Short Cases in Clinical Exams of Internal Medicine Wanis Hamad Ibrahim
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Cardiovascular Cases1

  • Wash your hands.
  • Shake hands with the patient, introduce yourself and take permission
  • Position the patient at a 45° angle and request the patient to remove their upper clothes.
  • Inform the patient to alert you in case you cause any discomfort or pain to him/her during the examination.
  • Start by inspecting the patient and the surrounding. Allow some time for a quick surveillance of the patient and their surroundings. This may give you important clues about the patient condition and diagnosis. A tall marfanoid habitus may suggest the diagnosis of aortic regurgitation due to Marfan's syndrome. Inability of the patient to move his or her neck (particularly while examining the Jugular venous pressure (JVP) should raise the suspicion of ankylosing spondylitis with associated aortic regurgitation. External appearance of Down's syndrome may suggest an atrioventricular septal defect. Similarly, a woman who looks short with a webbed neck may indicate the reason for cardiovascular system examination is coarctation of the aorta as a complication of Turner’ syndrome. A patient on an intravenous heparin infusion may suggest atrial fibrillation or presence of a metallic valve. A patient who is using oxygen may suggest the diagnosis of heart failure. A patient in a semi-sitting position from the start who appears in respiratory distress may suggest significant heart failure, while one lying comfortably in a flat position at the start of the examination suggests that significant pulmonary edema is unlikely. Look for cyanosis, malar flush due to mitral stenosis, obvious pedal edema, etc.2
  • Candidates may hear different instructions from different examiners such as examine the cardiovascular system, examine the heart or examine the precordium. Many candidates get confused whether to examine only the precordium or look for peripheral signs of cardiac diseases. I suggest that even if the instruction is to examine the heart, candidates should start by looking for peripheral signs of cardiovascular disease unless they are redirected by the examiners to examine only on the precordium. A common cause of failure is when candidates miss important peripheral signs such as clubbing or signs of infective endocarditis in a patient with valvular heart disease.
  • Hold the right hand of the patient and feel the pulse. Pay attention to the rhythm as an irregular pulse can be easily missed by the anxious candidate. Record the rate, rhythm, volume, any special character, the presence of a synchronous pulse on the other arm and feel for radiofemoral delay. Make sure that the patient does not have shoulder pain before you check for a collapsing pulse.
  • Examine the hands for clubbing, cyanosis, pallor, splinter hemorrhage, Janeway lesions and Osler's nodes (Figure 1.1).
  • Move to the face and mouth. Examine the eyes for pallor, cheeks for malar flush of mitral stenosis, cyanosis and dental caries (Figure 1.2).
  • Examine the neck for JVP, dancing carotid pulsations “Corrigan pulse” of aortic regurgitation and thyroid gland (particularly in a patient with atrial fibrillation).
  • Follow the steps of inspection, palpation and auscultation to examine the precordium.
  • Inspect for visible pulsations, shape of the chest, pectus excavatum (Figure 1.3) or carinatum (Figure 1.4).
  • Before you start palpating the chest ask the patient if he/she has any pain.
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    Figure 1.1: Finger clubbing and splinter hemorrhage in a patient with infective endocarditis
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    Figure 1.2: Facial appearance in mitral stenosis
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    Figure 1.3: Pectus excavatum
  • Feel for the apex beat; determine its location and character. Feel for a parasternal heave, thrill and palpable second heart sound.
  • Start listening at the apex and simultaneously place your free hand over the carotid to enable you to time the heart sounds, this is essential. First concentrate on the first and second heart sounds. Determine whether they are normal in intensity, muffled or loud. Check whether the splitting of second heart sound is normal wide, or fixed. Once you hear a murmur, determine the place in which you hear the murmur at its maximal intensity. This is usually the site of origin of the murmur. For example, if you hear a pansystolic murmur loudest at the mitral area, that murmur is most likely to be due to mitral valve disease. Determine also the character, radiation and effect of respiration on the murmur. Once you finish listening to the four areas, ask the patient to tilt to the left lateral position to listen for the mid-diastolic murmur of mitral stenosis then ask the patient to sit forward, breath out and hold breath to examine for the murmur of aortic regurgitation. Listen carefully over the left axilla for radiation of the mitral regurgitation murmur and over the carotids in the neck for the radiation of the murmur of aortic stenosis.4
    zoom view
    Figure 1.4: Pectus carinatum
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    Figure 1.5: Pitting edema of the legs (observe also the presence of diabetic dermopathy)
  • Finish your examination by listening to the lung bases and feeling for pitting pedal edema (Figure 1.5). Remember during the examination for pitting edema to enquire from the patient about leg pain before pressing over the legs and to direct your face towards the patient for any tenderness rather than towards the examiner.
