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Cardiology
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Compensations and Version 2 (2020)

Penalties Worldwide
System is Active

Corrected, Updated, Lighter

With the Most Recent Recalls and the UK Guidelines

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

1 elevation on ECG. What to Do Next?

→ Measure Cardiac Enzymes, especially (Troponin)

√ If Troponin is high → NON-STEMI Elevation MI

√ Immediate management → Give LMWH e.g. Fondaparinux √ recent

exam

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Points on Alcohol and Heart Disease

- Ankle swelling and orthopnea → features of Heart Failure.

- Excessive alcoholism → Alcoholic Cardiomyopathy (Cardiac Enlargement
on Chest X-ray) → Atrial Fibrillation.
- The commonest arrhythmia develops in patients with alcoholic
cardiomyopathy is → Atrial Fibrillation.
- Acute alcohol intake can lead to → AF or flutter ((Holiday heart Syndrome))
- AF presentation: Palpitation, Dyspnea, Dizziness or Syncope, Chest
discomfort or pain, Stroke or TIC, Irregularly irregular pulse.

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Key Cardiac Tamponade

2

• Beck’s Triad:

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

• Others: Dyspnea, Pulsus Paradoxus, Tachycardia.

• Cardiac Tamponade can develop as a complication of MI:

After MI → Acute pericarditis → Pericardial effusion → Cardiac Tamponade.

• Trauma is the most important cause for cardiac tamponade.

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

Either Pericardial effusion (OR) Cardiac Tamponade.

• Dx: Echo is diagnostic

• Tx: Urgent pericardiocentesis.

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Key Atrial Myxoma

3

- Benign tumours.
- 75% in the left atrium.
- Tend to grow on the wall (inter-atrial septum).
- 10% are inherited -> Familial myxoma

- Features:
◙ Obstruction of Mitral valve → Mid-diastolic murmur, Dyspnea, Syncope,
Congestive HF.
◙ Small pieces may break off and travel to arteries causing (ischemia) of
different parts of the body such as:

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♦ Lung → Can cause PE (Pulmonary Embolism)

♦ Brain →Can cause Stroke
♦ Peripheries → Clubbing and Blue fingers.
◙ Atrial Fibrillation

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

region of fossa ovalis (inter-atrial septum).

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

The likely Diagnosis → Cardiac Tamponade.

The most appropriate management → Pericardiocentesis

• Beck’s Triad: Hypotension, Muffled Heart Sounds, High JVP (Distended

neck veins).

Key Axis Deviation

5

- If ORS in lead I is up (+ve) and in lead II is down (negative) →

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Left axis deviation

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

Right axis deviation

These causes are important!

Causes of Left Axis Deviation Causes of Right Axis Deviation

Inferior MI Lateral MI
Left Ventricular Hypertrophy Right Ventricular Hypertrophy
Left Anterior Fascicular block (or Left Posterior Fascicular Block (or
hemiblock) hemiblock)
Obese Thin, Tall, Children

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Wolff Parkinson White Syndrome Chronic Lung Disease

(delta wave)
Pulmonary Embolism

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

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

Key Types of heart block

6

First degree heart block

• PR interval > 0.2 seconds (Only prolonged PR intervals).

Second degree heart block

• type 1 (Mobitz I, Wenckebach) → Progressive prolongation of the PR
interval until a dropped beat occurs.
• type 2 (Mobitz II) → PR interval is constant but the P wave is often not
followed by a QRS complex.

Third degree (complete) heart block

• There is no association between the P waves and QRS complexes.
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Key
7

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

Atrial Fibrillation:

- Beta-blockers (e.g. atenolol, metoprolol) → First line but Contraindicated

in Asthma.
- Calcium channel blockers (e.g. diltiazem) → used in Asthmatic patient.
- Digoxin → (not considered first-line anymore as they are less effective at
controlling the heart rate during exercise. However, they are the preferred
choice if the patient has coexistent heart failure)

• Atrial Flutter management → Cardioversion (Shock)

Key Ventricular tachycardia .

8

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

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

N.B:
• An ECG showing broad complex tachycardia in a (still) conscious patient
even if semiconscious ± atrial activity
→ Ventricular tachycardia → Give Amiodarone

• If the patient is Unconscious, Collapsed, or Not breathing

→ Ventricular Fibrillation → Defibrillation (Shock).

• Ventricular fibrillation is the most important shockable arrhythmia.

• Hypokalemia is the most important cause of ventricular tachycardia (VT)

clinically

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Atrial Fibrillation Palpitation, Tachycardia, Dyspnea, Fibrillatory

waves on the ECG. → Give Beta-Blocker.
If Asthmatic → Give Calcium Channel Blocker.
Atrial Flutter ‘’Fluttering Feeling in the chest’’, Sawtooth waves
on the ECG → Cardioversion.

Ventricular Regular and Fast rhythm.

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

Ventricular Older adult, Sudden collapse, Not breathing,

Fibrillation Unconscious, No pulse → Cardioversion
‘’defibrillation’’

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Sinus Lightheadness, hypotension, vertigo, syncope,

Bradycardia dizziness.
N.B. Sinus brady cardia is normal in young athletes.

Sinus Physiological situation (exercise, stress, anger).

Tachycardia Hx of infection.

