MEDICOSHARE NOTES FOR IMM & FCPS-II MEDICINE CARDIOLOGY SECTION

PREVENTION OF CARDIAC DISEASES: [CMDT 2023]

Several risk factors increase the risk of coronary artery disease. HIGH YIELD POINTS
These risk factors can be divided into modifiable and non-
modifiable risk factors.
 Smoking cessation
results in the
Modifiable risk factors. Non-modifiable risk
factors.
greatest immediate
 Hypertension (most  Age (> 45 for men improvement in
common). & > 55 for women). patient outcomes
 Diabetes mellitus (most  Gender. for CAD.
serious).  Family history of
 Hyperlipidemia. premature CAD.  Revascularization
 Cigarette smoking.  Renal disease. will not help in
 Obesity Takotsubo
cardiomyopathy,
SMOKING CESSATION: [CMDT 2023] since coronary
arteries are normal.

 Smoking is the second leading cause of disability adjusted life-years  Best mortality
lost overall and leading cause among men. benefit in chronic
 Almost 40% of smokers attempt to quit each year but only 4% are angina: aspirin and
successful.
beta blockers.
 Factors associated with successful cessation include having a rule
against smoking in the home, being older and having greater
education.
 Several effective clinical interventions are available to promote
smoking cessation, including counselling, pharmacotherapy and
combination of the two.
 Nicotine replacement therapy double the chance of successful
quitting. The nicotine patch, gum, and lozenges are available over the
counter and nicotine sprays and inhalers by prescription.
 The sustained release anti-depressant drug bupropion (150-300mg
/day orally) is an effective smoking cessation agent and associated
with minimal weight gain, although seizures are a contraindication.
 Varenicline, a partial nicotinic acetylcholine receptor agonist, has been
shown to improve cessation rates.
CORONARY ARTERY DISEASE (CAD):

 Coronary artery disease (also called atherosclerotic or ischemic heart

disease) describes insufficient perfusion of coronary arteries due to an
abnormal narrowing of the vessels, resulting in insufficient oxygen
delivery to the myocardial tissue.
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 Risk factors: DM (most serious), Hypertension (most common),

family history of premature CAD, hyperlipidemia, tobacco
smoking, age > 45 (men) and age > 55 (women), renal disease.
 Premature CAD is defined as male relative age < 55 or female HIGH YIELD POINTS
relative age < 65.
TAKOTSUBO CARDIOMYOPATHY: Patient having chest pain
on exertion but not on
rest, next step => do
 Takotsubo cardiomyopathy is acute myocardial damage most coronary angiography.
often occurring in postmenopausal women immediately following Holter mentoring is used
an overwhelming, emotionally stressful event. E.g. divorce, for rhythm disorder.
earthquake etc. Stress exercise tolerance
 This leads to “ballooning” and left ventricular dyskinesis. are used when etiology is
 Manage with beta blockers and ACE inhibitors. not clear and ECG is not
diagnostic. If you can't
ANGINA PECTORIS: read ECG in stress test
then use thallium scan or
Echo detection of wall
Angina is a symptom complex caused by transient myocardial ischemia. motion. If patient can't
It occurs whenever there is an imbalance between myocardial oxygen exercise then use
supply and demand. Atherosclerosis is by far the most common cause Dipyridamole with
of angina pectoris. Other causes include coronary artery vasospasm thallium scan it
and Syndrome X. Angina may also occur in aortic valve disease and Dobutamine with ECHO.
hypertrophic cardiomyopathy and when the coronary arteries are
involved with vasculitis or aortitis. When Inferior STEMI
presented with low BP, there
MANAGEMENT OF STABLE ANGINA: The management of stable angina
comprises lifestyle changes, medication, percutaneous coronary is usually associated right
intervention and surgery. NICE produced guidelines in 2011 covering ventricular infarction and you
the management of stable angina. would expect an
echocardiography to
Medication: demonstrate an inferior LV
wall RWMA with a dilated and
 All patients should receive aspirin and a statin in the absence of impaired RV.
any contraindication.
 Sublingual glyceryl trinitrate to abort angina attacks
 NICE recommend using either a beta-blocker or a calcium channel
blocker first-line based on 'comorbidities, contraindications and
the person's preference'
 If a calcium channel blocker is used as monotherapy a rate-limiting
one such as verapamil or diltiazem should be used. If used in
combination with a beta-blocker then use a longer-acting
dihydropyridine calcium channel blocker (e.g. amlodipine,
modified-release nifedipine). Remember that beta-blockers should
not be prescribed concurrently with verapamil (risk of complete
heart block).
 MEDICOSHARE NOTES FOR IMM & FCPS-II MEDICINE CARDIOLOGY SECTION

 If there is a poor response to initial treatment then medication should

be increased to the maximum tolerated dose (e.g. for atenolol 100mg
OD).
 if a patient is still symptomatic after monotherapy with a beta-blocker HIGH YIELD POINTS
add a calcium channel blocker and vice versa
 if a patient is on monotherapy and cannot tolerate the addition of a CARDIAC ENZYMES
calcium channel blocker or a beta-blocker then consider one of the RISE FOLLOWING MI
following drugs:
 Most specific
• A long-acting nitrate Troponin I and T.
• Ivabradine
 Most sensitive =
• Nicorandil
• ranolazine Myoglobin.
 Myoglobin rises first
 If a patient is taking both a beta-blocker and a calcium-channel blocker following MI.
then only add a third drug whilst a patient is awaiting assessment for  CK-MB is useful to
PCI or CABG. look for re-
infarction as it
Nitrate tolerance: Many patients who take nitrates develop tolerance and
experience reduced efficacy. NICE advises that patients who take standard- returns to normal
release isosorbide mononitrate should use an asymmetric dosing after 2-3 days.
interval to maintain a daily nitrate-free time of 10-14 hours to minimize the
Indications of Exercise
development of nitrate tolerance. This effect is not seen in patients who
tolerance test:
take once-daily modified-release isosorbide mononitrate.
1. To confirm the
diagnosis of angina.
ACUTE CORONARY SYNDROME (ACS):
2. To determine the
severity of limitation
ACS is characterized by typical chest pain, rise in cardiac biomarkers and of activity due to
ECG / ECHO changes. It generally develops in patients who have ischemic angina.
3. To assess prognosis in
heart disease, either known or previously undetected.
patients with known
Heart segment Artery involved ECG leads coronary disease,
Septal MI LAD V1 & V2 including those
Anterior wall MI LAD V3 & V4 recovering from MI,
Lateral wall MI LCX I, aVL, V5, V6 by detecting groups at
high or low risk.
Inferior wall MI RCA II, III & aVF
4. To evaluate responses
Posterior wall MI LCX or RCA
to therapy.

ACUTE CORONARY SYNDROME: INITIAL MANAGEMENT

The following is based on the 2020 update to the NICE ACS guidelines.
Acute coronary syndrome can be classified as follows:

 ST-elevation myocardial infarction (STEMI): ST-segment elevation +

elevated biomarkers of myocardial damage
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 Non ST-elevation myocardial infarction (NSTEMI): ECG changes but no ST-segment elevation +
elevated biomarkers of myocardial damage
 Unstable angina: Typical chest pain with ECG changes but normal biomarkers of myocardial
damage.

The management of ACS depends on the particular subtype. NICE management guidance groups the
patients into two groups:
1. STEMI
2. NSTEM / unstable angina
COMMON MANAGEMENT OF ALL PATIENTS WITH ACS
Initial drug therapy

 Aspirin 300mg
 Oxygen should only be given if the patient has oxygen saturations < 94% in keeping with British
Thoracic Society oxygen therapy guidelines
 Morphine should only be given for patients with severe pain.
 Nitrates, can be given either sublingually or intravenously. Useful if the patient has ongoing chest
pain or hypertension. Should be used in caution if patient hypotensive.

The next step in managing a patient with suspected ACS is to determine whether they meet the ECG
criteria for STEMI.

STEMI criteria: Clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with
persistent ECG features in ≥ 2 contiguous leads of:

 2.5 mm (i.e. ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e.
≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
 1.5 mm ST elevation in V2-3 in women
 1 mm ST elevation in all other leads (except V2-3)
 New LBBB (LBBB should be considered new unless there is evidence otherwise)

MANAGEMENT OF STEMI
Once a STEMI has been confirmed the first step is to immediately assess eligibility for coronary
reperfusion therapy. There are two types of coronary reperfusion therapy:

PERCUTANEOUS CORONARY INTERVENTION

 Should be offered if the presentation is within 12 hours of the onset of symptoms and PCI can be
delivered within 120 minutes of the time when fibrinolysis could ha ve been given (i.e. consider
fibrinolysis if there is a significant delay in being able to provide PCI).
 If patients present after 12 hours and still have evidence of ongoing ischemia then PCI should still
be considered.
 Drug-eluting stents are now used. Previously 'bare-metal' stents were sometimes used but have
higher rates of restenosis. Radial access is preferred to femoral access.

FIBRINOLYSIS / THROMBOLYSIS
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 Should be offered within 12 hours of the onset of symptoms if primary

PCI cannot be delivered within 120 minutes of the time when
fibrinolysis could have been given.
 A practical example may be a patient who presents with a STEMI to a HIGH YIELD POINTS
small district general hospital (DGH) that does not have facilities for
PCI. If they cannot be transferred to a larger hospital for PCI within 120 Glycemic control in
minutes then fibrinolysis should be given. If the patient's ECG taken 90 patients with diabetes
minutes after fibrinolysis failed to show resolution of the ST elevation mellitus:
then they would then require transfer for (rescue) PCI. If patients are  in 2011 NICE issued
eligible this should be offered as soon as possible. guidance on the
management of
PCI FOR PATIENTS WITH STEMI hyperglycemia in
Further antiplatelet therapy prior to PCI acute coronary
syndromes
 This is termed 'dual antiplatelet therapy', i.e. aspirin + another drug.  it recommends using
o If the patient is not taking an oral anticoagulant: prasugrel. a dose-adjusted
o If taking an oral anticoagulant: Clopidogrel. insulin infusion with
regular monitoring of
Drug therapy during PCI blood glucose levels
to glucose below 11.0
 patients undergoing PCI with radial access: unfractionated heparin mmol/l
with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of  Intensive insulin
using a GPI during the procedure when it was not intended from the therapy (an
outset, e.g. because of worsening or persistent thrombus intravenous infusion
 patients undergoing PCI with femoral access: bivalirudin with bailout of insulin and glucose
GPI with or without
potassium, sometimes
Other procedures during PCI referred to as
'DIGAMI') regimes are
 Thrombus aspiration, but not mechanical thrombus extraction, should not recommended
be considered. routinely.
 Complete revascularization should be considered for patients with
multi-vessel coronary artery disease without cardiogenic shock.
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FIBRINOLYSIS FOR PATIENTS WITH STEMI

 Fibrinolysis used to be the only form of coronary reperfusion therapy
available. However, it is used much less commonly now given the
widespread availability of PCI. HIGH YIELD POINTS
 Patients undergoing fibrinolysis should also be given an anti-thrombin
drug. ABSOLUTE
 An ECG should be repeated after 60-90 minutes to see if the ECG CONTRAINDICATIONS TO
changes have resolved. THROMBOLYTIC
 If patients have persistent myocardial ischemia following fibrinolysis THERAPY:
then PCI should be considered.  Major bleeding into
the bowel (melena) or
Myocardial infarction: secondary prevention brain (any type of CNS
NICE produced guidelines on the management of patients following bleeding).
myocardial infarction (MI) in 2013. Some key points are listed below  Recent surgery (within
All patients should be offered the following drugs: the last 2 weeks).
 Severe hypertension
 Dual antiplatelet therapy (aspirin plus a second antiplatelet agent) (BP > 180/110
 ACE inhibitor mmHg).
 Beta-blocker  Non-hemorrhagic
 Statin stroke within the last
6 months.
Some selected lifestyle points:

 Diet: Advice Mediterranean style diet, switch butter and cheese for
plant oil based products. Do not recommend omega-3 supplements or
eating oily fish.
 Exercise: advise 20-30 mins a day until patients are 'slightly breathless'
 Sexual activity may resume 4 weeks after an uncomplicated MI.
Reassure patients that sex does not increase their likelihood of a
further MI. PDE5 inhibitors (e.g. sildenafil) may be used 6 months after
a MI. They should however be avoided in patient prescribed either
nitrates or nicorandil.

Most patients who've had an acute coronary syndrome are now given dual
antiplatelet therapy (DAPT). Clopidogrel was previously the second
antiplatelet of choice. Now ticagrelor and prasugrel (also ADP-receptor
inhibitors) are more widely used. The NICE Clinical Knowledge Summaries
now recommend:

 Post-acute coronary syndrome (medically managed): add ticagrelor

to aspirin, stop ticagrelor after 12 months
 post percutaneous coronary intervention: add prasugrel or
ticagrelor to aspirin, stop the second antiplatelet after 12 months
 This 12 month period may be altered for people at a high-risk of
bleeding or those who at high-risk of further ischemic events.
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COMPLICATIONS OF MYOCARDIAL INFARCTION:

Patients are at risk of a number of immediate, early and late complications

following myocardial infarction (MI). HIGH YIELD POINTS
Cardiac arrest: This most commonly occurs due to patients developing
ventricular fibrillation and is the most common cause of death following  Post MI dizziness +/-
MI. Patients are managed as per the ALS protocol with defibrillation. palpitations => think
Cardiogenic shock: If a large part of the ventricular myocardium is of arrhythmias.
damaged in the infarction the ejection fraction of the heart may decrease  Complete heart block
to the point that the patient develops cardiogenic shock. This is difficult to from inferior
treat. Other causes of cardiogenic shock include the 'mechanical' myocardial infraction
complications such as left ventricular free wall rupture as listed below. does not need pacing
Patients may require inotropic support and/or an intra-aortic balloon unlike CHB from
pump. anterior MI.
Chronic heart failure: As described above, if the patient survives the acute  Dressler’s syndrome
phase their ventricular myocardium may be dysfunctional resulting in resistant to NSAIDs, is
chronic heart failure. Loop diuretics such as furosemide will decrease fluid treated with steroids.
overload. Both ACE-inhibitors and beta-blockers have been shown to  PVCs should not be
improve the long-term prognosis of patients with chronic heart failure. treated, even when
Tachyarrhythmias: Ventricular fibrillation is the most common cause of associated with an
death following MI. Other common arrhythmias including ventricular acute infarction.
tachycardia. Treatment of PVCs
Bradyarrhythmias: Atrioventricular block is more common only worsens
following inferior myocardial infarctions. outcome
Pericarditis: Pericarditis in the first 48 hours following transmural MI is (Reference: Master
common (10% of patients). The pain is typical for pericarditis (worse on the board, 6th ed).
lying flat etc), a pericardial rub may be heard and a pericardial effusion may
 In cardiogenic
be demonstrated with an echocardiogram.
shock, secondary to
Dressler's syndrome tends to occur around 2-6 weeks following MI. The anterior wall
underlying pathophysiology is thought to be an autoimmune reaction
against antigenic proteins formed as the myocardium recovers. It is myocardial
characterized by a combination of fever, pleuritic pain, pericardial effusion infarction, the
and a raised ESR. It is treated with NSAIDs. mainstay of
Left ventricular aneurysm: The ischemic damage sustained may weaken
the myocardium resulting in aneurysm formation. This is typically treatment includes
associated with persistent ST elevation and left ventricular failure. diuretics to reduce
Thrombus may form within the aneurysm increasing the risk of stroke. pulmonary
Patients are therefore anticoagulated.
Left ventricular free wall rupture: This is seen in around 3% of MIs and congestion and
occurs around 1-2 weeks afterwards. Patients present with acute heart inotropic support to
failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, enhance cardiac
diminished heart sounds). Urgent pericardiocentesis and thoracotomy are
required. output and
Ventricular septal defect: Rupture of the interventricular septum usually perfusion.
occurs in the first week and is seen in around 1-2% of patients. Features:
acute heart failure associated with a pan-systolic murmur. An
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echocardiogram is diagnostic and will exclude acute mitral regurgitation

which presents in a similar fashion. Urgent surgical correction is needed.
Acute mitral regurgitation: More common with infero-posterior infarction
and may be due to ischemia or rupture of the papillary muscle. Acute
hypotension and pulmonary oedema may occur. An early-to-mid systolic HIGH YIELD POINTS
murmur is typically heard. Patients are treated with vasodilator therapy but
often require emergency surgical repair. Which patients with
MANAGEMENT OF NSTEMI/UNSTABLE ANGINA NSTEMI/unstable
The management of NSTEMI/unstable angina is complicated and depends angina should have
on individual patient factors and a risk assessment. The summary below coronary angiography
provides an overview but the full NICE guidelines should be reviewed for (with follow-on PCI if
further details. necessary)?
Further drug therapy
 Immediate: patient
 Antiplatelet therapy:
who are clinically
unstable (e.g.
 Aspirin 300mg stat, then 75-81mg indefinitely if not
contraindicated. hypotensive)
 A P2Y12 receptor antagonists like ticagrelor (180 mg, followed by  Within 96 hours:
90 mg twice daily), prasugrel (60 mg, followed by 10 mg daily) or patients who have a
clopidogrel (300 mg, followed by 75 mg daily) should be given in predicted 6-months
combination with aspirin for up to 12 months. mortality > 3% i.e.
those at
 Antithrombin treatment: Fondaparinux should be offered to patients intermediate, high
who are not at a high risk of bleeding and who are not having or highest risk.
angiography immediately. If immediate angiography is planned or a  Coronary
patient creatinine is > 265 µmol/L then unfractionated heparin should angiography should
be given.
also be considered
 Intravenous Glycoproteins IIb/ IIIa receptors antagonists (Eptifibatide
for patients if
or tirofiban) should be given to patients who have an intermediate or
higher risk of adverse cardiovascular events (predicted 6-months ischemia is
mortality > 3%) and who are scheduled to undergo angiography within subsequently
96 hours of hospital admission. experienced after
 Coronary angiography admission.

