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(Corrected|, (Updated, Lighter]
 
 
 
ith the Most Recent Recalls and the UK Guideline:
 
ATTENTION: This file will be updated online on our website frequently!
(example: ec cu) , and so on)
 
 
Key Acute Coronary Syndrome (ACS)
 
 
 
 
Patients with Ischemic Chest Pain
 
 
Perform ECG
Y
 
 
 
No ST elevation sT elevation
 
 
 
 
 
 
 
40-60%
 
 
 
 
 
; Non ST elevation myocardial
Unstable angina (UA) infarction (NSTEMI)
 
 
 
 
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Acute Coronary Syndrome
\
Lv
| To
ceo see
 
a [Acute Coronary Syndrome includes;
V ST elevation myocardial infarction (STEMI).
 
V Non-ST elevation myocardial infarction (NSTEMI).
Vv Unstable angina.
 
 
 
 
The classic and most common feature of ACS is chest pain.
 
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V Typically, central/left-sided/ substernal/ epigastric.
V May radiate to the jaw, the left arm, the shoulder.
V Often described as ‘heavy’ or constricting, ‘like an elephant on my chest’
- Itshould 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:
 
[ may appear pa
  
 
« 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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ulinves igat Ns}
v|ECG|
V {cardiac markers e.g. [troponin]
 
 
 
 
 
 
 
 
ECG in ST-elevation MI
of the STEMI as follows:
Baud SS era)
Inferior Mt U1 Ill aVF
Lateral Mi |, aVL, V5, V6
Anterior or (Anteroseptal) == V1— V4
Anterolateral MI. |, aVL, V4, V5, V6
“ © tacctookcom/plabiteys  @) @plab.keys
 
> elevated ST segment in certain leads gives a clue about the site and type
Meer ent
it Coronary
Left Circumflex
LAD (Left Anterior Descending)
LAD or Left Circumflex
*
© Plabiteyscom "1"
 
 
 
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xample|:
 
OO
oy
Inferior MI: Note the ST elevation in leads If, I and aVF wa
(Likely: Right coronary artery occlusion) ey
 
 
ECG features of Left main coronary artery occlusion [LMCA]:
V Wide spread ST depression.
V ST elevation in aVR.
Do > [Emergency coronary angi graphy.
 
 
 
 
 
 
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Occluding thrombus Complete thrombus
Non occlusive aoe Sea eee occlusion
as tissue damage & mil
myocardial necrosis Savclevationsion
Non specific ECG or new LBBB
eG ST depression +/-
T wave inversion on ieicyarcdlcandiac
Normal cardiac Ee enzymes
enzymes 5
Elevated cardiac More severe
enzymes symptoms
 
 
 
Management of ST elevation MI (STEM )
a >
(IV Morphine, 02, Nitrates, Aspirin 300 mg)
 
 
+
Heparin (either unfractionated or LMW such as enoxaparin or
fondaparinux)
 
 
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+ If the patient presents within 12 hours of the onset of the symptoms
 
 
 
 
> Primary PCI (Percutaneous Coronary Intervention) “The gold standard”
 
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”.
 
 
Se, Long-term MI Rx = 5 Drugs: Aspirin, Clopidogrel, BB, ACEI, Statins,
 
 
(aaBcrs| > 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.
 
 
 
 
 
 
 
 
v Aspirin 300 mg.
V Nitrates or morphine to relieve chest pain if required
 
 
Vv 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
umol/I, unfractionated heparin should be given.
Fondaparinux and LMWH are given Si ly, whereas
Unfractionated Heparin is given Intravenously].
   
v Second antiplatelet: e.g. Clopidogrel, Prasugrel.
 
 
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Vv Intravenous glycoprotein lib/Illa receptor antagonists (eptifibatide or
tirofiban) should be given to patients who have an intermediate or higher risk
),
and who are scheduled to undergo angiography within 96 hours of hospital
admission.
 
v Coronary angiography should be considered within 96 hours of first
admission to hospital to patients who have a predicted 6-month mortality
/%. It should also be performed as soon as possible in patients who
are clinically unstable.
 
     
 
 
 
Examples of recent exams’ question
[Example 1)
A patient presents with (acute chest pain radiating to jaw and shoulder
+ other features suggesting ischemic heart disease...) However,
ST elevation on ECG. What to Do Next?
 
 
 
> Measure Cardiac Enzymes, especially ({Troponin||
 
V If Troponin is high > |NON-STEMI = Non-ST elevation MI
 
 
 
v Immediate management
 
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> Give Subcutaneous LMWH OR Fondaparinux| + |Aspirin 300 mg
 
 
 
Notes:
Low Molecular Weight Heparin
 
Examples > Dalteparin, Enoxaparin,
 
 
x (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.
 
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Since ECG is normal and Troponin is high > Non-STEMI
> Anti-coagulation (LMWH e.g. Dalteparin, Enoxaparin or Fondaparinux).
 
 
[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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aN SH TSE
" APH avL
 
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:
 
 
V [Aspirin 300 mg}.
 
 
 
 
Vv [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:
a i SN See
fy ar we v6
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|
 
Hypotension [| Muffled Heart Sounds [J High JVP (Distended neck veins).
® Others: Dyspnea, Pulsus Paradoxus, Tachycardia
After MI > Acute pericarditis > Pericardial effusion > Cardiac Tamponade
© Traumais the most important cause of cardiac tamponade.
 
