Rate control medications such as metoprolol should be given first as he is hemodynamically stable. If rate control medications fail, then we could try rhythm control. Digoxin as part of rate control should not be used as first-line unless there is evidence of congestive heart failure. Remember, the most important part of management for atrial fibrillation is preventing strokes and controlling the patient’s symptoms. Converting patients back to sinus rhythm is not always the main goal. 

The clinical presentation of atrial fibrillation can vary. Some patients are asymptomatic; others may have life-threatening complications (e.g. heart failure or angina). The management depends on the underlying cause and the presence of symptoms.

There are two wide categories for management:

1. Rhythm control (cardioversion)

2. Rate control

Rhythm Control : If the patient has signs of shock, syncope, acute cardiac failure, or ischaemia then perform electrical cardioversion under sedation. This is rarely necessary. There is also the option of chemically cardioverting with flecainide or amiodarone. If the patient has had symptoms for more than 48 hours, there is a risk of cardiac thromboembolism when cardioverted. So in these cases, rate control medications and low molecular weight heparin are better choices.

Rate control medications include beta blockers (metoprolol), rate-limiting calcium channel blockers (diltiazem or verapamil), and digoxin.

For rate control, beta-blockers or rate-limiting calcium channel blockers are the first choice. Digoxin 500 mcg is usually the choice of drug if the patient suffers from congestive heart failure.

This could be potentially a case of a myocardial infarction. A new LBBB in the context of cardiac chest pain is traditionally considered part of the criteria for thrombolysis. It is extremely important to recognize an LBBB on an ECG.

A common cause of left axis deviation is inferior myocardial infarction.

Remember, this question does not ask if this is an inferior myocardial infarction hence the ECG does not show the typical ST elevation in leads II, III, and aVF. This question is asking, what abnormalities could represent a left axis deviation of which inferior myocardial infarction is the only option.

Common causes of left axis deviation (LAD) : Left ventricular hypertrophy (LVH), Left anterior fascicular block (or hemiblock), Inferior myocardial infarction.

Less common causes of left axis deviation (LAD) : Obesity, Wolff Parkinson White syndrome.

Causes of right axis deviation : Right ventricular hypertrophy, Thin tall, Chronic lung disease, Pulmonary embolism, Left posterior hemiblock, Lateral myocardial infarction.

The lateral wall of the left ventricle is supplied by the left anterior descending. Infarction here would cause an axis deviation away from the site of infarction.

The widespread ST elevation and pericardial friction rub are seen in pericarditis. The chest X-ray showing an enlarged, globular heart points towards pericardial effusion.

Dressler’s syndrome would explain all the findings. Dressler’s syndrome tends to occur around 2-6 weeks following an MI.

The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterized by a combination of fever, pleuritic pain, pericardial effusion, and a raised ESR. It is treated with NSAIDs.

Mobitz type 1 block : Gradual prolongation of the PR interval followed by a dropped beat. 1st degree heart block is a prolongation of the PR interval (beyond 0.2 seconds). It is a benign condition that does not require additional follow-up or management. It is not usually associated with symptoms and does not progress to other forms of heart block. The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex.

Mobitz type 2 and complete heart block require permanent pacemakers.

The patient has been diagnosed with atrial fibrillation. The symptoms of stroke were probably due to atrial fibrillation. The main goals in managing AF are rate/rhythm control and anticoagulation.

As she was already managed with metoprolol which is a rate-limiting medication, the next step is to count her CHA2DS2-VASc score to determine if she requires anticoagulation. In her case, she would have a CHA2DS2-VASc score of 4 (1 for hypertension, 1 for age, 1 for stroke history, and 1 for sex). Anticoagulation such as warfarin would be of benefit to reduce the risk of stroke for her. Aspirin is no longer used for stroke prevention.

ATRIAL FIBRILLATION AND ANTICOAGULATION :

Guidelines suggests using the CHA2DS2-VASc score to determine the most appropriate anticoagulation strategy for atrial fibrillation.

The CHA2DS2-VASc score is used to assess a patient’s stroke risk. Offer anticoagulation to all people with a CHA2DS2-VASc of 2 or above, and consider offering it to men with a CHA2DS2-VASc of 1.

Risk factor : C - Congestive heart failure, 1 H - Hypertension, 1 A2 - Age 75 years , 2 Age 65-74 years, 1 D Diabetes, 1 S2 Prior stroke or TIA 2 V Vascular disease (including ischaemic heart disease and peripheral arterial disease), 1 S Sex (female). It may be quicker to remember when to give warfarin according to the below scenarios instead of writing out and calculating the whole CHA2DS2-VASc score.

This only applies to simple exam scenarios.

• < 65 years old and no comorbidities - No warfarin

•  65 years old or at least one comorbidity - Warfarin

Another alternative to warfarin which has gained much popularity over the past decade is DOAC (Direct-Acting Oral Anticoagulants) such as apixaban, edoxaban, and rivaroxaban. These medications are also licensed for use in stroke prevention with non-valvular atrial fibrillation and a CHA2DS2-VASc score 2 (consider for men with CHA2DS2-VASc score 1).

The benefits of using DOAC compared to warfarin include :

• Reduces the risk of intracranial haemorrhage

• No INR monitoring

• Faster onset anticoagulation (2-4 hours)

The disadvantages of using DOAC compared to warfarin include:

• No specific antidote

• Essential to be compliant

Newer questions for the exam may contain DOAC as an option so do read up on them.

SECONDARY PREVENTION AFTER STROKE OR TIA :

Stroke: A syndrome of the sudden onset of focal neurological loss of presumed vascular origin lasting more than 24 hours.

Transient Ischaemic Attack: A syndrome of the sudden onset of focal neurological loss of presumed vascular origin lasting less than 24 hours.

ATRIAL MYXOMA are benign tumours. Around three-quarters of atrial myxomas occur in the left atria and tend to grow on the wall (septum).

Sometimes small pieces of the tumour can break off and fall into the bloodstream. If this happens, they can block an artery elsewhere in the body such as the brain, which could cause a stroke, or in the lungs causing a pulmonary embolus. Around 10% of myxomas seem to be inherited (passed down through families). These are known as familial myxomas.

The symptoms occur due to obstruction of the mitral valve which results in syncope and heart failure.

Features :

• Symptoms of haemodynamic obstruction, embolization, or constitutional symptoms such as fever, malaise, tachycardia, and tachypnoea

• Symptoms and signs of ischaemia or infarction in the peripheries, due to embolization of adherent thrombus

• Atrial fibrillation

• Large myxomas may impair intracardiac blood flow, causing dyspnoea, syncope, or symptoms and signs of congestive cardiac failure.

• Echo: Pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum.

Start chest compressions.

This is clear that this is a myocardial infarction. Atypical presentations of myocardial infarction are common. They may present with abdominal pain in the question above. Atypical symptoms include abdominal discomfort or jaw pain. The remaining symptoms are quite characteristic of myocardial infarction.

• In pericarditis, the pain is aggravated by inspiration or lying flat and relieved by leaning forward. A pericardial rub may present and there may be a fever

• In pulmonary embolism, patients would present with dyspnoea and pleuritic chest pain.

The writers of the exam would also give other hints like having a history of immobilization or a long travel.

• In costochondritis, the pain is localized at the costochondral junction which is enhanced by motion, coughing, or sneezing. The writers would usually give a history of repeated minor chest injury or activities that one is unused to – perhaps decorating or moving furniture.

• In pneumothorax, the pain is not central but pleuritic and there are no signs that indicate that this is a pneumothorax in the given question The given picture of central chest pain for 45 minutes (more than 30 minutes), sweating, and dyspnoea with major risk factors of diabetes mellitus and hypertension suggest the diagnosis of myocardial infarction.

ACUTE MYOCARDIAL INFARCTION PRESENTATION :

Chest pain (central chest pain may not be the main symptom)

• Three-quarters of patients present with characteristic central or epigastric chest pain radiating to the arms, shoulders, neck, or jaw

• The pain is described as substernal pressure, squeezing, aching, burning, or even sharp pain

• Radiation to the left arm or neck is common

• Chest pain may be associated with sweating, nausea, vomiting, dyspnoea, fatigue and/or palpitations

• Shortness of breath

Atypical presentations are common and tend to be seen in women, older men, and people with diabetes. Atypical symptoms include abdominal discomfort or jaw pain. Elderly patients may even present with altered mental state.

ACUTE CHEST PAIN DIFFERENTIALS:

Ischaemic cardiac pain - Retrosternal “pressure”, tightness”, “constricting”, Radiates to shoulders, arms, neck, or jaw. Associated with diaphoresis, sweating, nausea, pallor.

Pericarditis - Atypical, retrosternal pain, Sometimes pleuritic, Positional (relieved on sitting forward).

Gastroesophageal reflux disease - Retrosternal “burning”, Associated with indigestion, Pain when supine, after consumption of food, alcohol, and NSAIDs, Relieved by antacids.

Aortic dissection - “Tearing” pain, sudden in onset. Radiates to back, Diaphoresis, hypotensive, tachycardic. Differences in blood pressures and/or pulses, Abnormal or absent peripheral pulses, New murmur (aortic regurgitation)

Pulmonary embolism - Acute respiratory distress, Diaphoresis, hypotensive, tachycardic, hypoxaemia, Pleural rub.

Pneumothorax - Pleuritic, sharp, positional, sudden in onset Associated with abrupt breathlessness, Diminished breath sounds, hyperresonance to percussion.

Pneumonia - Associated with cough, sputum, and fever.

Musculoskeletal - Sharp, positional, pleuritic aggravated by movement such as deep inspiration, coughing, twisting of neck or thoracic cage.

First-degree heart block :

• PR interval > 0.2 seconds

Second-degree heart block: Mobitz type I AV block (Wenckeback block/phenomenon)

• Progressive prolongation of the PR interval until a dropped beat occurs Mobitz type II AV block

• PR interval is constant but the P wave is often not followed by a QRS complex (dropped beat)

Third degree (complete):

• P waves will occur regularly, usually at heart block: a rate of around 75 beats per minute but are completely unconnected to the rhythm of the QRS complexes.

This question points towards cardiac tamponade. His chest is bilaterally clear thus we can therefore exclude pneumothorax or pleural effusion. Muffled heart sounds, distended neck veins and hypotension are called Beck’s triad and it is a classical finding in cardiac tamponade. This is diagnosed with an echocardiogram.

These are the most common features that are asked in exams .

ACUTE PERICARDITIS:

Causes include -

• Viral infections (Coxsackie)

• Tuberculosis

• Uraemia

• Trauma

• Post-myocardial infarction, Dressler’s syndrome

• Connective tissue disease

Clinical Features - Central chest pain is worse on inspiration or lying flat and relieved by sitting forward (Pericardial friction rub)

ECG classically shows concave (saddle-shaped) ST-segment elevation, Troponin may be raised.

Treatment NSAIDS.

PERICARDIAL EFFUSION:

Clinical features - Dyspnoea, Raised JVP

CXR shows an enlarged, globular heart ECG shows low-voltage QRS complexes and alternating.