CONSERVATIVE MANAGEMENT FOR PATIENTS WITH NSTEMI/UNSTABLE

ANGINA
Further drug therapy

 further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another

drug)
 if the patient is not at a high risk of bleeding: ticagrelor
 if the patient is at a high risk of bleeding: clopidogrel

INDICATIONS OF IMPLANTABLE CARDIAC DEFIBRILLATORS (IDC):

 Long QT syndrome
 Hypertrophic obstructive cardiomyopathy (HOCM)
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 Previous cardiac arrest due to VT/VF

 Previous myocardial infarction with non-sustained VT on 24 hour monitoring, inducible VT on
electrophysiology testing and ejection fraction < 35%.
 Brugada syndrome.

INDICATIONS FOR TEMPORARY PACEMAKER

 Symptomatic / hemodynamically unstable bradycardia not responding to atropine.
 Post anterior wall MI: type 2 or complete heart block.
 Trifascicular heart block prior to surgery.

CONGENITAL HEART DISEASES:

 CYANOTIC HEART DISEASES: TGA (most common at birth), TOF (most common overall), tricuspid
atresia and pulmonary valve stenosis. Patients with Fallot’s generally present at around 1-2 months.
 ACYANOTIC HEART DISEASES: VSD (most common), ASD, Patent ductus arteriosus, Coarctation of
aorta, and aortic valve stenosis.

PULMONARY VALVE STENOSIS

 Severe cases may present with right-sided heart failure.
 P2 delayed and soft or absent.
 Pulmonary ejection click often present and decreases with inspiration—the only right heart sound
that decreases with inspiration; all other right heart sounds increase.
 Echocardiography/Doppler is diagnostic.
 Severe pulmonic stenosis should be considered if the RV systolic pressure is greater than 80 mm Hg.
Management:
 Class I (definitive) indications for intervention include all symptomatic patients and all these with a
resting peak-to-peak gradient greater than 64 mm Hg or a mean greater than 35 mm Hg, regardless
of symptoms. Symptoms can include cyanosis due to right-to-left shunting via a patent foramen
ovale (PFO) or atrial septal defect (ASD).
 Percutaneous balloon valvuloplasty is highly successful in domed valve patients and is the treatment
of choice.
 Surgical commissurotomy can also be done, or pulmonary valve replacement (with either a
bioprosthetic valve or homograft) when pulmonary valve regurgitation is too severe or the valve is
dysplastic.
 Pulmonary outflow tract obstruction due to RV to PA conduit obstruction or to homograft
pulmonary valve stenosis can often be relieved with a percutaneously implanted pulmonary valve.
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COARCTATION OF AORTA:

Coarctation of aorta describes a congenital narrowing of the descending

aorta. It is more common in females (despite association with Turner's HIGH YIELD POINTS
syndrome).
Features
Coarctation of Aorta:
 Infancy: heart failure
 Adult: Systemic hypertension is usual presentation. Notching of the inferior
 Echocardiography / Doppler is diagnostic; a peak gradient of > 20 border of the ribs (due
mmHg may be significant due to collaterals around the Coarctation to collateral vessels) is
reducing gradient despite severe obstruction. not seen in young
 Radio-femoral delay children.
 Systolic blood pressure is higher in upper extremities than in lower
extremities; diastolic pressures are similar. Differential cyanosis:
 A continuous murmur heard superiorly and midline in the back or over with reversal of blood
the left anterior chest may be present when large collaterals are
flow in patent ductus
present and is a clue that the coarctation is severe.
 The coarctation itself may result in systolic ejection murmurs heard in arteriosus,
the left upper lung field anteriorly and near the spine on the left side deoxygenated blood is
posteriorly. shunted to the
Associations: descending aorta after
 Turner's syndrome, Bicuspid aortic valve (50-80% patients), Berry the origin of subclavian
aneurysms, Neurofibromatosis and accelerated Coronary Artery
Disease (CAD).
arteries, so cyanosis
Treatment: and clubbing occur in
 The percutaneous interventional procedure of choice is endovascular lower limbs.
stenting; when anatomically feasible, self-expanding and balloon-
expandable covered stents have been shown to be advantageous over Paradoxical emboli may
bare metal stents. be more common in
 Most coarctation repair in adults is percutaneous. Otherwise, surgical patients with a PFO
resection (usually with end-to-end anastomosis) should be performed. than a true ASD,
especially when there is
ATRIAL SEPTAL DEFECT
an atrial septal
Atrial septal defects (ASDs) are the most likely congenital heart defect to be aneurysm.
found in adulthood. Two types of ASDs are recognized, ostium secundum
and ostium primum. Ostium secundum are the most common
Ostium secundum (70% of ASDs)

 Associated with Holt-Oram syndrome (tri-phalangeal thumbs)

 ECG: RBBB with RAD

Ostium primum

 Present earlier than ostium secundum defects

 Associated with abnormal AV valves
 ECG: RBBB with LAD, prolonged PR interval.

Features:
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 Ejection systolic murmur, fixed splitting of S2.

 Emboli may pass from venous system to left side of heart causing a stroke.

Treatment:

 Both AHA/ACC and the ESC guidelines suggest that closure of all left-to-right shunts greater than
1.5:1 should be accomplished either by a percutaneous device or by surgery if any right heart
structures are enlarged at all.
 If the pulmonary systolic pressure is more than two-thirds the systemic systolic pressure, then
pulmonary hypertension may preclude ASD closure.
 The use of bosentan or sildenafil is recommended if the PVR is over 5 Wood units and there is a
right-to-left shunt.

VENTRICULAR SEPTAL DEFECT

A ventricular septal defect (VSD) is a defect in the interventricular septum resulting in the
communication between the ventricular cavities. VSDs occur in isolation or in combination with other
congenital heart defects such as atrioventricular canal, TOF and occasionally transposition of great
arteries.
Classification: VSDs may be classified as follow.
 Membranous VSDs  Malalignment VSDs  AV canal or inlet VSDs
 Muscular VSDs  Subpulmonic VSDs
Clinical Findings:
Small shunts are associated with loud, harsh holosystolic murmurs in the left third and fourth
interspaces along the sternum. A systolic thrill is common. Larger shunts may create both LV and RV
volume and pressure overload. If pulmonary hypertension occurs, high-pressure pulmonary valve
regurgitation may result. Right heart failure may gradually become evident late in the course, and the
shunt will begin to balance or reverse as RV and LV systolic pressures equalize with the advent of
pulmonary hypertension.
Treatment:
 Patients with a small VSD have a normal life expectancy except for the small risk of infective
endocarditis. Antibiotic prophylaxis after dental work is recommended only when the VSD is residual
from a prior patch closure or when there is associated pulmonary hypertension and cyanosis.
 Surgical repair of a VSD is generally a low-risk procedure unless there is significant Eisenmenger
physiology.
 Devices for nonsurgical closure of muscular VSDs are approved and those for membranous VSDs are
being implanted with promising results; however, conduction disturbance is a major complication.
 The medications used to treat pulmonary hypertension secondary to a VSD are similar to those used
to treat idiopathic (“primary”) pulmonary hypertension and at times can be quite effective in
relieving symptoms and reducing the degree of cyanosis.
 All patients who have a right-to-left shunt present should have filters placed on any intravenous
lines to avoid any contamination or air bubbles from becoming systemic.

EISENMENGER'S SYNDROME
Eisenmenger's syndrome describes the reversal of a left-to-right shunt in a congenital heart defect due
to pulmonary hypertension. This occurs when an uncorrected left-to-right leads to remodeling of the
pulmonary microvasculature, eventually causing obstruction to pulmonary blood and pulmonary
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hypertension.
Associations: Associated with VSD, ASD and PDA.

Features

 original murmur may disappear

 cyanosis
 clubbing
 right ventricular failure
 haemoptysis, embolism

Management: heart-lung transplantation is required

TETRALOGY OF FALLOT
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 mal-alignment of the aorticopulmonary septum.
The four Characteristic features are:

 ventricular septal defect (VSD)

 right ventricular hypertrophy
 right ventricular outflow tract obstruction, pulmonary stenosis
 Overriding aorta.

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

Other features:

 cyanosis
 unrepaired TOF infants may develop episodic hyper-cyanotic 'tet' spells due to near occlusion of the
right ventricular outflow tract
 features of tet spells include tachypnea and severe cyanosis that may occasionally result in loss of
consciousness
 they typically occur when an infant is upset, is in pain or has a fever
 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

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

 Most adult patients have had surgical repair, including VSD closure, resection of infundibular
muscle, and insertion of an outflow tract patch to relieve the subpulmonic obstruction.
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 Patients with pulmonary valve regurgitation should be monitored to ensure the RV volume does
not progressively increase. In patients with tetralogy of Fallot, transthoracic echocardiogram
monitoring of pulmonary valve regurgitation is recommended every 12–24 months based on the
degree of regurgitation.
 The RV volumes from cardiac MRI are important in deciding when to intervene if the patient is not
very symptomatic; an RV end-diastolic volume index of greater than 160 mm/m2 or an RV end-
systolic volume index of greater than 80 mm/m2 is recommended as the cutoff.

PATENT FORAMEN OVALE

 Patent foramen ovale (PFO) is present in around 20% of the population. It may allow embolus (e.g.
from DVT) to pass from right side of the heart to the left side leading to a stroke - 'a paradoxical
embolus'.
 There also appears to be an association between migraine and PFO. Some studies have reported
improvement in migraine symptoms following closure of the PFO.
 The management of patients with PFO who've had a stroke remains controversial. Options include
antiplatelet therapy, anticoagulant therapy or PFO closure.

RHEUMATIC FEVER:
Rheumatic fever develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus
pyogenes infection.
Diagnosis is based on evidence of recent streptococcal infection accompanied by 2 major criteria or 1
major with 2 minor criteria.
Major criteria Minor criteria
 erythema marginatum  raised ESR or CRP
 Sydenham's chorea: this is  pyrexia
often a late feature  arthralgia (not if arthritis a
 polyarthritis major criteria)
 carditis and valvulitis (eg,  prolonged PR interval
pancarditis)
 subcutaneous nodules

Evidence of recent streptococcal infection:

 Raised or rising streptococci antibodies,

 Positive throat swab
 Positive rapid group-A streptococcal antigen test.

Management:

General Measures: The patient should be kept at strict bed rest until the temperature returns to normal
(without the use of antipyretic medications) and the ESR, plus the resting pulse rate, and the ECG have
all returned to baseline.

Pharmacological treatment:
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 Salicylates: The salicylates markedly reduce fever and relieve joint pain and swelling. They have no
effect on the natural course of the disease. Adults may require large doses of aspirin, 0.6–0.9 g
every 4 hours; children are treated with lower doses.
 Penicillin: Penicillin (benzathine penicillin, 1.2 million units intramuscularly once, or procaine
penicillin, 600,000 units intramuscularly daily for 10 days) is used to eradicate streptococcal
infection if present. Erythromycin may be substituted (40 mg/kg/day).
 Corticosteroids: There is no proof that cardiac damage is prevented or minimized by corticosteroids.
A short course of corticosteroids (prednisone, 40–60 mg orally daily, with tapering over 2 weeks)
usually causes rapid improvement of the joint symptoms and is indicated when response to
salicylates has been inadequate.

Prevention of Recurrent Rheumatic Fever

 Recurrences of rheumatic fever are most common in patients who have had carditis during their
initial episode and in children, 20% of whom will have a second episode within 5 years.
 The preferred method of prophylaxis is with benzathine penicillin G, 1.2 million units intramuscularly
every 4 weeks. Alternatives are Oral penicillin, sulfadiazine (if patient is allergic to penicillin),
erythromycin, azithromycin or cephalosporin.
 Recurrences are uncommon after 5 years following the first episode and in patients over 21 years of
age.
 Prophylaxis is usually discontinued after these times except in groups with a high risk of
streptococcal infection—parents or teachers of young children, nurses, military recruits, etc.
 Current guidelines suggest that if there is no evidence for carditis, preventive therapy can be
stopped at age 21 years.
 If carditis has occurred but there is no residual valvular disease, it can be stopped at 10 years after
the acute rheumatic fever episode.
 If carditis has occurred with residual valvular involvement, it should be continued for 10 years after
the last episode or until age 40 years if the patient is in a situation in which reexposure would be
expected.

MITRAL STENOSIS:
Mitral stenosis describes the obstruction of blood flow across the mitral valve from the left atrium to the
left ventricle. This leads to increase in pressure within the left atrium, pulmonary vasculature and right
side of the heart.
Causes: It is said that the causes of mitral stenosis are rheumatic fever, rheumatic fever and rheumatic
fever. Rarer causes that may be seen in the exam include mucopolysaccharidoses, carcinoid and
endocardial fibroelastosis
Features:
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 Dyspnea: ↑ left atrial pressure → pulmonary venous hypertension

 Hemoptysis: due to pulmonary pressures and vascular congestion.
May range from pink frothy sputum to sudden haemorrhage
secondary to rupture of thin-walled and dilated bronchial veins HIGH YIELD POINTS
 Mid-late diastolic murmur (best heard in expiration)
 Loud S1, opening snap  Mid diastolic murmur
 Low volume pulse & loud first heart
 Malar flush sound are common
 Atrial fibrillation: secondary to ↑ left atrial pressure → left atrial findings &
enlargement.
pathognomonic of
Mitral stenosis.
Management:
 The papillary muscles
 Patients with associated atrial fibrillation require anticoagulation may be abnormally
 currently warfarin is still recommended for patients with close together,
moderate/severe MS sometimes so close
 there is an emerging consensus that direct-acting anticoagulants that they merge into a
(DOACs) may be suitable for patients with mild MS who develop atrial single papillary muscle
fibrillation (“parachute mitral
valve”).
Asymptomatic patients: Monitored with regular echocardiograms
Percutaneous/surgical management is generally not recommended. Features of severe MS:

Symptomatic patients: Percutaneous mitral balloon Valvotomy is used to  Length of murmur

treat sever M.S. It is contraindicated in moderate to severe mitral increases
regurgitation, left atrial thrombus, heavily calcified mitral valve and  Opening snap
concomitant coronary artery or other valve disease requiring surgery. becomes closer to S2
Other option is mitral valve surgery (commissurotomy, or valve  CXR findings: Left
replacement) atrial enlargement
may be seen.
MITRAL STENOSIS AND PREGNANCY:  ECHO: A 'tight' mitral
 Moderate to severe mitral stenosis: Valve should be replaced before stenosis implies a
pregnancy. cross-sectional area of
 Severe mitral stenosis in pregnancy: Balloon valvulplasty should be < 1 cm2 (Normal = 4-
done preferably in the third trimester. 6cm2).
 Mitral stenosis with
MITRAL VALVE PROLAPSE (MVP):
cross sectional area
Mitral valve prolapse is common, occurring in around 5-10 % of the of < 1cm2 warrants
population. It is usually idiopathic but may be associated with a wide surgical
variety of cardiovascular disease and other conditions intervention.
Associations: Congenital heart disease (PDA, ASD), cardiomyopathy,
Turner's syndrome, Marfan's syndrome, Fragile X syndrome, Osteogenesis
imperfecta, Pseudoxanthoma elasticum, WPW syndrome, Long-QT
syndrome, Ehlers-Danlos Syndrome and Polycystic kidney disease.

Features:
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 Patients may complain of atypical chest pain or palpitations

 Mid-systolic click (occurs later if patient squatting)
 Late systolic murmur (longer if patient standing)

Complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death

MITRAL REGURGITATION
Also known as mitral insufficiency, mitral regurgitation (MR) occurs when blood leaks back through the
mitral valve during systole. It is the second most common valve disease after aortic stenosis. The mitral
valve is located between the left atrium and ventricle, and regurgitation leads to a less efficient heart as
less blood is pumped through the body with each contraction.
As the degree of regurgitation becomes more severe, the body’s oxygen demands may exceed
what the heart can supply and as a result, the myocardium can thicken over time. While this may be
benign initially, patients may find themselves increasingly fatigued as a thicker myocardium becomes
less efficient, and eventually go into irreversible heart failure.

Risk factors include Female gender, lower body mass, age, renal dysfunction, prior myocardial
infarction, prior mitral stenosis or valve prolapse and collagen disorders e.g. Marfan's Syndrome and
Ehlers-Danlos syndrome
Causes

 Following coronary artery disease or post-MI: if the papillary muscles or chordae tendinae are
affected by a cardiac insult, mitral valve disease may ensue as a result of damage to its supporting
structures.
 Mitral valve prolapse: Occurs when the leaflets of the mitral valve is deformed so the valve does
not close properly and allows for backflow. Most patients with this have a trivial degree of mitral
regurgitation.
 Infective endocarditis: When vegetations from the organisms colonizing the heart grow on the
mitral valve, it is prevented from closing properly. Patients with abnormal valves are more likely to
develop endocarditis as opposed to their peers.
 Rheumatic fever: While this is uncommon in developed countries, rheumatic fever can cause
inflammation of the valves and therefore result in mitral regurgitation.
 Congenital

Symptoms: Most patients with MR are asymptomatic, and patients suffering from mild to moderate MR
may stay largely asymptomatic indefinitely. Symptoms tend to be due to failure of the left ventricle,
arrhythmias or pulmonary hypertension. This may present as fatigue, shortness of breath and oedema.
Signs: The murmur heard on auscultation of the chest is typically a pansystolic murmur described as
“blowing”. It is heard best at the apex and radiating into the axilla. S1 may be quiet as a result of
incomplete closure of the valve. Severe MR may cause a widely split S2
Investigations

 ECG may show a broad P wave, indicative of atrial enlargement

 Cardiomegaly may be seen on chest x-ray, with an enlarged left atrium and ventricle
 Echocardiography is crucial to diagnosis and to assess severity
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Treatment options

 Medical management in acute cases involves nitrates, diuretics,

positive inotropes and an intra-aortic balloon pump to increase cardiac HIGH YIELD POINTS
output
 If patients are in heart failure, ACE inhibitors may be considered along  Aortic stenosis co-
with beta-blockers and spironolactone occurs with
 Surgery is necessary when symptoms develop or when there is atherosclerotic
evidence for LV dysfunction, since progressive and irreversible disease => perform
deterioration of LV function can occur prior to the onset of symptoms. angiogram prior to
Early surgery is indicated even in asymptomatic patients with a reduced
surgical intervention.
EF (less than 60%) or marked LV dilation with reduced contractility (end
systolic dimension greater than 4.0 cm).
 The evidence for repair over replacement is strong in degenerative  Austin flint murmur
regurgitation, and is demonstrated through lower mortality and higher heard in severe AR is
survival rates. When this is not possible, valve replacement with either due to diastolic
an artificial valve or a pig valve is considered. displacement of
anterior leaflet of
AORTIC STENOSIS: (AS = SAD, syncope + angina + dyspnea) mitral valve by AR
stream. It is a mid-
Clinical features of symptomatic disease
diastolic murmur
heard at the apex.
 chest pain, dyspnea and syncope / pre-syncope (e.g. exertional
dizziness)
 Ejection systolic murmur (ESM), which classically radiates to the
carotids and is decreased following the Valsalva manoeuvre.  Surgery for aortic
regurgitation is
Features of severe aortic stenosis: Narrow pulse pressure, slow rising indicated if there is
pulse, delayed ESM, soft/absent S2, S4, thrill, change in duration of murmur significant
and left ventricular hypertrophy or failure. enlargement of the
ascending aorta,
Causes of aortic stenosis: severe regurgitation
with symptoms or if
 degenerative calcification (most common cause in older patients > 65 severe with an
years) ejection fraction of
 bicuspid aortic valve (most common cause in younger patients < 65
less than 50%.
years)
 William's syndrome (supravalvular aortic stenosis)
 post-rheumatic disease
 Subvalvular: HOCM.

