Criteria of Acute Pericarditis → Central sharp stabbing chest pain

relieved by sitting up and leaning forward and worsened by lying down +
Pericardial rub.
◙ Management of Pericarditis (imp):
√ A full-dose NSAID should be used (eg, aspirin, 2-4 g/d; ibuprofen 1200-1800
mg/d; indomethacin 75-150 mg/d); treatment should last at least 7-14 days.

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√ Colchicine (as an adjunct to NSAIDs to ↓ inflammation and recurrence).

Key A 50 YO man is to be started on Modafinil (to counter his extreme sleepiness). A

149 baseline ECG was requested and it shows:

What is the most appropriate management?

A) Atropine
B) Permanent pacing
C) Temporary pacing
D) Reassurance.

• The ECG shows PR prolongations followed by a dropped beat.

• This is a second-degree heart block (Mobitz type 1). Also called (Wenckebach).
• Asymptomatic patients with this type of heart block do not need specific Rx.

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Key A 58-year-old man had clinic blood pressure of 162/95 mmHg. He was asked to
150 record blood pressure at home (ABPM). He returns to the clinic next week with
an average ambulatory blood pressure reading of 155/92 mmHg. He does not
have a significant medical history. What is the most appropriate action?

A) Repeat ABPM for another week.

B) Prescribe enalapril.
C) Prescribe felodipine.
D) Prescribe indapamide.
E) No treatment is required, only encourage lifestyle modifications.

• Since his ambulatory BP is ≥ 150/95 (His SBP is the high portion in this case)
→ he needs treatment. (Confirmed stage 2 HTN).

(f ABPM or HBPM ≥ 150/95 mmHg (i.e., confirmed stage 2 or higher hypertension)

→ Always treat.)

• Since he is ≥ 55 YO → the first step is Calcium channel blocker (CCB).

→ Felodipine (Felodipine is a CCB).

Important notes regarding [When to treat Hypertension?]:

Stage Criteria
Stage 1 HTN Clinic BP ≥ 140/90
and subsequent ABPM daytime average or HBPM average
BP ≥ 135/85
Stage 2 HTN Clinic BP ≥ 160/100 and
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subsequent ABPM daytime or HBPM average BP ≥ 150/95

Stage 3 HTN Clinic systolic BP ≥ 180 mmHg,
or clinic diastolic BP ≥ 110 mmHg

◙ If a patient is completely free and has a stage 1 Hypertension

→ Lifestyle and Diet Modification + review (Follow up).

◙ In a patient with stage 2 hypertension at a clinic (Clinic BP ≥ 160/100)

→ Before commencing antihypertensive drugs, request either ABPM or HBPM.

◙ If ABPM or HBPM ≥ 150/95 mmHg (i.e., confirmed stage 2 or higher

hypertension) → Always treat.

◙ For patients < 40 years and with stage 2 hypertension or higher

→ Consider a specialist referral to exclude secondary causes of HTN.

Remember, the first step in managing HTN is as follows:

• White + < 55 YO → start with ACEi/ARBs as a step 1 management of HTN.
• White + > 55 YO → start with CCB as a step 1 management of HTN.
• Afro-Caribbean + any age → start with CCB as a step 1 management of HTN.

- Example of ACEi → Enalapril.

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- Example of ARBs → Valsartan.

- Example of CCB → Amlodipine, Felodipine.
- Examples of thiazide diuretics → chlorthalidone (12.5-25.0 mg once daily)
or indapamide (1.5 mg modified-release once daily or 2.5 mg once daily)
- Bendroflumethiazide is a thiazide like diuretic; however, it is no longer
recommended by NICE as an antihypertensive.

Key Patients with aortic stenosis (systolic murmur at the right second ICS) are liable to
151 fainting episodes that are called → Syncope.
Other features → Dyspnea, Angina.

Key After Myocardial Infarction, Mitral regurgitation may occur as a complication

152 (pansystolic murmur at the apex +Bi-basal crackles + Shortness of breath).

The most appropriate investigation to determine this mitral regurg is

→ Echocardiogram.

Key In diabetic patients who have heart failure “HF” with reduced ejection volume
153 Give → SGLT2 inhibitors such as Dapagliflozin, Empagliflozin

(When SGLT2 inhibitors are added to the medications of HF which are B-blockers,
ACE inhibitors, Aldosterone antagonist → they reduce cardiovascular death).
So, in DM with heart failure, use metformin and flozin family.