 
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N.B. Chest X-ray that shows Sree
> Think of either [EUR Msateen (OR) EERIEPeIone ners.
 
 
 
© Dx: Echocardiogram] is diagnostic
[Urgent pericardiocentesis.
 
 
e Rx
 
aCe eee OMe CLA Teta rere g)
“ae
CeCe
POPC s
ert?
bing
bet UTE Tals
Deal
 
 
 
 
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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 LIV fluid NS > bedside Pericardiocentesis.
 
 
 
Key lat Myxoma
 
o Benign tumours.
 
 
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© 75% in the left atrium.
o Tend to grow on the wall (inter-atrial septum).
o 10% are inherited > Familial myxoma
o Features:
B OC iececay — Mid-diastolic murmur, Dyspnea, Syncope,
Congestive HF.
[§Small pieces may break off and travel to arteriesfe-Wony-atulsui) kell
different parts of the body such as:
@ Lung > Can cause PE (Pulmonary Embolism)
¢ Brain >Can cause Stroke
@ Peripheries > Clubbing and Blue fingers.
a IX brillation’
 
 
 
 
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
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
lax is Deviation
 
© If QRS in lead | is up (+ve) and in lead II is down (negative) >
Left axis deviation
© If QRS in lead | is down (-ve) and in lead II is up (t+ve) >
 
Right axis deviation
 
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ae ee ea
Lead Il ae av ed ae isoelectric
Normal Left axis Right axis Right superior Indeterminate
axis deviation deviation axis deviation axis
—30° to +90° -30° to-90° +90°to +150° +150° to +270°
limb leads
 
 
 
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-90°
aVF
 
 
 
 
 
 
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Cardiology
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Lead | te
Lead Il Aka
Normal
axis
These causes are important!
Causes of Left Axis Deviation
{nferior MI
Left Ventricular Hypertrophy
Left Anterior Fascicular block (or
hemiblock)
Obese
Wolff Parkinson White Syndrome
(delta wave)
 
TL
1,
Left axis
deviation
Right axis
deviation
Causes of Right Axis Deviation
Lateral MI
Right Ventricular Hypertrophy
Left Posterior Fascicular Block (or
hemiblock)
Thin, Tall, Children
Chronic Lung Disease
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 | is up and
Lead II is down) or right axis deviation (Lead | is down and Lead Il is up) and
the causes of each (in the table above).
 
 
Key
 
Types of heart block
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 | = Wenckebach)|
 
 
 
> Progressive prolongation of the PR interval
 
 
[type 2 (Mobitz u)
> PR interval is constant but the P wave is often not followed by a QRS
complex.
 
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[thi ‘d degree (complete) heart block)
* There is no association between
 
 
 
First degree AV block
‘Second degree AV block (Mobitz! or Wenckebach)
SSS
Third degree AV block with junctional escape
4
CA
 
 
 
 
 
 
 
 
 
 
 
 
 
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Management;
 
 
 
@ 1% 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 (3 degree heart block)
> require permanent pacemaker
 
 
For your knowledge:
| square = p.o4 seq.
© 1 large square contains 5 small squares = p2 seq
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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Key
Atrial Fibrillation - fibrillatory waves
Atrial Flutter - sawtooth pattern
 
 
¢ Agents used to control rate (Rate Control) in patients with
° Beta-blockers (e.g. atenolol, bisoprolol, metoprolol) > First line but
Contraindicated in Asthma
° Calcium channel blockers [non-dihydropyridine CCB] (e.g. diltiazem,
verapamil) > used in Asthmatic patient.
° 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)
 
 
 
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v If haemodynamically unstable (e.g. SBP < 90) > [ardioversion| (Shock)
° Atrial Flutter management ~ |Cardioversion (Shock)
 
 
 
 
 
 
Key
 
entricui lar tachycardia|
 
V Ventricular tachycardia (VT) is broad-complex tachycardia originating from a
ventricular ectopic focus.
v It can develop into ventricular fibrillation and therefore requires urgent
treatment.
v P wave might be present or absent.
N.!
 
© ECG showing broad complex tachycardia in a (still) conscious patient even
if semiconscious + atrial activity and “haemodynamically ”
> Ventricular tachycardia] > Give famiodarone|He stable!
  
 
 
© ECG showing ventricular tachycardia in a haemodynamically u le (e.g.
SBP S 90) patient -> [DC cardioversion = shock. He is unstable but has a pulse.
 
 
 
 
 
© If the patient is
> Mentricular Fibrillation] > Defibrillation = Asynchronized shock
 
 
 
 
 
 
 
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[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.
 
tachycardia (VT) clinically.
Ventricular Tachycardia
 
 
 
° Ventricular fibrillation is the most important shockable arrhythmia}.
 
© Hypokalemia (J K’*) is the most important cause of ventricular
Ventricular Fibrillation
Atrial Flutter
avlwwlwhann
 
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Atrial Fibrillation Palpitation, Tachycardia, Dyspnea, Fibrillatory
waves on the ECG, Irregularly irregular rhythm
 
 
 
> Give Beta-Blocker,
If Asthmatic > Give Calcium Channel Blocker}.
 