WPWS Delta wave on the ECG

Key Management of Congestive Heart Failure

9

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

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

◙ The following drugs have all been shown to reduce mortality in patients
with left ventricular failure:

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

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How to manage? (Important)

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

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

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

• If the symptoms still persist → Add Spironolactone (Aldosterone

Antagonist).

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

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

• If HF + AF → Digoxin

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

hyperkalemia?

The answer is → No!

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

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

10

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

• If the patient presents within 12 hours of the onset of the symptoms → PCI
(Percutaneous Coronary Intervention) ‘’The gold standard’’

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

• (Chronic) Long-term Management of MI:

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Aspirin for life, Ticagrelor or Prasugrel for 12 months ‘’Clopidogrel

previously’’, Beta Blockers (for 12 months), ACE inhibitors, Statins

So, Long-term MI Rx = 5 Drugs: , , , ,

Key Patent Foramen Ovale:

11

TransOesophageal Echocardiography (TOE) with bubble contrast is the gold

standard in the diagnosis of Patent Foramen Ovale (PFO).

Key ◙ Pericarditis (Can occur as a Complication of MI, may develop shortly after
12 MI within 2 days) and Dressler's syndrome (presents 2-6 weeks after MI)
both
have the same features → Pleuritic chest pain that worsens on lying

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flat and during inspiration, Pericardial rub, Widespread Saddle

shaped ST elevation on the ECG.

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

Important Complications of MI

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

Chronic heart failure

If the patient survives the acute phase, their ventricular myocardium may
become dysfunctional resulting in chronic heart failure.
Management:
◙ For all patient for symptomatic relief and to reduce the volume overload →
Loop Diuretics (e.g. Furosemide)

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◙ Start with either ACEi or BB. (One drug at a time)

◙ If the symptoms persist → Add the other one (ACEi or BB).
◙ If the symptoms still persist → Add Spironolactone (Aldosterone
Antagonist).

Tachyarrhythmias
◙ Ventricular fibrillation, as mentioned above, is the most common cause of
death following a MI. Other arrhythmias can also occur e.g. ventricular
tachycardia.
◙ Management:
1) Check the patient’s pulse, if no pulse, commence the arrest protocol
immediately.
2) Administer Q2.
3) If the patient is hemodynamically unstable: Synchronised Cardioversion
followed by IV Amiodarone followed by further Shocks if needed.

Pericarditis
◙ Occurs within 48 hours (i.e. 2 days) after MI.
◙ Features → Pleuritic chest pain that is worse on lying flat and during
inspiration ± Fever ± pericardial rub
◙ Pericardial effusion may develop leading to enlarged globular heart on chest
X-ray and confirmed by echocardiogram.
◙ ECG → Widespread Saddle Shaped ST Elevation with upward concavity +
PR Depression.

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

Left ventricular aneurysm

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

Ventricular septal defect (VSD)

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◙ Rupture of the interventricular septum usually occurs in the first week after
a MI attack and is seen in around 1-2% of patients.
◙ Features: acute heart failure associated with a pan-systolic murmur.
◙ An echocardiogram is diagnostic and will exclude acute mitral regurgitation
which presents in a similar fashion.
◙ Urgent surgical correction is needed.

Acute mitral regurgitation (MR): pansystolic murmur

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

◙ Due to → Ischemia or rupture of the papillary muscles.

◙ An early-to-mid systolic or Pansystolic murmur is typically heard.
◙ Dx → Echocardiogram.
◙ Treatment → vasodilator therapy but often require emergency surgical
repair.
◙ May present with Hypotension, Tachycardia and Pulmonary edema.

Key Types of MI / Sites of Myocardial Infarction

13

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Key Any patient presents with STEMI, give MONA (Morphine, O2, Nitroglycerin,
14 Aspirin) and send immediately for PCI (Percutaneous Coronary
Intervention).

Key ◙ The first drug of choice for Symptomatic Bradycardia (Dizziness, feeling
15 unwell) is → Atropine (Given 0.5 mg IV push and may be repeated up to a
total dose of 3 mg).
◙ 2nd Line → Dopamine.
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◙ 3rd Line → Epinephrine.

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

Key • Beck’s Triad: Hypotension, Muffled “faint” Heart Sounds, High JVP
16 (Distended neck veins).
→ Cardiac Tamponade.
→ Echo for Dx and Pericardiocentesis for Rx

Key Infective Endocarditis (IE)

17

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

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

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

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

• Features and Diagnosis → Modified Duke criteria

Infective endocarditis diagnosed if

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

Major criteria

1) Positive blood cultures

◙ Two positive blood cultures showing typical organisms consistent with
infective endocarditis, such as Streptococcus viridans and the HACEK group,
(Or)

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◙ Persistent bacteraemia from two blood cultures taken > 12 hours apart or
three or more positive blood cultures where the pathogen is less specific such
as Staph aureus and Staph epidermidis.

2) Evidence of endocardial involvement

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

Minor criteria

1. Predisposing heart condition or intravenous drug use.

2. Microbiological evidence that does not meet the major criteria.
3. fever > 38°C.
4. Vascular phenomena → Major emboli, Splenomegaly, Clubbing, Splinter
haemorrhages, Janeway lesions, Petechiae or purpura.
5. Immunological phenomena → Glomerulonephritis, Osler's nodes, Roth
spots.