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Key A 72-year-old man presents to a GP clinic to complain of repetitive dizziness

154 and palpitations over the past few weeks. They mostly occur while walking
long distances and they resolve after a few minutes. He has a background
history of diabetes mellitus types 2 and hypertension. He is vitally stable. His
current ECG shows normal sinus rhythm. He denies any chest pain, fainting or
shortness of breath. What is the most appropriate investigation?

A) Echocardiogram.
B) Ambulatory 24-hour ECG (Holter monitor).
C) Exercise ECG (Stress test).
D) Random blood glucose.
E) Blood pressure monitoring.

• Exercise ECG (stress test) is preferred for stable angina. Here, no chest pain!

• Echo: could be requested if the current ECG is abnormal. Here, it is normal.

• Also, if you think this might be aortic stenosis (AS) that requires Echo to be
diagnosed, then you are mistaken. AS presents with ejection systolic murmur
over the right second intercostal space + Fainting episodes (syncope) ±
Dyspnea ± Angina (chest pain). None of these features are present!

• This patient has dizziness and PALPITATIONS mostly during walking, which
may indicate hidden arrhythmia which develops while walking.
• The arrhythmia can be detected by ECG. However, the current ECG is
normal. Thus, ambulatory 24-hour (Holter) ECG is needed.

Key A 60-year-old has just finished his appendectomy surgery and developed
155 dizziness, palpitations, tachycardia and hypotension (BP: 80/50). His ECG:
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What is the most appropriate diagnosis and management?

• The ECG + (palpitations, tachycardia. Dizziness) suggest atrial fibrillation.

• Since the AF has just started and the patient is hypotensive (ie,
haemodynamically unstable) → Cardioversion. √
• If cardioversion is not in the option → IV Amiodarone. √
• Another possible answer is IV Flecainide (IV, not Oral).
(Careful: beta-blockers are first line in STABLE patients with AF)!

Key • Remember that the initial treatment for symptomatic bradycardia

156 (lightheadness, syncope -fainting-, dizziness) is → IV atropine.

(Given 0.5 mg IV push and may be repeated every 3-5 minutes up to a total
dose of 3 mg).

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• Rx is required if the patient is symptomatic even if the ECG shows first-

degree heart block. As long as he has symptoms and bradycardic, start with
atropine.

• After initial stabilisation of the patient by atropine, he should then be

prepared for temporary pacemaker and assessed for whether or not he needs
a long-term permanent pacemaker.

Key Important Points to Remember on Ischemic Stroke

157

• The antihypertensive of choice in patients with diabetes mellitus is

→ ACE inhibitors (eg, ramipril).

• In patients with a history of ischemic stroke, the long-term management to

prevent further stroke (2ry prevention of ischemic stroke) is as follows:
√ Control Blood Pressure.
Remember, if he has diabetes, pick or add ACEi eg, ramipril.

√ Statins (for All patients regardless of their cholesterol baseline level).

√ Ani-platelets (or) Anti-coagulation: (Based on presence or absence of AF):

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• If there is Atrial Fibrillation → Anticoagulants: Warfarin [or] DOAC

(Dabigatran/ Apixaban/ Rivaroxaban/ Edoxaban). DOAC is now preferred.
(Warfarin is almost obsolete nowadays. DOAC is recommended instead).
• If No Atrial Fibrillation → Antiplatelets: Clopidogrel 75 mg OD.

Important: What if a patient with a history of stroke is already on warfarin and

presents with a new onset atrial fibrillation?
Since he is already on an anticoagulant, he should continue on warfarin and
should not be switched to DOAC (eg, Edoxaban) unless his INR is abnormal.

Scenario (1) that tests the above notes (important).

A 65 YO man presents for medication review. He has a history of ischemic
stroke a few months ago. His medical background includes atrial fibrillation,
hypertension and type 2 diabetes mellitus. His ECG still shows arterial
fibrillation. He is on warfarin, lercanidipine (CCB), atorvastatin, and
metformin. His current blood pressure is 160/100. What is the most
appropriate action?
A) Switch warfarin to Edoxaban (DOAC).
B) Continue warfarin and add clopidogrel.
C) Stop lercanidipine and start ramipril.
D) Continue lercanidipine and add ramipril.
E) Continue lercanidipine and add bendroflumethiazide.

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The right answer is (D): continue lercanidipine (CCB) and add ramipril (ACEi).
• Since he is diabetic, ACEi is of choice to control HTN.
• Since he is already on an antihypertensive (which is lercanidipine; a calcium
channel blocker) and his hypertension is still uncontrolled, go to step 2 and
add a second antihypertensive (ACE inhibitor eg, ramipril).
• We do not shift from warfarin to DOAC unless his INR is not normal. Here,
no mention of INR. Thus, continue on warfarin (option A is wrong).
• Since he has AF, an anticoagulant (eg, warfarin, DOAC) is given; Not an
antiplatelet (eg, clopidogrel).