 
 
Atrial Flutter “Fluttering Feeling in the chest”, Sawtooth waves
on the ECG > [cardioversion]
Ventricular Regular and Fast rhythm.
Tachycardia Ongoing lightheadness, Palpitations, Chest pain
> Give [Amiodarone|
 
If unstable (SBP <90, ) consciousness)
 
> |immediate Cardioversion|
 
 
 
 
Ventricular Older adult, Sudden collapse, Not breathing,
Fibrillation Unconscious, No pulse
 
> [’Immediate Defibrillation”
 
Sinus Lightheadness, hypotension, vertigo, syncope,
Bradycardia dizziness.
N.B. Sinus bradycardia is normal in young athletes.
 
 
 
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& The first drug of choice for Symptomatic
Bradycardia (Dizziness, feeling unwell) > Atropine
 
 
 
 
Sinus Physiological situation (exercise, stress, anger).
Tachycardia Hx of infection.
WPWS Delta wave on the ECG
 
 
 
Key
 
 
 
Management of Congestive Heart Failure,
 
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 !
in patients with le!
   
+ ACE-inhibitors
+ Beta-blockers
+ Angiotensin receptor blockers (ARBs)
« Aldosterone antagonists (e.g. Eplerenone, Spironolactone)
 
+ Hydralazine with nitrates
 
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How to manage CHF? (Important)
© For all patient, for symptomatic relief and to reduce the volume overload
> Diuretics (e.g. Furosemide I Lasix ™)
© Start with either an ACE inhibitor or Beta blocker (one drug at atime).
 
© |f the symptoms persist > Add the other one (ACEi or BB).
© If the symptoms still persist > Add Spironolactone
Side Note
Spironolactone is a p
  
agi
VA Ai: 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 AC! h DM in your
 
© 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
 
gin 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
 
 
 
 
 
> PC (Percutaneous Coronary Intervention)) “The gold standard”
 
+ If Not, or PCI is unavailable > Thrombolysis (Alteplase).
 
a (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 Ova' il
V The foramen allows blood to pass from the right atrium to the left atrium.
V 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.
v In most of these individuals, the PFO causes no problems and remains
undetected throughout life.
 
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v 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.
v [Transesophageal echocardiography, is considered the most accurate
investigation to demonstrate a patent foramen ovale.
vA 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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PFO: blood passes from Rt atrium > to Lt atrium
 
 
 
 
Key | [Important Complications of Ml
* This most commonly occurs due to patients developing ventricular
1 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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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)
@ If the symptoms persist > Add the other one (ACEi or BB).
@ If the symptoms still persist > Add Spironolactone (Aldosterone
Antagonist).
 
 
© 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)
 
 
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2) Administer 02.
 
PaRICaRaHIS “important v"
© Occurs within 48 hi 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.
BA full-dose ) should be used (aspirin, 2-4 g/d; ibuprofen 1200-1800
mg/d; indomethacin 75-150 mg/d); treatment should last at least 7-14 days.
 
 
 
DRESSIERSISRAROME “irrportant v"
@ 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
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.
 
 
 
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@ ECG: Widespread Saddle Shaped ST Elevation + PR Depression.
 
@ 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.
 
 
& Rupture of the interventricular septum usually occurs in the first week after
a Ml attack and is seen in around 1-2% of patients.
@ Features: acute heart failure associated with a pan-systolic murmur.
@ An echocardiogram is diagnostic and will exclude acute mitral regurgitation
which presents in a similar fashion.
@ Urgent surgical correction is needed.
 
 
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(eRHPETnTPaINPegUPTTOHEMICAR): “important v” pansystolie murmur
@ Occurs 2-15 days after the MI (Mostly inferior Ml).
@ 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 edemal.
@Dx—> Echocardiogram.
@ Treatment — vasodilator therapy but often requires emergency surgical
repair.
 
 
 
 
important Note:
 
 
 
 
® Pericarditis (Can occur as a Complication of Ml, 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,
 
 
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+ 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
Heart Sounds, High JVP).
 
 
Key
13 Types of MI / Sites of Myocardial Infarction
(ARREHISEIM (Left Anterior Descending LAD)
seen
[ieee ST elevated leads onECG | The likely Occluded Artery
Inferior ML 11M, aVF Right Coronary
Lateral MI 1, aVL, VS, V6 Left Circumflex
Anterioror (Anteroseptal) V1 V4 LAD (Left Anterior Descending)
AnteroLateral Ml |, aVL, V4, V5, V6 LAD or Left Circumflex
 
*H © taccrckeomblstites @)@rkb1tes © Plabtieyscom —*
 
 
 
 
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© Copyright plab1keys.com (Constantly updated for online subscribers)
 
 
Wide spread ST depression (+) ST elevation in aVR
 
 
 
 
> [Left main coronary artery [LMCA] occlusion]
 
 
> Emergency coronary angiography|
 
 
Key
14
 
 
 
 
 
For Theoretical Exams}
 
5 Any patient presents with S
 
> Give MONA (Morphine, O2, Nitroglycerin, and then:
 
 
 
 
> Send immediately for |PCI) (Percutaneous Coronary Intervention).
 
 
 
 
* If PCl is not obtainable = [Alteplase.. [i.e. thrombolysis]
 
 
 
 
+ If PCI and Alteplase are not given, pick >|Streptokinase.. [i.e. thrombolysis].
 
 
5 Any patient presents with N:
 
> After giving morphine, 2 medications should be given immediately:
v [Oral Aspirin 300 mg (+)
Vv SC |Low molecular weight heparin| “or” SC |Fondaparinux.
 