Treatment - Pericardiocentesis

CARDIAC TAMPONADE :

A life-threatening condition in which a pericardial effusion has developed so rapidly or has become so large that it compresses the heart.

Etiology : Usually penetrating or blunt chest trauma

Features :

• Dyspnoea

• Raised JVP – seen by having neck veins which are distended

• Tachycardia

• Hypotension

• Muffled heart sounds

• Pulsus paradoxus

Remember Beck’s triad: Muffled heart sounds, distended neck veins, and hypotension

Diagnosis - Echocardiography

Treatment - Pericardiocentesis.

This ECG shows supraventricular tachycardia. Carotid massage should be attempted before giving IV adenosine.

SUPRAVENTRICULAR TACHYCARDIA : Paroxysmal supraventricular tachycardia is manifested as a regular rhythm at a rate between 130 and 220 beats/min. Acute management if hemodynamically stable, this should be done in the following sequence :

• 1st : Valsalva manoeuvre, carotid massage

• 2nd : Adenosine 6 mg rapid IV bolus (or verapamil – but verapamil is rarely used for SVT now unless the patient is asthmatic in which case verapamil is used instead of adenosine)

If adenosine is unsuccessful in converting to normal sinus rhythm then give another 12 mg IV adenosine.

If still unsuccessful give a further 12 mg IV adenosine.

• 3rd : Electrical Cardioversion

Acute management if hemodynamically unstable -

• Direct current (DC) cardioversion

Prevention of episodes:

• Beta-blockers

• Radio-frequency ablation.

Non-steroidal anti-inflammatory drugs (NSAIDs) should be avoided in patients with chronic kidney disease, heart failure, or ischaemic heart disease. Selective COX-2 inhibitors should also be avoided in these patients. NSAIDs inhibit the synthesis of prostaglandins.

This in turn can lead to a reduction in sodium excretion, renal perfusion, and glomerular filtration rate. They can also reduce the effectiveness and increase the toxicity of ACE inhibitors and diuretics. This can result in an exacerbation of heart failure.

NSAIDs can cause the kidneys to retain more salt and water in the body which can increase your risk of heart failure.

They can also make some blood pressure-lowering medicines, such as ACE inhibitors and diuretics, less effective – and a rise in blood pressure is likely to worsen heart failure. It is also worth noting that thiazide diuretics increase the risk of gout due to reduced clearance of uric acid.

A racing heart or palpitation is a common phenomenon in alcoholics which is not serious or harmful. So reassure the patient.

The next step for management after trying carotid sinus massage would be intravenous adenosine. Verapamil is rarely used for SVT now unless the patient is asthmatic in which case verapamil is used instead of adenosine. The history of hypertension, type 2 diabetes mellitus, and angina have little or no significance in this question.

For junior doctors, the ECG pattern between ventricular tachycardia and ventricular fibrillation can be hard to distinguish. But here as the patient is still conscious, it cannot be ventricular fibrillation as V. fib would present without a pulse and the patient would not be conscious. Thus, ventricular tachycardia is the answer here. Since the patient is haemodynamically unstable, cardioversion would be the answer.

VENTRICULAR TACHYCARDIA :

Ventricular tachycardia may impair cardiac output with consequent hypotension, collapse, and acute cardiac failure. This is due to extreme heart rates and lack of coordinated atrial contraction (loss of “atrial kick”).The rate of V. Tach is from about 100-250 bpm. P Waves may be present or absent. P waves are usually not seen if the rate is increased. If present, the P waves have no relation to the QRS complexes.

V. Tach can present in two ways:

1. With Pulse : Haemodynamically stable or Haemodynamically unstable e.g. hypotension, chest pain, cardiac failure, decreased consciousness level.

2. Without Pulse : Management depends on how the patient presents.

With Pulse & Haemodynamically stable : Antiarrhythmics e.g. amiodarone, lidocaine, procainamide ; Haemodynamically unstable e.g. hypotension, chest pain, cardiac failure, decreased consciousness level - Immediate electrical cardioversion is indicated.

Without Pulse - Immediate electrical cardioversion is indicated.

ECG ARRHYTHMIA CLINCHERS :

These clinchers help point you towards an answer but you still need to read the whole stem and look at the ECG before you decide. The exam can be tricky.

Atrial Fibrillation:

• Palpitations

• Fast heart rate

• Dyspnoea

Atrial Flutter :

• The patient in the stem will describe it as a “fluttering feeling in the chest”

Ventricular Fibrillation :

• Older adult with sudden collapse

• Not breathing

Ventricular Tachycardia :

• Regular and fast

• Stem will mention a period of ongoing lightheadedness, palpitations, and chest pain (rarely will they present with collapsed in exams)

Sinus Bradycardia : Lightheadedness, dizziness, hypotension, vertigo and syncope

Note - Slow heart rate is completely normal in young athletes.

Sinus Tachycardia :

• Physiological situations, such as exercise or situations of stress or anger

• History of infection

Heart Block :

• Stem will mention an older patient who has suffered a previous MI or who has ACS.

Type 1 AV Block:  Lengthening of the PR interval

Type 2 AV Block Mobitz I: Progressive prolongation of PR interval until a P wave is dropped

Mobitz II: Randomly dropped P waves

Type 3 AV Block (Complete Heart Block): No P waves

Wolff-Parkinson White Syndrome : “Delta wave” on ECG.

This is simply a diagnosis of exclusion.

In pericarditis, the chest pain felt by patients is pleuritic and aggravated by inspiration, coughing, and a change to the upright position. The pain is relieved when the patient lies down – an important feature that was deliberately left out of the stem. The diagnosis of pericarditis involves the typical chest pain, pericardial friction rub on auscultation, and characteristic ECG changes this question stem only gives one part of a clue for diagnosis which is the pleuritic chest pain and a fever.

Remember, not all questions in exams are straightforward.

ACUTE PERICARDITIS :

• Chest pain is described as sharp, stabbing, central chest pain, with radiation to the shoulders and upper arm

• Chest pain may be pleuritic and is often relieved by sitting forwards

• Chest pain may be made by inspiration, cough, swallowing, or movement of the trunk

• Other symptoms include non-productive cough and dyspnoea

• Pericardial friction rub on auscultation

Clinically, the presence of a pericardial friction rub is pathognomic – often a rub can be heard even when a pericardial effusion is present.

Causes :

• Viral infections (Coxsackie)

• Tuberculosis

• Uraemia (causes ‘fibrinous’ pericarditis)

• Trauma

• Post-myocardial infarction, Dressler’s syndrome

• Connective tissue disease

Post-myocardial infarction is an extremely important cause to remember for the exam.

ECG changes : Widespread ‘saddle-shaped’ ST elevation (Saddle-shaped meaning concavity directed upwards) and PR segment depression.

Patients who have an unannounced loss of postural tone leading to a period of unconsciousness need to be investigated for three main causes which are:

• Irregular rhythms

• Low blood pressure or postural drop

• Seizures

The first two (irregular rhythms and low blood pressure or postural drop) are easy to investigate however seizures are a little bit more difficult and thus we would only suspect it if there was an eyewitness who saw the fit.

There is usually a period of post-ictal drowsiness or confusion if a seizure is to be considered. This stem mentions that he recovered completely within a few minutes which tells us that a seizure is unlikely. Cardiac syncopal events are the most likely here as they are usually abrupt in onset with rapid recovery with flushing. This is the reason that ECG is the answer here.

In many cases, it may be due to a vasovagal syncope which is a common response to an overwarm environment or a period of prolonged standing. It can also occur after a visual stimulus such as seeing blood on the floor. However, patients with vasovagal syncopes would normally feel dizzy and have ‘tunnel vision’ before the syncopal episode. This is not evident in this stem.

INVESTIGATIONS FOLLOWING SYNCOPE :

Things to do for patients who had a syncopal event and recovered

• Find witnesses – see if family members or friends have seen how the patient became unconscious or was there a seizure witnessed.

• Perform an ECG to look for arrhythmias

• Perform blood pressure supine and standing or sitting to look for a postural drop

• Check blood glucose to exclude hypoglycemia.

Although there are risk factors for myocardial infarction and pulmonary embolism, it is more likely a myocardial infarction that killed this man because in diabetics, myocardial infarction can be painless as the patient can develop autonomic neuropathy. We call this a “silent MI”. If one does not feel pain, he might not call for help. As this progresses, he collapses and dies.

Please see Q-10 for heart block

VENTRICULAR FIBRILLATION :

Ventricular Fibrillation means “sudden death”. The blood pressure drops immediately to zero and so does the cardiac output. Ventricular fibrillation (VF) is the most important shockable cardiac arrest rhythm. The ventricles suddenly attempt to contract at rates of up to 500 bpm. This rapid and irregular electricalactivity renders the ventricles unable to contract in a synchronized manner, resulting in immediate loss of cardiac output.

Unless advanced life support is rapidly instituted, this rhythm is invariably fatal. Prolonged ventricular fibrillation results in decreasing waveform amplitude, from initial coarse VF to fine VF and ultimately moving on to asystole due to progressive depletion of myocardial energy stores.

ECG Findings for V. Fib:

• Chaotic irregular deflections of varying amplitude

• No identifiable P waves, QRS complexes or T waves

• Rate 150 to 500 per minute

• There is no specific pattern to the discharge. There are different types of wavering baseline patterns.

This question is testing your management of hypertension with diabetes. Patients with type 2 diabetes mellitus have a considerably higher risk of cardiovascular morbidity and mortality, not to mention hypertension plays a major role in the development and progression of microvascular and macrovascular disease in people with diabetes.

Treatment in this group of patients is especially important. The management for a person with hypertension alone differs slightly when compared to the management of a patient with hypertension and diabetes. First-line antihypertensive drug treatment in a hypertensive patient with diabetes should be an ACE inhibitor unless the patient is Afro-Caribbean. Age here is irrelevant when the patient has diabetes.

Given the benefits of ACE inhibitors in terms of reno-protection and retinopathy, it is appropriate to recommend an ACE inhibitor as the first line for the treatment of hypertension in most adults with type 2 diabetes. This is partly due to the positive effect on glucose metabolism. For people of African or Caribbean family origin, an ACE inhibitor plus either a diuretic or a calcium channel blocker is the first line.

HYPERTENSION MANAGEMENT IN NONDIABETICS AND DIABETICS:

HYPERTENSION ALONE : First line :

• Age < 55 - ACE inhibitor 

• Age > 55 or of black African or Caribbean origin - calcium channel blocker

HYPERTENSION & TYPE 2 DM: First line :

• Any age - ACE inhibitor 

• Black African or Caribbean origin - ACE inhibitor plus either a diuretic or a calcium channel blocker.

Muscle weakness and cramping are features of low potassium. The potassium levels shown here are severely low. Low enough that management is likely going to be IV replacement in an area where there is cardiac monitoring. Thiazides such as bendroflumethiazide can increase potassium loss which results in hypokalemia. U waves are seen in hypokaleimia.

The other answers are less likely: J waves are usually observed in patients suffering from hypothermia.