Scenario (2) that tests the above notes (important).

A 61 YO man presents for medication review. He has a history of ischemic
stroke a few months ago. His medical background includes hypertension and
type 2 diabetes mellitus. His ECG now shows arterial fibrillation. He is on
clopidogrel, amlodipine, atorvastatin, and metformin. What is the most
appropriate action?
A) Switch amlodipine to ramipril.
B) Continue clopidogrel and add apixaban.
C) Stop clopidogrel and start edoxaban.
D) Continue amlodipine and add ramipril.
E) Continue amlodipine and add bendroflumethiazide.

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The right answer is ©: Stop clopidogrel and start a DOAC eg, edoxaban.
• He did not have atrial fibrillation before, that’s why he was on clopidogrel
(and not warfarin or DOAC).
• Since he is now having atrial fibrillation, switch clopidogrel to an
anticoagulant such as warfarin or DOAC (eg, edoxaban, apixaban). DOAC is
preferred over warfarin.
• His blood pressure is not mentioned so we assume it is controlled and
therefore no need to add an additional antihypertensive (even if he is diabetic,
he is already on amlodipine and controlled).

Key • In rhabdomyolysis, acute kidney injury and hyperkalemia can develop.

158

• A patient might be found on the floor after a fall for several hours.

• A patient can be found stuck under a heavy object for several hours.

• Hyperkalemia can develop and ECG may show tall tented T waves.

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Tall Tented T waves → Hyperkalemia

• Important: the investigation that would likely be abnormal in this case is

→ Urea and electrolytes.

Urea and electrolyte panel includes:

→ Urea, creatinine, sodium, potassium, eGFR.

Key • Consuming alcohol (and also tobacco) excessively can lead to transient
159 palpitations several times a day (holiday heart syndrome).

• The ECG in this case would be unremarkable.

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• The best action is to → Advise on lifestyle modifications (decreasing alcohol

and smoking would resolve palpitations completely).

Key • A patient with DM type 1 who presents with abdominal pain, vomiting,
160 lethargy, increased thirst and urination, and fruity smelling breaths is likely
suffering from a complication called diabetic ketoacidosis (DKA).

• One of the manifestations that would be seen in DKA is:

→ Hyperkalemia (ECG might show tall tented t waves)

Tall Tented T waves (Hyperkalemia).

Key ALS important points

161

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◙ Example (1):

A 50-year-old man was found unconscious with a absent pulse and

undetectable blood pressure. His ECG reading is flat. What is the best
management?

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→ Start CPR (Chest Compressions).

Important: If CPR is not among the options, what’s to pick?

→ Give adrenaline (Epinephrine) 1 mg IV.

(A flat ECG reading means asystole which is a non-shockable rhythm).

◙ Example (2):

A 50-year-old man was found unconscious with a absent pulse and

undetectable blood pressure. His ECG reading shows VT. What is the best
management?

→ Deliver a shock.

(VT in a pulseless patient and VF requires immediate shock delivery).

Key A few days after myocardial infarction (especially inferior MI):

162
• Pan-systolic murmur over the apex
Think → Mitral regurgitation.

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• Pan-systolic murmur over the lower left sternal border

Think → Tricuspid regurgitation Or ventricular septal rupture.

(This is due to a possible dysfunction of papillary muscles of the valve).

Q) Since these 2 conditions have the same type of murmur, how to

differentiate?
√ Ventricular septal defect occurs acutely (within a few days) after MI, and it
also presents with hypotension (shock).
√ Tricuspid regurgitation tends to develop over weeks to months after MI, and
hypotension is not a feature.

- In both conditions, do → Echocardiogram.

Key Important notes on the management of Atrial Fibrillation:

163
(Atrial fibrillation = narrow-complex irregularly irregular tachycardia).

• First line (if hemodynamic stable) → Beta-blockers (eg, metoprolol).

• If hemodynamic unstable (eg, hypotension, chest pain, altered mentation)

→ Start with electrical cardioversion.
If still not improved → IV amiodarone.

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Key An Important Question on Hypertension Management (Reminder):

164

A 67-year-old man presented to the GP surgery to check on his blood

pressure. It is found to be 155/95 mmHg. He was asked to measure his blood
pressure at home several times. On the next appointment, the average of his
home blood pressure measurements is 146/93 mmHg. His 10-year risk of
developing cardiovascular disease is calculated and is found to be 6%. He does
not smoke and otherwise healthy. What is the most appropriate
management?