 
 
 
 
 
 
 
 
 
i.e. (widespread ST depression + ST elevation in aVR):
 
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after giving morphine > [Emergency coronary angiography,
 
 
 
 
Key
15
@ The first drug of choice for BymptomaticBradycardil = tttS*«s@
(Dizziness, feeling unwell) is
> Atropine
(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}.
© 2" Line > Dopamine.
© 3" Line > Epinephrine.
4 N.B. If the question was “the next best step” (or) “the initial line’, the
Answer will be >
 
 
Key
16
 
v Hypotension,
Vv Muffled “faint = weak” Heart Sounds,
V High Jugular Venous Pressure [JVP] (= Distended neck veins).
> Cardiac Tamponade.
 
 
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> Echo for Dx and Pericardiocentesis for Rx
 
 
 
 
 
 
 
Key
17
 
Infective Endocarditis (IE)
New Murmur + Fever > think of [infective Endocarditis (IE)
+ Malaise, Rigors.
The initial step > Bieealeuiture v then > Echo]
VE ail
SA previous episode of endocarditis > the strongest risk factor.
& Rheumatic valve disease.
@ Prosthetic valves.
@ Congenital heart defects.
@ Intravenous drug users (IVDUs: typically causing tricuspid lesion).
CR RO Le ech cued
- Staph. Aureus is the commonest cause of IE in general.
 
- Staph. Epidermidis is the commonest cause after prosthetic valve surgery.
 
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- Strept. Viridans (especially sterpt. Mitis and strept. Sanguinis) are the
commonest cause in people with poor dental hygiene or following a dental
procedure.
CM Py ued
Infective endocarditis is diagnosed in any of the following situations:
* 2 major criteria, or
© 1 major and 3 minor criteria, or
© 5 minor 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)
 
 
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@ Positive echocardiogram (oscillating structures, abscess formation, new
valvular regurgitation or dehiscence of prosthetic valves). (Or)
& New valvular regurgitation
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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Splinter
sae Osler node
Roth's spot Janeway lesion
  
itial “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 +a new heart > suspect
and order until proven otherwise.
 
 
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Example 1|:
Aman 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 faneway lesions|(minor criteria of infective
endocarditis).
¢ Likely > Infective endocarditis}
> Do Blood culture then Echocardiogram
 
 
 
 
 
 
 
18
 
 
 
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“To determine the need to anticoagulants”.
 
 
 
 
 
 
 
 
 
Cc Congestive heart failure 1
(or LV dysfunction)
H Hypertension BP>140/90 1
or treated hypertension on medication
Ao Age =75 years 2
D Diabetes Mellitus |
So Prior Stroke or TIA or 2
Thromboembolism
Vv Vascular disease (e.g. MI, PVD, Aortic plaque) |
A Age 65-74 years |
Sc Sex category (female gender) I
 
 
 
 
 
 
 
Give Warfarin or DoAC (Direct-Acting Oral AntiCoagulants, such as
Apixaban, Rivaroxaban, Edoxaban, Dabigatran) To:
\ Consider giving Warfarin or DOAC to Men who score 2 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.
 
 
The
in apa
The
patien
The
@ The
patien
 
 
|cHA2Ds2-vase score’ is used to determine the need to anticoagulants
tient who has atrial fibrillation. V important
 
 
|ABCD2 score} (Prognostic) is used to identify the risk of future stroke in
its who have had a suspected TIA in the following 7 days. V Not advised
to be used now according to the recent 2019 CKS guidelines.
 
 
'HAS-BLED score estimates the risk of major bleeding for patients on
 
anticoagulation for atrial fibrillation.
 
 
 
DRAGON score predicts the 3-month outcome in ischaemic stroke
its receiving tissue plasminogen activator (tPA) e.g. alteplase.
 
 
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& The jarisK2 score] is used to determine the risk of a cardiovascular event in
the next 10 years.
 
 
 
Key
19
 
Pulmonary edema
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.
Desaturation (Low O2 Sat.),
Dyspnea (SOB),
Orthopnea (SOB worsens when lying down),
Auscultation > Crepitations “Crackles = rales”.
Tachycardia.
While aces usually shows features of pulmonary edema (The single
most appropriate Investigation), the underlying cause requires
 
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to be identified (e.g. Congestive Heart Failure, Complication
of MI > Acute Mitral Regurgitation due to papillary rupture, Ventricular
aneurysm, ...etc.)
@ The Most Appropriate Investigation > (Chest X-Ray}. “imp v”
& The Investigation Needed to Identify the Underlying Cause > [Echo “impv”
 
 
[Mona] (But the last A -Aspirin- is replaced by F -Furosemide-):
> Morphine, O02, Nitrates, i
 
 
 
 
 
> (Lasix).
1) Sit the patient up (Popup position) and give O2 (aim for O2 saturation of
2 95%, or 2 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.
Congestive Heart Failure — Heart unable to maintain circulation
Pulmonary Edema — Fluid build up in lungs
Pulmonary Edema
 
 
 
 
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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|
 
Important:
If pulmonary edema is cuased by existent hi
(Morphine, O2, Glyceryl Trinitrates,
 
 
 
 
 
Pulmonary Oedema -> Kerley Lines (Expansion of the interstitial space by fluid)
 
2, 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
ra
 
 
[The Typical Presentation of Acute MI (75% of cases)|:
 
@ 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:
Mf unequal pulses in upper ims
NAHx of Marfan Syndrome (tall, long slender limbs and fingers).
SAHx of Ehlers-Danlos syndrome/ turner syndrome
Se ee ee
WAHTN is the most important risk factorf
WaThe patient presents with Hypotension, SOB, tachycardia, sweatingh
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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.
eln settings > |
   
© Stanford classification of Aortic Dissection:
type
type B: descending aorta, distal to left subclavian origin, 1/3 of cases
 
ing aorta, 2/3 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
22
 
 
 
Left Bundle Branch Block (LBBB)
 
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:
SESTERES Shape) RPSREEORENORS sally n Lead), av. and ve but
not always.
(ibeepinvertedl(Negative)IGRS: usually in lead (v1).
@ Left Axis Deviation (Not always)
MU SSeS LUMO
v
tm “M” shaped QRS in Leads: 1, aVL, V6.
@ Deep (Negative) “Inverted” QRS in V1.
 
