1 | ||
2 | ||
3 | ||
4 | ||
5 | ||
6 | ||
7 | ||
8 | ||
9 | ||
10 | ||
11 | ||
12 | ||
13 | ||
14 | ||
15 | ||
16 | ||
17 | ||
18 | ||
19 | ||
20 | ||
21 | ||
22 | ||
23 | ||
24 | ||
25 | ||
26 | ||
27 | ||
28 | ||
29 | ||
30 | ||
31 | ||
32 | ||
33 | ||
34 | ||
35 | ||
36 | ||
37 | ||
38 | ||
39 | ||
40 | ||
41 | ||
42 | ||
43 | ||
44 | ||
45 | ||
46 | ||
47 | ||
48 | ||
49 | ||
50 | ||
51 | ||
52 | ||
53 | ||
54 | ||
55 | ||
56 | ||
57 | ||
58 | ||
59 | ||
60 |
A- ST elevation in Leads II, III and aVF | 0.9% | |
B- ST elevation in leads I, aVL, V5 and V6 | 0.2% | |
C- ST segment elevation in the anterior leads (V3 and V4) | 0.0% | |
D- no ecg changes | 0.0% |
1) dilated cardiomyopathy | 0.0% | |
2) Restrictive cardiomyopathy | 0.0% | |
3) Amyloidosis | 0.0% | |
4) sarcoidosis | 0.0% |
A. 0.6 sec | 0.0% | |
B. 0.5 sec | 0.0% | |
C. 1.1 sec | 0.0% | |
D. 0.0 sec | 0.0% |
EXPLANATION:
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 patient’s symptoms. Converting patients back to sinus rhythm is not always the main goal.
A. Adenosine | 0.0% | |
B. Metoprolol | 25% | |
C. Electrical cardioversion | 7% | |
D. Amiodarone | 7% | |
E. Digoxin | 0.0% |
A. Left bundle branch block | 0.0% | |
B. Right bundle branch block | 0.0% | |
C. Second degree heart block | 0.0% | |
D. Third degree heart block | 0.0% | |
E. Supraventricular tachycardia | 9% |
A) atrial depolarization | 0.0% | |
B) atrial repolarization | 0.0% | |
C) ventricle depolarization | 0.0% | |
D) ventricle repolarization | 0.0% |
A. Supraventricular tachycardia | 31% | |
B. Ventricular fibrillation | 0.0% | |
C. Ventricular tachycardia | 0.0% | |
D. Ectopic beats | 0.0% | |
E. Atrial fibrillation | 7% |
A) abstein anomaly | 5% | |
B) tetralogy of fallot | 0.0% | |
C) PDA | 2% | |
D) transposition of great vessels | 2% |
Warfarin
EXPLANATION:
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.
A. Aspirin | 13% | |
B. Warfarin | 0.0% | |
c. Clopidogrel | 0.0% | |
D. Propanolol | 0.0% | |
E. Simvastatin | 0.0% |
A) abstein anomaly | 10% | |
B) tetralogy of fallot | 0.0% | |
C) PDA | 0.0% | |
D) transposition of great vessels | 37% |
A. Patent ductus arteriosus | 46% | |
B. Tetralogy of Fallot | 0.0% | |
C. Transposition of great arteries | 2% | |
D. Atrial septal defect | 0.0% | |
E. Ventricular septal defect | 0.0% |
ANSWER:
Cardiac troponins
EXPLANATION:
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 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 troponinA. Cardiac troponins | 0.0% | |
B. Chest X-ray | 0.0% | |
C. Echocardiogram | 0.0% | |
D. Holter ECG | 0.0% | |
E. Exercise stress test | 7% |
ANSWER:
Transoesophageal echocardiography
EXPLANATION:
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. A transcranial Doppler (TCD) is also considered by some to be superior to both TOE and TTE. However, it cannot differentiate a intracardiac from a pulmonary shunt.