A) Start ACE inhibitors.

B) Start calcium channel blockers.
C) Offer lifestyle advice and modification.
D) Start statin.
E) Reassure and no intervention is required.

Answer → C.

Since his home blood pressure is ≥ 140/90, but < 150/95 mmHg.
→ He has stage (1) hypertension.

Stage Criteria

Stage 1 Clinic BP ≥ 140/90 mmHg and subsequent ABPM daytime

hypertension average or HBPM average BP ≥ 135/85 mmHg

Stage 2 Clinic BP ≥ 160/100 mmHg and subsequent ABPM daytime or

hypertension HBPM average BP ≥ 150/95 mmHg

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Stage 3 “Severe Clinic systolic BP ≥ 180 mmHg,

hypertension” or clinic diastolic BP ≥ 110 mmHg

♠ When to Treat Stage 1 Hypertension?

• Treat if the patient’s age is < 80 years AND + any of the following:
Target organ damage, established cardiovascular disease, renal disease,
diabetes (DM) or a 10-year cardiovascular risk equivalent to (QRISK2) ≥ 10%.

◙ Note: If a patient is completely free and has a stage 1 Hypertension

→ Lifestyle and Diet Modification + review (Follow up).

◙ Example: If a patient a stage 1 Hypertension and his QRISK2 ≥ 10?

→ Discuss initiating antihypertensive therapy.

Key A 53-year-old man from South Asia presents with headache and blurry vision
165 for sometimes. His blood pressure is found to be 149/ 101 mmHg. He was
asked to have blood pressure measurements at home. His average blood
pressure of 14 home readings is 153/97 mmHg. What is the most appropriate
management?

A) lifestyle modification only.

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B) No management required.

C) Ramipril.

D) Indapamide.

E) Amlodipine.

Answer → C.

• He has a stage 2 hypertension.

• Since he is < 55 YO → Start with ACE inhibitor (eg, ramipril).

Stage Criteria

Stage 1 Clinic BP ≥ 140/90 mmHg and subsequent ABPM daytime

hypertension average or HBPM average BP ≥ 135/85 mmHg

Stage 2 Clinic BP ≥ 160/100 mmHg and subsequent ABPM daytime or

hypertension HBPM average BP ≥ 150/95 mmHg

Stage 3 “Severe Clinic systolic BP ≥ 180 mmHg,

hypertension” or clinic diastolic BP ≥ 110 mmHg

• If ABPM (Ambulatory BP monitoring) or HBPM (Home BP monitoring) is ≥

150/95 mmHg (i.e., stage 2 or higher hypertension) → Always treat.

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◙ Step 1 in Hypertension Management:

√ Patients < 55-years-old → start with ACE inhibitor (A) or ARBs.

√ Patients ≥ 55-years-old or of Afro-Caribbean origin “of any age”
→ start with Calcium channel blocker.

In other words:
• White + < 55 YO → start with ACEi/ARBs as a step 1 management of HTN.
• White + > 55 YO → start with CCB as a step 1 management of HTN.
• Afro-Caribbean + any age → start with CCB as a step 1 management of HTN.

◙ Step 2 → Both: ACE inhibitor + Calcium channel blocker (A + C).

◙ Step 3 → Add a Thiazide Diuretic (D).

- Example of ACEi → Enalapril, Ramipril.

- Example of ARBs → Valsartan, Losartan, Candesartan.
- Example of CCB → Amlodipine, Felodipine.
- Examples of thiazide diuretics → chlorthalidone (12.5-25.0 mg once daily)
or indapamide (1.5 mg modified-release once daily or 2.5 mg once daily).

Answer: This patient has stage 2 hypertension, and he is < 55 years old, so →
start with an ACE inhibitor (eg, ramipril, enalapril).

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Key Remember (Regarding Hypokalemia):

166
√ Severe vomiting can cause hypokalemia.
√ Hypokalemia features include muscle weakness and cramping.
√ ECG features of hypokalemia involve:
U wave (an additional wave after the “T” wave).
Others: Inverted T wave, Depressed ST segment.

Management of hypokalemia
1) Oral or IV Potassium chloride (based on severity), e.g. if K+ <2.5 → IV.
2) Stop/ Treat the cause (e.g. stop furosemide, thiazide like diuretics).

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Key Important Notes on Hyperkalemia

167
A patient presents with both (Hyperkalemia; eg, potassium 6.9 mmol/L)
associated with broad QT complexes on ECG
AND
Bradycardia (HR is < 60 bpm).
What to treat first?