 
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Key ||[Ruptured Abdominal Aortic Aneurysm (AAA)
 
@ |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.
Git is a Ug es eutay: therefore, immediate jUltrasound[a the
most appropriate initial investigation.
@ If no U/Sin the options, go for Gen abdomen.
 
5 Screening for Abdominal Aortic Aneurysm (AAA) in the UK:
Vv Men only.
v Once only.
V In 65" year.
Vv 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 atime)
© If the symptoms persist > Add the other one (ACEi or BB).
e If still symptomatic > Add spironolactone “potassium sparing diuretics”.
 
. ana: the patient with Heart Failure has Diabetes, we start with
(e.g. Ramipril) instead of Beta-Blockers.
 
 
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.
 
 
 
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Key
25
[Coronary Artery Dominance}
 
» The artery that supplies the Posterior Descending Artery (PDA) determines
the coronary dominance.
» In 5%| of the population, the Right coronary artery (RCA) gives off the PDA
(Right Dominant).
 
 
 
 
 
 
+ In |159%| of the population, the left circumflex! gives off the PDA (Left
Dominant).
 
 
 
 
@ Hence, the artery that has artery dominance is the (RA), as it gives off the
PDA in 85% of people.
 
 
 
 
Key
26
 
 
Dressler’s syndro me|
@ 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.
@ It is characterised by a combination of fever, pleuritic pain worsens on
inspiration and on lying flat, pericardial effusion and a raised ESR.
 
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BECG > \
 
1 + 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|
 
 
 
 
 
[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 > |HypeRkalemial.
@ Loop diuretics, Thiazide like diuretics > HypOkalemial.
 
 
 
 
@ The ECG changes in HypUkalemia > U Wave
 
 
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Management of hypokalemia
 
U wave (hypokalemia) > an additional wave after (T-wave)
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).
 
 
 
 
 
 
 
Loop Diuretics (e.g. Furosemide)
° Thiazide-like diuretics
(e.g. bendroflumethiazide, indapamide)
© Vomiting and Diarrhea
 Villous Adenoma
¢ Renal tubular failure
* Cushing Syndrome
© Conn’s disease (1ry hyperaldosteronism)
 
© ACE inhibitors (e.g. enalapril).
* ARBs (e.g. losartan).
© Potassium-sparing diuretics
(e.g. Spironolactone/ Eplerenone)
* CKD/ Acute renal failure
© Addison’s (1ry Adrenal Insufficiency).
© Congenital Adrenal Hyperplasia (CAH).
 
 
 
 
Key | [Paroxysmal Supraventricular Tachycardia
28
E (Narrow-Complex SVT)
 
 
 
 
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= Usually in young patients
= Presents with Palpitations, Light-headedness, Recurrent, Young.
Management: imp V
* initia tine)
> (Carotid massage|.
+ Not improved?
> Intravenous jadenosine (6mg Rapid IV Bolus),
 
 
 
 
still not improved? — give additional 12mg adenosine,
still not improved? — give another 12mg adenosine.
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
> R-Blockers or Radio-frequency ablation.
 
In summary:
 
 
 
 
 
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B Carotid Massage and Valsalva Manoeuvre
B IV Adenosine 6 mg
8 IV Adenosine 12 mg
8 IV Adenosine 12 mg
8 Cardioversion (Shock)
errant eye
(Narrow/Complex\ViI),
1+ line > Carotid Massage
& Valsalva Manoeuvre.
2nd fine > 1V Adenosine. ~~
3r¢ ine -> Cardioversion.
 
 
 
 
 
Polymorphic (Broad-Complex) Ventricular Tachycardia
E Torsades De Pointes (TDP)
 
 
& Beat-to-beat variations with no uniform pattern of ventricular contractions.
 
 
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@ Broad QRS (except in resting status), Prolonged QT, Fainting episodes,
Patient might be a young athlete, Recurrent.
& Treatment - |v Magnesium Sulphatd > |V Magnesium Sulphate.
N.B. Verapamil should NOT be used in VT.
& =a
Ventricular sl achycardia
Ss Say
eek
eens
lly
ECG Indicating Torsades de Pointes
 
 
 
Key
29
 
For patients who present with STEMI, give MONA (Morphine, 02,
Nitroglycerin, Aspirin) and send immediately for Pa (Percutaneous
Coronary Intervention).
 