A. Transesophageal echocardiography | 0.0% | |
B. Electrocardiogram (ECG) | 0.0% | |
C. Stress test | 0.0% | |
D. Holter monitoring | 0.0% | |
E. Cardiac troponins | 3% |
A) Purkinji fibers | 47% | |
B) Atria | 3% | |
C) Ventricle | 2% | |
D) AV node | 2% |
A) medial inferior part of interatrial septum | 16% | |
B) lateral inferior part of interatrial septum | 0.0% | |
C) post inferior part of interatrial septum | 0.0% | |
D) anterior inferior part of interatrial septum | 15% |
Key: C
Explanation: Case of Congestive heart failure. In hypovolemic hyponatremia, both serum osmolality and blood volume decrease. Vasopressin (ADH) secretion increases despite a decrease in osmolality to maintain blood volume results in water retention increase plasma dilution and hyponatremia
A) Aldosterone | 0.0% | |
B) Angiotensin II | 0.0% | |
C) Antidiuretic hormone | 0.0% | |
D) AtriaI Natriuretic Peptide | 8% |
Key:C
Explanation: Pulse Pressure: The main determinants of the pulse pressure (Pp) are the stroke volume (SV) and arterial compliance (C), such that Pp = SV/C. Pulse pressure is highly dependent on stroke volume and is therefore influenced by all factors which determine stroke volume (preload, afterload, and contractility) For simplicity, pulse pressure can be calculated as; Pulse Pressure= Systolic- Diastolic
A) Greater compliance | 0.0% | |
B) Greater pressure | 0.0% | |
C) Greater compliance and Greater pressure | 0.0% | |
D) Greater compliance less pressure | 14% |
EXPLANATION:
The ECG revealing a broad complex tachycardia with 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 a wake as it is impossible to see a ventricular fibrillation in an awake patient. 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 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 conscious level. → immediate electrical cardioversion is indicated
2. Without Pulse → immediate electrical cardioversion is indicated
A. Stokes-Adams syndrome | 6% | |
B. Ventricular fibrillation | 10% | |
C. Ventricular tachycardia | 0.0% | |
D. Complete heart block | 0.0% | |
E. Atrial fibrillation | 0.0% |
Explanation: This patient's ECG reveals a narrow QRS complex tachycardia with a regular rhythm and nonvisible P waves. These findings are consistent with paroxysmal supraventricular tachycardia (PSVT), an episodic cardiac arrhythmia that originates at or above the atrioventricular (AV) node. ⦁ The most common type of PSVT is AV nodal reentrant tachycardia (AVNRT), which usually affects young patients (e.g., age <40) with an otherwise normal heart. This condition is usually treated with drugs that prolong AV conduction time as the major abnormality lies within AV node. One such short acting drug is adenosine what has the half-life of few seconds.
A) Lidocaine | 0.0% | |
B) Adenosine | 0.0% | |
C) Ivabradine | 0.0% | |
D Ranolazine | 0.0% |
Explanation: ▪️Coarctation of aorta at origin of subclavian artery causes hypertension in upper extremities and hypotension in lower extremities. ▪️On examination there is radio-femoral delay. ▪️Causes: Congenitally associated with TURNER SYNDROME and Acquired cause is TAKAYASU ARTERITIS. On X-ray: figure 3" appearance
A. Coarctation of aorta | 0.0% | |
B. Aortic aneurysm | 0.0% | |
C. Pheochromocytoma | 0.0% | |
D. Cushing syndrome. | 0.0% |
A) 0.50 | 0.0% | |
B) 0.55 | 0.0% | |
C) 0.60 | 0.0% | |
D) 0.77 | 3% |
A) Berry Aneurysm | 0.0% | |
B) Marfan Syndrome-Related Aneurysm | 0.0% | |
C) Aortic Dissection | 0.0% | |
D) Mycotic Aneurysm | 2% |
A) Crista Terminalis | 0.0% | |
B) Interventricular Septum | 0.0% | |
C) Tricuspid Valve | 0.0% | |
D) Interatrial Septum | 11% |
EXPLANATION:
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
• Basically 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
o Infant or child is asymptomatic with normal feeding and weight gain
o May be detected when a murmur is heard on routine examination
o Give louder murmurs
o Classically, a harsh pan-systolic murmur heard at the left sternal edge, with a systolic thrill, and
a left parasternal heave.
Most importantly is to 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
o Associated with signs of pulmonary hypertension
o These babies may develop a right to left shunt with cyanosis or Eisenmenger’s syndrome
A. Tetralogy of Fallot | 0.0% | |
B. Atrial septal defect | 0.0% | |
C. Ventricular septal defect | 21% | |
D. Patent ductus arteriosus | 9% | |
E. Transposition of the great arteries | 0.0% |
ANSWER:
Blood culture
EXPLANATION:
This is a case of infective endocarditis. The most appropriate investigation is blood cultures or echocardiogrm. Since echocardiogram is not one of the options, blood cultures should be picked.