→ Treat hyperkalemia first (by giving IV calcium Gluconate 10% or calcium

chloride or calcium carbonate ).
As initial intervention, treating hyperkalemia with IV calcium -which would
stabilize the cardiac membrane and prevent cardiac arrest- is more critical than
treating bradycardia with atropine.

Notes:
• If K+ is ≥ 6.5 mmol/L (ie, severe) → treat with IV calcium (even if ECG is
normal).
• If K+ is 6 – 6.4 (ie, moderate) → treat with IV calcium (if there is ECG changes).

Key Important Note on Primary Prevention of Cardiovascular Events

168
For all people ≤ 84 YO who have QRISK3 Score of ≥ 10
Offer → Statins (eg, atorvastatin) (for 1ry prevention of CVD).

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Key Systolic murmur at the left lower sternal border worsened by Valsalva
169 manoeuvre + ECG evidence of left ventricular hypertrophy (LVH)

Think → Hypertrophic cardiomyopathy (HOCM).

Key A few days after MI:

170
• Pansystolic murmur best heard at the left lower sternal border.
• Shock (hypotension and tachycardia).
• Heart failure/ pulmonary edema (eg, bibasilar crackles).
Think → Ventricular septal defect/ rupture.

Why NOT tricuspid regurgitation (TR)?

√ Tricuspid regurgitation can occur as a complication of MI, but it develops
over weeks to months, not acutely and within a few days after MI.
√ Also, hypotension and shock are another sign of ventricular septal defect,
not TR.

Key Quick Notes to Remember:

171
◙ If QRISK3 is ≥ 10% → Start atorvastatin “regardless of lipid profile level”.

◙ High doses of Citalopram, (a SSRI), can cause prolonged QT intervals, which

can lead to Torsade De Pointes.

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Key
Ventricular Septal Rupture (VSR) Post-Myocardial Infarction
172

Ventricular septal rupture (VSR) is a rare but serious mechanical complication

that occurs following a myocardial infarction (MI). It typically develops 3–5
days after the MI due to necrosis of the interventricular septum, which leads
to a communication between the left and right ventricles.

Key Features:

√ New Murmur: A characteristic pan-systolic murmur, best heard at the left

lower sternal border (LLSB).

√ Hemodynamic Instability: VSR often leads to cardiogenic shock, evidenced

by hypotension (e.g., blood pressure 90/60 mmHg), diaphoresis, and jugular
venous distension.

√ Respiratory Symptoms: Pulmonary crackles on auscultation, indicating

pulmonary edema due to the acute hemodynamic changes.

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Diagnosis:

→ Echocardiography: This is the definitive diagnostic tool. It confirms the

presence and severity of the septal rupture and helps in planning further
management.

Clinical Context:

• VSR should be suspected in any patient who develops a new pan-systolic

murmur a few days after an MI, especially if accompanied by signs of
hemodynamic instability.

• The murmur is typically loudest at the left sternal border.

• Immediate intervention is crucial as the condition rapidly progresses, often

requiring surgical repair.

Differential Diagnoses:

Acute Pericarditis: Usually presents with pleuritic chest pain and a pericardial
rub, not a murmur.

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Dressler Syndrome: A form of post-MI pericarditis that occurs weeks after the
event, presenting with fever and pleuritic chest pain.

Left Ventricular Aneurysm: Occurs weeks to months post-MI, presenting with

heart failure symptoms rather than a new murmur.

Mitral Regurgitation: While it may present with a pan-systolic murmur, the

murmur typically radiates to the axilla.

In summary, VSR post-MI is a critical diagnosis characterized by a pan-systolic

murmur at the left sternal border and hemodynamic instability. Early
diagnosis and intervention are essential to prevent fatal outcomes.

Key Long QT Syndrome and Ventricular Tachyarrhythmia

173
Overview:
A 19-year-old male presents with recurrent episodes of syncope, particularly
during exercise. His ECG reveals a prolonged QT interval, suggesting long QT
syndrome (LQTS), which is associated with a high risk of ventricular
tachyarrhythmias, such as torsades de pointes. This condition often presents
in childhood and is triggered by physical activity, which can precipitate
dangerous arrhythmias, leading to syncope or even sudden cardiac death.

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Key Features:

• Prolonged QT Interval: Identified on ECG, which increases the risk of life-

threatening arrhythmias.
• Syncope with Exercise: Episodes are commonly triggered by physical
exertion in patients with LQTS.
• Ventricular Tachyarrhythmias: The most likely arrhythmia in this case,
associated with the prolonged QT interval and syncope.