Delta waves are seen in Wolff Parkinson's White syndrome. PR interval in hypokalemia is prolonged. QT interval remains the same in hypokalemia although Q-T interval may be falsely seen as prolonged in hypokalaemia. It is usually the U wave that is mistaken for the T wave. These are situations that may falsely suggest a prolonged Q-T interval. This is an example of a prominent U wave.

A low T wave followed by a prominent U wave produces a ‘camel-hump’ effect. As hypokalaemia progresses to be more severe, the T wave decreases in amplitude and is flattened or becomes inverted. The U wave becomes more prominent. This may falsely be seen as a prolongation of the Q-T interval.

ECG features of hypokalaemia :

• Prominent U-waves

• Small or absent T waves

• Prolonged PR interval

• ST depression

Mnemonic: HypUkalaemia – U waves.

The patient has mitral regurgitation secondary to rheumatic fever. Some exam clinchers for mitral regurgitation:

• Previous disease that affects the mitral valve

• Signs and symptoms of pulmonary oedema will appear in the stem

• Panysystolic murmur at the cardiac apex is the murmur of mitral regurgitation

• Chest X-ray if given may show an enlarged left side of the heart.

MITRAL REGURGITATION :

Common scenarios in the exam are history of rheumatic fever.

• A few weeks after a myocardial infarction where the patient may be admitted for pulmonary oedema.

Clinical features of Left ventricular failure :

• Dyspnoea

• Orthopnoea

• Paroxysmal nocturnal dyspnoea

With severe and chronic mitral regurgitation, right-sided failure would eventually occur leading to:

• Oedema

• Ascites

Important clinical sign : Pansystolic apical murmur radiating to the axilla

ECG - signs of left ventricular hypertrophy and left atrial enlargement (e.g. broad P wave)

Chest X-ray - may show an enlarged left side of the heart

Diagnosis :

- Echocardiography.

Atropine is the first drug of choice for symptomatic bradycardia.

The dose in the bradycardia ACLS algorithm is 0.5 mg intravenous push and may repeat up to a total dose of 3 mg.

Pulmonary regurgitation is a common complication after surgical or percutaneous relief of pulmonary stenosis and following repair of Fallot's tetralogy. Pulmonary regurgitation is usually asymptomatic unless severe, when it may lead to signs of right heart failure. Patients can live for many decades following surgical repair of tetralogy of Fallot but a major problem encountered is the development of pulmonary regurgitation which may require pulmonary valve replacement.

This question points towards cardiac tamponade. Trachea is central thus tension pneumothorax is less likely. Muffled heart sounds, distended neck veins and hypotension are called Beck’s triad and are a clinical finding in cardiac tamponade. Please see Q-11

A polymorphic ventricular tachycardia is when there are beat-to-beat variations with no uniform pattern of ventricular contraction. This is also known as Torsades de points. Remember the ECG being described is one at rest, not during the fainting episode (when QRS would be broad due to the ventricular tachycardia) Prolonged QT syndrome is when the QT interval is abnormally long, predisposing individuals to ventricular arrhythmias (particularly Torsades de pointes), syncope, and sudden death.

There are no pre-syncope symptoms before fainting, which can be exacerbated by exercise, stress, medications, and electrolyte abnormalities. Sick sinus syndrome is a group of conditions affecting the function of the sinoatrial node.

It is usually associated with periods of sinus bradycardia, tachy-brady syndrome, atrial fibrillation, or flutter. It is not associated with a prolonged QT interval. The ECG demonstrates a sinus rhythm, which is not seen in a complete heart block (P waves not associated with QRS).

Aystole is not associated with a prolonged QT interval. Atrial fibrillation does not lead to fainting. Remember the atria only contributes to 15% of the overall blood ejected from the ventricle.

Angina is chest pain or discomfort that is caused when the heart muscle does not get enough blood. In stable angina, the pain is precipitated by predictable factors like exercise. This is relieved by rest.

Not all myocardial infarctions present with the typical cardiac chest pain symptoms. Some may present with atypical chest pain which can be described as an ache or discomfort. Other atypical symptoms include abdominal discomfort or epigastric pain. As there is ST elevation in leads I, II, and aVF, this confirms the diagnosis of a myocardial infarction. Percutaneous intervention (PCI) would be the best management for myocardial infarction.

POST-MANAGEMENT OF HEART FAILURE AND MYOCARDIAL INFARCTION (MI):

HEART FAILURE: Drugs that decreases mortality -

1. ACE inhibitor (Enalapril, Lisinopril, Ramipril)

2. Beta-blocker (Bisoprolol, Carvedilol, Nebivolol) (Initiate one at a time)

Manage symptoms - Furosemide add on if symptoms are not controlled; Spironolactone, or Digoxin.

ALL pts with MI on discharge:

Dual antiplatelet therapy: Aspirin + Clopidogrel

Note: Aspirin is continued lifelong Clopidogrel for 12 months.

• Beta Blockers : Offer BB to people who present acutely with MI as soon as they are haemodynamically stable. Continue a beta blocker for at least 12 months after an MI in people without heart failure. Continue a beta-blocker indefinitely in people with HF.

• ACEI : Offer ACEI to people who present acutely with MI as soon as they are haemodynamically stable. If intolerant to ACEi – use ARB.

• STATINS.

MYOCARDIAL INFARCTION MANAGEMENT: Myocardial infarction management is tricky and it is always changing. A good way to remember the first few steps of managing myocardial infarction is to remember the mnemonic.

MONA = Morphine, O2, Nitrates, Aspirin 300 mg. Morphine is given intravenously to manage the pain.

Oxygen is administered if there is evidence of hypoxia, pulmonary oedema, or continuing myocardial ischaemia. Nitrates such as GTN sublingual or by intravenous infusion are used to treat angina. Aspirin 300 mg should be given preferably before arrival at the hospital. Clopidogrel 300 mg should also be given. Heparin (unfractionated) or low molecular weight heparin (e.g. enoxaparin sodium) should also be considered.

STEMI management summary .

• If a patient presents to the hospital with symptom onset within 12 hours AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given - perform PCI.

• If PCI is not available and cannot be delivered within 120 minutes when fibrinolysis could have been given – Thrombolysis (Alteplase)

• Thrombolysis can only be done within 12 hours of symptom onset.

The most common cyanotic heart conditions presenting in the neonatal period are referred to as “The five T’s”

1. Tetrology of Fallot (TOF)

2. Transposition of the Great Arteries (TGA)

3. Truncus Arteriosus

4. Tricuspid Atresia

5. Total Anomalous Pulmonary Venous Connection (TAPVC)

By using the above mnemonic, we are down to 2 options : Tricuspid atresia or Tetralogy of Fallot

Tricuspid Atresia : Manifests early in life with severe cyanosis. Holosystolic murmurs are found along the left sternal border (Most have VSD)

Tetralogy of Fallot : This can also happen at birth but the symptoms depend on the severity. Ejection systolic murmur due to pulmonary stenosis is the common murmur to be heard.

The key word here to look out for is “investigation to determine the underlying cause”. A chest X-ray might show features of pulmonary oedema but will not show the underlying cause.

An echocardiogram is more likely to identify the underlying cause whether it be a post myocardial infarction complication such as ventricular aneurysm, infarct expansion, acute mitral regurgitation from papillary muscle rupture or ventricular septal rupture.

This man has had a cardiac arrest. The resuscitation guidelines state that if there are no signs of life, call the resuscitation team. Basic life support is an important topic for exam. Be sure to know the sequence of management.

The other choices in this question are less appropriate.

Get a defibrillator – The guidelines mention starting CPR and sending for a defibrillator as soon as possible. But given the choice, calling the resuscitation team would come first.

Nausea, vomiting, and diaphoresis (sweating) are symptoms that usually accompany cardiac chest pain. Percutaneous intervention (PCI) would be the best management for myocardial infarction. As PCI is not given in the option, thrombolysis would be the next best step. In terms of thrombolysis, Alteplase is preferred over streptokinase. However, alteplase is not given in the options thus the best option would be option B (streptokinase).

Pericarditis is one of the differentials of any patient presenting with chest pain. Pericarditis presents as sharp, pleuritic, and positional chest pain, usually 1 to 3 days post-infarct. The pain that is relieved when sitting forward is a clincher for pericarditis.

Tetralogy of Fallot is the most likely diagnosis here. It usually presents with an ejection systolic murmur. The low oxygen saturation and cyanosis are consistent with the Tetralogy of Fallot.

TETRALOGY OF FALLOT -

• The most common cause of cyanotic congenital heart disease

• Typically presents at around 1-2 months, although may not be placed until the baby is 6 months old The four characteristic features are:

• Ventricular septal defect (VSD)

• Right ventricular hypertrophy

• Pulmonary stenosis

• Overriding aorta Other features

• Cyanosis

• Causes a right-to-left shunt

• Ejection systolic murmur due to pulmonary stenosis (the VSD does not 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.

We can note that there is ST elevation in lead V2, V3, V4. This ECG shows a classical example of an anterior myocardial infarction.Those ECG findings are more than enough to answer the questions in the exam and it is highly unlikely that you would need to know more than that. For those who want to go into more details (probably noted needed for the exam), one can notice the following on this ECG :

• Q waves are present in the septal leads (V1-2)

• Note the subtle ST elevation in I, aVL, and V5, with reciprocal ST depression in lead III.

• There are hyperacute (peaked) T waves in V2, V3 and V4. These features indicate an anteroseptal STEMI.

ECG CHANGES IN MYOCARDIAL INFARCTION AND CORONARY ARTERIES :

MOST COMMONLY ASKED : 

Anteroseptal : V1-V4 - Left anterior descending (LAD)

Inferior : II, III, aVF  - Right coronary (RCA)

Lateral : I, aVL, V5-6 - Left circumflex

Although in many cases no cause is apparent, dilated cardiomyopathy is probably the result of damage to the myocardium. In this case, it was due to the fibrous change of the myocardium from a previous myocardial infarction. This is supported by the decreased ejection fraction and thinning of the septal walls seen on an echocardiogram.

DILATED CARDIOMYOPATHY :

• A disorder of heart muscle characterized by left ventricular and/or right ventricular dilation and impairment of systolic function.

• Presents as congestive heart failure, Dyspnoea, Oedema, Raised JVP, Pulmonary congestion, Cardiomegaly.

In Atrial flutter, you will see the characteristic “flutter waves” which are a “saw tooth” shape. The flutter waves replace the P waves. In general, this is managed in the same way as an atrial fibrillation.

ATRIAL FLUTTER VS ATRIAL FIBRILLATION :

ATRIAL FLUTTER: Atrial activity - Rate: 220-350 bpm, Visible flutter (F) waves

Ventricular activity - Rate: Regular, Constant R-R interval. Baseline - Sawtooth

ATRIAL FIBRILLATION: Atrial activity - Rate: > 350 bpm, Fine fibrillatory (f) waves

Ventricular activity - Rate: Variable, No relation to the atrial rate, Variable R-R interval. Baseline - ragged.

Her regular medications include multiple blood pressure-lowering agents (amlodipine, atenolol, bendroflumethiazide) which are known to cause postural hypotension. Blood pressure monitoring would be appropriate in this scenario to assess and review her medication therapy.