Management:

 if asymptomatic then observe the patient is a general rule

 if symptomatic then valve replacement
 if asymptomatic but valvular gradient > 40 mmHg and with features
such as left ventricular systolic dysfunction then consider surgery
 options for aortic valve replacement (AVR) include:
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 Surgical AVR is the treatment of choice for young, low/medium operative risk patients.
Cardiovascular disease may coexist. For this reason, an angiogram is often done prior to surgery so
that the procedures can be combined
 Transcatheter AVR (TAVR) is used for patients with a high operative risk
 balloon valvuloplasty
 may be used in children with no aortic valve calcification
 in adults limited to patients with critical aortic stenosis who are not fit for valve replacement

AORTIC REGURGITATION (AR):

Aortic regurgitation (AR) is the leaking of the aortic valve of the heart that causes blood to flow in the
reverse direction during ventricular diastole.
It can be caused either by disease of the aortic valve or by distortion or dilation of the aortic root and
ascending aorta

Causes of AR due to valve disease Causes of AR due to aortic root disease

 Rheumatic fever: the most common cause
 Bicuspid aortic valve (affects both the
in the developing world
valves and the aortic root)
 Calcific valve disease
 Aortic dissection
 Infective endocarditis
 Spondylarthropathies (e.g. ankylosing
 Connective tissue diseases e.g. rheumatoid
spondylitis)
arthritis/SLE
 Hypertension
 Bicuspid aortic valve (affects both the valves
 Syphilis
and the aortic root)
 Marfan's, Ehler-Danlos syndrome

Features:

 Early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
 Collapsing pulse & wide pulse pressure
 Quincke's sign (nailbed pulsation)
 De Musset's sign (head bobbing)
 mid-diastolic Austin-Flint murmur in severe AR
 Suspected AR should be investigated with echocardiography.

Management:

 Medical management of any associated heart failure

 Surgery: aortic valve indications include
 Symptomatic patients with severe AR
 Asymptomatic patients with severe AR who have LV systolic dysfunction.

TRICUSPID STENOSIS
 Female predominance.
 History of rheumatic heart disease most likely.
 Carcinoid disease and prosthetic valve degeneration are the most common etiologies in the US.
Clinical Findings:
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 Tricuspid stenosis is characterized by right heart failure with hepatomegaly, ascites, and dependent
edema. In sinus rhythm, a giant a wave is seen in the JVP, which is also elevated. The typical diastolic
rumble along the lower left sternal border mimics mitral stenosis, though in tricuspid stenosis the
rumble increases with inspiration. In sinus rhythm, a presystolic liver pulsation may be found. It
should be considered when patients exhibit signs of carcinoid syndrome.
Investigations:
 In the absence of atrial fibrillation, the ECG reveals RA enlargement.
 The chest radiograph may show marked cardiomegaly with a normal PA size. A dilated superior vena
cava and azygous vein may be evident.
 Echocardiography / Doppler is diagnostic.
Treatment:
 Initial therapy is directed at reducing the fluid congestion, with diuretics the mainstay.
 Aldosterone inhibitors also help, particularly if there is liver engorgement or ascites.
 Tricuspid valve replacement is the preferred surgical approach.

TRICUSPID REGURGITATION:

Signs:

 pan-systolic murmur
 prominent/giant V waves in JVP
 pulsatile hepatomegaly
 left parasternal heave

Causes:

 right ventricular infarction

 pulmonary hypertension e.g. COPD
 rheumatic heart disease
 infective endocarditis (especially intravenous drug users)
 Ebstein's anomaly
 carcinoid syndrome

Treatment:
 Mild tricuspid regurgitation is common and generally can be well managed with diuretics. When
severe tricuspid regurgitation is present, bowel edema may reduce the effectiveness of diuretics,
such as furosemide, and intravenous diuretics should be used initially.
 Aldosterone antagonists have a role as well, particularly if ascites is present.
 Since most tricuspid regurgitation is secondary, definitive treatment usually requires elimination of
the cause of the RV dysfunction.
 Guidelines suggest that tricuspid valve surgery may be considered when the tricuspid annular
dilation at end-diastole exceeds 4.0 cm and the patient is symptomatic.

PULMONARY STENOSIS:

 This can occur in the carcinoid syndrome but is usually congenital, in which case it may be isolated
or associated with other abnormalities such as tetralogy of Fallot.
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 Mild cases of pulmonary stenosis are asymptomatic; moderate to severe pulmonic stenosis may
cause symptoms of dyspnea on exertion, syncope, chest pain, and eventually right-sided heart
failure.
 On examination there is an ejection systolic murmur loudest at the left upper sternum and radiating
towards the left shoulder. There may a thrill, best felt when the patient leans forwards and breaths
out. The murmur is often preceded by an ejection click that decreases with inspiration—the only
right heart sound that decreases with inspiration. Severe pulmonic stenosis is characterized by a
loud harsh murmur, an inaudible pulmonary valve closure sound (P2), an increased right ventricular
heave and prominent “a” waves in the jugular pulse.
 ECG may show peaked “P” waves (right atrial overload), right axis deviation and RVH.
 Echocardiography/Doppler is diagnostic. Mild pulmonic stenosis is present if the peak gradient by
echocardiography/Doppler is less than 36 mm Hg, moderate pulmonic stenosis is present if the
peak gradient is between 36 mm Hg and 64 mm Hg, and severe pulmonic stenosis is present if the
peak gradient is greater than 64 mm Hg or the mean gradient is greater than 35 mm Hg.
 Patients with severe pulmonary stenosis should undergo intervention (percutaneous pulmonary
balloon valvulplasty or surgical Valvotomy) regardless of symptoms. Otherwise, operate for
symptoms or evidence for right ventricular (RV) dysfunction.

PULMONARY VALVE REGURGITATION

Pulmonary valve regurgitation can be divided into high pressure causes (due to pulmonary
hypertension) and low-pressure causes (usually due to a dilated pulmonary annulus, a congenitally
abnormal [bicuspid or dysplastic] pulmonary valve, plaque from carcinoid disease, surgical pulmonary
valve replacement, or the residual physiology following a surgical trans-annular patch used to reduce
the outflow gradient in tetralogy of Fallot).
Clinical findings:
 Most patients are asymptomatic. Those with marked pulmonary valve regurgitation may exhibit
symptoms of right heart volume overload.
 On auscultation, the second heart sound may be widely split due to prolonged RV systole or an
associated right bundle branch block.
 In high-pressure pulmonary valve regurgitation, the pulmonary diastolic (Graham Steell) murmur is
readily audible.
 Echocardiography may demonstrate evidence of RV volume overload (paradoxical septal motion and
an enlarged RV), and Doppler can determine peak systolic RV pressure and reveal any associated
tricuspid regurgitation.
Treatment:
 Pulmonary valve regurgitation rarely needs specific therapy other than treatment of the primary
cause.
 In low pressure pulmonary valve regurgitation due to surgical trans-annular patch repair of tetralogy
of Fallot, pulmonary valve replacement may be indicated if RV enlargement or dysfunction is
present.
 In high-pressure pulmonary valve regurgitation, treatment to control the cause of the pulmonary
hypertension is key.

PROSTHETIC VALVES:

The most common valves which need replacing are the aortic and mitral valve. There are two main
options for replacement: biological (bio-prosthetic) or mechanical.
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BIOPROSTHETIC VALVES MECHANICAL VALVES

 Usually bovine or porcine in origin  The most common type now implanted is the
 Major disadvantage is structural bileaflet valve.
deterioration and calcification over time.  Mechanical valves have a low failure rate.
Most older patients ( > 65years for aortic  Major disadvantage is the increased risk of
valves and > 70 years for mitral valves) thrombosis meaning long-term anticoagulation
receive a bio-prosthetic valve is needed.
 Long-term anticoagulation not usually  Aspirin is normally given in addition unless
needed. there is a contraindication.
 Warfarin may be given for the first 3  Target INR
months depending on patient’s factors.  Aortic: 2.0-3.0
 Low-dose aspirin is given for long-term.  Mitral: 2.5-3.5

HEART MURMURS:

 There is holosystolic murmur in three condition.

o MR, radiates to axilla
o TR, radiates to back
o VSD.
 Continous machinary like murmur: patent ductus arteriosus.
 MNEMONIC: If you don’t remember anything about murmur, just memorize “PASS” & “PAID”

PASS: “P” for pulmonary, “A” for aortic, “S” for stenosis and “S” for systolic murmur.

 Pulmonary and aortic stenosis = systolic murmurs and vice versa for mitral and tricuspid stenosis
i.e. diastolic murmurs.

PAID: “P” for pulmonary, “A” for aortic, “I” for insufficiency / regurgitation and “D” for diastolic
murmur.

 Pulmonary and aortic insufficiency / regurgitation = diastolic murmurs and vice versa for mitral and
tricuspid regurgitation i.e. systolic murmurs.
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Murmur—hypertrophic Systolic ejection murmur heard along lateral sternal border that
obstructive cardiomyopathy ↑ with ↓ preload (Valsalva maneuver).
Murmur—aortic insufficiency Austin Flint murmur, a diastolic, decrescendo, low-pitched,
blowing murmur that is best heard sitting up. ↑ With ↑
afterload (handgrip maneuver).
Murmur—aortic stenosis Systolic crescendo/decrescendo murmur that radiates to neck.
↑ With ↑ preload (squatting maneuver)
Murmur—mitral regurgitation Holosystolic murmur that radiates to axilla. ↑ With ↑ afterload
(handgrip maneuver).
Murmur—mitral stenosis Diastolic, mid to late, low-pitched murmur preceded by an
opening snap

DYNAMIC MANEUVERS AND SYSTOLIC MURMURS

Maneuvers HOCM MVP AS MR
Valsalva strain phase Louder Longer Softer Softer
Squatting or leg raise Softer Shorter Louder Louder
Hand grip Softer Shorter Softer Louder

INFECTIVE ENDOCARDITIS:
The strongest risk factor for developing infective endocarditis is a previous episode of endocarditis.
The following types of patients are affected:

 Previously normal valves (50%, typically acute presentation).

 Rheumatic valve disease (30%)
 prosthetic valves
 congenital heart defects
 intravenous drug users (IVDUs) e.g. typically causing tricuspid lesion)
 others: recent piercings

Causes:

 Staphylococcus aureus: now the most common cause of infective endocarditis particularly
common in acute presentation and IVDUs.
 Streptococcus viridans: The two most notable viridans streptococci are Streptococcus
mitis and Streptococcus sanguinis. They are both commonly found in the mouth and in particular
dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or
following a dental procedure.
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 Coagulase-negative Staphylococci such as Staphylococcus epidermidis

commonly colonize indwelling lines and are the most cause of
endocarditis in patients following prosthetic valve surgery, usually the
result of perioperative contamination. After 2 months the spectrum of HIGH YIELD POINTS
organisms which cause endocarditis return to normal
(i.e. Staphylococcus aureus is the most common cause). Mitral valve is most
 Streptococcus bovis: associated with colorectal cancer. The
commonly affected in
subtype Streptococcus gallolyticus is most linked with colorectal
infective endocarditis if
cancer.
 Non-infective causes include systemic lupus erythematosus (Libman- valves are previously
Sacks endocarditis), malignancy (marantic endocarditis). normal.
 Culture negative causes: prior antibiotic therapy, Coxiella burnetii,
Bartonella, Brucella and HACEK group (Haemophilus, Actinobacillus, The BNF now recommend
Cardiobacterium, Eikenella, Kingella). Flucoloxacillin
monotherapy for native-
SCENARIO SUGGESTED ANTIBIOTIC THERAPY valve endocarditis caused
Native valve: Amoxicillin, consider adding low- by staphylococci.
dose gentamicin.
If penicillin allergic, MRSA or severe sepsis: INFECTIVE
Initial blind therapy ENDOCARDITIS: Poor
Vancomycin + low-dose gentamicin
If prosthetic valve: Vancomycin + rifampicin + prognostic factors
low-dose gentamicin include:
Native valve  Flucoloxacillin
endocarditis caused If penicillin allergic or MRSA: Vancomycin +  Staphylococcus
by staphylococci rifampicin aureus infection.
 Flucoloxacillin + rifampicin + low-dose  Prosthetic valve
Prosthetic valve
gentamicin (especially 'early',
endocarditis caused
If penicillin allergic or MRSA: Vancomycin + acquired during
by staphylococci
rifampicin + low-dose gentamicin
surgery).
Endocarditis caused
 Benzylpenicillin  Culture negative
by fully-sensitive
If penicillin allergic: Vancomycin + low-dose endocarditis
streptococci (e.g.
gentamicin  Low complement
viridans)
Endocarditis caused Benzylpenicillin + low-dose gentamicin levels.
by less sensitive If penicillin allergic: Vancomycin + low-dose
streptococci gentamicin Trans esophageal ECHO
(TEE) should be done
Current antibiotic guidelines (source: British National Formulary) for endocarditis as it
Indications for surgery detects vegetations in
more than 90% of
 severe valvular incompetence patients with definitive
 aortic abscess (often indicated by a lengthening PR interval) endocarditis.
 infections resistant to antibiotics/fungal infections
 cardiac failure refractory to standard medical treatment
 Recurrent emboli after antibiotic therapy.
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CARDIAC ARRHYTHMIAS:

An abnormality of the cardiac rhythm is called cardiac arrhythmia. There

are two main types of arrhythmias HIGH YIELD POINTS
 Bradycardia: The heart rate is slow (less than 60 bpm).
 Tachycardia: The heart rate is fast (greater than 100 bpm). FEATURES SUGGESTING
VT RATHER THAN SVT
WITH ABERRANT
Sinus Arrhythmias: The normal increase in heart rate that occurs during CONDUCTION:
inspiration. This is a natural response and is more accentuated in children  AV dissociation.
than adults.  Fusion or capture
beats.
ANTIARRHYTHMIC MEDICATIONS:  Positive QRS
concordance in chest
Class-I antiarrhythmic (Na channel blockers): leads.
Class-IA: quinidine, procainamide, disopyramide  Marked left axis
Class-IB: lidocaine, mexiletine. deviation.
Class-IC: Flecainide, propafenone)  History of IHD.
Class-II antiarrhythmic (Beta-blockers): Esmolol, metoprolol and  Lack of response to
propranolol. adenosine or carotid
Class-III antiarrhythmic: Amiodarone, dronedarone, sotalol, dofetilide, sinus massage.
ibutilide  QRS > 160 ms.
Class-IV antiarrhythmic (calcium channel blockers): Diltiazem and
verapamil
Miscellaneous: Adenosine, digoxin and ivabradine.  Sotalol should be
avoided in WPW
ATRIOVENTRICULAR BLOCK Syndrome if there is
co-existent AF.
In atrioventricular (AV) block, or heart block, there is impaired electrical  Adenosine, verapamil
conduction between the atria and ventricles. There are three types: and digoxin are
First-degree heart block
contraindicated in
WPW syndrome.
 PR interval > 0.2 seconds
 Asymptomatic first-degree heart block is relatively common and does
not need treatment.
 Second-degree heart block:
o Mobitz Type 1 (Wenckebach): progressive prolongation of the PR
interval until a dropped beat occurs.
o Mobitz type 2: PR interval is constant but the P wave is often not
followed by a QRS complex.
 Third-degree (complete) heart block: There is no association between
the P waves and QRS complexes.
Treatment of Heart blocks:

 First degree heart block: Asymptomatic require no treatment. If

symptomatic give atropine.

 Second degree Heart block

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o Mobitz type-I: Asymptomatic => Discharge home.

If symptomatic => permanent pacemaker

o Second degree Heart block Mobitz Type 2: transvaneous cardiac HIGH YIELD POINTS
pacing.
 The most
 Third degree / complete heart block: permanent pacemaker. characteristic ECG
 Atropine is not useful in type 2 block and complete heart block. finding in
arrhythmogenic
SUPRAVENTRICULAR TACHYCARDIA (SVT):
right ventricular
The term supraventricular tachycardia refers to any tachycardia that is not dysplasia (ARVD) is
ventricular in origin. Episodes are characterized by the sudden onset of a the epsilon wave (a
narrow complex tachycardia, typically an atrioventricular nodal re-entry small positive
tachycardia (AVNRT). Other causes include atrioventricular re-entry
deflection at the
tachycardia (AVRT) and junctional tachycardia.
Treatment of SVT: end of the QRS
 Vagal maneuvers (carotid sinus massage contraindicated in carotid complex).
vascular disease).
 IV adenosine 6 mg then 12mg (contraindicated in Asthma, use  Sick sinus syndrome
verapamil instead). is a contraindication
 Electrical cardioversion. to ivabradine and
SVT Prophylaxis: Beta blockers, radiofrequency ablation. calcium channel
blocker.
MULTIFOCAL ATRIAL TACHYCARDIA:
 It is defined as irregular cardiac rhythm caused by at least three  SVT + asthma: Give
different sites in the atria, which may be demonstrated by verapamil
morphologically distinctive P waves.  SVT in Pregnancy:
 It is more common in elderly patients with chronic lung disease (e.g. Give Adenosine
COPD). (Avoid BETA
Management: BLOCKERS in 1st
 Correction of hypoxia and electrolyte disturbances trimester of
 Rate-limiting calcium channel blockers are often used first-line. pregnancy).
 Cardioversion and digoxin are not useful in the management of MAT.