A. Computed tomography scan of the chest | 0.0% | |
B. Abdominal ultrasound | 0.0% | |
C. Chest X-ray | 0.0% | |
D. Blood culture | 0.0% |
Atheroma | 0.0% | |
B. Congenital | 1% | |
C. Regeneration of tissue | 0.0% | |
D. Infection | 0.0% |
ANSWER:
Ultrasound abdomen
EXPLANATION:
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 or CT scan can be performed. Although, it may be safer and quicker to perform USS in the ED, rather than transfer the patient for CT scan
A. Laparoscopy | 0.0% | |
B. sigmoidoscopy | 0.0% | |
C. Ultrasound pelvis | 0.0% | |
D. Ultrasound abdomen | 39% |
8.
Explanation
The answer is B When a person moves to a standing position, blood pools in the leg veins, causing decreased venous return to the heart, decreased cardiac output, and decreased arterial pressure. The baroreceptors detect the decrease in arterial pressure, and the vasomotor center is activated to increase sympathetic outflow and decrease parasympathetic outflow. There is an increase in heart rate (resulting in a decreased PR interval), contractility, and total peripheral resistance (TPR). Because both heart rate and contractility are increased, cardiac output will increase toward normal.
(A) Decreased heart rate | 0.0% | |
(B) Increased contractility | 0.0% | |
(C) Decreased total peripheral resistance (TPR) | 0.0% | |
(D) Decreased cardiac output | 0.0% | |
(E) Increased PR interval | 1% |
Explanation
The answer is B The absent P wave indicates that the atrium is not depolarizing and, therefore, the pacemaker cannot be in the sinoatrial (SA) node. Because the QRS and T waves are normal, depolarization and repolarization of the ventricle must be proceeding in the normal sequence. This situation can occur if the pacemaker is located in the atrioventricular (AV) node. If the pacemaker were located in the bundle of His or in the Purkinje system, the ventricles would activate in an abnormal sequence (depending on the exact location of the pacemaker) and the QRS wave would have an abnormal configuration. Ventricular muscle does not have pacemaker properties.
(A) sinoatrial (SA) node | 0.0% | |
(B) atrioventricular (AV) node | 0.0% | |
(C) bundle of His | 0.0% | |
(D) Purkinje system | 0.0% | |
(E) ventricular muscle | 1% |
(A) 3.45 L/min | 0.0% | |
(B) 4.55 L/min | 0.0% | |
(C) 5.25 L/min | 0.0% | |
(D) 8.00 L/min | 0.0% | |
(E) 9.85 L/min | 0.0% |
(A) an exaggerated response of the renin–angiotensin–aldosterone system | 0.0% | |
(B) a suppressed response of the renin–angiotensin–aldosterone system | 0.0% | |
(C) an exaggerated response of the baroreceptor mechanism | 0.0% | |
(D) a suppressed response of the baroreceptor mechanism | 23% |
The answer is D The PR segment (part of the PR interval) and the ST segment are the only portions of the electrocardiogram (ECG) that are isoelectric. The PR interval includes the P wave (atrial depolarization) and the PR segment, which represents conduction through the atrioventricular (AV) node; during this phase, the ventricles are not yet depolarized. The ST segment is the only isoelectric period when the entire ventricle is depolarized
(A) PR interval | 0.0% | |
(B) QRS complex | 0.0% | |
(C) QT interval | 0.0% | |
(D) ST segment | 0.0% | |
(E) T wave | 2% |
A. -55 to -60 | 0.0% | |
B. 70 to 80 | 4% | |
C. -80 to -90 | 0.0% | |
D. 90 to 100 | 0.0% |
ANSWER:
Hyperkaleimia
EXPLANATION:
Acute renal failure is one of the causes of hyperkalemia. Together with the ECG findings points 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
Hypercalcemia:
Shortened QT intervals
Hypocalcemia:
Prolonged QT intervals
A. Hypophosphatasemia | 0.0% | |
B. Hyperkalemia | 0.0% | |
C. Hypokalemia | 0.0% | |
D. Hypercalcinemia | 0.0% | |
E. Hypocalcemia | 2% |
EXPLANATION:
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 include having a pansystolic murmur radiating to the axilla which is seen in this stem
A. Papillary muscle rupture | 16% | |
B. Ventricular aneurysm | 0.0% | |
C. Pericarditis | 0.0% | |
D. Pericardial effusion | 6% | |
E. Ventricular septal defect | 7% |
ANSWER:
Atrial fibrillation
EXPLANATION:
Ankle swelling and orthopnea are features of heart failure. These features in combination with the history of alcoholism gives us the 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 decompensaitons 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 is increased following weekends and during holiday seasons
A. Ventricular tachycardia | 0.0% | |
B. Paroxysmal supraventricular tachycardia | 0.0% | |
C. Ventricular fibrillation | 0.0% | |
D. Atrial fibrillation | 10% | |
E. Ventricular ectopic | 2% |
The words “yellow haloes” are a clincher for 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, hypokalemia 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
A. Digoxin | 24% | |
B. Amlodipine | 0.0% | |
C. Aminophylline | 2% | |
D. Propanolol | 6% | |
E. Diltiazem | 4% |
EXPLANATION:
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
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
Mnemonic (SAD)
Remember, the murmur for aortic stenosis is an ejection systolic murmur loudes in aortic area (2nd intercostal space, right sternal border), radiates to carotids, and louder in expiration.