  • Many candidates feel the time given for cardiovascular cases in the clinical examination is not enough. Frequent timed practice of the cardiovascular system examination under supervision of a registrar or a consultant will be very helpful.
  • A systolic murmur that radiates to the neck is due to aortic stenosis.
  • A systolic murmur that radiates to the axilla is due to mitral regurgitation.
  • If you find a displaced apex beat in a patient with mitral stenosis, search carefully for other coexistent valvular lesions.
  • The early diastolic murmur of aortic regurgitation may mimic breath sounds. Make sure that you ask the patient to hold breath when you listen for this murmur.
  • When you find pure aortic regurgitation in the examination make sure you identify ankylosing spondylitis or Marfan's syndrome, if present.
  • Do not forget to examine for peripheral signs of aortic regurgitation when you find an early diastolic murmur in the aortic area.
  • Aortic stenosis murmur may be harsh and heard also in the mitral area and might be confused with a systolic murmur of mitral regurgitation (Gallavardin phenomenon). The clue is in the radiation to the neck and an absence of radiation to the axilla.
  • In Eisenmenger syndrome, the murmur of the ventricular septal defect (VSD) may disappear. If you are asked to examine the cardiovascular system of a patient with cyanosis, clubbing and elevated JVP, think of Eisenmenger syndrome even if you cannot hear a murmur (other differential diagnosis include chronic lung diseases) (Figure 1.6).
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    Figure 1.6: Finger clubbing and cyanosis in a patient with Eisenmenger complex
  • If you do not feel the apex beat and you do not hear heart sounds keep in mind dextrocardia. Some candidates developed a good habit of feeling both sides of the chest for the apex beat as they begin their examination.
  • Remember that the indications for infective endocarditis prophylaxis in valvular heart disease have been modified recently.
Common Pitfalls
  • Candidates fail to recognize that the patient has stroke due to systemic embolization.
  • Candidates fail to recognize signs of infective endocarditis.
  • Candidates miss the presence of atrial fibrillation (AF).
  • Candidates find a displaced apex beat and do not think of other coexistent valvular lesion aortic regurgitation (AR)/mitral regurgitation (MR).
Examiner Instructions
  • Examine this patient's cardiovascular system
  • Examine this patient's precordium
  • Listen to this patient's heart.
Well, this gentleman has features to suggest mitral stenosis as evidenced by a low pulse volume, tapping apex, loud S1, opening snap and mid-diastolic rumbling murmur. There were no signs to suggest infective endocarditis or pulmonary hypertension.
Examiner: Why should the pulse volume be low in MS?
Candidate: Due to reduced stroke volume.
Examiner: Did you notice anything in this patient's face?
Candidate: He has malar flush (pinkish–purple cheeks) resulting from decrease cardiac output (reduced stroke volume) leading to vasoconstriction (Figure 1.2).
Examiner: Why is S1 loud in MS?
Candidate: It is due to the increase in left atrial pressure leading to closure of the mitral valve from a wide distance.
Examiner: What does it mean if S1 is soft in pure MS?
Candidate: It indicates that the valve is heavily calcified.
Examiner: What happens to S2 in MS?
Candidate: S2 may be normal or it may becomes loud if there is pulmonary hypertension.7
Examiner: What is the mechanism of the opening snap in MS and what are its clinical implications?
Candidate: It is heard after S2 at the apex and is best heard at the left sternal border. It is caused by sudden and rapid opening of the mitral valve in early diastole due to the high pressure in the left atrium. The opening snap helps in determining the severity of mitral stenosis; when the valve becomes severely stenotic or heavily calcified, the interval between S2 and opening snap becomes shorter and the opening snap may disappear.
Examiner: Which sound is usually confused for the opening snap and how would you differentiate them?
Candidate: Splitting of S2 (For example, due to pulmonary hypertension). Variation with respiration may help in differentiation.