WOLFF-PARKINSON WHITE (WPW) SYNDROME:

WPW syndrome is caused by a congenital accessory conducting pathway

between the atria and ventricles leading to atrioventricular re-entry
tachycardia.

ECG features include

 Short PR interval.
 Wide QRS complex with a slurred upstroke- “delta waves”.
 Left axis deviation if right-sided accessory pathway.
 Right axis deviation if left-sided accessory pathway.
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Associations of WPW syndrome: HOCM, mitral valve prolapse, Epstein’s anomaly, thyrotoxicosis,
secundum ASD.

Medical treatment include sotalol, amiodarone and Flecainide.

Definitive treatment is radiofrequency ablation of the accessory pathway.

ACCELERATED IDIOVENTRICULAR RHYTHM

Accelerated idioventricular rhythm (AIVR) is a benign ectopic rhythm of ventricular origin. It usually
occurs following the reperfusion of an ischemic myocardium. It has a rate of 50 -110 beats per minute
(which helps differentiate it from ventricular bradycardia or ventricular tachycardia) and, therefore, the
patient tends to be hemodynamically stable. However, if the rate is fast or there is extensive damage to
the myocardium, the patient can become unstable.
Causes:

 Reperfusion following myocardial infarction – by far the most common cause

 Beta-sympathomimetics (e.g. adrenaline)
 Drug toxicity (digoxin/cocaine)
 Electrolyte imbalance
 Cardiomyopathy, congenital heart disease, myocarditis

AIVR is diagnosed based on electrocardiography (ECG) findings:

 AIVR has a gradual onset and termination as the ventricular rate is only slightly faster than sinus
rhythm. This may result in ventricular fusion beats on ECG.
 Atrioventricular dissociation - P waves present but not associated with QRS complexes.
 The ECG will show wide QRS complexes >120ms.
 Rate between 50-110 beats per minute.

Treatment: AIVR is usually self-limiting and therefore treatment is not necessary, however, occasionally
atropine can be used to increase the sinus rate to overcome AIVR.

BRUGADA SYNDROME

Brugada syndrome is a form of inherited cardiovascular disease with may present with sudden cardiac
death. It is inherited in an autosomal dominant fashion.

ECG changes

 Convex ST segment elevation > 2mm in > 1 of V1-V3, followed by a negative T wave
 Partial right bundle branch block.
 ECG changes may be more apparent following the administration of flecainide or ajmaline- this is
investigation of choice in suspected cases of Brugada syndrome.

Management: Implantable cardioverter-defibrillator.

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ATRIAL FIBRILLATION:

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. ECG shows absent P waves and
irregular QRS complexes.

AF is classified as follow.

 Paroxysmal AF: AF that terminates spontaneously in <7 days and <48 hours in duration.
 Persistent AF: Sustained for >7 days, but can be terminated by chemical or electrical cardioversion.
 Permanent AF: Typically >1 y and when cardioversion has failed or in which clinical judgment has led
to a decision not to pursue cardioversion.

Symptoms: Palpitations, dyspnea and chest pain

Signs: An irregularly irregular pulse

Investigations: An ECG is essential to make the diagnosis as other conditions can also give irregular
pulse, such as ventricular ectopics or sinus arrhythmia.
Management: There are two key parts of managing patients with AF:

1. Rate/rhythm control
2. Reducing stroke risk

Rate vs. rhythm control: There are two main strategies employed in dealing with the arrhythmia
element of atrial fibrillation:

 Rate control: accept that the pulse will be irregular, but slow the rate down to avoid negative effects
on cardiac function
 Rhythm control: try to get the patient back into, and maintain, normal sinus rhythm. This is termed
cardioversion. Drugs (pharmacological cardioversion) and synchronized DC electrical shocks
(electrical cardioversion) may be used for this purpose

NICE advocate using a rate control strategy except in a number of specific situations such as coexistent
heart failure, first onset AF or where there is an obvious reversible cause.

Rate control: A beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem) is used first-line
to control the rate in AF.
If one drug does not control the rate adequately NICE recommend combination therapy with any 2 of
the following:
A beta blocker, Diltiazem and Digoxin.
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Rhythm control: As mentioned above there are a subgroup of patients for whom a rhythm control
strategy should be tried first.
When considering cardioversion it is very important to remember that the moment a patient switches
from AF to sinus rhythm presents the highest risk for embolism leading to stroke. Imagine the thrombus
formed in the fibrillating atrium suddenly being pushed out when sinus rhythm is restored. For this
reason patients must either have had a short duration of symptoms (less than 48 hours) or be
anticoagulated for a period of time prior to attempting cardioversion.

Reducing stroke risk: Some patients with AF are at a very low risk of stroke whilst others are at a very
significant risk. Clinicians use risk stratifying tools such as the CHA2DS2-VASc score to determine the
most appropriate anticoagulation strategy.

ANTICOAGULATION IN AF: NICE updated their guidelines on the management of atrial fibrillation (AF) in
2021.

Does the patient need anticoagulation?

The need for anticoagulation should be considered in patients with any history of AF, not just if they are
in AF currently, i.e. the following groups should be assessed:

 Symptomatic or asymptomatic paroxysmal, persistent or permanent atrial fibrillation

 Atrial flutter
 A continuing risk of arrhythmia recurrence after cardioversion back to sinus rhythm or catheter
ablation.

NICE suggest using the CHA2DS2-VASc score to determine the most appropriate anticoagulation
strategy. This scoring system superceded the CHADS2 score. The table below shows a
suggested anticoagulation strategy based on the score:

CHA2DS2-VASc Scoring
Risk factors Points
C Congestive heart failure 1
H Hypertension (or treated hypertension) 1
A2 Age > = 75 years 2
D Diabetes 1
S2 Prior Stroke, TIA or thromboembolism 2
V Vascular disease (including IHD and PAD) 1
A Age 65-74 years 1
S Sex (female gender) 1
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 Remember that if a CHA2DS2-VASc score suggests no need for anticoagulation it is important to

ensure a transthoracic echocardiogram has been done to exclude valvular heart disease, which in
combination with AF is an absolute indication for anticoagulation.
 NICE recommend that we offer patients a choice of anticoagulation, including warfarin and the
novel oral anticoagulants (NOACs).
 Assessing bleeding risk
Doctors have always thought carefully about the risk/benefit profile of starting someone on
warfarin. A history of falls, old age, alcohol excess and a history of previous bleeding are common
things that make us consider whether anticoagulation is in the best interests of the patient., but
NICE warn us not to withhold anticoagulation solely on the grounds of age or risk of falls. NICE now
recommend we formalize this risk assessment using the ORBIT scoring system. Previously the HAS-
BLED scoring system was recommended.

Score Anticoagulation
0 No treatment
Males: Consider anticoagulation
1 Females: No treatment (this is because their
score of 1 is only reached due to their gender)
2 or more Offer anticoagulation

If treatment is indicated, which anticoagulant?

For many years warfarin was the anticoagulant of choice in atrial fibrillation. This changed following the
development of direct oral anticoagulants (DOACs). These have the advantage of not requiring regular
blood tests to check the INR and now recommended as the first-line anticoagulant for patients with AF.
If a patient was previously started on warfarin, NICE recommend discussing switching to a DOAC during
a routine follow-up appointment.
The following DOACs are recommended by NICE for reducing stroke risk in AF:

 Apixaban
 Dabigatran
 Edoxaban
 Rivaroxaban

Warfarin is now used second-line, in patients where a DOAC is contraindicated or not tolerated. Aspirin
is not recommended for reducing stroke risk in patients with AF.

ATRIAL FIBRILLATION: CARDIOVERSION:

There are two scenarios where cardioversion may be used in atrial fibrillation:

 Electrical cardioversion as an emergency if the patient is hemodynamically unstable.

 Electrical or pharmacological cardioversion as an elective procedure where a rhythm control
strategy is preferred.
 Electrical cardioversion is synchronized to the R wave to prevent delivery of a shock during the
vulnerable period of cardiac repolarization when ventricular fibrillation can be induced.
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 The notes below refer to cardioversion being used in the elective scenario for rhythm control. The
wording of the 2014 NICE guidelines is as follows: “Offer rate or rhythm control if the onset of the
arrhythmia is less than 48 hours, and start rate control if it is more than 48 hours or is uncertain”

Onset < 48 hours

If the atrial fibrillation (AF) is definitely of less than 48 hours onset patients should be heparinized.
Patients who have risk factors for ischemic stroke should be put on lifelong oral anticoagulation.
Otherwise, patients may be cardioverted using either:

 Electrical - 'DC cardioversion'

 Pharmacology - amiodarone if structural heart disease, flecainide or amiodarone in those without
structural heart disease.

Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further
anticoagulation is unnecessary.

Onset > 48 hours

 If the patient has been in AF for more than 48 hours then anticoagulation should be given for at
least 3 weeks prior to cardioversion. An alternative strategy is to perform a transesophageal echo
(TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinized
and cardioverted immediately. NICE recommend electrical cardioversion in this scenario, rather than
pharmacological.

 If there is a high risk of cardioversion failure (e.g. previous failure or AF recurrence) then it is
recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion
 Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this
time decisions about anticoagulation should be taken on an individual basis depending on the risk of
recurrence
Atrial fibrillation: pharmacological cardioversion
NICE published guidelines on the management of atrial fibrillation (AF) in 2014. The following is also
based on the joint American Heart Association (AHA), American College of Cardiology (ACC) and
European Society of Cardiology (ESC) 2016 guidelines
Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation

 amiodarone
 flecainide (if no structural heart disease)
 others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone

Less effective agents include beta-blockers (including sotalol), calcium channel blockers, digoxin,
disopyramide & procainamide.

ATRIAL FIBRILLATION: RATE CONTROL AND MAINTENANCE OF SINUS RHYTHM

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NICE updated its guidelines on the management of atrial fibrillation (AF) in 2021. The following is also
based on the joint American Heart Association (AHA), American College of Cardiology (ACC) and
European Society of Cardiology (ESC) 2012 guidelines

Patients presenting acutely with AF

If a patient has signs of hemodynamic instability (e.g. hypotension, heart failure) they should
be electrically cardioverted, as per the peri-arrest tachycardia guidelines.
For hemodynamically stable patients, the management depends on how acute the AF is:

 < 48 hours: rate or rhythm control

 ≥ 48 hours or uncertain (e.g. patient not sure when symptoms started): rate control if considered for
long-term rhythm control, delay cardioversion until they have been maintained on therapeutic
anticoagulation for a minimum of 3 weeks

Rate control
Rate control should be offered as the first-line treatment strategy for atrial fibrillation except in people:

 whose atrial fibrillation has a reversible cause

 who have heart failure thought to be primarily caused by atrial fibrillation
 with new-onset atrial fibrillation (< 48 hours)
 with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus
rhythm
 for whom a rhythm-control strategy would be more suitable based on clinical judgement

Medications
Agents used to control rate in patients with atrial fibrillation

 beta-blockers
 a common contraindication for beta-blockers is asthma
 calcium channel blockers
 digoxin
o not considered first-line anymore as they are less effective at controlling the heart rate during
exercise
o should only be considered if he person does no or very little physical exercise or other
rate-limiting drug options are ruled out because of comorbidities
o may have a role if there is coexistent heart failure

Rhythm control
Agents used to maintain sinus rhythm in patients with a history of atrial fibrillation

 beta-blockers
 dronedarone: second-line in patients following cardioversion
 amiodarone: particularly if coexisting heart failure
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Catheter ablation
NICE recommends the use of catheter ablation for those with AF who have
not responded to or wish to avoid, antiarrhythmic medication.
Technical aspects HIGH YIELD POINTS

 The aim is to ablate the faulty electrical pathways that are resulting in SUMMARY OF ATRIAL
atrial fibrillation. This is typically due to aberrant electrical activity FIBRILLATION:
between the pulmonary veins and left atrium
 the procedure is performed percutaneously, typically via the groin  Atrial fibrillation +
 both radiofrequency (uses heat generated from medium frequency Valvular disease:
alternating current) and cryotherapy can be used to ablate the tissue Give Warfarin

 Atrial fibrillation +
Anticoagulation
Stroke or TIA: Give
warfarin
 Should be used 4 weeks before and during the procedure
 It should be remember that catheter ablation controls the rhythm but  Atrial fibrillation +
does not reduce the stroke risk, even if patients remain in sinus CHADS score zero:
rhythm. Therefore, patients still require anticoagulation as per their No treatment
CHA2DS2-VASc score
 if score = 0: 2 months anticoagulation recommended  Pharmacological
 if score > 1: long term anticoagulation recommended cardio version If
no structural heart
Outcome: notable complications include cardiac tamponade, stroke, and disease: Flecainide
pulmonary vein stenosis.
 In case of
INDICATIONS OF DC CARDIO VERSION IN AF ARE: structural heart
 Blood pressure less than 90 mmHg diseases: Give
 chest pain Amiodarone
 heart failure
 Impaired consciousness.
 HR more than 200

NOTE:
 Don't use rhythm control in asymptomatic atrial fibrillation patients nor
in patients with permanent atrial fibrillation.
 Don't use antiplatelet for stroke prevention in Atrial fibrillation
 History of Atrial fibrillation + enlarged left atrial size with previous DC
cardio version: the best long term treatment will be radiofrequency
ablation.
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ATRIAL FLUTTER

Atrial flutter is a form of supraventricular tachycardia characterized by a

succession of rapid atrial depolarization waves. HIGH YIELD POINTS
ECG findings  IV magnesium
 'Sawtooth' appearance. sulfate is used to
 As the underlying atrial rate is often around 300/min the
treat torsades de
ventricular or heart rate is dependent on the degree of AV block.
For example if there is 2:1 block the ventricular rate will pointes.
be 150/min
 flutter waves may be visible following carotid sinus massage or
adenosine  Sotalol may
Management exacerbate long QT
syndrome.
 Treatment of atrial flutter is similar to that of atrial fibrillation
although medication may be less effective.
 Atrial flutter is more sensitive to cardioversion however so lower  Verapamil should
energy levels may be used never be given to a
 Radiofrequency ablation of the tricuspid valve isthmus is curative patient with a
for most patients broad complex
tachycardia as it
VENTRICULAR TACHYCARDIA
may precipitate
Ventricular tachycardia (VT) is broad-complex tachycardia originating from ventricular
a ventricular ectopic focus. It has the potential to precipitate ventricular fibrillation in
fibrillation and hence requires urgent treatment. patients with
There are two main types of VT: ventricular
1. Monomorphic VT: most commonly caused by myocardial infarction
tachycardia.
2. Polymorphic VT: A subtype of polymorphic VT is torsades de pointes
which is precipitated by prolongation of the QT interval. The causes of a
long QT interval are listed below.
 Inherited long QT
CAUSES OF LONG QT SYNDROME
syndrome +
CONGENITAL DRUGS OTHERS sensorineural
deafness - Jervell
Jervell- Includes amiodarone, Electrolyte imbalance
and Lange-Nielsen
Lange- sotalol, Class-I including Hypocalcaemia,
Nielsen antiarrhythmic, TCA, hypokalemia,
syndrome.
syndrome SSRIs, methadone, hypomagnesaemia.
and Romano- chloroquine,
Acute MI, myocarditis,
ward terfenadine,
hypothermia and
syndrome erythromycin and
subarachnoid hemorrhage.
haloperidol.
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Management: Avoid drug causing long QT interval, give beta blockers and implantable defibrillators in
high risk cases.

Ventricular tachycardia: management: Whilst a broad complex tachycardia may result from a
supraventricular rhythm with aberrant conduction, the European Resuscitation Council advise that in a
peri-arrest situation it is assumed to be ventricular in origin.
If the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure, syncope) then
immediate cardioversion is indicated. In the absence of such signs antiarrhythmics may be used. If these
fail, then electrical cardioversion may be needed with synchronized DC shocks

Drug therapy

 amiodarone: ideally administered through a central line

 lidocaine: use with caution in severe left ventricular impairment
 Procainamide

If drug therapy fails

 Electrophysiological study (EPS)

 Implantable cardioverter-defibrillator (ICD) - this is particularly indicated in patients with
significantly impaired LV function

VENTRICULAR TACHYCARDIA IN DIGOXIN TOXICITY:

 Treat with lidocaine and phenytoin

 Avoid Amiodarone and Procainamide (D/C shock when all measures fail (but usually unsuccessful).
If drug therapy fails

 Electrophysiological study (EPS)

 Implantable cardioverter-defibrillator (ICD)
 significantly impaired LV function

TORSADES DE POINTES:

It is a rare arrhythmia associated with a long QT interval. It may deteriorate into ventricular fibrillation
and hence lead to sudden death.
Risk factors:
 Female gender, low HR, CHF, digoxin, Prolonged QT & Subclinical long QT syndrome, severe alkalosis
and recent conversion from AF
Management
 IV magnesium sulphate
 Correct K+ if there is hypokalemia
 Override pacing (set pacemaker to be faster than patient rate then decrease the rate).
 D/C shock.
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HYPOTENSION AND SHOCK

 Acute circulatory failure leading to inadequate tissue perfusion which, if prolonged, results in
irreversible organ failure.
 It is often defined by low BP- Systolic BP < 90 mmHg or mean arterial pressure (MAP) < 65 mmHg with
evidence of tissue hypoperfusion e.g. mottled skin, urine output of < 0.5mL/Kg/hr, serum lactate of >
2 mmol/L.
 Signs of shock: Low GCS / agitation, pallor, cool peripheries, tachycardia, slow capillary refill,
tachypnea, oliguria / anuria.
 Shock can result from inadequate cardiac output or a loss of systemic vascular resistance or both.
INADEQUATE CARDIAC OUTPUT
 Hypovolemia:
 Bleeding: trauma, ruptured aortic aneurysm, GI bleed.
 Fluid loss: Vomiting, burns, third space losses e.g. pancreatitis, heat exhaustion.
Note: Do not underestimate hypovolemia. Signs of shock may not become evident until a 50% loss of
blood volume in adults.