A. Tricuspid regurgitation | 2% | |
B. Mitral regurgitation | 5% | |
C. Mitral stenosis | 3% | |
D. Aortic stenosis | 27% | |
E. Aortic regurgitation | 0.0% |
ANSWER:
Dressler’s syndrome
EXPLANATION:
The widespread ST elevation and pericardial friction rub is 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 characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.
A. Cardiac tamponade | 0.0% | |
B. Mitral regurgitation | 0.0% | |
C. Dressler’s syndrome | 0.0% | |
D. Atrial fibrillation | 1% | |
E. Pulmonary embolism | 2% |
ANSWER:
Mobitz type 1 block
EXPLANATION:
Mobitz type 1 block→Gradual prolongation of 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.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 requires permanent pacemakers.
A. Sinus bradycardia | 2% | |
B. 1st degree heart block | 0.0% | |
C. Mobitz type 1 block | 0.0% | |
D. Mobitz type 2 block | 11% | |
E. Complete heart block | 0.0% |
ANSWER:
Atrial myxoma
EXPLANATION:
ATRIAL MYXOMA
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 tumor 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 value which results in syncope and heart failure.
A. Mitral regurgitation | 0.0% | |
B. Ventricular ectopics | 0.0% | |
C. Pulmonary regurgitation | 0.0% | |
D. Atrial myxoma | 0.0% | |
E. Complete heart block | 0.0% |
A. Get a defibrillator | 0.0% | |
B. Give two rescue breaths immediately | 2% | |
C. Check notes for a Do Not Attempt Resuscitation (DNAR) order | 3% | |
D. Insert two wide-bore cannulas into each antecubital fossa | 0.0% | |
E. Start chest compressions at a rate of 30:2 | 0.0% |
ANSWER:
Complete heart block
EXPLANATION:
HEART BLOCK
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.
A. Complete heart block | 29% | |
B. First degree heart block | 0.0% | |
C. Mobitz type 1 AV block | 3% | |
D. Mobitz type II AV block | 0.0% |
EXPLANATION:
This question clearly points towards cardiac tamponade. His chest is bilaterally clear thus we can therefore exclude pneumothorax or pleural effusion. Muffled heart sounds, distended neck veins, hypotension are called Beck’s triad and it is a classical finding in cardiac tamponade. This is diagnosed with an echocardiogram.
A. Echocardiogram | 25% | |
B. Chest X-ray . | 0.0% | |
C. CTPA | 4% | |
D. Blood cultures | 2% |
EXPLANATION:
Non-steroidal anti-inflammatory drugs (NSAIDs) should be avoided in patients with chronic kidney disease,heart failure or ischemic 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. Prednisolone | 9% | |
B. Paracetamol | 0.0% | |
C. Ibuprofen | 6% | |
D. Colchicine | 15% | |
E. Beta blockers | 0.0% |
A. Myocardial infarction | 9% | |
B. Pericarditis | 0.0% | |
C. Pneumonia | 0.0% | |
D. Oesophagitis | 3% |
ANSWER:
ACE inhibitor
EXPLANATION:
This question is really 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 macro-vascular 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 renal-protection and retinopathy, it is appropriate to recommend an ACE inhibitor as 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 first lineA. ACE inhibitor | 0.0% | |
B. Thiazide diuretic | 0.0% | |
C. Insulin | 0.0% | |
D. Beta blocker | 0.0% | |
E. Calcium channel blocker | 0.0% |
ANSWER:
U wave
EXPLANATION:
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 hypokalemia The other answers are less likely:J waves are usually observed in patients suffering from hypothermia.Delta waves are seen in Wolff Parkinson White syndrome.PR interval in hypokalemia is prolonged.