N.B.
- Osler’s Nodes: painful, red nodules on the hands or feet that can persist for
hours to days.

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- Janeway lesions: Non-tender, small, erythematous or hemorrhagic macular

or nodular lesion on the soles or palms. (they occur due to septic micro-
emboli that deposit the bacteria under the skin).

Endocarditis: initial “Empirical” “Blind” therapy

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

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The most important note to remember is that in any patient

presenting with Fever + a new heart Murmur → suspect Infective
Endocarditis and order Blood Culture until proven otherwise.

Key In a Patient with Atrial Fibrillation

18
We Calculate the CHA2DS2-VASc Score

To determine the need to anticoagulants.

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

Apixaban, Rivaroxaban, Edoxaban, Dabigatran) To →
◙ All patients with score 2 or more.
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◙ Consider giving Warfarin or DOAC to Men whose scores are 1 or more.

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

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

Important Score Systems to Know:

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

in a patient who has atrial fibrillation. √ important
◙ The ABCD2 score (Prognostic) is used to identify the risk of future stroke in
patients who have had a suspected TIA. √ important

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

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

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

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

the next 10 years.

Key Pulmonary edema

19

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

Features:
Desaturation (Low O2 Sat.), Dyspnea, Orthopnea (SOB worsens when lying
down), Auscultation → Crepitations, Tachycardia.

Investigations:
While chest X-ray usually shows features of pulmonary edema (The single
most appropriate Investigation), the underlying cause requires
Echocardiogram to be identified (e.g. Congestive Heart Failure, Complication
of MI→ Acute Mitral Regurgitation due to papillary rupture, Ventricular
aneurysm, …etc.)
Therefore, pay attention to the question words!
◙ The Most Appropriate Investigation → Chest X-Ray.

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◙ The Investigation Needed for Identifying the Underlying Cause → Echo.

Management:

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

Morphine, O2, Nitrates, Furosemide (Lasix).

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

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

is that Pulmonary Oedema can be diagnosed by Chest X-ray while Pulmonary
Embolism needs D-Dimer, CTPA (CT Pulmonary Angiogram). This might be a
hint in the question.

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

fluid)

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

20

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

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

Key Scenario
21
20 days after MI, a patient developed sudden Dyspnea. O/E →
Tachycardia, Desaturation (88% on Room Air), Hypotension and
Bilateral Chest Crackles.

◙ The likely Dx → Pulmonary Oedema.

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

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

Key left bundle branch block (LBBB).

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

LBBB features on ECG:

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

Important Note A new onset LBBB is characteristic for Myocardial

Infarction (MI).

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Key Ruptured Abdominal Aortic Aneurysm (AAA)

23

◙ The classical picture: a triad of:

Pain, Hypotension, pulsatile tender abdominal mass.

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

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

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

appropriate initial investigation.

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

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

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

Key In a patient with Heart Failure (LL Edema, Dyspnea, Orthopnea, Ejection
24 fraction less than 40%), the management would be:

• For symptomatic relief and to reduce the volume overload → Loop

Diuretics (e.g. Furosemide)
• Start with either ACEi or BB. (One drug at a time)
• If the symptoms persist → Add the other one (ACEi or BB).

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

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

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Key Coronary Artery Dominance

25

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

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

Key Dressler's syndrome

26 ◙ It tends to occur around 2-6 weeks following a MI. The underlying
pathophysiology is thought to be an autoimmune reaction against antigenic
proteins formed as the myocardium recovers.
◙ It is characterised by a combination of fever, pleuritic pain worsens on
inspiration and on lying flat, pericardial effusion and a raised ESR.
◙ It is treated with NSAIDs.

◙ ECG: Widespread Saddle Shaped ST Elevation + PR Depression

Key Hypokalemia
27
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◙ Muscle weakness and cramps + U wave on ECG

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

◙ Spironolactone, ACE inhibitors → HypeRkalemia.

◙ Loop diuretics, Thiazide diuretics → HypOkalemia.

◙ The ECG changes in HypUkalemia → U Wave

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

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Key Paroxysmal Supraventricular Tachycardia (Narrow-Complex SVT)

28

◙ Usually in young patients

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

◙ Management:
♠ Initial line → Valsalva manoeuvre, Carotid massage.
♠ Not improved? → Intravenous adenosine (6mg Rapid IV Bolus), still not
improved? → give another 12mg, still not improved? → give another 12mg.
N.B. Adenosine is contraindicated in asthmatics – Verapamil (CCB) is the
preferred option in Asthma.
♠ Not improved? → Electrical DC Cardioversion

• Prevention of the episodes → ß-Blockers or Radio-frequency ablation.

In summary:
Carotid Massage and Valsalva Manoeuvre → IV Adenosine 6 mg
→ IV Adenosine 12 mg → IV Adenosine 12 mg → Cardioversion

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Polymorphic (Broad-Complex) Ventricular Tachycardia

= Torsades De Pointes (TDP)

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

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

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Key Any patient presents with STEMI, give MONA (Morphine, O2, Nitroglycerin,
29 Aspirin) and send immediately for PCI (Percutaneous Coronary
Intervention).

What if PCI was not given in the options?