 Pump failure:
 Cardiogenic shock e.g. ACS, arrhythmias, aortic dissection, acute valve failure
 Secondary causes e.g. PE, tension pneumothorax, and cardiac tamponade.

PERIPHERAL CIRCULATORY FAILURE (LOSS OF SVR)

 Septic shock:
 Infection with any organism can cause acute vasodilation from inflammatory cytokines.
Classically patients with shock are warm and vasodilated.
 Sepsis is defined as life threatening organ dysfunction caused by dysregulated host response to
infection.
 Septic shock: Sepsis in combination with
 Either lactate > 2mmol/L despite adequate fluid resuscitation.
 OR the patient is requiring vasopressors to maintain MAP > 65 mmHg.
 Anaphylactic shock:
 Type-I IgE-mediated hypersensitivity reaction. Release of histamine and other agents cause
capillary leak, wheeze, cyanosis, oedema (larynx, lids, tongue, and lips), and urticaria.
 Examples are drugs like penicillin & contrast media in radiology, latex, stings like egg, fish, and
peanuts.
 Neurogenic shock: e.g. spinal cord injury, epidural or spinal anesthesia.
 Endocrine failure: Addison disease or hypothyroidism.
 Others: Drugs e.g. anesthetics, anti-hypertensives, cyanide poisoning.

General principles of Management of shock:

 Early recognition of the state of shock and rectification of the underlying cause are vital in the
management of shock.
 Intravenous access, cardiac monitoring, pulse oximetry, oxygen administration along with urgent
clinical and diagnostic workup is mandatory in all cases.
 Whenever indicated, the principles of basic and advance cardiac life support (BLS & ACLS) should be
followed while managing these patients.
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Hemodynamic targets: Blood pressure should be individualized in each patient. For instance, a mean
MAP of around 65 mmHg is sufficient in most patients with septic shock while it should be on the lower
side in patients with uncontrolled external bleeding e.g. following an RTA (with no head injury) and a
little higher in previously hypertensive patients

Fluids management: Optimal fluid management is one of the cornerstones of hemodynamic

management in shock. Apart from hypovolemic shocks with severe intravascular volume depletion (e.g.
due to bleeding, diarrhea or vomiting), with the exception of cardiogenic shock, almost all circulatory
shock states require IV fluid replacement. The need for IV fluids may be evaluated by observing the
response to a volume challenge (unless there are obvious signs of dehydration and evidence of fluid loss
on clinical grounds).

Types of IV fluids used in the treatment of shock:

Isotonic crystalloid solutions (e.g. 0.9% normal saline [NS] or Ringer’s lactate [RL]) are typically used
for intravascular repletion during shock and hypovolemia. Both NS and RL are equally effective;
however, RL may be preferred in hemorrhagic shock because it somewhat minimizes acidosis and will
not cause hyperchloremia.

Colloid solutions (eg, Polygelene [Haemaccel], Hydroxyethyl starch, Albumin, Dextrans), though not
ideal, may be used effectively for volume replacement during major hemorrhage in the absence of
blood transfusions availability.
Properly cross-matched Blood transfusions are ideal as replacement fluid in shock due to blood
loss. However in an urgent situation, 1 to 2 units of O-negative blood is an acceptable alternative. When
more than 1 to 2 units are transfused (e.g. in major trauma), blood is warmed to 37°C. Patients receiving
6 units may require Inj calcium chloride and replacement of clotting factors like fresh frozen plasma or
cryoprecipitate and platelet transfusions.

Patients not responding to adequate fluid challenge and rehydration are a candidate for
vasopressors administration.

INOTROPIC VASOACTVE CATECHOLAMINES

Drug dosage Hemodynamic action
α adrenergic
4mg/500 ml D5W vasoconstriction β-
Norepinephrine infusion @ 8-12 µg/m Adrenergic inotropic
initially then 2-4 and chronotropic
µg/m maintenance effects.

400 mg/500ml D5W α adrenergic

Dopamine @ 2.5-20 µg/kg/min vasoconstriction

250mg/250 ml D5W
Dobutamine @ 2.5-10 µg/kg/min β-Adrenergic inotropic
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Mechanical ventilatory support: Isolated hypoxic or mixed hypoxemic/ventilatory respiratory failure

may critically jeopardize the tissues oxygenation further in a patient with circulatory shock. Therefore,
not only the measures to increase cardiac output (IV infusions and vasopressors) are taken but also the
threshold for tracheal intubation and mechanical ventilation should be kept very low especially in
patients with slow recovery. Normally, respiratory muscles utilize < 5% of total cardiac output and total
body oxygen consumption. However, patients in shock with respiratory distress (due to pulmonary
edema, acidosis and anemia) may require ≥ 40% of the cardiac output to meet their metabolic needs
and if due to shock body is unable to fulfill this high metabolic demand, respiratory muscles start getting
exhausted leading to ventilatory failure, called type IV respiratory failure. Mechanical ventilation not
only relieves the patient of respiratory distress by taking over the functions of respiratory muscles but
also helps in better oxygenation by administering 100% FiO2 and by appropriately applying positive end-
expiratory pressure (PEEP). The latter, however may be associated with a reduction in venous return and
consequently further reduction in MAP. Therefore, measures should be taken to counteract hypotension
by careful fluids resuscitation and by keeping PEEP as low as possible (must never be >12 cmH2O).
During a positive pressure breath, RV filling has been shown to decrease by 20-70 %, leading to a
decrease in stroke volume that may get worsened by an increasing degree of hypovolemia. Therefore, to
maintain hemodynamic stability, it is important to ensure that these patients are adequately (and not
over) hydrated and, if needed, MAP is maintained around 65 mmHg with judicious use of vasopressors.

Specific management of different types of shock: Shock can be associated with four underlying
patterns, of which three are associated with a low flow (hypovolemic, cardiogenic, obstructive) and the
fourth one (distributive) is associated with a hyperkinetic state.
Hypovolemic shock: (see above for details).
Cardiogenic shock: Due to the failure of cardiac pump function resulting from acute coronary syndrome
(ACS), myopathy, myocarditis or major arrhythmias (such as ventricular tachycardia or ventricular
fibrillation). A cardiac index of < 2.2 l/min/m2 and pulmonary artery occlusion (wedge) pressure of >
18mmHg are usually taken as a cut off index to define cardiogenic shock. Typical chest pain with ECG
changes of ACS may be evident at presentation. Such patients, though hypotensive, are not usually
volume depleted (may rather be overhydrated) and may have peripheral edema, jugular venous
distension (JVD), S 3 &/or S4 gallop and bibasal pulmonary crackles (signs of pulmonary edema). Chest X-
ray and Echocardiogram may be diagnostic (see the chapter on “the management of chest pain and
ACS” for the management of cardiogenic shock).

Obstructive Shock:

Pulmonary Embolism (PE): Apart from massive PE, such type of shock also occurs due to tension
pneumothorax or cardiac tamponade. Such states either lead to a mechanical obstruction of forward
blood flow or prevent adequate ventricular filling leading to a reduced cardiac output and shock. High
degree of clinical suspicion and timely diagnosis usually leads to the definitive therapy of the underlying
disorder.
Management of PE: If PE is suspected, ECG (S1, Q3 T3 pattern), CXR and echocardiogram (showing acute
right ventricular strain) may help in establishing the diagnosis. D-dimers should be checked Immediately
(a negative D-dimer excludes PE) along with baseline PT/aPTT and platelet count and if clinical suspicion
on objective grading by Wells scoring system (see below) is high, urgent contrast enhanced spiral
(helical) CT chest or CTPA using multidetector CT gives the best yield for the diagnosis of PE. Once
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confirmed urgent Heparinization along with Warfarin should be instituted. In patients with persistent
shock and low risk of bleeding, thrombolysis (using Alteplase or rTPA) should be considered. Surgical
option (embolectomy) should be considered in patients with massive PE, persistent shock and
contraindication for thrombolysis. (See the chapter on “the management of chest pain and ACS” for the
management of tension pneumothorax and cardiac tamponade).
Distributive shock: Loss of vascular sympathetic tone due to loss of vasoregulatory control resulting in
maldistribution of blood flow is responsible for this type of shock. It takes place in cases of anaphylaxis,
septicemia, liver failure, neurogenic causes like high spinal injury, spinal or general anesthesia, acute
adrenergic crisis or vasovagal syncope due to fright or sudden emotional trauma. Besides, any condition
that might elicit systemic inflammatory response syndrome (SIRS) like pancreatitis, burns and other
trauma may also lead to onset of such type of shock.
Septic shock: Due to septicemia (or bacteremia proven on blood culture) leading to generalized
activation of intravascular inflammatory mediators and endothelial injury. It is associated with fever
(temp > 380 C or 100.40 F) or even hypothermia (< 360 C or < 96.80 F), tachypnea (RR > 24 breaths/min),
tachycardia (> 90 BPM), diaphoresis, peripheral vasodilatation and capillary leak that often leads to a
further loss of intravascular volume. Because of these features, as against other types of shock, septic
shock presents initially as a hyperdynamic state and therefore labelled as “warm shock”. However, if
untreated in time septic shock also leads to hypodynamic features (as discussed above in hypovolemic
shock). Hematological investigations may reveal leukocytosis (> 12,000) or even leukopenia (<4000) or >
10% band cells. Besides, thrombocytopenia (< 80,000/µl or 50% reduction from the baseline over the
past three days) may also be present. Disseminated intravascular coagulation (DIC) may also complicate
septic shock (indicated by the presence of D-dimers, thrombocytopenia of < 50,000/µl, prolonged
thrombin time and decreased Fibrinogen) that must be kept in mind and managed accordingly. The
mainstay of the management of septic shock is fluid resuscitation to keep MAP >65 mmHg, failing which,
vasopressors (Norepinephrine or Dopamine infusions) can be used as well. Steroids can be used as a
treatment of last resort in cases who are fully fluids resuscitated and are vasopressors dependent.
Besides, administration of appropriate broad spectrum antibiotics according to the underlying clinical
circumstances (e.g. acute abdomen, urosepsis, post splenectomy status, neutropenia, endocarditis or
compromised immune status) should also be considered after taking at least 20 ml peripheral blood for
culture. Tight control of diabetes with Insulin to lower blood glucose levels to 100-120 mg/dl is no more
recommended and it is prudent to keep blood sugar to ~180 mg/dl range. Besides, nutritional support
and prophylaxis for DVT (compression stockings, physiotherapy, early mobilization and if not
contraindicated using low dose Heparin) should also be considered in all critically ill patients.
Goals and principles of treatment of septic shock: The treatment of patients with septic shock has the
following major goals:
 Identify the source of infection, and treat with antimicrobial therapy, surgery, or both (source
control) after taking blood cultures.
 Fluid resuscitation: (see above).
 Administer vasopressors for hypotension that does not respond to initial fluid resuscitation to
maintain a mean arterial pressure (MAP) of 65 mm Hg.
 If CVP is used to target resuscitation, it should be used as a stopping rule. If, during fluid
resuscitation, CVP rapidly increases by more than 2 mm Hg, absolute CVP greater than 8-12 mm Hg,
or signs of volume overload (dyspnea, basal pulmonary crackles, or pulmonary edema on chest
radiograph) occur, fluid infusion as primary therapy needs to be stopped.
 Resuscitate the patient, using supportive measures to correct hypoxia, hypotension, and impaired
tissue oxygenation (hypoperfusion).
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 Maintain adequate organ system function, guided by cardiovascular monitoring, and interrupt the
progression to multiple organ dysfunction syndrome (MODS).
Anaphylactic shock: It is a generalized, severe (may be life-threatening) hypersensitivity reaction
characterized by rapid onset of shock and respiratory distress (chest discomfort, dyspnea and/or
wheezing). Skin manifestations in the form of generalized urticarial rash and pruritus may also ensue at
the same time. Anaphylactic hypersensitivity reaction leading to shock can take place by administration
of certain drugs like IV antibiotics (e.g. Penicillin), Thiamine (B1), antisera (e.g. anti-snake venom),
neuromuscular blocking drugs, administration of Aspirin or NSAIDs, bee/wasp sting, certain foods like
eggs, fish, cow milk protein and peanuts. It is prudent to have resuscitation facilities available before
embarking upon IV administration of drugs likely to cause anaphylaxis. Patients may develop acute
cardiac arrest and must be managed on BLS & ACLS protocol (see chapter on CPR). Other resuscitative
measures include laying the patients flat on a flat surface with legs elevated to increase the venous
return or in recovery position if they are retching and unconscious but breathing spontaneously).
Immediate IM Adrenaline (0.5 ml of 1:1000 i.e. 500 µg) is administered on first recognition of
anaphylaxis and repeated every 5 minutes according to the response of the patient in terms of blood
pressure, pulse and respiratory status of the patient. Remember that patients already taking β-blockers
may not respond to adrenaline and in such cases IV salbutamol should be considered. If the patient is
not responding to IM Adrenaline due to inadequate peripheral perfusion and absorption, IV Adrenaline
should be considered in a dose of 0.5 ml of 1:10,000 dilution i.e. 50 µg by slow IV injection. However, the
patient must be on continuous cardiac monitoring with all resuscitative facilities available before
embarking upon IV Adrenalin. Adrenaline is followed by IV or IM Inj of 10mg of Chlorphenamine and 100
mg Hydrocortisone as an adjunctive therapy. Patients with severe respiratory distress with wheezing not
responding to this regime should be managed on management of acute severe asthma guidelines (see
chapter on “management of acute severe asthma). High flow Oxygen and IV fluids should also be
administered together with above mentioned definitive therapy in all such cases.
Acute adrenergic insufficiency: It may occur in an already diagnosed patient of adrenal insufficiency
(tuberculous or autoimmune adrenalitis) or in patients with sudden withdrawal following long term use
of steroids especially under stressful circumstances like in postoperative and/or post-traumatic period,
ACS or in sepsis. Hemorrhagic adrenal infarction may take place in coagulation disorders, hyper-
coagulable states and in meningococcemia (Waterhouse-Friedrichsen syndrome). If acute adrenal
insufficiency is suspected in patients presenting with shock, urgent steroids administration should be
considered. In an already diagnosed patient of Addison’s disease presenting with shock, 100 mg
Hydrocortisone IV stat and q8h is given after collecting a blood sample for serum electrolytes, blood
sugar and cortisol estimation. As hypoglycemia may take place in acute adrenal insufficiency.
Continuous dextrose saline infusion is also administered until hypotension and hypoglycemia are
corrected. However, if hypo-adrenalism is being suspected in a patient presenting with shock with
previously unknown adrenal status, and the urgency of clinical situation does not allow time for
corticotropin stimulation test, Injection Dexamethasone 4-8 mg IV stat is given along with dextrose
saline IVI. Dexamethasone is administered instead of Hydrocortisone because the former does not
interfere with subsequent serum cortisol estimation in future.
Neurogenic shock: The classic presentation of this type of shock is hypotension without compensatory
tachycardia and/or cutaneous vasoconstriction. Neurogenic shock takes place due to some neurological
insults like high cervical or thoracic spinal cord injury (above T6 level), inadvertently high spinal or
general anesthesia or devastating head injury (however, per se only head injury is unlikely to lead to
neurogenic shock). Such causes lead to a loss of vascular sympathetic tone leading to a reduction in
afterload due to arteriolar and a reduction in venous return due to venous capacitance vessels’
dilatation respectively. The situation is complicated by the absence of compensatory tachycardia leading
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to profound hypotension precipitating early cerebral or myocardial ischemic damage. Initial

management includes establishing IV access, ensuring patent airway and adequate ventilation/
breathing, bleeding control and fluids resuscitation (usually under CVP monitoring).
Shock in poly-trauma patents: There may be several causes of shock in a poly trauma patient e.g.
following a motor vehicle crash, fall from height, fire-arm injuries and victim of bomb blasts (including
severe burns). The causes include external bleeding secondary to open wounds (lacerations, cuts or
stabs), open or closed long bone fractures or internal / concealed bleeding in the form of
hemoperitonium, accumulation of blood in pelvic cavity or in thigh after pelvic or femur fracture
respectively or rarely as a result of large hemothorax. Apart from blood loss, these patients are also
prone to develop systemic inflammatory response syndrome (SIRS) that may lead to a fall in systemic
vascular resistance (SVR) aggravating the shock by precipitating severe hypotension.
Importance of bedside sonography in shock and trauma: Bedside abdominal sonography in patients
with trauma has a special role in managing such patients especially in taking decisions regarding
laparotomy; commonly referred to as FAST (Focused Assessment by Sonography in Trauma), it has been
shown to be invaluable in detecting pericardial fluid (? Tamponade), peri-hepatic or splenic and pelvic
hematomas helping in making a diagnosis of intraperitoneal bleeding, most likely, due to organ or viscus
rupture or vascular trauma needing urgent laparotomy. FAST has been shown to have a sensitivity of
94.6% and specificity of 95.1% with an overall accuracy of 94.9% in identifying the presence of intra-
abdominal injuries.

In extended-FAST (eFAST), USG can even be utilized to look for the presence and quantification of
pneumothorax (? Tension pneumothorax). Apart from its use in trauma patients, FAST along with
diagnostic peritoneal lavage (DPL) has been proven to be quite useful in diagnosing intraperitoneal
bleed and septic peritonitis (? Perforated DU or typhoid enteric perforation). FAST and DPL assisted
rapid diagnosis helps in managing these patients early with rapid IV volume repletion and antibiotics and
stopping further losses by taking appropriate measures (e.g. laparotomy in perforated DU or ileum and
ruptured ectopic pregnancy). Timely diagnosis and management are usually sufficient to manage shock
in such patients. All hemodynamically unstable patients with positive FAST must undergo immediate
laparotomy. On the other hand a CT abdomen should be considered in hemodynamically stable patients.