POSTURAL HYPOTENSION (ORTHOSTATIC HYPOTENSION):

Postural hypotension should always be considered in an elderly patient especially if he is on multiple medications and presents with dizziness. The baroreflex mechanisms that control heart rate and vascular resistance decline with age (particularly in patients with hypertension) who thus display lability in BP. They are particularly prone to postural hypotension and to the effects of drugs. It may present with dizziness or sudden loss of consciousness after getting up from a chair, with recovery within a minute.

Diagnosis :

• Blood pressure is taken when lying down and standing up. Postural hypotension is defined as a drop in BP of more than 20 mmHg after 3 minutes of standing. One of the most common causes of postural hypotension is dehydration. This is the reason that U&Es are always requested if one presents to the hospital with collapse with the likely reason being postural hypotension. A raised creatinine and urea would support dehydration. Hydration using intravenous fluids would be key if dehydration was the cause.

GOLDEN POINTS FOR DIZZINESS :

• Dizzy when rolling over the bed – Benign paroxysmal positional vertigo

• Light sensitivity during dizzy spells – Migraine

• First attack severe vertigo lasting hours with vomiting – Vestibular neuritis

• Lightheaded when getting up from bed – Orthostatic hypertension

• One ear feels full before or during the dizzy attack – Meniere’s disease

Aortic stenosis is the most common type of valvular heart disease in patients over the age of 65 years. Remember that a congenital bicuspid value predisposes to both aortic stenosis and aortic regurgitation. A normal aortic valve has three cusps or leaflets. A clincher for exam would be an elderly patient who is complaining of exercise intolerance or who is otherwise asymptomatic. They will mention a type of systolic murmur THAT IS LOUDER WHEN THE PATIENT SITS UPRIGHT. Remember, the murmur for aortic stenosis is an ejection systolic murmur loudest in the aortic area (2nd intercostal space, right sternal border), radiates to carotids, and louder in expiration.

AORTIC STENOSIS causes :

• Degenerative calcification (most common cause in older patients above 65)

• Bicuspid aortic valve (2nd most common cause, usually in the younger age group)

Clinical features :

• Dyspnoea

• Angina

• Syncope

Remember, the murmur for aortic stenosis is an ejection systolic murmur loudest in the aortic area (2nd intercostal space, right sternal border), radiates to carotids and is louder in expiration.

The words “yellow haloes” are a clincher for digoxin toxicity. For exam, if you see any question with yellow-green colour vision with arrhythmia, it is most likely digoxin toxicity. Digoxin is now mainly used for rate control in the management of atrial fibrillation.

As it has positive inotropic properties it is sometimes used for improving symptoms (but not mortality) in patients with heart failure. Also remember, hypokalaemia predisposes to toxicity because potassium and digoxin bind to the same site on the sodium-potassium ATPase pump, leading to increased intracellular calcium and increased cardiac contractility.

Features of digoxin toxicity :

• Gastrointestinal symptoms are most common. These are nausea, vomiting, diarrhea, and anorexia

• Neurologic and visual symptoms include blurred vision, yellow-green vision, hallucinations and confusion

• Arrhythmias – Bradycardia, premature contractions, ventricular tachycardia, and any other type of arrhythmias may be seen. A serum digoxin level should be ordered in patients you suspect of being toxic (history, etc.)

Management of digoxin toxicity :

• Digibind - Correct arrhythmias

• Monitor potassium.

The artery that supplies the posterior descending artery (PDA) determines coronary dominance. If the posterior descending artery is supplied by the right coronary artery (RCA), then the coronary circulation can be classified as “right-dominant”.

If the posterior descending artery is supplied by the circumflex artery (CX), a branch of the left artery, then the coronary circulation can be classified as “co-dominant”. Approximately 85% of the general population are right-dominant In 85% of patients (Right Dominant), the RCA gives off the posterior descending artery (PDA). In the other 15% of cases (Left Dominant), the PDA is given off by the left circumflex artery. The PDA supplies the inferior wall, ventricular septum, and the posteromedial papillary muscle.

Atrial myxomas are benign tumours. Around three-quarters of atrial myxomas occur in the left atria, and tend to grow on the wall (septum). Sometimes small pieces of the tumour can break off and fall into the bloodstream. If this happens, they can block an artery elsewhere in the body such as the brain, which could cause a stroke, or in the lungs causing a pulmonary embolus. Around 10% of myxomas seem to be inherited (passed down through families). These are known as familial myxomas.

The symptoms occur due to obstruction of the mitral valve which results in syncope and heart failure.

Features :

• Symptoms of haemodynamic obstruction, embolization, or constitutional symptoms such as fever, malaise, tachycardia, and tachypnoea

• Symptoms and signs of ischaemia or infarction in the peripheries, due to embolization of adherent thrombus

• Atrial fibrillation

• Large myxomas may impair intracardiac blood flow, causing dyspnoea, syncope, or symptoms and signs of congestive cardiac failure

• ECHO : Pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum.

Ankle swelling and orthopnea are features of heart failure. These features in combination with the history of alcoholism give us hints of an alcoholic cardiomyopathy which is a type of dilated cardiomyopathy. Atrial fibrillation is the most common arrhythmia that develops in patients with dilated cardiomyopathy.

Acute decompensation can occur especially in patients with asymptomatic LV dysfunction who develop atrial fibrillation. In some scenarios, there is a setting of acute alcohol use or intoxication followed by palpitations, dizziness, and syncope which can be attributed to arrhythmias such as atrial fibrillation or flutters. This is known as holiday heart syndrome because the incidence increases following weekends and during the holiday seasons.

ATRIAL FIBRILLATION PRESENTATION :

• Dyspnoea

• Palpitation

• Syncope or dizziness

• Chest discomfort or pain

• Stroke or transient ischaemic attack

• An irregularly irregular pulse.

Rupture of a papillary muscle is a rare but well-known complication of myocardial infarction. Papillary muscle rupture may lead to worsening of mitral regurgitation features including having a pansystolic murmur radiating to the axilla which is seen in this stem.

From the given options the most likely answer is ventricular ectopics. This is a classic scenario where the patient would complain of having “missed beats”. They are usually otherwise asymptomatic. If ventricular ectopics occur in a normal heart (i.e. no cardiomyopathy or ischaemic heart disease) though symptomatic, it is benign and are of no clinical significance.

VENTRICULAR ECTOPICS: Aetiology:

• Ischaemic heart disease

• Cardiomyopathy

• Stress, alcohol, caffeine, medication, cocaine, or amphetamines

• Occurs naturally Patients may be symptomatic with palpitations often described as "skipped or missed beats" but they may also have symptoms of dyspnoea or dizziness. Over half the population have silent, or asymptomatic, ventricular ectopics which are discovered incidentally on a routine ECG.

In clinical practice, it is important to identify the presence of an underlying cardiomyopathy or ischaemic heart disease. If neither of these are present then it is likely that these ventricular ectopics are benign. Patients with no ischaemic heart disease or cardiomyopathy have an excellent prognosis however, if ventricular ectopics are secondary to heart disease like myocardial infarction, it may precipitate more life-threatening arrhythmias like ventricular fibrillation.

Acute renal failure is one of the causes of hyperkalemia. Together the ECG findings point towards hyperkalemia as the answer.

ECG CHARACTERISTICS IN ELECTROLYTE DISBALANCE:

Hyperkalaemia: Tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern and asystole.

Hypokalemia: Flat T waves, ST depression, and prominent U waves

Hypercalcaemia: Shortened QT intervals

Hypocalcaemia: Prolonged QT intervals

Please see Q-40

This is a classic picture of a ruptured abdominal aneurysm. An ultrasound scan is the only appropriate investigation given the options. Questions would usually have either an ultrasound or CT abdomen as one of the choices for a ruptured aortic aneurysm. Both choices are correct. It is important to note that both USS and CT scans can be performed. Although, it may be safer and quicker to perform USS in the ED, rather than transfer the patient for a CT scan.

As this patient is already on an ACE inhibitor, the next most appropriate class of medications would be a beta-blocker (i.e. bisoprolol, carvedilol, nebivolol) to manage his symptoms of chronic heart failure. Start with a low-dose beta blocker and titrate up once the low dose is tolerated. Remember, when starting a beta blocker, “start low and go slow”. 

MANAGEMENT OF CHRONIC HEART FAILURE :

The general management of chronic heart failure can be summarized below -

• ACE-inhibitor and a beta-blocker (e.g. Carvedilol)  

1st line - Spironolactone  

2nd line - Digoxin  

Only if heart failure is in combination with atrial fibrillation.

Both an angiotensin-converting enzyme (ACE) inhibitor and a beta-blocker are licensed to treat heart failure but it is good practice to only start one drug at a time. Clinical judgement is used when deciding which drug to start first.

For example, the preferred initial treatment might be :

• An ACE inhibitor if the person has diabetes mellitus or has signs of fluid overload

• A beta-blocker, if the person has angina.

The question points towards cardiac tamponade. His chest is bilaterally clear thus we can therefore exclude pneumothorax or pleural effusion. Muffled heart sounds, distended neck veins and hypotension are called Beck’s triad and it is a classical finding in cardiac tamponade.

Signs and consistent with infective endocarditis. A dental extraction is a known source of infection-causing bacteraemia.

INFECTIVE ENDOCARDITIS :

Fever + new murmur = endocarditis until proven otherwise

Risk Factors :

• Valve replacement

• Recreational drug abuse and invasive vascular procedures

Note: Dentistry interventions are a common cause of bacteremia leading to infective endocarditis.

Cause Strep viridans is a common cause (more than 35%)

Presentation :

• Septic signs: Fever, rigors, night sweats, malaise

• Cardiac lesion: New murmur

• Immune complex deposition: Roth spots (boat-shaped retinal haemorrhage with pale center); splinter haemorrhages, Osler’s nodes (painful pulp infarcts in fingers or toes)

• Embolic phenomena: e.g. Janeway lesions (painless palmar or plantar macules) Some patients may present with congestive cardiac failure.

Diagnosis :

Infective endocarditis is diagnosed if:

• 2 major criteria present or

• 1 major and 3 minor criteria present or

• 5 minor criteria present

Major criteria:

• Positive blood cultures

• Positive echocardiogram - showing abscess formation, new valvular regurgitation

Minor criteria:

• IV Drug user, predisposing heart condition

• Fever >38°C

• Vascular phenomena: e.g. major emboli, clubbing, splinter haemorrhages, Janeway lesions

• Immunological phenomena: Glomerulonephritis, Osler's nodes, Roth spots

• Microbiological evidence does not meet major criteria.

These characteristics are classic in myocardial infarction. Do not get fooled into picking dissecting aneurysm. Although the pain of a myocardial infarction can be somewhat similar to a dissecting aneurysm, a myocardial infarction is much more common than a dissecting aneurysm.

The examiners would have to include something specific to dissecting aneurysms for that to be the answer such as a history of severe, tearing chest pain radiating to the back with a history of Marfan syndrome and unequal pulses in upper extremities. If you see any of these key phrases, you should stop and consider dissecting an aneurysm as the answer.