Differential Diagnosis:

• Sick Sinus Syndrome: Causes bradyarrhythmias and syncope due to slow

heart rates, but not associated with prolonged QT intervals.
• Ventricular Ectopics: Extra heartbeats that are common in young
individuals and often benign. These are not linked to syncope or prolonged
QT interval unless very frequent.

In summary, this patient's presentation is highly suggestive of long QT

syndrome, and the likely arrhythmia responsible for his symptoms is
ventricular tachyarrhythmia such as Torsades de Pointes. Early identification
and management are crucial to prevent severe complications, including
sudden cardiac death.

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Important Note:

Torsades de pointes is a type of ventricular tachyarrhythmia that is

associated with a prolonged QT interval. It is the hallmark and most dangerous
complication of congenital long QT syndrome (LQTS).

Key Simplified Hypertension Management Summary

174

Classification of Hypertension:

1. Stage 1 Hypertension:
o Clinic BP: ≥ 140/90 mmHg.
o Confirmed by Ambulatory BP Monitoring (ABPM) or Home BP Monitoring
(HBPM): Daytime average BP ≥ 135/85 mmHg.
2. Stage 2 Hypertension:
o Clinic BP: ≥ 160/100 mmHg.
o Confirmed by ABPM or HBPM: Daytime average BP ≥ 150/95 mmHg.
3. Stage 3 (Severe) Hypertension:
o Clinic systolic BP: ≥ 180 mmHg OR
o Clinic diastolic BP: ≥ 120 mmHg.

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Stage Clinic BP ABPM/HBPM Average

Stage 1 Daytime average BP ≥

≥ 140/90 mmHg
Hypertension 135/85 mmHg

Stage 2 Daytime average BP ≥

≥ 160/100 mmHg
Hypertension 150/95 mmHg

Stage 3 (Severe) Systolic BP ≥ 180 mmHg OR

N/A
Hypertension Diastolic BP ≥ 120 mmHg

Management of Hypertension:

1. For Stage 1 Hypertension:

√ Treat if <80 years of age and one or more of the following conditions:

• Target organ damage.

• Established cardiovascular disease.
• Renal disease.
• Diabetes.
• 10-year cardiovascular risk of ≥10%.

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√ For patients >80 years of age, treatment decisions are individualized,

considering overall health, frailty, and potential risks of treatment.

√ If the patient is "completely healthy" and has no significant comorbidities,

lifestyle modifications (such as salt reduction, regular exercise, and smoking
cessation) are recommended. Antihypertensive treatment is generally not
required unless additional risk factors (e.g., organ damage or high
cardiovascular risk) are present.

2. For Stage 2 Hypertension:

o Patients <55 years: Treat with an ACE inhibitor.
o Patients ≥55 years or of Afro-Caribbean origin: Start with a calcium
channel blocker.
o If the patient's blood pressure remains above 140/90 mmHg on
treatment, escalate to step 2.

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Management of Stage 1 and Stage 2 Hypertension

Condition/Patient Type Treatment Approach

Stage 1 Hypertension

Treat with antihypertensives if one or more of the

following:
- Target organ damage.
Age < 80 years with risk
- Cardiovascular disease.
factors
- Renal disease.
- Diabetes.
- 10-year cardiovascular risk ≥ 10%.

Individualized treatment based on overall health, frailty,

Age > 80 years
and potential risks.

No comorbidities Advice on lifestyle modifications (e.g., diet, exercise, no

("completely healthy") smoking); no antihypertensive treatment unless high risk

Stage 2 Hypertension

Patients < 55 years Start with an ACE inhibitor

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Patients ≥ 55 years or
Start with a calcium channel blocker.
Afro-Caribbean origin

If BP remains >140/90 mmHg after initial treatment,

Escalation
move to step 2 treatment as in the following table.

Stepwise Drug Treatment for Essential Hypertension in Non-Diabetic Patients :

Step Patient Characteristics Treatment Options

Step 1 Age <55 Start with ACE inhibitor.

Age ≥55 or Start with Calcium Channel Blocker (CCB).

Afro-Caribbean origin

Step 2 BP uncontrolled in Step 1 Add a second drug: ACE inhibitor, CCB, or

Thiazide-like diuretic.

Step 3 BP uncontrolled in Step 2 Combine all three: ACE inhibitor + CCB +

Thiazide-like diuretic.

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Key Notes:

• Patients with diabetes: Start with ACE inhibitors or ARBs, regardless of

age or ethnicity, to protect kidney function.
• Lifestyle Modifications: Encourage lifestyle changes in all patients,
including:
o Salt reduction.
o Regular exercise.
o Stress management.
o Limiting alcohol intake.
o Smoking cessation.