Examiner: Is opening snap pathognomonic for MS?
Candidate: No. It can be heard in tricuspid stenosis and left atrial myxoma. (Remember: In the examination opening snap is always due to mitral stenosis).
Examiner: In which condition will you not be able to hear presystolic accentuation of the MS murmur?
Candidate: If the patient has atrial fibrillation.
Examiner: What are the factors that indicate the severity of MS?
  • A short S2-OS interval
  • Signs of pulmonary arterial hypertension
  • Long mid-diastolic murmur
  • Mitral valve area less than 1.5 cm2.
Examiner: What are the causes of MS?
  • Rheumatic heart disease
  • Congenital MS/Lutembacher's syndrome atrial septal defect (ASD) with mitral stenosis (MS)
  • Mitral annular calcification [For example, in patients with end-stage renal disease (ESRD)]
  • Systemic lupus erythematosus (SLE).
Examiner: What are the complications of MS?
  • Systemic embolization
  • PA hypertension
  • Infective endocarditis
  • Hemoptysis.
Examiner: What if this patient comes with hoarseness of his voice?
Candidate: Compression of the left recurrent laryngeal nerve against the pulmonary artery by an enlarged left atrium may rarely cause hoarseness.
Examiner: How would you manage this patient?
  • Perform transthoracic echocardiogram (TTE) to confirm the diagnosis, quantify hemodynamic severity, PA hypertension and assess concomitant valvular lesions.
  • Surgical intervention is indicated in
    • Very severe MS with a mitral valve area < 1.0 cm2
    • Severe MS with a mitral valve area <1.5 cm2with:
      • Severe symptoms: NYHA III or IV
      • Presence of pulmonary hypertension (PA systolic pressure ≥ 25 mm Hg)
      • Possibly in new onset AF or multiple systemic embolization despite adequate anticoagulation
  • Anticoagulation for prevention of thromboembolism (high risk groups include prior embolic event, AF, small mitral valve area, presence of AR and left atrial thrombus).
  • Management of AF.
  • Prevention of rheumatic fever recurrence.
Examiner: Would you recommend routine antibiotic prophylaxis for infective endocarditis (IE) in this patient before procedures?
Candidate: The prophylaxis against IE has recently been updated and not all valvular lesions or procedures require prophylaxis. (See infective endocarditis section).
Common Pitfalls
  • Candidates hear radiation of a systolic murmur to the axilla and fail to diagnose MR.
  • Candidates confuse harsh AS with MR.
Examiner Instructions
  • Examine this patient's cardiovascular system.
  • Examine this patient's precordium.
  • Listen to this patient's heart.
This patient has brisk pulse, displaced apex beat, systolic thrill in the mitral area, soft S1 and a loud pansystolic murmur heard best in the mitral area which radiates to the axilla. He has MR with no signs of heart failure.9
Examiner: How would you differentiate a high volume pulse in AR from that of MR?
Candidate: In MR the pulse pressure will be normal while in AR it will be wide.
Examiner: What are the causes of MR?
  • Mitral valve prolapse (most common cause in developed countries)
  • Rheumatic heart disease
  • Infective endocarditis
  • Acute MR in ischemic heart disease (rupture papillary muscle)
  • Left ventricular failure (dilatation of valve)
  • Hypertrophic cardiomyopathy.
Examiner: What are the main complications of MR?
  • Development of left ventricular dysfunction
  • Atrial fibrillation
  • Infective endocarditis.
Examiner: Which factors indicate severity of MR?
  • Acute MR (from acute coronary syndrome)
  • Development of symptoms and signs of left ventricular dysfunction
  • Regurgitant fraction >50%
  • Regurgitant volume > 60 mL
  • Left ventricular ejection fraction (LVEF) <60%
  • Left ventricular end systolic dimension(LVESD) >40 mm (LV dilatation).
Examiner: In the presence of coexisting MS, how would you determine the predominant valvular lesion?
Candidate: Presence of displaced apex beat; high volume pulse and muffled first heart sound suggest that MR is the predominant lesion.
Examiner: What are the indications for surgical intervention in MR?
  • Patients with acute MR who are symptomatic
  • Symptomatic severe MR (regurgitant fraction >50% or volume > 60 mL) with LVEF> 30% [ejection fraction (EF) should be reasonable to go for surgery]
  • Asymptomatic severe MR with one of the following:
    • LVEF between 30% and 60%
    • LVESD < 40 mm
    • Development of AF
    • Development of pulmonary hypertension
Examiner: How would you manage this patient?