ALL PATIENTS WITH MI ON DISCHARGE:

• Dual antiplatelet therapy: Aspirin + Clopidogrel

Note: Aspirin is continued lifelong Clopidogrel for 12 months

• Beta Blockers : Offer BB to people who present acutely with MI as soon as they are hemodynamically stable.

Continue a beta-blocker for at least 12 months after an MI in people without heart failure. Continue a beta-blocker indefinitely in people with HF.

• ACEi Offer ACEi to people who present acutely with MI as soon as they are hemodynamically stable. If intolerant to ACEi  use ARB

• STATINS

Mnemonic: Once the patient is discharged, he can take the CAB or BAS(BUS) home.

C - Clopidogrel

A - Aspirin

B - Beta Blockers

A - ACEi

S – Statins

This is a case of infective endocarditis. The most appropriate investigation is blood cultures or echocardiogram. Since an echocardiogram is not one of the options, blood cultures should be picked.

Percutaneous intervention (PCI) would be the best management for myocardial infarction. As PCI is not given in the option, thrombolysis would be the next best step. In terms of thrombolysis, Alteplase is preferred over streptokinase.

Chest pain and ECG findings of widespread ST elevation with an upward concavity are diagnostic of acute pericarditis. The history of a myocardial infarction supports this as one of the causes of acute pericarditis is a recent myocardial infarction. Fever, night sweats, and other constitutional symptoms may be present, depending on the underlying cause.

An echocardiogram would be the best option here. It is used to identify structural cardiac abnormalities and assess left ventricular function. It may show a clot in the atrial appendage responsible for syncope which could be due to a transient ischaemic attack secondary to atrial fibrillation.

The most common valvular cause for a syncope is aortic stenosis which needs an echocardiogram to diagnose it. A Holter ECG (24-hour ECG) is not needed as the ECG is already said to have an irregular rhythm.

If they did not state that the rhythm was irregular, then 24-hour ECG would be an option. CT and MRI may be performed in selected cases (eg, aortic dissection and haematoma, pulmonary embolism, cardiac masses, pericardial and myocardial diseases, congenital anomalies of coronary arteries). However, as he has recovered fully, it is unlikely to be any of the causes requiring a CT or MRI. Exercise testing is for patients who have experienced episodes of syncope during or shortly after exertion. There was no mention of exertion in this question.

A key mnemonic that can help you get through the exam cardio question is: Pan-systolic  MR, TR, VSD. Hence, when you see the words pan-systolic murmur in the question, straight away, you can cut out any options that ARE NOT mitral regurgitation, tricuspid regurgitation, and ventricular septal defect.

Ventricular septal defect :

• A hole connecting the ventricles

Causes :

• Congenital 

• Acquired (post-MI)

Symptoms:

• May present with severe heart failure in infancy, or remain asymptomatic and be detected incidentally in later life.

Signs: These depend on size and site

• Small holes : Infant or child is asymptomatic with normal feeding and weight gain  May be detected when a murmur is heard on routine examination  Give louder murmurs. Classically, a harsh pan-systolic murmur was heard at the left sternal edge, with a systolic thrill, and a left parasternal heave. Most importantly, remember the term “pan-systolic murmur” as often that alone can give you the answer provided mitral regurgitation and tricuspid regurgitation are not one of the options.

• Large holes : Associated with signs of pulmonary hypertension. These babies may develop a right to left shunt with cyanosis or Eisenmenger’s syndrome. The diagnosis and management. Not so important for the exam.

-

DRESSLER’S SYNDROME tends to occur around 2-6 weeks following an MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterized by a combination of fever, pleuritic pain, pericardial effusion, and a raised ESR.

It is treated with NSAIDs.

The patient is suffering from acute pulmonary oedema brought upon by heart failure. While it is true that an ECG is important to look for arrhythmia, a chest X-ray would be a better answer given that it would be able to confirm pulmonary oedema.

This question is very debatable but the clinical picture here fits pulmonary oedema slightly better than a myocardial infarction. In reality, both will be performed.

The scenario depicted here describes a typical complication of a myocardial infarction – a tachyarrhythmia. As is clear from the stem, the patient is haemodynamically unstable.

In addition, there is the presence of a broad complex tachycardia on ECG. Therefore to answer this question correctly, it is important to know about the management of a broad complex tachycardia.

STEPS OF BROAD COMPLEX TACHYCARDIA MANAGEMENT:

1. Check the patient’s pulse - if there is no pulse, follow the arrest protocol immediately.

2. Administer oxygen

3. If the patient is haemodynamically unstable, then commence synchronized cardioversion followed by IV amiodarone and further shocks as needed In the above case, the first two steps have already been performed so the next appropriate step in management would be synchronized cardioversion.

The diagnosis here is atrial fibrillation. A completely irregular rhythm.

When looking at any ECG, try to use a stepwise approach :

Step 1: Calculate rate

Step 2: Determine regularity

Step 3: Assess the P waves

Step 4: Determine the PR interval

Step 5: Determine QRS duration

Step 6: Determine the axis

Step 7: Look at morphology

In this ECG, at step 2 (determine regularity), we can already see irregularity here just by looking at the R-R intervals. We will not discuss management here but the initial thoughts when seeing an ECG like this are :

1. Are they stable?

2. Is there rate control?

3. What is the patient’s CHA2DS2-VASc score?

The ECG revealing a broad complex tachycardia with the absence of atrial activity in a conscious person can only be ventricular tachycardia. The hypotension seen here supports this. Cardiac arrhythmias are more common in patients with Ischaemic heart disease hence the given history.

Occasionally, in the exam, they may include a picture of an ECG showing a broad complex tachycardia. Again, pick ventricular tachycardia if the patient is still awake as it is impossible to see ventricular fibrillation in an awake patient.

Ventricular tachycardia may impair cardiac output with consequent hypotension, collapse, and acute cardiac failure.

This is due to extreme heart rates and lack of coordinated atrial contraction (loss of “atrial kick”).

The rate of V. Tach is from about 100-250 bpm. P Waves may be present or absent. P waves are usually not seen if the rate is increased. If present, the P Waves have no relation to the QRS complexes of the V. Tach.

V. Tach can present in two ways.

1. With Pulse

a) Haemodynamically stable or

b) Haemodynamically unstable — e.g. hypotension, chest pain, cardiac failure, decreased conscious level.

2. Without Pulse Management depends on how the patient presents:

1. With Pulse

a) Haemodynamically stable antiarrhythmics e.g. amiodarone, lidocaine, procainamide

b) Haemodynamically unstable — e.g. hypotension, chest pain, cardiac failure, decreased consciousness level.  immediate electrical cardioversion is indicated

2. Without Pulse,  immediate electrical cardioversion is indicated.

The patient is suffering from acute pulmonary oedema brought upon by heart failure. It is worth noting that this stem is a little tricky as there were no risk factors of heart failure mentioned and the information that the woman had a recent C-section makes physicians (especially if you have worked in an obstetric unit), think of a pulmonary embolism. However, it is important to be aware that cardiac causes of breathlessness do occur in pregnancy and post-delivery as well. This stem gives the history of orthopnea which points towards heart failure as the reason for the shortness of breath.

In terms of the management of acute pulmonary oedema, 4 important steps need to be done:

1. Sit the patient up, and give oxygen – aim for saturations. 95% (>90% in those with COPD)

2. Glyceryl trinitrate (GTN) spray two puffs sublingual

3. Furosemide 40 mg intravenously (slowly) produces transient venodilation and subsequent diuresis

4. Diamorphine 2.5-5 mg intravenously slowly (or morphine 5-10 mg intravenously slowly) can be used to relieve anxiety, pain, and distress.

It is clear from the stem that this patient has mitral regurgitation.

There are two types of mitral regurgitation: Primary (degenerative) MR and secondary (functional) MR. From the patient’s past medical history, we can see that she has had a relatively recent myocardial infarction. The most important complications of a myocardial infarction that we need to recognize in this stem are mitral valve dysfunction and atrial arrhythmia.

VALVULAR HEART DISEASE :

We have listed the common heart valve disorders here. There are certain keywords that if you see in the exam, would help point you towards a specific heart valve disorder.

Aortic valve stenosis is the most common valvular heart disease, hence the most commonly asked heart valve question. The two most common pathogenesiss are age-related degenerative sclerocalcific changes to valves (the most common cause, usually an elderly patient) and congenital bicuspid aortic valve (seen in a younger person with aortic stenosis).

Signs : Ejection systolic murmur is best heard at the 2nd intercostal space, at the right sternal border which radiates to carotid arteries.

Mitral regurgitation (MR), which is also known as mitral insufficiency, is the second most common heart valve disorder.

Signs : Soft S1 and S2, pan systolic murmur at the 5th intercostal space in the left midclavicular line which radiates to the axilla.

A useful method to remember is to remember this phrase “When cooking, you do not want to regurgitate onto the cooking pan”. This is a good way to remember pan systolic murmurs are found in mitral and tricuspid regurgitation (and also in ventricular septal defects).

Mitral valve prolapse is a common inheritable connective tissue disorder like Marfan’s syndrome, Ehlers-Danlos syndrome, and osteogenesis imperfecta. Most patients are asymptomatic. The classical case would be a slim young female with low blood pressure. Mitral valve prolapse is a risk factor for mitral regurgitation.

Signs: Mid-systolic click, best heard at the 5th intercostal space in the left midclavicular line, followed by a mid or late-systolic murmur with findings accentuated in the standing position. 

Mitral stenosis : Rheumatic heart disease is the most common cause of mitral stenosis worldwide.

Signs : Mid-diastolic murmur with an opening click (the click represents the mitral valve opening) is best heard at the 5th intercostal space in the left midclavicular line.

Aortic regurgitation causes include rheumatic heart disease, infective endocarditis, and Marfan syndrome amongst others.

Signs : Early diastolic murmur, best heard at left sternal edge

Pulmonary stenosis Signs : Ejection systolic murmur best heard over the pulmonary area, radiates to the left shoulder or infraclavicular region.

Tricuspid regurgitation Signs : Pansystolic murmur is best heard over the tricuspid region.

Other common mnemonics that can help you remember heart murmurs are:

Left-sided murmurs louder with expiration

Right-sided murmurs louder with inspiration.

This question points towards cardiac tamponade. Muffled heart sounds, distended neck veins and hypotension are called Beck’s triad and it is a classical finding in cardiac tamponade.

CARDIAC TAMPONADE : A life-threatening condition in which a pericardial effusion has developed so rapidly or has become so large that it compresses the heart.

Aetiology -

• Usually penetrating or blunt chest trauma

Features -

• Dyspnoea

• Raised JVP - seen by having neck veins which are distended

• Tachycardia

• Hypotension

• Muffled heart sounds

• Pulsus paradoxus

Remember Beck’s triad: Muffled heart sounds, distended neck veins, and hypotension

Diagnosis -

• Echocardiography

Treatment - Pericardiocentesis.