Common Antihypertensive Examples:

• ACE Inhibitors: Ramipril, Lisinopril.

• Angiotensin II Receptor Blockers (ARBs): Losartan, Candesartan.
• Calcium Channel Blockers (CCBs): Amlodipine, Diltiazem.
• Thiazide-like Diuretics: Indapamide, Chlorthalidone.

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Extra Question – Resistant Hypertension:

What is the next step in managing resistant hypertension according to NICE UK
guidelines if blood pressure remains uncontrolled after trying an ACE
inhibitor/ARB, a calcium channel blocker, and a thiazide-like diuretic (ie, after
trying all steps 1, 2, and 3 but hypertension remains uncontrolled)?

Answer:
According to NICE UK guidelines (NG136), if blood pressure remains
uncontrolled after steps 1, 2, and 3, the next step in managing resistant
hypertension (Step 4) involves the following:

1. Add Low-Dose Spironolactone:

o If the patient’s potassium levels are ≤ 4.5 mmol/L, add spironolactone at a
dose of 25 mg once daily.
2. Alternative Option:
o If the patient’s potassium levels are > 4.5 mmol/L or if spironolactone is
not tolerated, consider using an alpha-blocker (e.g., Doxazosin) or a beta-
blocker (e.g., Atenolol).
3. Referral to Specialist:
o If the blood pressure remains uncontrolled despite these interventions,
refer the patient to a hypertension specialist for further evaluation and
management.

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4. Monitoring:
o Regular monitoring of potassium levels and renal function is necessary,
especially when using spironolactone.

This approach is based on the NICE NG136 guidelines for managing resistant
hypertension in adults.

Hypertension Case Study Scenarios:

Scenario 1:

Patient: A 65-year-old man presents with a clinic blood pressure of 155/95

mmHg. He has a history of type 2 diabetes and is of Afro-Caribbean origin.

Answer: Start with an ACE inhibitor (e.g., Ramipril, Lisinopril) or an ARB (e.g.,
Losartan, Candesartan).

Reasoning: For diabetic patients, ACE inhibitors or ARBs are the first-line
treatment regardless of age or ethnicity due to their kidney-protective effects.
The presence of diabetes takes precedence over ethnicity in this case.

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Scenario 2:

Patient: A 45-year-old woman presents with a clinic blood pressure of 150/95

mmHg. She has no history of organ damage, cardiovascular disease, renal
disease, or diabetes. She is otherwise healthy and does not smoke.

Answer: Recommend lifestyle modifications such as reducing salt intake,

increasing exercise, and quitting smoking.

Reasoning: In a healthy patient without risk factors or comorbidities,

antihypertensive medication is not required for Stage 1 hypertension (clinic BP ≥
140/90 mmHg but <160/100 mmHg). Lifestyle changes are the first
recommendation unless there are additional risk factors like organ damage,
diabetes, or cardiovascular disease.

Scenario 3:

Patient: A 50-year-old woman has been on Ramipril (ACE inhibitor) for 6 months
for her Stage 2 hypertension (clinic BP ≥ 160/100 mmHg), but her blood
pressure remains elevated at 160/95 mmHg. Her doctor added Amlodipine

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(calcium channel blocker), but her blood pressure is still above 140/90 mmHg
after another 3 months.

Answer: Add a thiazide-like diuretic (e.g., Indapamide, Chlorthalidone).

Reasoning: After trying an ACE inhibitor and a calcium channel blocker (Step 1
and Step 2), adding a third drug, such as a thiazide-like diuretic, is the next step
to achieve better blood pressure control.

Scenario 4:

Patient: A 40-year-old man presents with a clinic blood pressure of 170/100

mmHg. He has no significant medical history, no diabetes, and no organ damage.

Answer: Start with an ACE inhibitor (e.g., Lisinopril, Enalapril).

Reasoning: For patients under 55 years with Stage 2 hypertension (BP ≥ 160/100
mmHg), the first-line treatment is typically an ACE inhibitor unless there are
contraindications. His age and absence of other risk factors point toward this
approach.
Note: If the patient were ≥55 years or Afro-Caribbean of any age, the first-line
treatment would be a calcium channel blocker (CCB).

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Scenario 5:

Patient: An 82-year-old woman presents with a clinic blood pressure of 145/90

mmHg. She has mild frailty but no history of cardiovascular disease, diabetes, or
renal impairment.

Answer: Individualized treatment based on overall health, considering her

frailty.

Reasoning: For patients over 80 years old, treatment decisions should be

personalized. In this case, the patient's frailty means that the risks and benefits
of medication need careful consideration, and lifestyle modifications might be a
reasonable alternative if her health allows.