A. U wave | 23% | |
B. J wave | 0.0% | |
C. Delta waves | 0.0% | |
D. Short PR interval | 0.0% | |
E. Prolonged QT interval | 0.0% |
ANSWER:
Tetralogy of Fallot
EXPLANATION:
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 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 piced 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
A. Tetralogy of Fallot | 0.0% | |
B. Atrial septal defect | 0.0% | |
C. Patent ductus arteriosus | 6% | |
D. Transposition of great arteries | 0.0% | |
E. Ventricular septal defect | 0.0% |
ANSWER:
Percutaneous intervention (PCI)
EXPLANATION:
Not all myocardial infarction presents 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.
A. Low molecular weight heparin | 0.0% | |
B. Percutaneous intervention (PCI) | 0.0% | |
C. Warfarin | 3% | |
D. Streptokinase | 0.0% |
ANSWER:
Tricuspid atresia
EXPLANATION:
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 is found along the left sternal border (Most have VSD)
Tetralogy of Fallot – 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.
A. Atrial septal defect | 0.0% | |
B. Ventricular septal defect | 16% | |
C. Tricuspid atresia | 0.0% | |
D. Patent ductus arteriosus | 0.0% | |
E. Tetralogy of Fallot | 0.0% |
A. Unstable angina | 6% | |
B. Decubitus angina | 0.0% | |
C. Stable angina | 0.0% | |
D. Coronary spasm | 0.8% | |
E. Myocardial infarction | 0.0% |
ANSWER:
Pericardiocentesis
EXPLANATION:
This question clearly points towards cardiac tamponade. Trachea is central thus tension pneumothorax is less likely. Muffled heart sounds, distended neck veins, hypotension are called Beck’s triad and is a clinical finding in cardiac tamponade.
A. Chest drain | 2% | |
B. IV fluids | 0.0% | |
C. Pericardiocentesis | 0.0% | |
D. Large-bore cannula into second intercostal space in midclavicular line | 0.0% | |
E. Blood transfusion | 0.0% |
Explanation: Inferior wall myocardial infarction (MI) occurs from a coronary artery occlusion with resultant decreased perfusion to that region of the myocardium.
A. anterior wall MI | 3% | |
B. posterior wall MI | 0.0% | |
C. inferior wall MI | 33% | |
D. lateral wall MI Key: C | 2% |
Key: B
Cannon A waves, or cannon atrial waves, are waves seen occasionally in the jugular vein of humans with certain cardiac arrhythmias. When the atria and ventricles happen to contract simultaneously, the right atrium contracts against a closed tricuspid valve, resulting in back pressure into the venous system that can be seen in the jugular venous pulse as a high- amplitude "cannon wave".
Associated with heart block, in particular third-degree (complete) heart block. It is also seen in pulmonary hypertension. Cannon A waves may also be seen in ventricular tachycardia due to the inherent AV dissociation of the arrhythmia
A. sinus bradycardia | 0.0% | |
B. complete heart block | 0.0% | |
C. pulmonary stenosis | 2% | |
D. atrial fibrillation | 9% |
Key: A
Aortic disease
• Caused by aortic necrosis (cystic medial degeneration) → weakening of the elastic artery
• Manifestations include:
• Aortic aneurysm
Thoracic or abdominal aortic aneurysm
Aortic root dilation: aneurysm of the proximal thoracic aorta
• Aortic regurgitation
• Aortic dissection (typically of the thoracic aorta)
Mitral valve prolapse
Berry aneurysms: rupture leads to subarachnoid hemorrhage
A. Marfan’s | 29% | |
B. SLE | 0.0% | |
C. Klinefelter | 5% | |
D. Fragile X syndrome | 2% |
A. R wave is smaller than 12 mm in amplitude. | 0.0% | |
B. R wave is greater than 12 mm in amplitude. | 21% | |
C. P wave not present. | 0.0% | |
D. p wave is larger than normal | 0.0% |
Explanation:
S1Q3T3 pattern was defined as the presence of S wave in lead I and Q wave and inverted T wave in lead III. Pathological conditions which can cause S1Q3T3 electrocardiographic abnormality are pneumothorax, pulmonary embolism, cor pulmonale, acute lung disease, and left posterior fascicular block
A. S1Q3T3 | 27% | |
B. U wave | 4% | |
C. delta wave | 6% | |
D. missed beats | 0.0% |
Key: B
Explanation:The Bainbridge reflex is a compensatory reflex resulting in an increase in heart rate following an increase in cardiac preload so prevents venous congestionA. Chemoreceptor reflex | 0.0% | |
B. Bainbridge reflex | 0.0% | |
C. Stress relaxation | 6% | |
D. Renin release | 8% |
A. 30:1 | 5% | |
B. 30:2 | 0.0% | |
C. 20:1 | 0.0% | |
D. 10:1 | 0.0% |