This is a classical ECG showing an inferior myocardial infarction. See the leads II, III, and aVF which show an ST elevationPercutaneous intervention (PCI) would be the best management for myocardial infarction.

Acute mitral regurgitation post- MI. This is a mitral regurgitation due to ischaemic papillary muscle dysfunction or partial rupture. It is usually seen 2-10 days post myocardial infarction. It is more commonly associated with inferior myocardial infarction than anterior myocardial infarction. ‘Silent MR’ is quite frequent and must be suspected in any post-MI patient with unexplained haemodynamic deterioration.

Diagnosis- Echocardiogram

Treatment- Acute MR is treated with vasodilator therapy but often requires emergency surgical repair.

One of the many known adverse effects of thiazides is postural hypotension. Common adverse effects of thiazides worth remembering include:

• Postural hypotension

• Hyponatraemia, hypokaleimia

• Gout

Transoesophageal echocardiography (TOE) with bubble contrast is the gold standard for the diagnosis of patent foramen ovale. In the absence of TOE, transthoracic echocardiography (TTE) may also be considered. However, a bubble contrast is essential to evaluate a functional right-to-left shunt. 

However, it cannot differentiate an intracardiac from a pulmonary shunt.

We are suspecting a myocardial infarction in this patient. Cardiac enzymes would need to be ordered. Measurement of cardiac troponins helps to predict which patients are at risk of a cardiac event, and who can be safely discharged early. The risk of death from an ACS is directly related to troponin level and patients with no detectable troponins have a good short-term prognosis.

Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days. Troponin levels may therefore be normal initially and should be repeated.

Myocardial muscle creatine kinase (CK-MB) is found mainly in the heart. CK-MB levels increase within 3-12 hours of the onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours. Sensitivity and specificity are not as high as for troponin levels.

Myocardial infarction is a painful condition seen as tightness, pressure, or squeezing pain in the chest. The ECG shows that he is having an inferior myocardial infarction. Pain relief with GTN sublingual or spray and/or an intravenous opioid 2.5-5 mg diamorphine or 5-10 mg morphine intravenously with an anti-emetic is often used as part of the pre-hospital management. Remember, nitrates bring relief to many patients, but up to one-third of those who experience a myocardial infarction have nitrate-resistant chest pain and should receive morphine to help manage the pain.

Avoid intramuscular injections of opioid medication even while in the ambulance, as absorption is unreliable. In addition, the injection site may bleed if the patient later receives thrombolytic therapy.

Please see Q-16

Please see Q-40

The clincher here is the chest X-ray that shows a straight left heart border. This is classic for mitral stenosis where the left atrium enlarges. The rest of the symptoms also match the diagnosis of mitral stenosis. The history of stroke given in this question is a clue that she has had atrial fibrillation for a while and had a systemic embolism (due to stagnation of blood in an enlarged left atrium).

MITRAL VALVE STENOSIS :

• Most commonly due to rheumatic fever

• Results in right ventricular failure

Aetiology: Most cases are secondary to rheumatic fever (This is extremely important to remember for the exam)

Pathogenesis:

• Mitral valve stenosis impedes left ventricular filling

• Increased left atrial pressure is referred to the lungs, causing pulmonary congestion

• Forward cardiac output becomes reduced, secondary pulmonary vasoconstriction occurs, and eventually right ventricular failure results

Clinical symptoms: Usually manifest slowly over the years

• Dyspnoea

• Orthopnoea

• Paroxysmal nocturnal dyspnoea

• Right-sided heart failure

• Hepatomegaly

• Ascites

• Peripheral oedema

The following are presentations that are rare and unlikely to be asked:

• Haemoptysis (due to rupture of pulmonary vessels due to raised atrial pressure)

• Systemic embolism (due to stagnation of blood in an enlarged left atrium)

Physical signs:

• Malar flush on the cheeks

• Atrial fibrillation

Pulmonary rales

• Loud S1 (This is particularly important to note for the exam)

• Diastolic rumble (low-pitched apical murmur)

Diagnosis:

1. ECG -

• May show signs of right ventricular hypertrophy

• Atrial fibrillation may be seen

• P mitrale 

2. Chest X-ray -

• Large left atrium, Straightening of the left heart border

• Pulmonary hypertension, including Kerley B lines and increased vascular markings

3. Echocardiography -

• Thickening of mitral valve leaflets.

This patient is suffering from chronic heart failure. Given that this patient has diabetes mellitus, an ACE-inhibitor like ramipril would be more appropriate when compared to a beta blocker.

PDAs are very common in preterm babies and they also may close spontaneously and can have significant physiological effects. 

• The continuous murmur (rarely heard)

• There may be a rough systolic murmur along the left sternal border

• Bounding peripheral pulses

• The diagnosis is confirmed by echocardiography which not only allows the PDA to be visualised but also assesses the haemodynamic significance of the PDA

• PDA may close spontaneously

• Indomethacin closes the connection in the majority of cases.

LEFT BUNDLE BRANCH BLOCK (LBBB):

It is always good to be able to recognize a LBBB on an ECG. LBBB is best seen in lead V6, where you would see a broad complex with an “M” morphology. This broad complex “M” morphology can also be seen in leads I and aVL.

Other ECG features of LBBB include:

• Left axis deviation

• Deep S-wave in V1Below are some ECG examples with LBBB seen

• Broad complex “M” morphology seen in leads I and aVL

• Broad complex in V6

• Deep S-wave in V1

• Broad complex “M” morphology seen in leads I

• Broad complex in V6

• Deep S-wave in V1.

The two closest options here are left ventricular aneurysm and Dressler’s syndrome. One needs to understand them for the exam. Left ventricular aneurysm is usually a complication resulting from a myocardial infarction. When the cardiac muscle partially dies during a myocardial infarction, a layer of muscle may survive, and being severely weakened, start to become an aneurysm. It usually presents four to six weeks post-myocardial infarction which fits this stem and ECG shows persistently raised ST segments.

Dressler’s syndrome is a secondary form of pericarditis that occurs post-myocardial infarction. It usually presents one-week post myocardial infarction but may also occur several months after a myocardial infarction. Clinical features consist of fever, pleuritic pain, pericardial and pleural effusion. The pleuritic pain is usually the main complaint. As we can see from the presenting symptoms of the patient, a left ventricular aneurysm fits best.

This patient is suffering from acute pulmonary oedema brought upon by heart failure.

This patient is stable.

Treatment for SVT in stable patients always begins with Valsalva maneuvers followed by carotid massage followed by adenosine provided there are no contraindications for it.If this patient had asthma, verapamil would be a better option. DC cardiovert only if the patient is haemodynamically unstable or if you have given 3 doses of adenosine and the patient is still in SVT.

Smoking is the number one factor for all-cause mortality of coronary artery disease and peripheral arterial disease. To reduce his risk of getting heart disease, the best referral for him would be a smoking cessation clinic. This man is well within the allowed consumption of alcohol per week so referring him to an alcohol support group is correct.

The diagnosis here is atrial fibrillation.

The hallmark of atrial fibrillation is the absence of P waves. Instead, irregular fibrillatory waves called “f waves” are seen which produced a ragged baseline. Atrial fibrillation can be differentiated from atrial flutter by the irregular ventricular rate.

Atrial flutter has a more regular ventricular rate. Atrial flutter also has the classical “saw tooth pattern”. 

Chest pain and ECG findings of widespread ST elevation with an upward concavity are diagnostic of acute pericarditis. The cardiac shadow seen on a chest X-ray is not enlarged in dry pericarditis. A pericardial friction rub is frequently heard in acute pericarditis.

This is a superficial, scratchy, grating sound that is best heard in the second to fourth intercostal spaces when pressure is exerted on the diaphragm of the stethoscope.

The two top choices here are acute myocardial infarction (a silent MI) or pulmonary embolism due to immobilization which may result in deep vein thrombosis. 

Given the history of immobilization, pulmonary embolism should be suspected. 

A myocardial infarction can cause acute pericarditis which can lead to pericardial effusion. A chest X-ray shows an enlarged globular heart at this stage. A pericardial effusion of a significant amount can cause cardiac tamponade which shows up as a sign of shock.

One can expect his blood pressure to be low and his JVP to be high.

Please see Q- 60

Inferior myocardial infarction is frequently associated with conduction defects.

Mobitz type I AV block (also known as Wenckebach’s phenomenon) There is a progressive prolongation of the P-R interval following each atrial impulse until an atrial impulse fails to be conducted to the ventricles causing a ‘dropped beat’.

Since the patient has Afro-Caribbean origins calcium channel blockers would be the best antihypertensive medication to start. Afro-Caribbeans tend to develop low-renin, salt-sensitive type hypertension.

Monotherapy for hypertension with beta-blockers or ACE inhibitors is less effective than calcium channel blockers in this particular ethnicity.

This patient is at high risk of stroke with a CHA2DS2-VASc score of 3 (2 for age and 1 for diabetes). Anticoagulation using warfarin is the most appropriate long-term management in these options to prevent stroke.

The given history of palpitations, lightheadedness with tachycardia plus a history that this has occurred before, gives the likely diagnosis of supraventricular tachycardia.

Firstly, we must define what a non-disabling ischaemic stroke is. It is defined as an ischaemic stroke with symptoms that last for more than 24 hours but later resolve, leaving no permanent disability. The reason this is important is often anticoagulation treatment is deferred for at least 14 days from the onset in people with disabling ischaemic stroke for a fer of a haemorrhagic event. In the interim aspirin 300 mg daily will be used.

For non-disabling ischaemic strokes, it depends on specific circumstances. Nonetheless, in this question, they are asking for a long-term prophylactic regimen and thus warfarin is still the best option whether it started in 14 days or right away. He has atrial fibrillation which could lead to another stroke which is the reason that anticoagulation is extremely important. If atrial fibrillation was not included in this question, then the answer would be aspirin for 2 weeks and clopidogrel long-term for stroke prevention.

You should be able to recognize that the patient is currently on Step 1 of the NICE hypertension treatment pathway. Persons aged over 55 or black persons of African or Caribbean family origin of any age with hypertension, offer antihypertensive treatment with a CCB.

If a CCB is not suitable, for example, because of oedema or intolerance, or if there is evidence of heart failure or a high risk of heart failure, offer a thiazide-like diuretic. He should therefore commence with Step 2 by adding an ACE inhibitor or an angiotensin-II receptor blocker. An increase in his Indapamide dose is not recommended as doses larger than 2.5 mg daily showed no appreciable antihypertensive effect but a diuretic effect may become apparent.

This is a classic picture of a ruptured abdominal aneurysm. An ultrasound scan is the only appropriate investigation given the options. Questions would usually have either an ultrasound or CT abdomen as one of the choices for a ruptured aortic aneurysm.

Both choices are correct. It is important to note that both USS and CT scans can be performed. Although, it may be safer and quicker to perform USS in the ED, rather than transfer the patient for a CT scan.

Atrial septal defect.

Most adult patients with a large defect present with (some or all) symptoms including fatigue, exercise intolerance, palpitations, syncope, shortness of breath, peripheral oedema, thromboembolic manifestations, and cyanosis. Arrhythmias are more common after 40 years of age. The common arrhythmias are atrial flutter and atrial fibrillation.