Stress ulcer prophylaxis and use of steroids in shock: All severely ill bed-ridden patients with shock,
SIRS or MODS ( especially if they require mechanical ventilation) must receive IV proton pump inhibitors
(PPIs) to prevent stress peptic ulceration and UGI bleed till the recovery takes place.
Low-dose steroids (200-300 mg of hydrocortisone for 5-7 days) improved survival and the reversal
of shock in vasopressor-dependent patients. Low-dose steroids should be considered on an individual
basis for patients with refractory hypotension (e.g. septicemic shock) despite adequate fluid
resuscitation and appropriate vasopressor administration. Prior to initiating steroid therapy, however,
physicians must consider the potential risks of steroids, such as stress ulcers and hyperglycemia.
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BASIC LIFE SUPPORT

It is the initial set of responses and actions taken by a untrained lay rescuer
or health care professionals immediately after an observed cardio-
HIGH YIELD POINTS
pulmonary arrest (CPA), to sustain perfusion to the vital organs, especially
brain.
When to terminate CPR:
1. Unresponsive, no pulse, and not breathing
 BLS should be
a) Activate emergency response
terminated if there
b) Obtain defibrillator; when available, attach and activate
are no signs of life 15-
c) Begin CAB resuscitation (compressions, airway, breathing)
i. Compressions: 100/min, 2 inches depth, allow recoil, 20 minutes after
minimize interruptions commencing CPR.
ii. Airway: Head tilt, chin lift; jaw thrust if trauma  No ROSC (return of
iii. Breathing: Compressions only; if second trained rescuer spontaneous
available,30:2 ratio; with advanced airway, 8-10 breaths per circulation) achieved
minute before transport, no
d) Every 2 minutes, reassess, rotate compressors, and resume shock delivered, no
compressions promptly. bystander initiated
CPR
ADVANCED CARDIAC LIFE SUPPORT  CPA was unwitnessed
or CPR was
commenced
The following is based on the 2021 Resus Council guidelines. Please see the inadvertently by an
link for more details, below is only a very brief summary of key points.
ULR in an already
It should be remembered that the algorithm divides patients into those
dead person with no
with:
signs of life.
 'shockable' rhythms: ventricular fibrillation/pulseless ventricular IMP points in ATLS:
tachycardia (VF/pulseless VT)
 'non-shockable' rhythms: asystole/pulseless-electrical activity  Atropine is no longer
(asystole/PEA) recommended for
routine use in asystole
Major points include: or pulseless electrical
activity (PEA).
 Chest compressions:  Following successful
o the ratio of chest compressions to ventilation is 30:2 resuscitation oxygen
o chest compressions are now continued while a defibrillator is should be titrated to
charged achieve saturations of
 Defibrillation: 94-98%. This is to
o A single shock for VF/pulseless VT followed by 2 minutes of
address the potential
CPR
harm caused by
o If the cardiac arrested is witnessed in a monitored patient
(e.g. in a coronary care unit) then the 2015 guidelines hyperoxaemia.
recommend 'up to three quick successive (stacked) shocks',
rather than 1 shock followed by CPR
 Drug delivery:
o IV access should be attempted and is first-line
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o if IV access cannot be achieved then drugs should be given via the intraosseous route (IO)
o delivery of drugs via a tracheal tube is no longer recommended
 Adrenaline:
o adrenaline 1 mg as soon as possible for non-shockable rhythms
o during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have
restarted after the third shock
o repeat adrenaline 1mg every 3-5 minutes whilst ALS continues
 Amiodarone:
o Amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3
shocks have been administered.
o a further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT
after 5 shocks have been administered
o lidocaine used as an alternative if amiodarone is not available or a local decision has been
made to use lidocaine instead
 Thrombolytic drugs:
o Should be considered if a pulmonary embolus is suspected
o If given, CPR should be continued for an extended period of 60-90 minutes.

REVERSIBLE CAUSES OF CARDIAC ARREST

The 'Hs' The 'Ts'
 Hypoxia
 Hypovolemia
• Thrombosis (coronary or pulmonary)
 Hyperkalemia, hypokalaemia, hypoglycaemia,
• Tension pneumothorax
hypocalcaemia, acidemia and other metabolic
• Tamponade – cardiac
disorders
• Toxins
 Hypothermia

HEART FAILURE:

Acute heart failure (AHF) is a term used to describe the sudden onset or worsening of the symptoms of
heart failure. AHF is usually caused by a reduced cardiac output that results from a functional or
structural abnormality. The most common precipitating causes of acute AHF are acute coronary
syndrome, hypertensive crisis, acute arrhythmia and valvular disease. There is generally a history of pre-
existing cardiomyopathy. It usually presents with signs of fluid congestion, weight gain, orthopnea and
breathlessness.

Symptoms Signs
Breathlessness Cyanosis
Reduced exercise tolerance Tachycardia
Oedema Elevated jugular venous pressure
Fatigue Displaced apex beat
Chest signs: classically bibasal crackles but may also
cause a wheeze
S3-heart sound
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The diagnostic workup for patients with AHF includes:

 Blood tests – this is to look for any underlying abnormality such as HIGH YIELD POINTS
anemia, abnormal electrolytes or infection.
 Chest X-ray – findings include pulmonary venous congestion, interstitial  Nifedipine is
oedema and cardiomegaly contraindicated in
 Echocardiogram – this will identify pericardial effusion and cardiac heart failure.
tamponade
 BNP – raised levels (>100mg/litre) indicate myocardial damage and are

supportive of the diagnosis.

Heart failure: drug management

 The first-line treatment for all patients is both an ACE-inhibitor and

a beta-blocker. ACE-inhibitors and beta-blockers have no effect on
mortality in heart failure with preserved ejection fraction.
 Second-line treatment is an aldosterone antagonist. These are
sometimes referred to as mineralocorticoid receptor antagonists.
Examples include spironolactone and eplerenone.
 Third-line treatment should be initiated by a specialist. Options include
ivabradine, sacubitril-valsartan, hydralazine in combination with
nitrate, digoxin and cardiac resynchronization therapy
o Ivabradine
 Criteria: sinus rhythm > 75/min and a left ventricular
fraction < 35%

o Sacubitril-valsartan
 Criteria: left ventricular fraction < 35%
 is considered in heart failure with reduced ejection
fraction who are symptomatic on ACE inhibitors or
ARBs
 should be initiated following ACEIs or ARBs wash-out
period
o Digoxin
 Digoxin has also not been proven to reduce mortality in
patients with heart failure. It may however improve
symptoms due to its inotropic properties
 it is strongly indicated if there is coexistent atrial
fibrillation
o Hydralazine in combination with nitrate
 this may be particularly indicated in Afro-Caribbean
patients
o Cardiac resynchronization therapy
 indications include a widened QRS (e.g. left bundle
branch block) complex on ECG

Other treatments: Vaccinations

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 Offer annual influenza vaccine

 Offer one-off pneumococcal vaccine. Adults usually require just one dose but those with asplenia,
splenic dysfunction or chronic kidney disease need a booster every 5 years

Heart failure: non-drug management

CARDIAC RESYNCHRONIZATION THERAPY

 for patients with heart failure and wide QRS

 biventricular pacing
 improved symptoms and reduced hospitalization in NYHA class III patients

Exercise training: improves symptoms but not hospitalization/mortality.

PULMONARY EDEMA:
 Pulmonary edema is rapid onset of fluid accumulating in the lungs. It is the worst (more severe)
form of CHF.
 Usually present with SOB, orthopnea, JVD, S3 gallop and edema.
 Diagnostic tests:
o Brain natriuretic peptide (BNP) if the etiology of SOB is not clear.
o X-ray chest
o Oximetry / arterial blood gases
o ECG
o Echocardiography
 Treatment: Oxygen, morphine, loop diuretics, ACEIs / ARBs and nitrates.
 Dobutamine, digoxin, nitroprusside and IV hydralazine can be used whenever required.

MYOCARDITIS:
Myocarditis describes inflammation of the myocardium.
Causes

 viral: coxsackie B, HIV

 bacteria: diphtheria, clostridia
 spirochaetes: Lyme disease
 protozoa: Chagas' disease, toxoplasmosis
 autoimmune
 drugs: doxorubicin

Presentation

 usually young patient with an acute history

 chest pain
 Dyspnea
 Arrhythmias

Investigations
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 bloods
o ↑ inflammatory markers in 99%
o ↑ cardiac enzymes
o ↑ BNP HIGH YIELD POINTS
 ECG
o tachycardia
 HOCM murmur
o arrhythmias
o ST/T wave changes including ST-segment elevation become soft with
and T wave inversion rapid squatting as
venous return to the
Management heart is increased
and outflow tract
 treatment of underlying cause e.g. antibiotics if bacterial
obstruction become
cause
 supportive treatment e.g. of heart failure or arrhythmias less severe.

Complications

 heart failure
 arrhythmia, possibly leading to sudden death
 dilated cardiomyopathy: usually a late complication

HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY:

Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal

dominant disorder of muscle tissue caused by defects in the genes
encoding contractile proteins. HOCM is important as it is the most
common cause of sudden cardiac death in the young.

Features

 often asymptomatic
 exertional dyspnea
 angina
 syncope
o typically following exercise
o due to subaortic hypertrophy of the ventricular
septum, resulting in functional aortic stenosis
 sudden death (most commonly due to ventricular
arrhythmias), arrhythmias, heart failure
 jerky pulse, large 'a' waves, double apex beat
 ejection systolic murmur
o increases with Valsalva manoeuvre and decreases on
squatting.
o hypertrophic cardiomyopathy may impair mitral valve
closure, thus causing regurgitation
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Associations

 Friedreich's ataxia
 Wolff-Parkinson White

Echo findings - mnemonic - MR SAM ASH

 mitral regurgitation (MR)

 systolic anterior motion (SAM) of the anterior mitral valve leaflet
 asymmetric hypertrophy (ASH)

ECG

 left ventricular hypertrophy

 non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
 deep Q waves
 atrial fibrillation may occasionally be seen

Management

 Amiodarone
 Beta-blockers or verapamil for symptoms
 Cardioverter defibrillator
 Dual chamber pacemaker
 Endocarditis prophylaxis*

Drugs to avoid

 nitrates
 ACE-inhibitors
 inotropes

DILATED CARDIOMYOPATHY:

Dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy, accounting for 90% of
cases.
Causes:

 idiopathic: the most common cause

 myocarditis: e.g. Coxsackie B, HIV, diphtheria, Chagas disease
 ischemic heart disease
 Peripartum cardiomyopathy
 hypertension
 iatrogenic: e.g. doxorubicin
 substance abuse: e.g. alcohol, cocaine
 inherited: either a familial genetic predisposition to DCM or a specific syndrome e.g. Duchenne
muscular dystrophy
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o around a third of patients with DCM are thought to

have a genetic predisposition
o a large number of heterogeneous defects have been
identified HIGHYIELD POINTS
o the majority of defects are inherited in an autosomal
dominant fashion although other patterns of Signs and symptoms of
inheritance are seen right sided heart failure
 infiltrative e.g. haemochromatosis, sarcoidosis
with bi-atrial enlargement
+ these causes may also lead to restrictive cardiomyopathy and low voltage ECG with
elevated JVP & absent Y
 nutritional e.g. wet beriberi (thiamine deficiency) descent on JVP are
characteristics of
Features restrictive
cardiomyopathy.
 classic findings of heart failure
 systolic murmur: stretching of the valves may result in mitral
and tricuspid regurgitation
 S3
 'balloon' appearance of the heart on the chest x-ray

Treatment:
 ACEIs / ARBs, beta blockers, diuretics and digoxin. Hydralazine
and nitrates can also be used.
 Biventricular pacemaker if QRS is wide (> 120 ms). The wider the
QRS, the greater the benefit of biventricular pacemaker.
 Automated implantable cardioverter / defibrillator if low
ejection fraction.

RESTRICTIVE CARDIOMYOPATHY:
Causes

 amyloidosis (e.g. secondary to myeloma) - most common cause

in UK
 haemochromatosis
 post-radiation fibrosis
 Loffler's syndrome: endomyocardial fibrosis with a prominent
eosinophilic infiltrate
 endocardial fibroelastosis: thick fibroelastic tissue forms in the
endocardium; most commonly seen in young children
 sarcoidosis
 scleroderma

Features

 similar to constrictive pericarditis

 low-voltage ECG
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Features suggesting restrictive cardiomyopathy rather than constrictive pericarditis

 prominent apical pulsev

 absence of pericardial calcification on CXR
 the heart may be enlarged
 ECG abnormalities e.g. bundle branch block, Q waves

Investigations

 Echocardiography
 cardiac MRI

Management:
 Treat the underlying cause
 Diuretics, cardiac maneuvers, amyl nitrate and ACEIs / ARBs.

PERICARDITIS:

Pericarditis is one of the differentials of any patient presenting with chest pain.
Features

 Chest pain: may be pleuritic. Is often relieved by sitting forwards

 other symptoms include non-productive cough, dyspnea and flu-like symptoms
 pericardial rub, tachypnea and tachycardia.

Causes include viral infections (Coxsackie), tuberculosis, uraemia (causes 'fibrinous' pericarditis),
trauma, post-myocardial infarction (Dressler's syndrome), connective tissue disease, hypothyroidism
and malignancy
Investigations

 ECG changes
o the changes in Pericarditis are often global/widespread, as opposed to the 'territories'
seen in ischemic events
o 'saddle-shaped' ST elevation
o PR depression: most specific ECG marker for pericarditis
 all patients with suspected acute pericarditis should have transthoracic echocardiography

Management

 treat the underlying cause

 a combination of NSAIDs and colchicine is now generally used for first-line for patients with
acute idiopathic or viral pericarditis

CARDIAC TAMPONADE

Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure.

Classical features - Beck's triad: Hypotension + raised JVP + muffled heart sounds.
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Other features:

 dyspnea & tachycardia

 an absent Y descent on the JVP - this is due to the limited right ventricular filling
 pulsus paradoxus - an abnormally large drop in BP during inspiration
 ECG: electrical alternans.

The key differences b/w constrictive pericarditis & cardiac tamponade are summarized below:

Cardiac Constrictive
tamponade pericarditis

JVP Absent Y X + Y present

descent

Pulsus Present Absent

paradoxus

Kussmaul's sign Rare Present

Characteristic Pericardial
features calcification on CXR

Management: urgent pericardiocentesis

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
Associations:

 Hypertension: the most important risk factor

 Trauma
 Bicuspid aortic valve
 Collagens: Marfan's syndrome, Ehlers-Danlos syndrome
 Turner's and Noonan's syndrome
 Pregnancy
 Syphilis

Features: x

 Chest pain: typically severe, radiates through to the back and 'tearing' in nature
 Aortic regurgitation
 Hypertension
 Other features may result from the involvement of specific arteries. For example coronary
arteries → angina, spinal arteries → paraplegia, distal aorta → limb ischemia.
 The majority of patients have no or non-specific ECG changes. In a minority of patients, ST-
segment elevation may be seen in the inferior leads
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Classification
Stanford classification

 type A - ascending aorta, 2/3 of cases

 type B - descending aorta, distal to left subclavian origin, 1/3 of cases

DeBakey classification

 type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond
it distally
 type II - originates in and is confined to the ascending aorta
 type III - originates in descending aorta, rarely extends proximally but will extend distally

Aortic dissection: management

Type A is managed surgically but blood pressure should be controlled to a target systolic of 100-120
mmHg whilst awaiting intervention

Type B is managed conservatively. Bed rest is advised and blood pressure is reduced with IV labetalol to
prevent progression.
Complications:
Complications of backward tear include aortic incompetence/regurgitation and MI (inferior pattern
often seen due to right coronary involvement)

Complications of forward tear are unequal arm pulses and BP, stroke, & renal failure.

HYPERTENSION:

Hypertension: secondary causes

It is thought that between 5-10% of patients diagnosed with hypertension have primary
hyperaldosteronism, including Conn's syndrome. This makes it the single most common cause of
secondary hypertension.
Renal disease accounts for a large percentage of the other cases of secondary hypertension. Conditions
which may increase the blood pressure include:

 glomerulonephritis
 pyelonephritis
 adult polycystic kidney disease
 renal artery stenosis

Endocrine disorders (other than primary hyperaldosteronism) may also result in increased blood
pressure:

 phaeochromocytoma
 Cushing's syndrome
 Liddle's syndrome
 congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
 acromegaly
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Drug causes:

 steroids
 monoamine oxidase inhibitors
 the combined oral contraceptive pill
 NSAIDs
 leflunomide

Other causes include:

 Pregnancy
 coarctation of the aorta

Blood pressure classification: This becomes relevant later in some of the management decisions that
NICE advocate.

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
hypertension average or HBPM average BP >= 150/95 mmHg
Severe Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120
hypertension mmHg

Diagnosing hypertension
 Firstly, NICE recommend measuring blood pressure in both arms when considering a diagnosis
of hypertension. If the difference in readings between arms is more than 20 mmHg then the
measurements should be repeated. If the difference remains > 20 mmHg then subsequent blood
pressures should be recorded from the arm with the higher reading. It should of course be
remember that there are pathological causes of unequal blood pressure readings from the arms,
such as supravalvular aortic stenosis. It is therefore prudent to listen to the heart sounds if a
difference exists and further investigation if a very large difference is noted.
 NICE also recommend taking a second reading during the consultation, if the first reading is >
140/90 mmHg. The lower reading of the two should determine further management.
 NICE suggest offering ABPM or HBPM to any patient with a blood pressure >= 140/90 mmHg.
 If the blood pressure is >= 180/120 mmHg:

 admit for specialist assessment if:

o signs of retinal haemorrhage or papilledema (accelerated hypertension) or
o life-threatening symptoms such as new-onset confusion, chest pain, signs of heart
failure, or acute kidney injury
 NICE also recommend referral if a phaeochromocytoma is suspected (labile or postural
hypotension, headache, palpitations, pallor and diaphoresis)
 if none of the above then arrange urgent investigations for end-organ damage (e.g. bloods,
urine ACR, ECG)
o if target organ damage is identified, consider starting antihypertensive drug
treatment immediately, without waiting for the results of ABPM or HBPM.
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o if no target organ damage is identified, repeat clinic blood pressure measurement

within 7 days

Ambulatory blood pressure monitoring (ABPM)

 at least 2 measurements per hour during the person's usual waking hours (for example,
between 08:00 and 22:00)
 use the average value of at least 14 measurements

If ABPM is not tolerated or declined HBPM should be offered.