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en in the options?
Pick > Alteplase “preferred” or Streptokinase| (Tissue Plasminogen Activator)
®
 
 
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 LIMWH OR Fondaparinux{ + [Aspirin 300 mg]
 
 
 
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Patients with Ischemic Chest Pain
Perform ECG
 
 
 
 
y
 
NoST elevation ST elevation
ED
Non ST elevation myocardial ST elevation myocardial
infarction (NSTEMI) infarction (STEMI)
 
 
 
 
 
 
 
 
¥
 
 
Unstable angina (UA)
 
 
 
 
 
 
 
 
 
 
 
Key
31
 
6 weeks after MI, a patient returns with SOB when walking long distance
and his ECG shows ST elevation in V1-V5 leads.
(Persistent ST elevation post-MI > Think of:
 
@ 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.
 
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& 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.
 
 
Key
32
 
Hypertension Management
Hypertension classification
Stage Criteria
Stage 1 Clinic BP > 140/90 mmg 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”
 
 
clinic diastolic BP 2 110 mmHg
Keys:
ABPM ~ Ambulatory Blood Pressure Monitoring.
 
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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|
should not be forgotten:
© 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:
 
  
diabetes ora. 10-vear. cardiovascular risk equivalent to > 20%.
& Note: Ifa patient is completely free and has a stage 1 Hypertension
 
 
 
> Lifestyle and Diet Modification + review (Follow up).
 
 
 
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& 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
 
 
> {Consider a specialist referral to exclude secondary causes of the HTN.
 
If ABPM or HBPM 2 150/95 mmhg (i.e. confirmed stage 2 or higher
hypertension) — [We¥eset
The Steps of The Management of Hypertension
* Patients < 55-years-old — start with ACE inhibitor (A) or ARBs.
 
* Patients > 55-years-old lor] of Afro-Caribbean origin “of any age”
= start with Calcium channel blocker.
In other words:
 
 
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White + < 55 YO) > start with lacei/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 ece} as a step 1 management of HTN.
 
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 > |ACEil + kcal
+
[Thiazide like Diuretid (A+C+D).
 
- Example of ACEi > Enalapril.
- Example of CCB > Amlodipine.
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.
 
 
 
 
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* 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.
¢ If further diuretic therapy is not tolerated or is contraindicated or
ineffective, consider an alpha- or beta-blocker.
ll 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) k 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
 
 
 
 
 
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lypertension + Diabetes (V. Imp.
@ Always treat hypertension in a DIABETIC patient with
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 >
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
33
 
 
Postural Hypotension (Orthostatic Hypotension)
 
- Adrop in systolic blood pressure of at least 20 mm Hg within three
minutes of standing.
 
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ww.plab1keys.com (Constantly updated for online subscribers)
 
 
 
- ora drop in diastolic blood pressure of at least 10 mm Hg within three
minutes of standing.
- BP is measured on lying position, then on standing position.
 
 
- Dx: |Monitor BP).
 
 
@ Postural hypotension is common in elderly people especially those who
take multiple drugs (/Polypharmacy) and those with hypertension.
 
 
 
 
® Anti-hypertensive medications can cause postural hypotension as well.
& The
(Vascular resistance) decl
hypertension.
 
 
5 that control HR (Heart Rate) and VR
ith age, particularly in patients with
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.
 
 
 
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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}
Blood pressure moni a
Management >
 
 
 
 
 
 
Key
34
Again, any patient of any age and any ethnic group presents with
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
35
 
 
 
 
(Absent “P” wave on ECG + [irregularly Irregular Rhythm|
 
 
+ Palpitation|
 
Diagnosis? > [atrial Fibrillation).
Management?
V First line >
v If asthmatic > Avoid beta-blockers and give
v If the patient has associated HF > give |digoxin.
+
 
 
 
beta-blockers,
 
 
 
 
calcium channel blockers}.
 
 
 
 
 
 
> Calculate ‘CHAZDS2-VASCc Score (Key number 18) and accordingly:
 
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> Give (Warfarin) or (DOAC) or nothing according to the Cha2ds2vasc score.
& Examples of DOAC “Direct-Acting Oral AntiCoagulants” -important v-
 
(Apixaban]| Rivaroxaban, Edoxabanl, [Dabigatran)’.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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 |Ment r Ectopics|
37
 
= Three-beat patterns = Ventricular Trigeminy.
@ Asense 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.
 
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@ 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
38
 
 
 
{The Typical Presentation of Acute MI (75% of cases)|
 
& 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.
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.
 
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Key
39
Long term medications post-Myocardial Infarction = 5 Drugs
Aspirin, Clopidogrel, 8- Blockers, ACEi, Statins
AABCS > Aspirin, ACEi, BB, Clopidogrel, Statin (e.g. Atorvastatin)
 
 
Key
40
 
A patient with chronic heart failure developed gout. A medication for his
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.
Important Notes
& Never give NSAIDs (e.g. Ibuprofen) nor selective COX-2 inhibitors (e.g.
Celecoxib) to the following patients:
(Chronic Kidney Disease, Chronic Heart Failure, Ischemic Heart Disease).
 
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@ 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
41
 
in-Hospital Cardiac Arrest algo hy]
If. No Signs of Life (i.e. No breathing, No detectable Pulse):
1) Ring the emergency bell and call resuscitation team| (Code Blue) first. Then >
2) Start CPR30:2). Then >
3) (Get defibrillator. Then >
4) ALS when the resuscitation team arrives)
 
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Collapsed/Sick patient
Shout for help and
i Ce Ce Tue
Are there signs of life?
(Breathing, Pulse, Movement)
 
ABCDE — recueciation _fardovertote,
team
 
 
Key
42
In STEMI patient, what if PCI is not given in the options?
Pick > Alteplase| “oreferred” or Streptokinase| (Tissue Plasminogen Activator)
= ie. [Thrombolysig,
 
 
Key
 
 
 
Diabetic patients may develop “Silent MI” i.e. painless MI. Thus, they may
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.
 