Auscultatory findings are:  Loud P2 with fixed splitting of 2nd heart sound.

A left-to-right shunt caused increased loading on the right ventricle, leading to delayed emptying and therefore delayed closure of the pulmonary valve which caused this splitting. Soft systolic ejection murmur in the pulmonary area at the upper left sternal border.  

A diastolic rumble over the left lower sternum because of increased flow through the tricuspid valve. Classic auscultatory findings as described above are not present unless the shunt is reasonably large.

Citalopram.

Depression is common among patients recovering from a myocardial infarction. Approximately 1 in 6 patients with MI experience major depression and at least twice as many as that have significant symptoms of depression soon after the event.

Post -MI depression is an independent risk factor for increased mortality (as depression is associated with poor compliance with risk-reducing recommendations).

For treating this depression SSRIs are recommended as first-line agents and among SSRIs Sertraline is the drug of choice for ischemic heart disease. The next choice is citalopram (as it is often related to torsades de pointes it is not 1st choice). If SSRI cannot be used Mirtazapine is recommended as the next antidepressant.

This is a case of exercise-related syncope.

Exercise-related syncopes are of 2 types,

i) Syncope during exercise or exertional syncope (this is ominous)

ii) Post exercise syncope (this is benign).

A few examples of Syncope during exercise- are arrhythmia, valvular heart disease, structural heart disease like hypertrophic cardiomyopathy, coronary artery disease, myocarditis, etc.

Example of Syncope following exercise- orthostatic hypotension as in the case of exercise in a hot environment with vasodilation and increased sweating, prolonged standing, vasovagal related to a sudden decrease in venous return, etc.

Given cause is exertional syncope and systolic murmur indicate valvular lesions (particularly aortic stenosis) in this elderly man.

Abdominal aortic aneurysm (AAA or triple A) is a localized enlargement of the abdominal aorta such that the diameter is greater than 3 cm or more than 50% larger than normal. They usually cause no symptoms, except during rupture. Occasionally, abdominal, back, or leg pain may occur. A single most discriminating investigation is abdominal ultrasound.

Depression is common among patients recovering from a myocardial infarction. Post -MI depression is an independent risk factor for increased mortality.

For treating this depression SSRIs are recommended as first-line agents and among SSRIs Sertraline is the drug of choice for ischemic heart disease. The next choice is citalopram (as it is often related to torsades de pointes it is not 1st choice). As the patient has insomnia and citalopram can cause insomnia too, it should be taken in the morning. If SSRI cannot be used Mirtazapine is recommended as the next antidepressant.

Pulsus bisferiens, is a sign where, on palpation of the pulse, a double peak per cardiac cycle can be appreciated. Bisferious means striking twice.

Classically, it is detected when aortic insufficiency exists in association with aortic stenosis, but may also be found in hypertrophic obstructive cardiomyopathy.

The diagnosis is infective endocarditis.

Fever + new murmur suggest endocarditis until proven otherwise.

Important risk factors: dermatitis, IV injections, renal failure, organ transplantation, DM, post-operative wound.

Risk of developing endocarditis in following abnormalities of valves: aortic or mitral valve disease, tricuspid valve in IV drug users, prosthetic valves.

Diagnosis is ASD with atrial fibrillation.

i) Atrial fibrillation = irregularly irregular pulse.

ii) ASD = SOB, fixed splitting with loud P2, ESM in pulmonary area]. This picture is typical. One should not misdiagnose SOB, ESM in the pulmonary area, and loud P2 as pulmonary hypertension (though in the elderly this can develop with ASD).

Antibiotic prophylaxis points towards rheumatic fever. Present complaints of breathlessness and orthopnea suggest probable valvular disease. Mitral stenosis is the most common valvular complication of rheumatic fever.

In acute AF (<48h) if stable, rate control by verapamil or bisoprolol.

In chronic AF (>48h) rate control with beta-blocker or rate limiting CCB.

Ischaemic mitral regurgitation > raised pulmonary capillary pressure > pulmonary oedema. Inferior myocardial infarction causes left ventricular remodeling, which displaces posterior papillary muscle away from its normal position, leading to ischemic mitral regurgitation.

Points in favour of rheumatic valve stenosis:

i) Dyspnoea on exertion

ii) Straight left border of the cardiac silhouette. Straightening the left heart border requires underfilling of the left ventricle and aorta, which occurs in mitral stenosis.

iii) Atrial fibrillation is a common association.

Atherosclerotic narrowing of vessels produces these symptoms.

Why atherosclerosis? There is other vasculopathy as IHD. Smoking is a risk factor for atherosclerosis.

Now if we think of exclusion:

i) It is not sciatica as sciatica pain is worse when sitting. There may be weakness, numbness, or difficulty moving the leg or foot. A constant pain on one side of the rear. A shooting pain that makes it difficult to stand up.

ii) It is not DVT as no swelling, warmth or redness of the skin is there

iii) It is not thromboangitis obliterans as pulses are ok, no colour change or reduced hair growth, no ulceration or gangrene

iv) Not embolism as no pain (rest pain), no numbness, not pale or blue, no rash, no ulceration of skin.

Beck's triad is a collection of three medical signs associated with acute cardiac tamponade, an emergency condition wherein fluid accumulates around the heart and impairs its ability to pump blood. The signs are low arterial blood pressure, distended neck veins, and distant, muffled heart sounds.

Coarctation of the aorta :

Headache and nosebleeds - >hypertension, pain in lower limb on exertion -> as reduced blood supply to leg due to coarctation.

Radio-femoral delay, cold legs with a weak pulse and mid-systolic murmur are all features of coarctation of the aorta.

Tricuspid regurgitation.

Long standing complication of mitral valve replacement is tricuspid regurgitation. In tricuspid regurgitation there is recurrent breathlessness (mostly exertional), prominent pulsation in the neck (giant V wave), abdominal pain due to the enlarged congested liver (due to CHF), and ankle oedema due to right heart failure.

Diabetes mellitus and obesity are risk factors for developing MI. In diabetics, MI pain is not felt if there occurs autonomic neuropathy. But if there are no autonomic neuropathy diabetics will feel the pain of MI.

A small ventricular septal defect may cause no problems, and many small VSDs close on their own.

Medium or larger VSDs may need surgical repair early in life to prevent complications. If not treated may cause symptoms like shortness of breath, a feeling of tiredness or weakness (especially during exercise), poor appetite, and trouble gaining weight. left parasternal heave and systolic thrill with a harsh pan-systolic murmur at the left parasternal edge are examination findings of moderate to severe ventricular septal defect.

Statin + ACEi.

Offer all people who have had an acute MI treatment with the following drugs: ACE (angiotensin-converting enzyme) inhibitor dual antiplatelet therapy (aspirin plus a second antiplatelet agent) beta-blocker statin.

If the posterior descending artery is supplied by the circumflex artery then it is left dominant and if the posterior descending artery is supplied by the right coronary artery then it is right dominant. As in 85% of population posterior descending the artery is supplied by the right coronary artery which is called the dominant that is right coronary artery is dominant.

Dressler syndrome is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium such as heart attack (myocardial infarction), heart surgery, heart procedure, or chest trauma due to an accident or injury. It is also known as post-myocardial infarction syndrome, post-cardiac injury syndrome, or post-pericardiotomy syndrome.

Dressler’s syndrome is characterized by combinations of pericarditis, pleuritis, and pneumonitis.

This pleuritis is responsible for pleural effusion leading to loss of margin at the costo-vertebral angle. The disease consists of a persistent low-grade fever, chest pain (usually pleuritic), pericarditis (usually evidenced by a pericardial friction rub, chest pain worsening when recumbent, and diffuse ST elevation with PR segment depression), and/or a pericardial effusion.

The symptoms tend to occur 2–3 weeks after myocardial infarction but can also be delayed a few months. It tends to subside in a few days, and very rarely leads to pericardial tamponade.

It causes postural hypotension by volume depletion.

Dilated cardiomyopathy (DCM) is a condition in which the heart becomes enlarged and cannot pump blood effectively. Symptoms vary from none to feeling tired, leg swelling, and shortness of breath. It may also result in chest pain or fainting.

Causes include genetics, alcohol, cocaine, certain toxins, complications of pregnancy, and certain infections. Coronary artery disease and high blood pressure may play a role, but are not the primary cause.

Metoprolol.

P waves are replaced by fibrillatory f-waves. Irregular R-Rintervals. The diagnosis is atrial fibrillation.

Atrial flutter.

Saw-tooth-like waves, normal QRS complex of 80 ms (normal range 70-100 ms), ventricular rate of 150/min, and regular R-R intervals are diagnostic of atrial flutter.

The patient has a +ve two-level PE.

Wells score (if it was negative we should do D-Dimer) and there is no renal impairment or history suggestive of allergy to contrast media (if these were present we should have gone for VQ scan) the investigation of choice is PTCA. 

24h ECG.

Episodic breathlessness, chest pain, and palpitations are suggestive of paroxysmal arrhythmia. As paroxysmal arrhythmia it will only be evident during the attack and in between attacks ECG will be normal (as in the given case). So to confirm the diagnosis 24h ECG should be done.

Indications of 24 h ambulatory heart monitoring:

1. To evaluate chest pain not reproduced with exercise testing

2. To evaluate other signs and symptoms that may be heart-related, such as fatigue, shortness of breath, dizziness, or fainting

3. To identify arrhythmias or palpitations

4. To assess risk for future heart-related events in certain conditions, such as idiopathic hypertrophic cardiomyopathy, post-heart attack with weakness of the left side of the heart, or Wolff-Parkinson-White syndrome

5. To assess the function of an implanted pacemaker

6. To determine the effectiveness of therapy for complex arrhythmias.

If no time limit is mentioned it is assumed that the patient has reached within the time required for primary PCI. There is general agreement that PCI should be considered if there is an ST-elevation. ACS if symptoms started up to 12 hours previously.

Nature of pain i.e. sharp pain increased by breathing and relieved by sitting forward is suggestive of pericarditis.

Nature of pericardial pain: the most common symptom is sharp, stabbing chest pain behind the sternum or in the left side of your chest. However, some people with acute pericarditis describe their chest pain as dull, achy, or pressure-like instead, and of varying intensity.

The pain of acute pericarditis may radiate to your left shoulder and neck. It often intensifies when you cough, lie down, or inhale deeply. Sitting up and leaning forward can often ease the pain.

Cold peripheries due to reduced blood flow to distal parts of dissection. Paraperesis or paraplegia due to spinal cord ischemia and infarction as a presenting manifestation of aortic dissection has been found in 2 to 5 % of patients.

Usual management for type A dissection is surgery and for type B is conservative.

Management of SVT:

i) Vagal manoeuvres (carotid sinus message, Valsalva manoeuvre) transiently increase AV-block, and unmask the underlying atrial rhythm. If unsuccessful then the first medicine used in SVT is adenosine, which causes transient AV block and works by : Transiently slowing ventricles to show the underlying atrial rhythm.

ii) Cardioverting a junctional tachycardia to sinus rhythm.