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

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

→ Measure Cardiac Enzymes, especially (Troponin)

If Troponin is high → NON-STEMI Elevation MI

→ Give LMWH e.g. Fondaparinux

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

The likely cause → Left Ventricular Aneurysm.

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

Left ventricular aneurysm

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

Key Hypertension Management

32

Blood pressure classification

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

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

“Severe
hypertension”

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

Management of hypertension

Lifestyle advice should not be forgotten:

• Low salt diet.
• Caffeine intake should be reduced.
• Stop smoking, drink less alcohol, eat a balanced diet rich in fruit and
vegetables, exercise more, lose weight.

♠ When to Treat Stage 1 Hypertension (ABPM or HBPM ≥

135/85 mmHg)?

• Treat if < 80 years of age AND any of the following apply:

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Target organ damage, established cardiovascular disease, renal disease,

diabetes or a 10-year cardiovascular risk equivalent to 20% or greater

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

Lifestyle and Diet Modification and review.

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

160/100 → Before commencing antihypertensive medications, record either
ABPM or HBPM.
◙ Note: For patients < 40 years and with stage 2 hypertension or higher →
Consider a specialist referral to exclude secondary causes of the HTN.

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

→ Always treat.

The Steps of The Management of Hypertension

Step 1

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

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• patients ≥ 55-years-old or of Afro-Caribbean origin “of any age” → Calcium

channel blocker.

Step 2
• ACE inhibitor + Calcium channel blocker (A + C)

Step 3
• Add a Thiazide Diuretic (D) → ACEi + CCB + Thiazide Diuretic (A+C+D).

- Example of ACEi → Enalapril.

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

Step 4 (For resistant hypertension) (For Reading)

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

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

ineffective, consider an alpha- or beta-blocker.

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

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

Blood pressure targets

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

Hypertension and Diabetes (V. Imp)

◙ Always treat hypertension in a DIABETIC patient with ACE inhibitor
regardless of the age. “Unless if the eGFR is <30”
◙ However, if this diabetic patient is Afro-Caribbean, start with both ACE
inhibitor + Calcium Channel Blocker.

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

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

Why ACE inhibitors is used for Diabetic hypertensive patients?

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

Key Postural Hypotension (Orthostatic Hypotension)

33
- It is a drop in the BP of >20 mmHg within 3 minutes after standing.
- BP is measured on lying position, then on standing position.
- Dx: Monitor BP.
◙ Postural hypotension is common in elderly people especially those who
take multiple drugs (Polypharmacy) and those with hypertension.
◙ Anti-hypertensive medications can cause postural hypotension as well.
- Why? Because the Baroreflex mechanisms which control the HR (Heart
Rate) and the VR (Vascular resistance) decline with age, particularly in
patients with hypertension.

Q) An elderly complains of difficult mobilisation as he feels dizzy upon trying

to stand ± Recurrent Falls.
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- Treatment → Blood pressure monitoring & → Assess and review the

patient’s Medications.

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

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

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

35 → Atrial Fibrillation.

→ Calculate CHA2DS2-VASc Score (Key number 18) → Give (Warfarin) or

(DOAC such as Apixaban, Rivaroxaban, Edoxaban, Dabigatran) Accordingly.

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

36
So, the reason is → Infection “infective” endocarditis.

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

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

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Key Ventricular Ectopics = Three-beat patterns = Ventricular Trigeminy.

37 ◙ A sense of a missed/skipped beat, unsustained palpitation ± Dyspnea and
Dizziness due to immature discharge of a ventricular ectopic focus which
produces → an early and broad QRS complex.
◙ Causes → IHD (MI), Cardiomyopathy, Stress, Alcohol, Caffeine, Cocaine,
Medications OR Naturally.
◙ Over half the population have silent, or asymptomatic ventricular ectopics
which are discovered incidentally on a routine ECG.
◙ If No underlying Heart disease (IHD, Cardiomyopathy) → Benign, no clinical
significance.
◙ If these ventricular ectopics are due to IHD or Cardiomyopathy → may
precipitate to more life-threatening arrhythmias like Ventricular Fibrillation.

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

38

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

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

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

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Key Long term medications post-Myocardial Infarction = 5 Drugs →

39

, , , ,

(You need to memorise these 5 drugs)!

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

- The likely cause of this patient’s gout → Thiazide or Loop Diuretics (Both
can cause hyperuricemia (Gout) and both can be used to treat volume
overload caused by Heart Failure)

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

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

Important Notes:

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

decrease the eGFR, retain more salt and water (risk factor for HF).
◙ N.B. Thiazide like diuretics and Loop diuretics decrease the clearance of
Uric Acid → leading to Gout (Hyperuricemia)
◙ N.B. NSAIDs such as Ibuprofen are used for the treatment of Gout. If given
for a patient with chronic heart failure, they would worsen the symptoms
(Orthopnea and Dyspnea).

Key In-Hospital Cardiac Arrest algorithm

41

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

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

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Key In MI patient, what if PCI was not given in the options?

42 Pick → Alteplase or Streptokinase (Tissue Plasminogen Activator) =

Thrombolysis.

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

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Key An elderly male presents with Palpitations and Shortness of breath on

44 exertion. The ECG is as follows. What is the diagnosis?

Answer:

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

Key • Beck’s Triad in Cardiac Tamponade:

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

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

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• Dx: Echocardiography is diagnostic.