Home blood pressure monitoring (HBPM)

 for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart
and with the person seated
 BP should be recorded twice daily, ideally in the morning and evening
 BP should be recorded for at least 4 days, ideally for 7 days
 discard the measurements taken on the first day and use the average value of all the remaining
measurements

Hypertension: management: NICE published updated guidelines for the management of hypertension in
2019. Some of the key changes include:

 lowering the threshold for treating stage 1 hypertension in patients < 80 years from 20% to 10%
 angiotensin receptor blockers can be used instead of ACE-inhibitors where indicated
 If a patient is already taking an ACE-inhibitor or angiotensin receptor blocker, then a calcium
channel blocker OR a thiazide-like diuretic can be used. Previously only a calcium channel
blocker was recommended

Managing hypertension
Lifestyle advice should not be forgotten and is frequently tested in exams:

 a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in
the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt
intake can have a significant effect on blood pressure. For example, reducing salt intake by
6g/day can lower systolic blood pressure by 10mmHg
 caffeine intake should be reduced
 the other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich
in fruit and vegetables, exercise more, lose weight

ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)

 treat if < 80 years of age AND any of the following apply; target organ damage, established
cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to
10% or greater
 in 2019, NICE made a further recommendation, suggesting that we should 'consider
antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with
stage 1 hypertension and an estimated 10-year risk below 10%. '. This seems to be due to
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evidence that QRISK may underestimate the lifetime probability of

developing cardiovascular disease

ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension) HIGH YIELD POINTS
 offer drug treatment regardless of age New drugs
direct renin inhibitors
For patients < 40 years consider specialist referral to exclude secondary
causes.  e.g. Aliskiren
Step 1 treatment (branded as Rasilez)
by inhibiting renin
 patients < 55-years-old or a background of type 2 diabetes
blocks the
mellitus: ACE inhibitor or a Angiotensin receptor blocker (ACE-i
or ARB): (A) conversion of
o angiotensin receptor blockers should be used where ACE angiotensinogen to
inhibitors are not tolerated (e.g. due to a cough) angiotensin-I
 patients >= 55-years-old or of black African or African–Caribbean 
origin: Calcium channel blocker (C)
o ACE inhibitors have reduced efficacy in patients of black
African or African–Caribbean origin are therefore not used
first-line

Step 2 treatment

 if already taking an ACE-i or ARB add a Calcium channel blocker or a

thiazide-like Diuretic
 if already taking a Calcium channel blocker add an ACE-i or ARB
o for patients of black African or African–Caribbean origin
taking a calcium channel blocker for hypertension, if they
require a second agent consider an angiotensin receptor
blocker in preference to an ACE inhibitor
 (A + C) or (A + D)

Step 3 treatment

 add a third drug to make, i.e.:

o if already taking an (A + C) then add a D
o if already (A + D) then add a C
 (A + C + D)

Step 4 treatment

 NICE define step 4 as resistant hypertension and suggest either

adding a 4th drug (as below) or seeking specialist advice
 first, check for:
o confirm elevated clinic BP with ABPM or HBPM
o assess for postural hypotension.
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o discuss adherence
 if potassium < 4.5 mmol/l add low-dose spironolactone
 if potassium > 4.5 mmol/l add 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 if it has not yet been obtained.
Blood pressure targets

Clinic BP ABPM / HBPM

Age < 80 years 140/90 mmHg 135/85 mmHg
Age > 80 years 150/90 mmHg 145/85 mmHg

HYPERTENSION IN PREGNANCY:
 Hypertension usually falls in the first trimester (particularly the diastolic) and continue to fall
until 20-24 weeks.
 If patient is pregnant and there is risk of developing pre-eclampsia or eclampsia, start her on
low dose (75mg daily) aspirin from 12 weeks onwards.
 Never give ACEIs or ARBs to pregnant patients or patients with renal artery stenosis.

Pre-existing Hypertension Pregnancy induced Pre-eclampsia

hypertension
History of hypertension Occurring in 2nd half of Pregnancy induced hypertension
before pregnancy or an pregnancy i.e. after 20 in association with proteinuria (>
elevated BP (> 140/90) weeks. 3gm/24 hours).
before 20 weeks gestation. No proteinuria, no oedema Oedema may occur.

PULMONARY HYPERTENSION:

 A sustained elevation in mean pulmonary arterial pressure of greater than 25 mmHg at rest or 30
mmHg after exercise.
 Presentation: Exertional dyspnea, chest pain and syncope.
 On examination there is loud P2 and left parasternal heave (due to right ventricular hypertrophy).
 It is diagnosed by cardiac catheterization.
 Management:
o Treat the underlying condition.
o Acute vasodilator testing.
 Positive vasodilator response: Calcium channel blockers.
 Negative vasodilator response: prostacyclin analogues (treprostinil, iloprost),
endothelin receptor antagonists (bosentan), and phosphodiesterase inhibitors
(sildenafil).
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CARDIAC MANIFESTATIONS OF SYSTEMIC DISEASES

SYSTEMIC DISORDER COMMON CARDIAC MANIFESTATIONS

Diabetes mellitus CAD, atypical angina, CMP, systolic or diastolic CHF.

Protein calorie Dilated CMP, CHF.

malnutrition

Thiamine deficiency High output failure, dilated CMP.

Hyperhomocysteinemia Premature atherosclerosis.

Obesity CMP, systolic or diastolic CHF.

Hyperthyroidism Palpitations, SVT, atrial fibrillation and hypertension

Hypothyroidism Hypotension, bradycardia, dilated CMP, CHF and pericardial effusion.

Malignant carcinoid Tricuspid and pulmonary valve disease, right heart failure.

pheochromocytoma Hypertension, palpitations and CHF.

Acromegaly Systolic or diastolic heart failure.

Rheumatoid arthritis Pericarditis, pericardial effusion, coronary arteritis, myocarditis,

valvulitis.

Seronegative Aortitis, aortic and mitral insufficiency, conduction abnormalities

arthropathies

SLE Pericarditis, Libman Sacks endocarditis, myocarditis, arterial and venous

thrombosis.

HIV Myocarditis, dilated CMP, pericardial effusion.

Amyloidosis CHF, restrictive CMP, valvular regurgitation and pericardial effusion.

Sarcoidosis CHF, dilated or restrictive CMP, ventricular arrhythmias and heart block.

Hemochromatosis CHF, arrhythmias and heart block.

Marfan syndrome Aortic aneurysm and dissection, aortic insufficiency, mitral valve
prolapse.

Ehler-Danlos syndrome Aortic and coronary aneurysm, mitral and tricuspid valve prolapse.

Abbreviations: CAD, coronary artery disease: CHF, congestive heart failure: CMP, Cardiomyopathy:
SVT, supraventricular tachycardia.
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CARDIAC PATIENT AND PREGNANCY

The Cardiac Disease in Pregnancy Investigation (CARPREG I) scoring system for risk from cardiac events
for women with heart disease noted four major risk factors:
1. NYHA FC III or IV heart failure,
2. Prior cardiac events
3. Mitral or aortic obstruction, and
4. LVEF less than 40%.

CARDIOVASCULAR COMPLICATIONS OF PREGNANCY: Pregnancy-related hypertension (eclampsia and

preeclampsia) is already discussed.

CARDIOMYOPATHY OF PREGNANCY (PERIPARTUM CARDIOMYOPATHY):

 Peripartum cardiomyopathy (PPCM) develops during the last trimester or within the first 5
months after pregnancy.
 Heart failure after pregnancy is most likely due to PPCM.
 More common in older women, greater parity and multiple gestations
 Treatment options include beta blockers, diuretics, hydralazine and nitrates.
 Sotalol is acceptable for ventricular or atrial arrhythmias if other beta blockers are ineffective.
 In severe cases, transient use of extracorporeal membrane oxygenation (ECMO) has been lifesaving.
 Delivery of the baby is important, though the peak incidence of the problem is in the first week after
delivery and a few cases appear up to 5 weeks after delivery.
IMPORTANT POINTS REGARDING PULSE
 PULSUS PARADOXUS (abnormal decrease in pulse volume during inspiration) => severe asthma and
cardiac tamponade
 SLOW RISING PULSE => Aortic stenosis.
 COLLAPSING PULSE => Aortic regurgitation and PDA.
 IRREGULARLY IRREGULAR PULSE => AF and multiple ectopic.
 REGULARLY IRREGULAR PULSE => digoxin toxicity.
 HYPERKINETIC PULSE => Exercise, Pregnancy, Thyrotoxicosis, and anemia.
 PULSUS ALTERNANS (alternating strong & weak beats) => Severe LVF.
 BISFERIESN PULSE (Also known as biphasic pulse, a cardiac cycle with two peaks, a small one
followed by a strong & broad one) => mixed aortic valve disease.
 JERKY PULSE => HOCM.
 ABSENT RADIAL PULSE => Dissection of aorta with subclavian involvement, post catheterization,
Takayasu arteritis and trauma.

JUGULAR VENOUS PULSE

As well as providing information on right atrial pressure, the jugular vein waveform may provide clues to
underlying valvular disease. A non-pulsatile JVP is seen in superior vena caval obstruction. Kussmaul's
sign describes a paradoxical rise in JVP during inspiration seen in constrictive pericarditis.
 JVP is raised in heart failure, obstruction of vena cava, supraclavicular lymph node enlargement and
increased thoracic pressure.
 “A” wave = Atrial contraction.
o Prominent “A” wave => Pulmonary Hypertension. Large “A” also seen in tricuspid and
pulmonary stenosis.
o Absent “A” wave => Atrial Fibrillation.
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 Canon A-waves: Caused by atrial contractions against a closed tricuspid valve.

o Irregular => Complete heart block.
o Regular => junctional bradycardia, SVT and VT.
 'C' wave: Caused by closure of tricuspid valve and is not normally visible
 'V' wave: Due to passive filling of blood into the atrium against a closed tricuspid valve.
o Giant v waves in tricuspid regurgitation
 'X' descent = fall in atrial pressure during ventricular systole.
 'Y' descent = opening of tricuspid valve.
o Absent Y descent in JVP => Cardiac Tamponade.

DRUGS USED FOR THE MANAGEMENT OF CARDIOVASCULAR DISORDERS

DRUGS SIDE EFFECTS NOTES

ACE INHIBITORS Cough, angioedema (without  Pregnancy and breastfeeding - avoid
urticaria), hyperkalemia and  Reno-vascular disease - may result in renal
first-dose hypotension. impairment
 Aortic stenosis - may result in hypotension
 Hereditary idiopathic angioedema
 Specialist advice should be sought before
starting ACE inhibitors in patients with a
potassium >= 5.0 mmol/L.

ADENOSINE Chest pain, bronchospasm,  Commonly used in SVTs.

transient flushing and can  The effects of adenosine are enhanced by
enhance conduction down dipyridamole (antiplatelet agent)
accessory pathways, resulting and blocked by theophyllines.
in increased ventricular rate  It should be avoided in asthmatics due to
(e.g. WPW syndrome). possible bronchospasm.

BETA-BLOCKERS Bronchospasm, cold Contraindications include uncontrolled heart

e.g. atenolol peripheries, fatigue, sleep failure, asthma, sick sinus syndrome and
and propranolol disturbances, including concurrent use of verapamil (may precipitate
nightmares and erectile severe bradycardia).
dysfunction.
IVABRADINE Visual disturbances including Ivabradine is a class of anti-anginal drug which
phosphenes & green works by reducing the heart rate. It acts on
luminescence, headache, the If ('funny') ion current which is highly
bradycardia, & heart block. expressed in the sinoatrial node, reducing cardiac
pacemaker activity.
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ANTIPLATELETS: SUMMARY OF LATEST GUIDANCE

Diagnosis 1st line 2nd line

Acute coronary Aspirin (lifelong) & ticagrelor If aspirin contraindicated, clopidogrel
syndrome (12 months) (lifelong)
Percutaneous coronary Aspirin (lifelong) & prasurgrel If aspirin contraindicated, clopidogrel
intervention or ticagrelor (12 months) (lifelong)
TIA Clopidogrel (lifelong) Aspirin (lifelong) & dipyridamole
(lifelong)
Ischaemic stroke Clopidogrel (lifelong) Aspirin (lifelong) & dipyridamole
(lifelong)
Peripheral arterial Clopidogrel (lifelong) Aspirin (lifelong)
disease

DABIGATRAN:

Dabigatran is an oral anticoagulant (direct thrombin inhibitor). Dabigatran is currently used for two main
indications.

 Prophylaxis of venous thromboembolism following hip or knee replacement surgery.

 For prevention of stroke in patients with non-valvular AF who have one or more of the following risk
factors present:
o Previous stroke, transient ischemic attack or systemic embolism
o Left ventricular ejection fraction below 40%
o Symptomatic heart failure of New York Heart Association (NYHA) class 2 or above
o Age 75 years or older
o Age 65 years or older with one of the following: diabetes mellitus, coronary artery disease
or hypertension

Side-effects: hemorrhage is the major adverse effect.

Dose should be reduced in chronic kidney disease and it should not be prescribed if the creatinine
clearance is < 30 ml/min.
Reversing the effects: Idarucizumab can be used for rapid reversal of the anticoagulant effects of
dabigatran.

STATINS:

Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol
synthesis.
Adverse effects include myopathy, liver impairment and may increase the risk of intracerebral
haemorrhage in patients who've previously had a stroke. For this reason the Royal College of Physicians
recommend avoiding statins in patients with a history of intracerebral haemorrhage.

Contraindications include pregnancy and concurrent use of macrolides (e.g. erythromycin,

clarithromycin).
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Who should receive a statin?

 all people with established cardiovascular disease (stroke, TIA, ischemic heart disease, peripheral
arterial disease)
 following the 2014 update, NICE recommend anyone with a 10-year cardiovascular risk >= 10%
 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. NICE
currently recommends the following for the prevention of cardiovascular disease:

 Atorvastatin 20mg for primary prevention

o increase the dose if non-HDL has not reduced for >= 40%
 Atorvastatin 80mg for secondary prevention.

THIAZIDE DIURETICS

Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of the distal convoluted
tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter. Potassium is lost as a result of more
sodium reaching the collecting ducts. Thiazide diuretics have a role in the treatment of mild heart failure
although loop diuretics are better for reducing overload. 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.
Common adverse effects include dehydration, postural hypotension,
hyponatremia, hypokalaemia, hypercalcemia, gout, impaired glucose tolerance and impotence.
Rare adverse effects include thrombocytopenia, agranulocytosis, photosensitivity rash and pancreatitis.
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COMMONLY TESTED FACTS IN EXAM