Ventricular fibrillation is when the heart quivers instead of pumping due to disorganized electrical activity in the ventricles.

Diagnosis is by an electrocardiogram (ECG) showing irregular unformed QRS complexes without any clear P waves.

The likely diagnosis is SVT. 1st vagal maneuvers (carotid sinus massage, Valsalva manoeuvre), if fails then next is to give iv adenosine.

Pulmonary embolism.

Immobilization due to hip pain may result in DVT and later pulmonary embolism.

The given picture of central chest pain for 45 minutes (more than 30 minutes), sweating, and dyspnoea with major risk factors of DM and HTN suggest the diagnosis of MI.

In pericarditis pain is aggravated by inspiration or lying flat and relieved by leaning forward.

A pericardial rub may present and there may be fever. In pneumothorax pain is not central but pleuritic. Pulmonary embolism causes dyspnoea and pleuritic chest pain. In costochondritis, localized pain / tenderness at the costochondral junction is enhanced by motion, coughing, or sneezing.

Probable diagnosis is MI. In MI often ECG doesn’t show the changes in the early stage. Cardiac enzymes will help in such cases.

The features described are insufficient and can be seen in both aortic dissection and MI. However, dissection pain is described as tearing and crushing pain and is often used for MI pain. Both dissection and MI can cause pain radiation to the neck.

The history of diabetes goes with MI as it is a recognized risk factor for MI. Some may argue that DM MI will be painless! But it is not always the case. MI is only painless when autonomic neuropathy becomes well established.

Wells score is >4. So single most appropriate investigation is CTPA.

In any case of IHD, the most important initial management is aspirin (unless decided to go for thrombolysis). Aspirin, the most widely used anti-platelet agent, is effective, safe, and inexpensive and is recommended for all patients undergoing PCI.

Patients already on daily aspirin therapy should be given 75–325 mg of aspirin before PCI; those not taking aspirin should be given 500 mg at least 3 hours before the procedure or 300 mg intravenously immediately before the procedure. After PCI, aspirin should be continued at 75–160 mg/day indefinitely.

Gingival hyperplasia is a recognized side effect of calcium channel blockers.

Contrast media that are pushed in blood are nephrotoxic and IV normal saline will help to maintain adequate hydration to pass it out with urine.

Infective endocarditis (IE) is defined as an infection of the endocardial surface of the heart which may include one or more heart valves, the mural endocardium, or a septal defect. Its intracardiac effects include severe valvular insufficiency, which may lead to intractable congestive heart failure and myocardial abscesses. If left untreated, IE is almost inevitably fatal. Dental extraction is a risk factor for infective endocarditis.

If age less than 55 years In general ACEI or Beta blockers are preferred. But in the case of Afro-Caribbean origin, CCB is chosen even in younger age as it gives better results in this ethnic group.

High blood sugar is a well-known side effect of thiazide (here bendroflumethiazide).

Atrial myxomas are the most common primary heart tumors. Two-dimensional echocardiography is the diagnostic procedure of choice. Most atrial myxomas are benign and can be removed by surgical resection. Constitutional symptoms that include fever, weight loss, arthralgias, and the Raynaud phenomenon. These symptoms may be related to the overproduction of interleukin-6. Left heart failure may cause dyspnea on exertion caused by obstruction at the mitral valve orifice.

Valve damage may result in mitral regurgitation. Jugular venous pressure may be elevated, and a prominent A wave may be present. An early diastolic sound called a tumor plop, is heard.

A diastolic atrial rumble may be heard if the tumor is obstructing the mitral or tricuspid valve. Systemic or pulmonary embolization may occur from left- or right-sided tumors. Embolization to the central nervous system may result in transient ischemic attack, stroke, or seizure.

Mobitz type I 2nd-degree heart block.

Inferior MI is frequently associated with conduction defect.

ACEI and ARB are known to raise the serum potassium level.

Chest pain, raised temperature and ECG findings of widespread ST elevation with upwards concavity are diagnostic of acute pericarditis, particularly after MI.

Left ventricular aneurysm is defined as a localized area of the myocardium with abnormal outward bulging and deformation during systole and diastole. Clinically, ventricular aneurysms may be recognized late with features of heart failure and persistent ST elevation, recurrent ventricular arrhythmias, or recurrent embolization.

Risk factors for these aneurysms after acute MI include the following: Female sex, Total occlusion of the left anterior descending (LAD) coronary artery,  Single-vessel coronary artery disease (CAD), Absence of previous angina pectoris.

Any condition that causes the walls of the arteries to weaken can lead to an aneurysm. Atherosclerosis is the leading cause. Others are high blood pressure and smoking. Deep wounds, injuries, or infections can also cause blood vessels to bulge.

Stable angina is chest pain or discomfort that most often occurs with activity or emotional stress and lasts for <30 minutes, relieved by rest or nitroglycerine. Symptoms of angina occur when the blood supply to the heart muscle is reduced. This happens when the coronary arteries are narrowed or blocked by atherosclerosis or by a blood clot.

Here sudden unconsciousness without any provocation makes arrhythmia the most likely cause; hence we should do an ECG.

Here ST elevation in L1, aVL, v2,v3,v4 and v5. So the diagnosis is anterior MI (as L1 and aVL and v2-v5, anterolateral would be more appropriate description).

IV fluids 0.9%. NS crystalloids to bring SBP to 90 mmHg.

Probable ruptured aortic aneurism. Immediate IV normal saline to raise the BP to 90 mmHg to keep the vital organs perfused till definitive measures are taken.

There is ST elevation in leads II, III and aVF and pathological Q wave in lead III.

History of surgery (particularly when patients are immobile like hip surgery) followed by chest pain and breathlessness strongly suggests diagnosis of pulmonary embolism.

This is a test that can help identify a Patent Foramen Ovale. Pictures are taken of the heart in the same way a normal echocardiogram is performed. A small thin plastic cannula will be inserted into a vein in the patient’s arm.

A small amount of sterile salty water (saline) will be mixed with a small amount of the patient’s blood and then injected into the vein in the patient’s arm. The salty water contains tiny harmless bubbles which can be tracked on the echocardiogram scan revealing any potential abnormal flow through patent foramen ovale.

Chronic bronchitis is a well-known cause of congestive cardiac failure. Leg oedema and transudative fluid in the liver are suggestive of congestive cardiac failure.

All these drugs (particularly prolonged use of thiazide and amlodipine) are well-established causes of postural hypotension. So 24-hour BP monitoring should be done.

Sudden papillary muscle rupture or VSD may be the likely cause (ventricular aneurism may take a slower course), so echo is a more logical approach.

Clue - h/o immobilisation.

There are features of shock with a pulse of 120 bpm and BP 70/40 mmHg and the sudden collapse of the patient with a pulsatile mass in the abdomen makes the likely diagnosis of ruptured aortic aneurysm.

Dressler’s syndrome is a form of pericarditis or inflammation of the pericardium. Dressler’s syndrome can occur after a heart attack (myocardial infarction), heart surgery, heart procedure, or chest trauma due to an accident or injury.

It is also known as post-myocardial infarction syndrome, post-cardiac injury syndrome, or postpericardiotomy syndrome. Dressler’s syndrome usually occurs within two to six weeks after heart surgery or a heart attack, but it can take up to several months for symptoms to develop. It is characterized by pleuritic chest pain which is worse on inspiration, low-grade fever, and pericarditis.

This range is appropriate for the prophylaxis or treatment of venous thromboembolism and reduction of the risk of systemic embolism for people with atrial fibrillation and valvular heart disease.

An ectopic rhythm is an irregular heart rhythm due to a premature heartbeat. Ventricular ectopic rhythm is also known as premature ventricular contraction and ventricular extrasystole. When a patient's heart experiences an early beat, a brief pause usually follows. Ventricular-ectopics If occurs in a normal heart though symptomatic it is benign but if it is secondary to heart disease like MI it may precipitate to more life-threatening arrhythmia like ventricular fibrillation.

Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise. The condition is a medical emergency, the complications of which include pulmonary edema, shock, and death. Distended neck vein, clear breath sound, no tracheal shift, and BP of 60/0 points towards cardiac tamponade.

This is a case of diuretic resistance. Heart failure represents the most common clinical situation in which diuretic resistance is observed. In mild CHF, diuretic resistance is not commonly encountered, as long as renal function is preserved. However, in moderate and severe CHF patients, diuretic resistance occurs more frequently and often becomes a clinical problem. In diuretic resistance, another diuretic is added to get optimal or desirable results.

As the patient is still in heart failure and pulmonary edema with the usage of a loop diuretic (frusemide), a thiazide diuretic could be added with frusemide when the response is inadequate. This will reduce the volume overload and improve breathing.

History of surgery, left ventricular pain, fever, and murmur suggest a diagnosis is infective endocarditis. Therefore the next appropriate investigation is blood culture.

QRS complex is chaotic, wide, bizarre, and irregular which is characteristic of ventricular fibrillation.

Beta blockers can precipitate asthma attacks even though cardioselective.

Bendroflumethiazide causes hyponatremia and hypokalemia. But the findings are the opposite which is probably the error of the test. Hence blood tests should be repeated to confirm the level of potassium and sodium.

Ambulatory BP to document low BP as the cause of presenting symptoms. The case seems to be of postural hypotension and low BP as a result of the given antihypertensive.

Swelling, tenderness, and enlarged calf diameter are features of DVT supported by positive Homan’s test (pain on passive movement).

Ankle swelling suggests alcoholic cardiomyopathy and alcoholism is also a well-known cause of atrial fibrillation.

In the present day, some patients with tetralogy of Fallot have survived for longer than 15-20 years after their first operation. The major problem encountered by these individuals is the development of pulmonary valvular regurgitation. It appears that a number of these individuals require pulmonary valve replacement.

Sinus Tachycardia

The general rule is occlusion occurs in proximal bifurcation.

Left common iliac artery. That is an occlusion in the bifurcation of the left common iliac artery (as the femoral artery bifurcates more distally to superficial and deep branches).

Pansystolic murmur in apex radiating to the axilla may be due to mitral regurgitation secondary to papillary muscle rupture.

Low Na+, Low K+.

Frusemide causes hyponatremia, hypochloremic alkalosis, hypokalemia, hypomagnesemia and hypocalcemia.

In patients >55 yrs - CCB.

If CCB is not suitable (oedema, heart failure) thiazide is preferred.

In patients <55yrs - ACEI or ARB.

Now if the patient is on CCB or Thiazide and 2nd drug is to be added it should be one of ACEI or ARB and not one from CCB or Thiazide.

Mobitz type 1 block.

Gradual prolongation of PR interval followed by a drop beat.

Digoxin toxicity causes diarrhea, vomiting, dehydration, xanthopsia (yellow halos around light), bradycardia. History of atrial fibrillation is also a clue of digoxin use.

The patient is diabetic and has a pass history of MI. In both of these situations ACEI is the antihypertensive of choice.

Papillary muscle rupture causes mitral regurgitation causing pancystolic murmur leading to features of heart failure like breathlessness.