• Tx: Urgent pericardiocentesis.

Key Remember that:

47

◙ In Atrial Myxoma → Mitral valve obstruction → Mitral Stenosis → Early or

Mid-diastolic murmur, Dyspnea, Syncope.

◙ In Atrial Myxoma → Breakdown of small emboli from the mass can travel
down the blood and cause ischemia (e.g. Pulmonary Embolism, Stroke,
Clubbing, Blue fingers)

Therefore, in a patient with Hx of syncope, SOB, Pulmonary Embolism and

early-mid diastolic murmur → Think of Atrial Myxoma.

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

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

Key Scenario:
49

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

→ The likely Dx → Mitral Regurgitation.

→ The likely Cause → Rupture of Papillary Muscles.

Acute mitral regurgitation (MR): pansystolic murmur

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

◙ Causes → Ischemia or Rupture of the papillary muscle.

◙ An early-to-mid systolic or Pansystolic murmur is typically heard.

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◙ Treatment → vasodilator therapy but often require emergency surgical

repair.

Key Scenario
50 2 days after MI, an elderly patient presents with fever and chest pain. ECG
shows ST elevation with upward concavity.

→ Acute Pericarditis.

Pericarditis Post-MI
◙ Occurs within 48 hours after MI.
◙ Features → Pleuritic chest pain that is worse on lying flat and during
inspiration ± Fever ± pericardial rub
◙ Pericardial effusion may develop leading to enlarged globular heart on chest
X-ray and confirmed by echocardiogram.
◙ ECG → Widespread Saddle Shaped ST Elevation with upward concavity +
PR Depression

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

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

Morphine, Oxygen, Nitrates, Aspirin.

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MI Analgesia while in an ambulance (Pre-Hospital)

1) Glyceryl Trinitrate (GTN) sublingual or spray.
2) +/- Opioids (INTRAVASCULAR): 2.5-5 mg Diamorphine or 5-10 mg
Morphine.
- N.B. Around 1/3 of the patients with MI have nitrate-resistant chest pain;
therefore, morphine is given IV.
- Why IV and not IM? IM absorption is unreliable + if the patient
receives thrombolysis later on, the site of IM injection might bleed.

Key Ventricular Old adult, Sudden collapse, Not breathing,

52 Fibrillation Unconscious → Cardioversion ‘’defibrillation’’

Broad Complex Tachycardia

◙ Tachyarrhythmia is one of the complications of MI.
♠ An ECG showing broad complex tachycardia in a (still) conscious patient ±
atrial activity → Ventricular tachycardia → IV Amiodarone.

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

breathing → Ventricular Fibrillation →

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1) Check the patient’s pulse, if no pulse, commence the arrest protocol

immediately.
2) Administer Q2.
3) If the patient is hemodynamically unstable: Synchronised Cardioversion
followed by IV Amiodarone followed by further Shocks if needed.

• N.B. HypOkalemia is the most important cause of ventricular

tachycardia (VT) clinically

Key Treatment of Cardiac Tamponade → Pericardiocentesis.

53

Key ◙ Tall Tented T-wave → HypeRkalemia.

54 ◙ U-wave → HypOkalemia.

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

55
→ The initial line treatment → Calcium Channel Blocker (CCB)

(First Step Management of hypertension in African-Caribbean

patients is CCB regardless of the age).

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Key Remember that:

56

LBBB is associated with acute MI.

Key Heart Murmurs:

57

Defect Type of Murmur Where is it Symptoms

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

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Aortic Early Diastolic Right 2nd ICS just Symptoms of

Regurgitation lateral to Heart Failure
sternum
Mitral Stenosis Mid-Late Apex (left 5th ICS Symptoms of
Diastolic, with MCL) Heart Failure
opening click
Mitral Pan-Systolic Apex (left 5th ICS Symptoms of
Regurgitation MCL), radiates to congestive Heart
Axilla Failure; edema,
Ascites
Pulmonary Ejection Systolic Left 2nd ICS just Systemic
Stenosis lateral to Cyanosis
sternum, radiates
to left shoulder
of infraclavicular
area
Pulmonary Early-Diastolic Left 2nd ICS just Symptoms of
Regurgitation lateral to Right-Sided Heart
sternum Failure
Tricuspid Diastolic Rumble 4th-5th ICS over Fluttering
Stenosis the left sternal Discomfort in the
border. neck
Tricuspid Pan-Systolic 4th-5th ICS over Symptoms of
Regurgitation the left sternal Right-Sided Heart
border. Failure

Example:

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A patient with Hx of MI presents with Orthopnea (Cannot lie down flat),

Bibasilar crepitations, Pan-systolic murmur.

→ Mitral Regurgitation

→ do Echo

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

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

Polymorphic (Broad-Complex) Ventricular Tachycardia

= Torsades De Pointes (TDP)

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

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

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Key An elderly patient with a Hx of stroke presents with exertional dyspnea. ECG
59 → AF. Chest X-ray → Straight left heart border.

→ Mitral Stenosis.

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

fever and rheumatic fever.

Pathogenesis of Mitral Stenosis:

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

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Features
• Mid-late diastolic murmur (best heard on expiration) ‘’low pitched’’ Note:
left murmurs best heard in expiration whereas Right murmurs (Aortic) best
heart in inspiration
• Loud S1, opening snap
• Low volume pulse
• Malar flush
• Atrial fibrillation

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

Chest x-ray

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

heart.