  • Serial echocardiography to follow LVEF
  • Afterload reduction by diuretics and nitrates
  • Infective endocarditis prophylaxis is not routinely recommended in mitral and aortic rheumatic heart disease (RHD) except in high-risk groups (see MS)
  • Treat AF.
Common Pitfalls
  • Failure to recognize clinical features of Marfan's syndrome or ankylosing spondylitis in a patient with AR
  • Failure to diagnose AR in a patient with dancing carotid pulsation
  • Failure to examine for peripheral signs of AR
  • Missing AR murmur as breath sound particularly when there is another valvular lesion.
Examiner Instructions
  • Examine this patient's cardiovascular system
  • Examine this patient's precordium
  • Listen to this patient's heart
Candidate: This patient has a collapsing pulse, there is a dancing carotid (Corrigan's sign) and a blowing early diastolic murmur heard best at the left second intercostal space, which suggests AR.
Examiner: What are the causes of AR?
  • Valve disease: Rheumatic heart disease—Infective endocarditis—Congenital bicuspid valve
  • Aortic root disease: Marfan's syndrome—Long standing hypertension—Syphilitic aortitis—Ankylosing spondylitis—Ehlers–Danlos syndrome—Aortic dissection
Examiner: How could you identify the cause of AR from the site of the murmur?
Candidate: AR due to valvular disease is usually heard at the third and fourth intercostal space of the left sternal border, while that due to aortic root disease is heard best at the right sternal border.
Examiner: If you hear an ejection systolic murmur at the aortic area, what could it be?
Candidate: It could be due to coexisting AS or a functional stenosis resulting from the large volume of blood passing through the aortic valve because of AR.11
Examiner: If you hear an associated mid-diastolic murmur at the apex, what could it be?
Candidate: It can be an associated MS or an Austin-Flint murmur.
Examiner: How would you differentiate MS from an Austin-Flint murmur?
Candidate: An Austin-Flint murmur occurs because of the turbulence of blood at the mitral valve due to regurgitation of blood from the aorta into the left ventricle. In Austin-Flint, S1 will be normal and there is no opening snap.
Examiner: What are the peripheral signs of AR?
  • Becker sign: Visible systolic pulsations of the retinal arterioles
  • Corrigan pulse (dancing carotid pulsation)
  • de Musset sign: Bobbing of the patient's head with each heartbeat
  • Hill sign: Popliteal cuff systolic blood pressure 40 mm Hg higher than brachial cuff systolic blood pressure
  • Duroziez sign: Systolic and diastolic murmur over the femoral artery with mild compression of the artery
  • Müller sign: Visible systolic pulsations of the uvula
  • Quincke sign: Visible capillary pulsations of the fingernail bed
  • Pistol-shot sign: Systolic and diastolic sounds heard over the femoral artery.
Examiner: Why do these signs occur in AR?
Candidate: All these signs result from widened pulse pressure (exaggerated difference between systolic and diastolic blood pressure) because of elevated stroke volume during systole that falls significantly during diastole due to the incompetent aortic valve.
Examiner: What are the main complications of chronic AR and what is the single-most important prognostic factor?
Candidate: Progressive LV dysfunction and failure, angina, arrhythmia, and sudden death. Patients with AR and New York Heart Association (NYHA) class III or IV heart failure have an annual mortality of about 25%. The single-most important prognostic factor is LV function.
Examiner: What are the factors indicating severity of AR?
  • Clinical factors: Displaced apex beat, longer AR murmur, presence of peripheral signs that suggest wider pulse pressure (see above)
  • Echocardiographic factors: LVEF < 50% and LVESD > 50 mm (Remember the number 50. They all represent dilatation or poor function of LV).
Examiner: How would you manage this patient?
  • Serial echocardiography to assess LVEF and LVESD
  • Exercise stress test12
  • Cardiac catheterization to assess the presence of coronary artery disease (CAD) and severity of AR
  • Vasodilator drugs like angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers to decrease afterload
  • Infective endocarditis prophylaxis is not routinely recommended in mitral and aortic RHD except in the high risk groups (see MS).