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Key |A scenario to test your knowledge on a previous topid
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?
Eee errr
 
Sp I
(EEE ESE IESE IE Eee Bee
 
 
Answer:
 
 
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ardiology] ©Copyright www.plabikeys.com (Constantly updated for online subscribers)
 
 
Cia
fathetke <
@ Irregularly Irregular Rhythm.
Absent “P” wave.
1 Fine Fibrillatory waves.
 
Palpitation, Tachycardia, Dyspnea (SOB), Fibrillatory waves on
e ECG, Irregul im = Absent “P” wave.
    
 
Key Remember;
 
45
 
 
@ In Supraventricular tachycardia] (Narrow QRS Complex)
 
If thi
gin
> We firstly perform {Carotid Massage] and WValsalva Manoeuvre}.
 
 
 
 
 
 
 
is fails > We give |lV Adenosine.
 
 
 
 
 
polymorphic ventricular tachycardia| (i.e. torsade’s de pointes)
 
~> IV magnesium sulfated.
 
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Plabikeys.com861 P ogy] ©Copyright www.plabikeys.com (Constantly updated for online subscribers)
 
P wave bued iT wave
Wr
 
@ First line > Carotid massage
and Valsalva Manoeuvre
Then > IV Adenosine
 
 
 
Key Beck’s Triad in Cardiac Tamponade|
46 Hypotension,
Muffled Heart Sounds,
High JVP (Distended neck veins).
© Trauma (e.g. stab in the chest) is the most important cause for cardiac
tamponade.
 
 
 
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© Dx: Echocardiography is diagnostic.
 
 
e Tx:
x
 
 
Urgent pericardiocentesis|.
 
 
Key ||Remember that:
47
 
 
 
 
@ In Atrial Myxoma| > Mitral valve obstruction > Mitral Stenosis
 
 
 
 
> Early or Mid-diastolic murmur, Pyspneal, byncope|
 
 
 
 
@ 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)
 
 
Therefore, in a patient with Hx of syncope, SOB, Pulmonary Embolism and
early-mid diastolic murmur — Think of [Atrial Myxomal.
 
 
 
 
 
 
Key ||Points on Alcohol
48
 
UK guidelines recommend that a person should drink
 
- No more than 14 units a week,
 
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- 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
49
 
 
 
 
JA scenario to test your knowledge on a previous topid
 
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.
> The likely Dx > [Mitral Regurgitation).
> The likely Cause > |Rupture of Papillary Muscles).
 
 
 
 
 
(CRPETRTPaINPegUPaTTGHOMICAR): “important v" pansystolie murmur
@ Occurs 2-15 days after the MI (Mostly inferior Ml).
 
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@ Due to — Ischemia or ri of the mitral valve.
 
@An early-to-mid systolic or Pansystolic murmur is typically heard.
 
 
 
 
 
 
 
@ May present with |Hypotension|, [Tachycardia] and Pulmonary edema.
gDx—> Echocardiogram.
@ Treatment — vasodilator therapy but often requires emergency surgical
repair
 
 
 
 
 
Key
50
 
 
[A scenario to test your knowledge on a previous topid
 
2 days after MI, an elderly patient presents with fever and chest pain. ECG
shows ST elevation with upward concavity.
  
> cute Pericardi
PREREMEIPERCGREY “imcortant v"
@ Occurs within 2-
 
is 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.
 
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BA full-dose N ) should be used (aspirin, 2-4 g/d; ibuprofen 1200-1800
mg/d; indomethacin 75-150 mg/d); treatment should last at least 7-14 days.
 
 
 
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.
 
 
 
 
 
IMI Analgesia while in an ambulance (Pre-Hospital)
 
1) Glyceryl Trinitrate (GTN) sublingual or spray.
2) + Opioids (
 
.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.
oaWhy IV and not IMy
v IM absorption is unreliable +
 
 
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v 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.
# An ECG showing broad complex tachycardia in a (still) conscious patient +
atrial activity > Ventricular tachycardia > .
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 02.
3) If the patient is hemodynamically unstable: Shock followed bylv
Amiodarone followed by further Shocks if needed.
@ N.B. HypOkalemia is the most important cause of ventricular tachycardia
(VT) clinically.
 
 
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Key | Treatment of Cardiac Tamponade > Pericardiocentesis.
53
 
 
Key | Tall Tented T-wave > HypeRkalemia.
54 & U-wave > HypOkalemia.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Vi
ve
aye
i as:
| i a
f\
LAT fe Sa
‘Vel Vented VeWare
aRtedcanta Plabi eyscom|
 
 
 
 
 
 
 
 
 
 
 
 
 
Important Causes of HypeRkalemia:
ACE inhibitors, Spironolactone, NSAIDs, Renal Failure, Acidosis,
Adrenal Insuffici , Addison's disease.
Firstly > Protect the cardiac membrane by giving IWiealeium|eluconate (OR:
Calcium Chloride).
Then > Reduce the serum Potassium by giving Insulin with Dextrose OR sometimes
salbutamol inhalation.
ot ©) tactoctsomettton G@riabikoo © Plabtteyscom *H#
 
 
 
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ardiology] ©Copyright
 
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Key
55
 
[A scenario to test your knowledge on a previous topid
 
45 Y/O African patient has BP 160/90 on three separate occasions.
What is the initial line of treatment?
> {Calcium Channel Blocker (CCB)
 
(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 kecB| as a step 1 management of HTN.
 