ECG (may show):

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

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Echocardiography
(Thickening of Mitral valve leaflets)

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

60

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

61 Dilated Cardiomyopathy

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

Hypertrophic Cardiomyopathy.

Dilated cardiomyopathy (DCM) basics (For READING ONLY)

• dilated heart leading to systolic (± diastolic) dysfunction
• all 4 chambers are affected but Left Ventricle is more affected than Right
Ventricle.
• features include arrhythmias, emboli, mitral regurgitation
• absence of congenital, valvular or ischaemic heart disease

◙ Causes often considered separate entities

• alcohol: may improve with thiamine
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• postpartum
• hypertension

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

◙ Inherited dilated cardiomyopathy

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

Key A Summary on Arrhythmias Management

62

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

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

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

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

◙ In Polymorphic Ventricular Tachycardia (Broad-Complex)

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

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

◙ In Ventricular Tachycardia →

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Give Amiodarone.

(Haemodynamically Unstable → e.g. Hypotension, Confusion,

Altered Mentation, ↓ Urine Output)
→ DC Cardioversion.

Key An elderly patient suddenly fell unconscious, he recovered completely within a

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

The best Investigation → 12-lead ECG

Analysis and Causes of Falls.

Causes are usually:

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

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

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

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

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

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

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

Stokes Adam attack [Reading]:

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

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Key Murmurs in Paediatrics:

64 - Preterm baby with continuous or machinery murmur → PDA
- Cyanotic baby with ejection systolic murmur (due to pulmonary stenosis)
→ TOF (Tetralogy of Fallot).
- Progressive (Severe) Cyanosis + Poor feeding + Holosystolic murmur along
the left sternal border → Tricuspid Atresia.
- Acyanotic, Pan-systolic murmur → VSD (Others: Poor feeding and poorly
gaining weight)

Congenital Heart Diseases

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Patent Ductus Arteriosus (PDA)

Overview

• A form of congenital heart defect

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

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Features

• left subclavicular thrill (sometimes rough systolic murmur along

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

Diagnosis → Echo

Management

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• Indomethacin (a NSAID) (ind=end=closes the duct) (inhibits

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

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

→ Tetralogy of Fallot.

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

the four criteria of TOF).

Tetralogy of Fallot (TOF)

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

heart disease

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

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

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

until the baby is 6 months old

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

The four characteristic features are:

1) Ventricular septal defect (VSD)

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

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

Other features

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

Management

• Surgical repair is often undertaken in two parts.

• Cyanotic episodes may be helped by beta-blockers to reduce
infundibular spasm.
Key Familial Hypercholesterolemia
66

It is Autosomal dominant

Q) When to highly suspect it?

1) If Cholesterol is > 7.5 (Normal: <5 mmol/L)

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2) Family History of “MI” in a first degree relative before the age of 60 or 2nd
degree below 50.

First degree relatives: Parents and siblings.

Second degree relatives: Grandparents, aunts, uncles

Key Ventricular Fibrillation

67

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

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

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

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Key Pan-Systolic murmur could be:

69

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

VSD (Ventricular Septal Defect):

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

systolic thrill.

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

Key ◙ Myocardial Infarction (Weak dead part of the cardiac muscle)

70
→ Congestive Heart Failure
→ Backflow of the blood to the lungs
→ Pulmonary Oedema
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→ Desaturation, Dyspnea, Orthopnea, Crepitations

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

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

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

71

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

Key A hypertensive patient on Enalapril (ACE inhibitor) developed annoying

72 dry cough.

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

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

Key Pansystolic murmur at the apex + Hx of Rheumatic fever

73

→ Mitral Regurgitation (MR).

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

◙ MR can occur 2ry to Rheumatic fever.

◙ MR may lead to → Pulmonary oedema

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

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

We can decide based on clinical features.

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

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

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

The likely underlying cause of the recurrent falls

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→ Postural Hypotension.

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

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

Key
75

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

◙ A Holter ECG (24-hour ECG) will not be beneficial as the ECG already shows
Irregular Rhythm; hence, there is no point of using it again.
◙ Echo should be done to identify the underlying cause of this irregular
rhythm so the treatment can be decided accordingly.
◙ The most common Valvular heart disease that causes Syncopal attacks is →
Aortic Stenosis (ejection systolic murmur).

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

Stenosi Systolic to sternum, radiates to Anginal chest pain,
s Carotid artery syncope

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

→ Tricuspid Atresia.

Key - Preterm, continuous murmur → PDA

78

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

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

Key Before prescribing amiodarone

79

→ Serum Electrolytes and Urea measurements should be obtained.

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

Monitoring of patients taking amiodarone

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

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Adverse effects of amiodarone use

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

◙ Amiodarone is (p450 inhibitor) e.g. Decreases metabolism of warfarin.

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

80 is not serious or harmful.

→ Reassurance.

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Key Pulmonary Early- Left 2nd ICS just Symptoms of

81 Regurgitation Diastolic lateral to sternum Right-Sided Heart
Failure

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

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

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

Suspect → pulmonary regurgitation (on top of the corrected pulmonary

stenosis as a child – due to TOF)

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

New murmur + Fever → Infective Endocarditis.