Scenario 6:

Patient: A 58-year-old man presents with a clinic blood pressure of 160/100

mmHg. He has no significant medical history and is of Afro-Caribbean descent.

Answer: Start with a calcium channel blocker (e.g., Amlodipine, Diltiazem).

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Reasoning: For patients ≥55 years or Afro-Caribbean of any age, the first-line
treatment for Stage 2 hypertension is a calcium channel blocker. This is because
CCBs have been shown to be more effective in these populations compared to
ACE inhibitors or ARBs.

Scenario 7:

Patient: A 52-year-old woman started on Ramipril (ACE inhibitor) for her Stage 2
hypertension. After 3 months, her blood pressure remained elevated, so her
doctor added Amlodipine (calcium channel blocker). However, she developed
significant ankle swelling after starting the CCB.

Answer: Stop the calcium channel blocker due to the side effects and replace it
with a thiazide-like diuretic (e.g., Indapamide, Chlorthalidone).

Reasoning: Ankle swelling (peripheral edema) is a common side effect of

calcium channel blockers. In this case, the CCB should be discontinued and
replaced with a thiazide-like diuretic.
The four most common side effects of calcium channel blockers are:

1. Peripheral edema (ankle swelling).

2. Gingival hyperplasia (gum overgrowth).

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3. Headache.
4. Flushing.

Key Management of Hyperkalemia

175
in Hypertensive Patients on ACE Inhibitors

Overview:

A 58-year-old man with a history of well-controlled hypertension on Ramipril

(an ACE inhibitor) presents for a routine follow-up. Recent blood tests show a
potassium level of 6.0 mmol/L (normal: 3.5-5.0 mmol/L), indicating moderate
hyperkalemia. The patient is currently asymptomatic, with normal renal
function and no significant past medical history.

Next Step in Management:

The most appropriate next step is to arrange an ECG to check for any
electrocardiographic changes that may indicate life-threatening arrhythmias
due to hyperkalemia.

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Explanation:

Even though the potassium level of 6.0 mmol/L represents moderate

hyperkalemia, the patient is asymptomatic. An ECG is necessary to assess for
changes such as:

• Peaked T waves.
• Widened QRS complex.
• Prolonged PR interval.

These changes can indicate a risk for life-threatening arrhythmias.

If ECG abnormalities are present, urgent treatment with calcium gluconate

may be required to stabilize the cardiac membrane.

Post-ECG Management:

1. If ECG is Normal (No Significant Changes):

• Stop or reduce Ramipril: ACE inhibitors like Ramipril can increase

potassium levels by reducing aldosterone activity, which promotes
potassium excretion. Discontinuing or reducing Ramipril can help prevent
further hyperkalemia.

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• Do not switch to an ARB: ARBs (e.g., Losartan, Candesartan) also increase

potassium levels by a similar mechanism and should be avoided in patients
with hyperkalemia.
• Switch to an alternative antihypertensive:
o Calcium channel blockers (CCBs) (e.g., Amlodipine) or
o Thiazide-like diuretics (e.g., Indapamide) can be considered to control
hypertension while promoting potassium excretion.
• Monitor potassium levels: Recheck potassium levels after discontinuing or
changing medications to ensure they normalize.

2. If ECG Shows Abnormalities (e.g., Peaked T Waves, Widened QRS, Prolonged

PR Interval):

• Administer intravenous calcium gluconate: This stabilizes the cardiac

membranes and reduces the risk of arrhythmias.
• Give treatments to lower potassium levels:
o Insulin and dextrose: To shift potassium into the cells.
o Nebulized salbutamol: Another method to shift potassium intracellularly.
o Sodium bicarbonate: If acidosis is present, it helps reduce serum
potassium levels.

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• Stop Ramipril: Discontinue ACE inhibitors to prevent further increases in

potassium levels.
• Do not switch to an ARB: ARBs should also be avoided as they pose a
similar risk of hyperkalemia.
• Close monitoring: Regular monitoring of ECG and potassium levels is
crucial to track improvement and prevent complications.

Summary:

First, arrange an ECG, then in both scenarios (normal or abnormal ECG):

• Discontinue ACE inhibitors like Ramipril.

• Avoid ARBs, as they also contribute to hyperkalemia.

(So, both ACE inhibitors and ARBs can cause hyperkalemia).

• Switch to safer alternatives such as calcium channel blockers or thiazide-

like diuretics.
• Continue monitoring renal function and potassium levels to ensure
effective management of hyperkalemia and maintain blood pressure
control.

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