 
 
 
(Any ethnicity + Any age + Diabetes|
 
> start with ceil ARBs|as a step 1 management of HTN
 
 
Key
 
[Remember that}
 
 
 
 
 
 
LBBB is associated with acute Ml.
 
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hy a Af Lat
=" ralebed QRS in Leads: |, aVL, V6.
@ Deep (Negative) “Inverted” QRS in V1.
| ©
(acca isc) N\A A ire
 
 
Key
57
 
Heart Murmurs,
 
 
 
 
 
 
Defect Where is it Symptoms
heard?
Aortic Ejection Systolic Right 2°¢ICS just Dyspnea on
si . lateral to activity, Anginal
persis sternum, radiates chest pain,
to Carotid artery syncope
Aortic Early Diastolic Right 2™71CS just Symptoms of
Regurgitation lateral to Heart Failure
sternum
Pulmonary Ejection Systolic Left 2"¢ICSjust Systemic
Stenosis lateral to Cyanosis
 
 
 
sternum, radiates
 
 
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Pulmonary Early-Diastolic
Regurgitation
Mitral Stenosis Mid-Late
Diastolic, with
opening click
Mitral Pan-Systolic
Regurgitation
Tricuspid Diastolic Rumble
Stenosis
Tricus Pan-Systolic
 
 
Regurgitation ‘opyright
plab1keys.com
 
Example!
 
 
> Mitral Regurgitation
 
to left shoulder
of infraclavicular
area
Left 2°4 ICS just
lateral to
sternum
Apex (left 5 ICS
midclavicular
line)
Apex (left St" ICS
MCL), radiates to
Axilla
4-5" ICS over
the left sternal
border.
4-5 ICS over
the left sternal
border.
Symptoms of
Right-Sided Heart
Failure
Symptoms of
Heart Failure
Symptoms of
congestive Heart
Failure; edema,
Ascites
Fluttering
Discomfort in the
neck
Symptoms of
Right-Sided Heart
Failure
A patient with Hx of MI presents with Orthopnea (Cannot lie down flat),
Bibasilar crepitations, Pan-systolic murmur.
 
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> do Echi
 
 
 
 
Key ||A scenario to test your knowledge on a previous topid
58
   
A Young adult presents with f od
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)
 
 
 
@ 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.
 
 
 
5 Treatment] — |v Magnesium Sulphate
 
N.B. Verapamil should NOT be used in VT.
 
 
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[Polymorphic Cert ‘complex
VentricularysTachycardia’
es Say
Ee
1V Magnesium Sulphate
clbry
 
 
Key
59
 
An elderly patient with a Hx of stroke presents with exertional dyspnea.
ECG shows Atrial Fibrillation. Chest X-ray shows Straight left heart border.
> Mitral Stenosis).
 
+ 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 I ial h hy; therefore, CXR shows Straight left
side heart border) > Blood returns Back to lungs > Pulmonary Congestion >
Right Ventricular Failure (Hepatomegaly, Ascites, Oedema)
   
 
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© Copyright
 
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Features
© Mid-late diastolic murmur (best heard on expiration) “low pitched”
© Loud $1, 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
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
 
 
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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) > B-Blockers (e.g. Metoprolol)|
 
 
 
Key | \ Ejection Fraction (+) | Septal Wall Thickness >
*" | Ditated Cardiomyopathy
@ 7 Ejection Fraction (+) 7’ Septal Wall Thickness >
 
 
 
 
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* 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
SS Causes often considered separate entities
* alcohol: may improve with thiamine
* postpartum
* hypertension
S Other causes
* 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
 
 
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Inherited dilated cardiomyopathy
* around a third of patients with DCM are thought to have a genetic
predisposition
* alarge number of heterogeneous defects have been identified
* the majority of defects are inherited in an a
although other patterns of inheritance are seen
 
ant fashion
 
 
Key
62
 
PUTA ACS Latere Cat A
 
In Supraventricular tachycardia (Narrow-Complex) (SVT)
 
 
4 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 [Adenos | 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.
 
4 If the patient is Jlaaemodynamically Unstable| > start with Cardioversion.
 
 
 
 
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In Polymorphic Ventricular Tachycardia (Broad-Complex)|
= (Torsade De Pointe)|
> Give IV MgSO4 (Magnesium Sulphate)
 
Ue
- Start with B-Blockers (e.g. Metoprolol).
- If Asthmatic patient > Calcium Channel Blockers.
- If Associated Heart Failure > Digoxin.
TA eu Lae Coah ec Li Leiee
Give Amiodarone.
 
 
Haemodynamically Unstable| — e.g.
\ Hypotension (SBP < 90),
\ Loss of Consciousness,
Others:
V HR > 150.
\ Severe dizziness or syncope.
V Ongoing chest pain.
 
 
 
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V increasing SOB.
 
— Immediate DC Cardioversion\.
 
 
 
 
[Any arrhythmia in an unstable patient + DC Cardioversion]
 
 
 
Key
 
An elderly patient suddenly fell unconscious, he recovered completely
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.
The best Investigation > A2lead ECG
Analysis and Causes of Falls.
1) Cardiac cause (e.g. Arrhythmia).
2) Postural (Orthostatic) Hypotension.
3) Hypoglycemia.
4) Seizure.
 
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