Investigation → Blood Culture or Echocardiogram.

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Key Young Adult + Recurrent Palpitations + Light-headedness +

83 Tachycardia

→ Think of SVT (Paroxysmal Supraventricular Tachycardia) = Narrow

Complex.

→ Valsalva manoeuvre and Carotid massage

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

N.B. Adenosine is contraindicated in asthmatics – Verapamil (CCB) is the

preferred option in Asthma.

Key ◙ 1st Degree Heart Block and Mobitz type 1 usually do not require treatment
84 (As long as the patient is Asymptomatic).
◙ Mobitz type 2 and Complete heart block (3rd degree heart block) require
permanent pacemaker.

Key Aortic Stenosis:

85 - The commonest valvular disease in the elderly (Over 65).

- Usually Asymptomatic apart of exercise intolerance (often mild).

- It can cause syncopal fainting.

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- Ejection systolic murmur at the right 2nd ICS, louder on sitting upright and
radiates to carotid.
A scenario of an elderly presents with mild exercise intolerance or
is asymptomatic but visiting for the purpose of cockup found to
have ejection systolic murmur.

Key Investigations following Syncope

86 Patients who have unannounced loss of postural tone leading to a period of
unconsciousness need to be investigated for 4 main causes:
1) Irregular rhythm (Cardiac syncopal events): Usually abrupt, with rapid
recovery and flushing → 12 Lead ECG
2) Low blood pressure or postural drop → Measure BP while lying and 3
minutes after standing (Blood Pressure Monitoring).
3) Seizures → need eyewitness to confirm, as there is usually post-ictal
drowsiness or confusion.
4) Hypoglycemia → Check blood glucose
N.B. A vasovagal attack is usually due to overwarm environment, or prolonged
standing period, or after visual stimuli e.g. seeing blood. The patients usually
feel dizzy and ‘’tunnel vision’’ before the attack.

Other explanation:

DDx of Sudden Falls.

• Drop attacks → Sudden falls without losing consciousness.

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• Stokes Adam → Unconscious + Abnormal ECG.

• Hypoglycemia → Unconscious (or) ↓ level of consciousness + Sweating, do
not recover unless given glucose.
• Vasovagal attacks → Unconscious + Hx of prolonged standing, straining,
pooping, heavy weight lifting or after visual stimuli e.g. seeing blood. The patients
usually feel dizzy and ‘’tunnel vision’’ before the attack. Usually in a YOUNG
FEMALE (with NO chest pain, palpitation and with Normal ECG)
• Epilepsy → Unconscious ± Post-seizure confusion

Key Digoxin Toxicity

87

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

• Neurological: Hallucination, Confusion.
• Visual: Yellow green vision, (Yellow haloes), blurred vision.
• Arrhythmias: Bradycardia, V tach, Premature contractions.

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

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Key Thiazide like diuretics

88

◙ Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of

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

Common adverse effects

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

A patient with hypertension on treatment presents complaining of

recurrent falls especially when trying to get up.

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

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

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

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

→ Acute Mitral Regurgitation.

Acute mitral regurgitation (MR) after MI: pansystolic murmur

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

◙ Due to → Ischemia or rupture of the papillary muscles.

◙ An early-to-mid systolic or Pansystolic murmur is typically heard.
◙ Dx → Echocardiogram.
◙ Treatment → vasodilator therapy but often require emergency surgical
repair.
◙ May present with Hypotension, Tachycardia and Pulmonary edema.

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Key Stable Angina

91
√ In the case of stable Angina, the pain is precipitated by predictable factors
such as exercise and emotional stress. This is because while exercising, the
Oxygen demand is more than the Oxygen supply.

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

Unstable Angina: occurs mostly at rest, unpredictable, random. It is an

emergency.

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

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

Tricuspid Atresia → Cyanotic.

VSD → Acyanotic.

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

→ Tall Tented T-Waves → Hyperkalemia (Likely 2ry to ACE inhibitors being

used to control his Hypertension)

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Remember that:
◙ Spironolactone and ACE inhibitors → HypeRkalemia.
◙ Loop diuretics, Thiazide diuretics → HypOkalemia.

Key
94

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U wave in → Hypokalemia “HypUkalemia”, an additional wave after the T

wave.

Tall Tented T-wave in → Hyperkalemia

J wave (Osborn wave) in → Hypothermia.

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

Widespread Saddle Shaped ST Elevation with upward concavity + PR

Depression in → Pericarditis.

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

Diagnosis 1st line

Acute coronary Aspirin (lifelong) & ticagrelor (12 months)
syndrome (medically
treated) (MI)
Percutaneous coronary Aspirin (lifelong) & prasugrel or ticagrelor (12 months)
intervention (PCI)
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TIA: Transient Ischemic Aspirin 300 mg 2 weeks then Clopidogrel 75 mg

Attack (lifelong)
Ischaemic stroke Aspirin 300 mg 2 weeks then Clopidogrel 75 mg
(lifelong)
Peripheral arterial Clopidogrel (lifelong)
disease
AF + Ischemic Stroke Aspirin 300 mg for 2 weeks then start Anticoagulation
(e.g. Warfarin or DOAC- apixaban, rivaroxaban)

Who should receive a statin?