1. Heparin prevents clots formation whereas angioplasty and thrombolytic open clots that have
already formed.
2. Stopping smoking has greatest benefit in reducing cardiovascular risk factors.
3. Worst prognosis of carcinoid syndrome => Valvular heart disease
4. ECG of LVH = R wave in V5 or V6 plus S wave in V1 or V2 exceeds 35mm
5. 3 vessel disease or 2 vessel disease in diabetes needs CABG. 1 or 2 vessel disease needs stent
placement.
6. Classic ECG finding in atrial flutter => “Sawtooth” P waves
7. Antihypertensive for a diabetic patient with proteinuria => ACEIs / ARBs.
8. Beck triad for cardiac tamponade => Hypotension, distant heart sounds, and JVD.
9. Drugs that slow heart rate => β-blockers, calcium channel blockers, digoxin, and amiodarone.
10. Hypercholesterolemia treatment that leads to flushing and pruritus => Niacin.
11. Treatment for atrial fibrillation and atrial flutter: If hemodynamically unstable, cardiovert. If
stable or chronic, rate control with CCBs or β blockers.
12. Treatment for ventricular fibrillation: Immediate defibrillation.
13. Classic ECG findings in pericarditis: Low-voltage, diffuse ST-segment elevation.
14. Dressler syndrome: Autoimmune reaction with fever, pericarditis, and ↑ ESR occurring 2–4
weeks post-MI. Treatment with analgesics and steroids.
15. IV drug use with JVD & a holosystolic murmur at the left sternal border: Treat existing heart
failure, & replace tricuspid valve.
16. Diagnostic test for HOCM: Echocardiogram (showing a thickened left ventricular wall & outflow
obstruction).
17. Pulsus paradoxus: Decrease in systolic BP of > 10 mm Hg with inspiration. Seen in cardiac
tamponade
18. Eight surgically correctable causes of hypertension: Renal artery stenosis, coarctation of the
aorta, pheochromocytoma, Conn syndrome, Cushing syndrome, unilateral renal parenchymal
disease, hyperthyroidism, hyperparathyroidism.
19. MR angiography is the investigation of choice for renal artery stenosis.
20. Evaluation of a pulsatile abdominal mass and bruit: Abdominal ultrasound and CT
21. Indications for surgical correction of abdominal aortic aneurysm: size > 5.5 cm, rapidly enlarging,
symptomatic, or ruptured.
22. 50-year-old man with stable angina can exercise to 85% of maximum predicted heart rate,
appropriate diagnostic test => Exercise stress treadmill with ECG.
23. 65-year-old woman with left bundle branch block and severe osteoarthritis has unstable angina,
appropriate diagnostic test = Pharmacologic stress test (eg, Dobutamine echocardiogram).
24. Signs of active ischemia (Angina) during stress testing = ST-segment changes on ECG, or ↓ BP.
25. ECG findings suggesting MI: ST-segment elevation (depression means ischemia), flattened T
waves, and Q waves.
26. Coronary territories in MI: Anterior wall (LAD/diagonal), inferior (PDA), posterior (left circumflex/
oblique, RCA/marginal), septum (LAD/diagonal).
27. Young patient with angina at rest and ST-segment elevation with normal cardiac enzymes =
Prinzmetal angina.
28. Diagnostic test for pulmonary embolism: CT pulmonary angiogram.
29. Protamine: Reverses the effects of heparin.
30. Young patient with family history of sudden death collapses and dies while exercising. Probable
diagnosis => Hypertrophic cardiomyopathy.
31. Endocarditis prophylaxis regimens:
o Oral surgery—amoxicillin for certain situations.
o GI or GU procedures— endocarditis prophylaxis not recommended.
32. Virchow triad: Stasis, hypercoagulability, endothelial damage.
33. Most common cause of hypertension in young women = OCPs.
34. Most common cause of hypertension in young men = Excessive Ethyl alcohol.
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35. Water bottle–shaped heart pericardial effusion: Look for pulsus paradoxus.
36. Swan Ganz catheter does not measure cardiac output directly.
37. Reversal of shunt in PDA causes cyanosis in lower limbs.
38. Most common cause of death in infective endocarditis is LVF.
39. Oliguric lung fields / absent lung markings + RV dilation on echocardiography => think of
pulmonary stenosis.
40. Rapid replacement of IV potassium results in cardiac arrest in diastole because potassium is
involved in repolarization.
41. Most accurate way of determining the ejection fraction is MUGA scan.
42. Diagnostic feature of coarctation of aorta is absent femoral pulses.
43. Pulmonary capillary wedge pressure is approximation of pressure in left atrium.
44. Dyspnea is the most common presentation in mitral stenosis. It is due to pulmonary congestion.
45. Syncope is the most common presentation in aortic stenosis.
46. Palpitations are most common presentation of atrial fibrillation.
47. Young man, sport injury, presenting with clinical features of heart failure => Fat embolism. Treat
with oxygen, IV fluids, and CPAP.
48. VT 2ndry to digoxin toxicity: Give phenytoin 250mg IV over 5 min, or lidocaine.
49. WPW syndrome with narrow complex tachycardia: Give adenosine, then IV flecanide, if unstable
DC cardioversion. (Avoid verapamil & digoxin as they increase conduction through the accessory
pathway).
50. New onset AF: First anticoagulate with LMWH then flecainide 300 mg, if patient becomes
hypotensive or CP or heart failure then DC cardioversion.
51. Stent thrombosis occurs 2 days post angioplasty, treat with IV abciximab, heparin, and aspirin then
do urgent angioplasty.
52. Pericarditis: chest pain worse on lying down, ST elevation in ECG, raised inflammatory markers &
CK, Rx. NSAID. PR depression in lead II & V6 = specific ECG feature.
53. Indication to temporary transvenous wiring post MI: Mobitz type 2, Mobitz type 1 or sinus
bradycardia not responding to atropine, asystole, and trifascicular block.
54. Carotid sinus hypersensitivity: patients present with collapse. Treat with Dual chamber pacemaker.
55. Endocarditis following colonic resection may be caused by Bacillus fragilis.
56. Aortic dissection: is associated with inferior wall MI.
o Type-A (proximal): require surgery.
o Type B (distal): conservative management, control BP with labetalol.
57. ACE inhibitors are contraindicated in aortic stenosis as they may precipitate heart failure.
58. Polymorphic VT: if patient is stable treat with IV magnesium, & overriding pacing. If patient is
unstable treat with DC cardioversion.
59. Dentistry in warfarinised patients: check INR 72 hours before procedure, proceed if INR is less
than 4.0
60. Bendroflumethiazide - inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the
beginning of the distal convoluted tubule
61. B-type natriuretic peptide is mainly secreted by the ventricular myocardium
62. Statins inhibit HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis
63. Patients with very poor dental hygiene – cause of endocarditis => Viridans streptococci e.g.
Streptococcus sanguinis
64. Primary percutaneous coronary intervention is the gold-standard treatment for ST-elevation
myocardial infarction
65. Prosthetic heart valves - antithrombotic therapy:
o Bioprosthetic: aspirin
o Mechanical: warfarin + aspirin
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66. Endothelin receptor antagonists decrease pulmonary vascular resistance in patients with primary
pulmonary hypertension
67. IV magnesium sulfate is used to treat torsades de pointes.
68. J-waves in ECG are associated with hypothermia.
69. HOCM is the most common cause of sudden cardiac death in the young
70. Prosthetic valve endocarditis caused by staphylococci → Give Flucoloxacillin + rifampicin + low-
dose gentamicin.
71. When treating angina, if there is a poor response to the first-line drug (e.g. a beta-blocker), the
dose should be titrated up before adding another drug.
72. Infective endocarditis - indications for surgery:
o Severe valvular incompetence
o Aortic abscess (often indicated by a lengthening PR interval)
o Infections resistant to antibiotics/fungal infections
o Cardiac failure refractory to standard medical treatment
o Recurrent emboli after antibiotic therapy.
73. Gallop rhythm (S3) is an early sign of LVF
74. Young man with AF, no TIA or risk factors, no treatment is now preferred to aspirin.
75. Ischemic changes in leads V1-V4 - left anterior descending.
76. With Magnesium sulphate therapy, Monitor => reflexes + respiratory rate.
77. A single episode of paroxysmal atrial fibrillation, even if provoked, should still prompt consideration
of anticoagulation
78. A prolonged PR interval in ECG => aortic root abscess.
79. Hypocalcemia is associated with QT interval prolongation; Hypercalcemia is associated with QT
interval shortening
80. Infective endocarditis - streptococcal infection carries a good prognosis
81. Nitrates should be avoided in the likely diagnosis of right ventricular myocardial infarct because
they cause reduced preload
82. Infective endocarditis causing congestive cardiac failure is an indication for emergency valve
replacement surgery
83. A beta-blocker or a calcium channel blocker is used first-line to prevent angina attacks
84. Furosemide - inhibits the Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle
85. People with cardiac syndrome X have normal coronary angiograms despite ECG changes on
exercise stress testing.
86. Patients with recurrent venous thromboembolic disease may be considered for an inferior vena
cava filter
87. AV block can occur commonly following an inferior MI
88. Aortic stenosis - S4 is a marker of severity
89. Labetalol is first-line for pregnancy-induced hypertension
90. Paradoxical embolus - PFO most common cause - do TOE
91. Risk of falls alone is not sufficient reason to withhold anticoagulation
92. DVLA advice post MI - cannot drive for 4 weeks
93. Pulmonary arterial hypertension patients with negative response to vasodilator testing should be
treated with prostacyclin analogues, endothelin receptor antagonists or phosphodiesterase
inhibitors. Often combination therapy is required
94. A potassium above 6mmol/L should prompt cessation of ACE inhibitors in a patient with CKD (once
other agents that promote hyperkalemia have been stopped)
95. Hypokalaemia - U waves on ECG
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96. Rate-limiting CCBs should be avoided in patients with AF + heart failure with reduced EF (HFrEF)
due to their negative inotropic effects
97. Dipyridamole is a non-specific phosphodiesterase inhibitor and decreases cellular uptake of
adenosine
98. The main ECG abnormality seen with hypercalcemia is shortening of the QT interval
99. Beta-blockers e.g. bisoprolol should not be used with verapamil due to the risk of bradycardia,
heart block, congestive heart failure
100. HOCM - poor prognostic factor on echocardiography => septal wall thickness of > 3cm
101. Second heart sound (S2)
o Loud in hypertension.
o Soft in AS.
o Fixed split in ASD.
o Reversed split in LBBB.
102. ALS - give adrenaline in non-shockable rhythm as soon as possible
103. Patients with stable CVD who have AF are generally managed on an anticoagulant and the
antiplatelets stopped
104. In management of STEMI if primary PCI cannot be delivered within 120 minutes then thrombolysis
should be given
105. HOCM is usually due to a mutation in the gene encoding β-myosin heavy chain protein or myosin
binding protein C
106. Ticagrelor has a similar mechanism of action to clopidogrel - inhibits ADP binding to platelet
receptors
107. Atrial myxoma - commonest site = left atrium
108. Patients with a suspected pulmonary embolism should be initially managed with low-molecular
weight heparin
109. Patients with VT should not be prescribed verapamil
110. Contrast-enhanced CT coronary angiogram is the first line investigation for stable chest pain of
suspected coronary artery disease etiology
111. Aortic regurgitation - early diastolic murmur, high-pitched and 'blowing' in character
112. Patients with SVT who are hemodynamically stable and who do not respond to vagal manoeuvre,
next step => treat with adenosine.
113.
114. Atrioventricular dissociation suggests VT rather than SVT with aberrant conduction
115. Bisferiens pulse is suggestive of mixed aortic valve disease
116. Patients on warfarin undergoing emergency surgery - give four-factor prothrombin complex
concentrate
117. Aschoff bodies are granulomatous nodules found in rheumatic heart fever
118. Streptococcus bovis endocarditis is associated with colorectal cancer
119. Most common cause of endocarditis:
o Staphylococcus aureus
o Staphylococcus epidermidis if < 2 months post valve surgery
120. Left parasternal heave is a feature of tricuspid regurgitation.
121. Hypertension in diabetics - ACE-inhibitors are first-line regardless of age
122. New onset AF is considered for electrical cardioversion if it presents within 48 hours of
presentation
123. Takotsubo cardiomyopathy is a differential for ST-elevation in someone with no obstructive
coronary artery disease
124. DVLA advice following angioplasty - cannot drive for 1 week
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125. PCI - patients with drug-eluting stents require a longer duration of clopidogrel therapy
126. Pulsus alternans is seen in left ventricular failure
127. Cocaine induced MI should be treated with PCI if available as cocaine causes vasospasm with
platelets activation and acute arterial blockage.
128. Massive PE + hypotension => thrombolysis.
129. Major bleeding while using warfarin => stop warfarin, give intravenous vitamin K, and
prothrombin complex concentrate
130. Complete heart block following an inferior MI is NOT an indication for pacing, unlike with an
anterior MI
131. Pulmonary arterial hypertension patients with positive response to vasodilator testing should be
treated with calcium channel blockers
132. Pulmonary embolism and renal impairment → V/Q scan is the investigation of choice
133. Takayasu's arteritis is an obliterative arteritis affecting the aorta
134. Palpitations should first be investigated with a Holter monitor after initial bloods/ECG
135. Tricuspid valve endocarditis can cause tricuspid regurgitation, which may manifest with a new pan-
systolic murmur, large V waves and features of pulmonary emboli.
136. Asymmetric septal hypertrophy and systolic anterior movement (SAM) of the anterior leaflet of
mitral valve on echocardiogram or cardiac MR support the diagnosis of HOCM.
137. The recommended dose of adrenaline to give during advanced ALS is 1mg
138. Bendroflumethiazide can worsen glucose tolerance
139. PCI: stent thrombosis - withdrawal of antiplatelets is the biggest risk factor.
140. Antibiotic prophylaxis to prevent infective endocarditis is not routinely recommended in the UK for
dental and other procedures
141. ACE-inhibitors should be avoided in patients with HOCM
142. Renal dysfunction (eGFR <60) can cause a raised serum natriuretic peptides
143. A stable patient presenting in AF with an obvious precipitating cause may revert to sinus rhythm
without specific antiarrhythmic treatment
144. Witnessed cardiac arrest while on a monitor => up to three successive shocks before CPR
145. Ventricular tachycardia - verapamil is contraindicated
146. Thiazide diuretics can cause hyponatremia, metabolic alkalosis, hypokalemia and hypocalciuria
147. Percutaneous mitral commissurotomy is the intervention of choice for severe mitral stenosis.
148. Ivabradine use may be associated with visual disturbances including phosphenes and green
luminescence
149. Myoglobin rises first following myocardial infarction
150. Ischemic changes in leads I, aVL +/- V5-6 - left circumflex artery
151. Mechanical valves - target INR:
o Aortic: 3.0
o Mitral: 3.5
152. Unprovoked' pulmonary embolisms are typically treated for 6 months
153. INR > 8.0 (no bleeding) while using warfarin- stop warfarin, give oral vitamin K 1-5mg, repeat dose
of vitamin K if INR high after 24 hours, restart when INR < 5.0.
154. VF/pulseless VT should be treated with 1 shock as soon as identified.
155. In the context of a tachyarrhythmia, a systolic BP < 90 mmHg → DC cardioversion.
156. S1Q3T3 is a classic but uncommon ECG finding in PE.
157. Pleuritic chest pain at <48hrs after MI -> pericarditis.
158. RBBB +left anterior or posterior hemiblock + 1st-degree heart block = Trifascicular block.
159. Bleeding on dabigatran => use idarucizumab to reverse.
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160. Myocarditis presents with ST elevation and acute pulmonary oedema in a young patient with a
recent flu-like illness.
161. Patients who've had a catheter ablation for atrial fibrillation still require long-term anticoagulation
as per their CHA2DS2-VASc score.
162. The most appropriate medication in patients with acute heart failure and a preserved ejection
fraction who have signs of volume overload is addition/up-titration of a loop diuretic.
163. Following elective DC cardioversion for AF, anticoagulation should be continued even if sinus
rhythm is maintained
164. New AF in mitral regurgitation => refer for mitral valve replacement
165. Elderly male patients who present with pre-syncope/syncope and are on alpha-blockers as
treatment for BPH should be assessed for orthostatic hypotension as a first step in evaluation.
166. Complete heart block following an anterior MI suggests significant damage to the myocardium and
will likely require pacing, in contrast to complete heart block following an inferior MI.
167. Statins are the only lipid-regulating drugs that are used in secondary prevention of cardiovascular
disease (with the exception of ezetimibe which is used in cases of primary hypercholesterolemia).
168. Acute heart failure not responding to treatment => consider CPAP.
169. In hypertensive urgency, treatment aims to lower blood pressure with the use of oral anti-
hypertensive medication.
170. Heyde syndrome is a triad of aortic stenosis, coagulopathy and GI bleeding.
171. Electrical alternans is suggestive of cardiac tamponade.
172. In coronary vasospasm (Prinzmetal’s angina, or variant angina), the ECG shows ST elevation that is
very similar to an acute STEMI. However, unlike acute STEMI the ECG changes are transient,
reversible with vasodilators and not associated with myocardial necrosis.
173. First line management of acute pericarditis involves combination of NSAID and colchicine.
174. Thiazide diuretics can cause hypercalcemia and hypocalciuria.
175. ECG changes in Brugada syndrome are more apparent following the administration of flecainide or
ajmaline - this is the investigation of choice in suspected cases.
176. In patient with BBB and unexplained syncope but an ejection fraction >35% proceed with further
testing (e.g. carotid sinus massage, electrophysiological studies) prior to initiation of management.
177. Accelerated idioventricular rhythm is common and unconcerning following recent MI
178. Digoxin administration is not recommended in cardiac amyloidosis owing to a higher risk of digoxin
toxicity, as the drug binds avidly to amyloid fibrils.
179. Multiple episodes of inappropriate shocks from an ICD can be both unpleasant and dangerous.
Ultimately the device will need interrogated from a pacemaker technician, however the most
immediate management should be to place a ring magnet over the ICD to prevent further
inappropriate shocks.
180. AV blocking drugs and vagal maneuvers are absolutely contraindicated in patients with AF and
pre-excitation.
181. AKI following angiography can be caused by contrast-induced nephropathy or cholesterol emboli.
182. Ischemic changes in leads II, III, aVF - right coronary artery involved.
183. Hydrazine and nitrate should be considered for Afro-Caribbean patients with heart failure who are
not responding to ACE-inhibitor, beta-blocker and aldosterone antagonist therapy.
184. Cardiac magnetic resonance imaging has been shown to be very useful in diagnosing myocarditis
by visualizing markers for inflammation of the myocardium.
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185. In patients with Mobitz type II AV block, or complete heart block, a DDD or DDDR pacemaker is
indicated.
186. Wellens’ syndrome is a pattern of deeply inverted or biphasic T waves in V2-3. It is highly specific
for critical stenosis of the left anterior descending artery (LAD). It should be treated as a STEMI with
urgent angiography and revascularization.
187. In pre-excited AF don’t give anything that blocks conduction at AV node (including calcium channel
blockers, adenosine or digoxin) as this can cause ventricular tachycardia.
188. Cardiac MRI is the investigation of choice alongside echocardiography in order to identify the
potential cause of cardiomyopathy.
189. If a cardiac MIBI scan shows that the defect is present on both stress and rest, this is suggestive of
a fixed defect such as myocardial necrosis and fibrosis secondary to infarction.
190. ACE inhibitors offer prognostic benefit in chronic heart failure.
191. Females with Turner's syndrome have just one X chromosome. Therefore they have the same
probability of being affected by an X linked recessive disease as males.
192. Distinguishing between VT and SVT with BBB can be challenging. The presence of RBBB and RAD
favors the diagnosis of SVT with BBB.
193. Aortic stenosis - a soft S2 is a feature of severe disease.
194. First degree heart block and Wenckebach phenomenon are normal variants in an athlete. They do
not require intervention.
195. In pure sinus node dysfunction without AF or evidence of AV block, an AAIR or DDDR pacemaker
can be used. Most cardiologists would choose a DDDR pacemaker since many of these patients go
on to develop AV block.
196. IV vancomycin + rifampicin + low-dose gentamicin is the empirical treatment of choice in prosthetic
valve endocarditis with penicillin allergy.
197. Patients with ventricular ectopics can usually be managed by reassurance and lifestyle
modifications. If pharmacological management is required, then beta blockers are first line.
198. Posterior wall MI typically present on ECG with tall R waves V1-2.
199. The presence of ST elevation without reciprocal depression following myocardial infarction is
suggestive of a left ventricle aneurysm. Left ventricle aneurysms predispose to both ventricular
arrhythmias and cardiac thrombo-embolisms.
200. Twiddling refers to pacemaker dysfunction due to patients interfering with the wires.
201. Delivery of the baby is the treatment of HELLP syndrome.
202. Methadone is a common cause of QT prolongation.
203. During a cardiology clinical examination, a sustained apical impulse is consistent with left
ventricular hypertrophy, which can be verified on an ECG by identifying deep S waves in V1 and V2
and tall R-waves in V5 and V6.
204. Dextrocardia is associated with an inverted P wave in lead I, right axis deviation, and loss of R wave
progression.
205. Peripheral edema is considered to be a common and annoying adverse effect of calcium channel
blockers. Diuretics don’t relieve the edema caused by calcium channel blockers.
206. Radiographic evidence of aortic disruption or dissection => Widened mediastinum (> 8 cm), loss of
aortic knob, pleural cap, tracheal deviation to the right, depression of left main stem bronchus.
207. The most common ECG change in hypocalcaemia is prolongation of the QTc interval.
208. Turner's syndrome - most common cardiac defect is bicuspid aortic valve (more common than
coarctation of the aorta).