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

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

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Key Atrial fibrillation in an unstable patient → Immediate DC Cardioversion

96

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

failure)

Scenario,

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

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

The next step in management is → Immediate DC Cardioversion

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

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

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

The most appropriate management → [Pericardiocentesis].

• Cardiac Tamponade:

• Beck’s Triad: Hypotension, Muffled Heart Sounds, High JVP

(Distended neck veins).

• Others: Dyspnea, Pulsus Paradoxus, Tachycardia.

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• Cardiac Tamponade can develop as a complication of MI:

After MI → Acute pericarditis → Pericardial effusion → Cardiac

Tamponade.

• Trauma is the most important cause for cardiac tamponade.

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

Either Pericardial effusion (OR) Cardiac Tamponade.
• Dx: Echo is diagnostic

• Tx: Urgent pericardiocentesis.

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Key Ventricular Old, Sudden collapse, confusion, severe

98
Fibrillation hypotension, Not breathing, Unconscious
→ Immediate DC Cardioversion ‘’defibrillation’’

Key Atrial fibrillation in an unstable patient → Immediate DC Cardioversion

99

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

failure)

Scenario,

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

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

The next step in management is → Immediate DC Cardioversion

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

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

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

100 elevation on ECG. What to Do Next?

→ Measure Cardiac Enzymes, especially (Troponin)

√ If Troponin is high → NON-STEMI Elevation MI

√ Immediate management → Give LMWH e.g. Fondaparinux √ recent

exam

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

101

→ Adenosine.

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

Key Loop diuretic Thiazide-like Potassium-sparing

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

Hyponatremia Hyponatremia Hyponatremia

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Hypokalemia Hypokalemia HypeRkalemia

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

Key
103

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

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What is the most appropriate investigation?

→ Blood Culture

These lesions are likely Janeway lesions (minor criteria of infective

endocarditis).

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

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

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initial line → give Calcium Chloride (or Calcium Gluconate)

(to prevent cardiac arrhythmia).

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

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

→ Withhold (stop) ACE inhibitors.

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

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

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→ Rivaroxaban (or any other DOAC e.g. Apixaban, Rivaroxaban, Edoxaban,

Dabigatran)

Remember:

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

√ Control Blood Pressure.

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

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

AF):

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

(Dabigatran/ Apixaban/ Rivaroxaban/ Edoxaban).

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

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

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→ ABCD2 Score.

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

patient who has atrial fibrillation.

♦ The ABCD2 score (Prognostic) is used to identify the risk of stroke in patients
who have had a suspected TIA.

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

→ Furosemide.

(Loop diuretics such as furosemide can cause hypokalemia).

HypOkalemia HypeRkalemia

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

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• Thiazide-like diuretics • Potassium-sparing diuretics

(e.g. bendroflumethiazide, indapamide) (e.g. Spironolactone/ Eplerenone)
• Vomiting and Diarrhea • CKD.
• Villous Adenoma • Addison’s (1ry Adrenal Insufficiency).
• Renal tubular failure • Congenital Adrenal Hyperplasia.
• Cushing Syndrome
• Conn’s disease (1ry hyperaldosteronism)

Key A patient with hypertension on treatment presents complaining of ankle

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

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

Diltiazem) to be remembered:

◙ Ankle Swelling

◙ Gingival Hyperplasia

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

Key Before prescribing amiodarone, what investigation should be ordered?

111

→ Serum Electrolytes and Urea.

Remember (do not mix thing up):

The 2 most important tests to be done before initiating lithium are:
Thyroid Function Tests.
Kidney Function Tests.

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

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→ Beta-blockers (e.g. metoprolol)

Agents used to control rate (Rate Control) in patients with Atrial Fibrillation
(AF):

- Beta-blockers (e.g. atenolol, metoprolol) → First line but Contraindicated in

Asthma.
- Calcium channel blockers (e.g. diltiazem) → if Asthmatic patient.
- Digoxin → (not considered first-line anymore as they are less effective at
controlling the heart rate during exercise. However, they are the preferred
choice if the patient has coexistent heart failure).

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

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

◙ The first drug of choice for Symptomatic Bradycardia (Dizziness, feeling

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

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

A. Amiodarone

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

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

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

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

Patient unstable, SBP < 90 → Shock.

Broad complex tachycardia + low BP (unstable) → Cardioversion (DC Shock).

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

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

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

± Malaise, Rigors, Fever

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The initial step → Blood Culture. Then → Echo

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

A. Pericarditis
B. Pulmonary Embolism
C. Pleural Effusion

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

within 2 days) and Dressler's syndrome (presents 2-6 weeks after MI) both
have the same features → Pleuritic chest pain that worsens on lying flat and
during inspiration, Pericardial rub, Widespread Saddle shaped ST elevation on
the ECG.
◙ They can also lead to Pericardial effusion (Enlarged globular heart on chest
X-ray) and if severe enough, Cardiac Tamponade can also develop (also
enlarged globular heart on the X-ray).
Cardio

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

118 complaining of 25 minutes left side dull aching chest pain radiating to his
jaw. He was given Aspirin 300 mg by his GP and then sent to medical services

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in a local hospital. He is no longer in pain. The ECG is normal. The troponin is

elevated 202 ng/L (Normal: < 5 ng/L). What is the next step in management?

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

Since the ECG is normal, alteplase is wrong.

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

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

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