Examiner: What are the indications for surgery in AR?
  • Acute AR from IE or aortic dissection
  • Symptomatic patient
  • Asymptomatic patient, with a resting EF <50%
  • Asymptomatic patient, with LV dilation LVESD >50 mm
  • Asymptomatic patient with AR who is undergoing coronary bypass or other cardiac surgery.
Common Pitfalls
  • Failure to differentiate aortic sclerosis from aortic stenosis
  • Misdiagnosing aortic stenosis (AS) MR in a patient whose murmur radiates to the neck (misinterpretation of the Gallavardin phenomenon)
  • Failure to look for AR as it is commonly associated with AS (in 80% of cases)
Examiner Instructions
  • Examine this patient's cardiovascular system
  • Examine this patient's precordium
  • Listen to this patient's heart
This patient has a displaced heaving apex beat, with a slow rising pulse (pulsus parvus tardus), S4 and a harsh ejection systolic murmur which is heard best in the right second intercostal space and radiates to the neck. I could hear the same murmur which was a bit softer at the apex in the mitral area but there was no radiation to the axilla, I would suggest pure AS (without coexistent MR) – Gallavardin phenomenon. There are no signs of heart failure.
Examiner: What do you mean by Gallavardin phenomenon?
Candidate: An aortic stenosis murmur sometimes has two components, a noisy harsh component which is heard in the right second or third intercostal space and radiates to the neck and a musical component that radiates to the apex (mitral area). This musical component may be mistaken for MR.13
Examiner: Then how do you differentiate between the Gallavardin phenomenon and the presence of true MR?
Candidate: The murmur of MR usually radiates to the axilla, whereas that due to Gallavardin does not.
Examiner: Which cause of AS usually produces the Gallavardin phenomenon?
Candidate: Degenerative aortic stenosis.
Examiner: What are the common causes of AS?
  • Congenital aortic stenosis: Unicuspid, bicuspid and tricuspid valve.
    In adults, bicuspid aortic valve is the most common cause of AS
    In children, a unicuspid valve predominates
  • Acquired aortic stenosis:
  • Degenerative calcific AS: The most common cause in older patients (risk factors include: DM, hypertension, hypercholesterolemia and smoking)
  • Rheumatic heart disease.
Examiner: How would you differentiate between aortic stenosis and aortic sclerosis?
Candidate: In aortic sclerosis, the murmur usually does not radiate to the neck and the volume of the pulse is usually high rather than slow rising. Also, in aortic stenosis there is usually a reduced pulse pressure (difference between systolic and diastolic < 40 mm Hg).
Examiner: What do you mean by pulsus parvus tardus and how would you check for its presence?
Candidate: Parvus means low volume and tardus means rising slowly. You need to place one hand over the apex beat and the other over the carotid pulse. In addition to being low in volume, there will be delay in the upstroke of the carotid pulse compared to the apex beat. Tardus is more specific than parvus in AS.
Examiner: What are the classic triad of symptoms in AS?
Candidate: Angina, dyspnea and syncope or dizziness
Examiner: What is the incidence of sudden cardiac death in AS?
Candidate: About 30% in symptomatic AS.
Examiner: If this patient presents with bleeding per rectum, what do you suspect as a cause?
Candidate: Colonic angiodysplasia. Aortic valve replacement may cure angiodysplasia and recurrent bleeding.14
Examiner: What factors indicate the severity of AS?
  • Presence of symptoms
  • Prolonged louder murmur
  • Paradoxical splitting of S2 (due to delayed closure of A2)
  • Presence of S4
  • Pulsus parvus tardus
  • Valve area < 1 cm2
  • Pressure gradient across the valve > 40 mm Hg
Examiner: How would you manage this patient?
  • Request echocardiography to assess valve area and pressure gradient
  • Caution when prescribing blood pressure lowering medications to avoid excessive lowering of preload (diuretics, beta blockers, vasodilators such as nitrates, hydralazine and nifedipine should be used with caution and in smaller doses)
  • Instruct patient to avoid standing suddenly from a sitting or recumbent position
  • No routine endocarditis prophylaxis is indicated in valvular AS except in the high-risk groups mentioned in the infective endocarditis section
  • Cardiac catheterization to look for coexistent CAD.
Examiner: What are the indications for surgery in AS?
  • Surgery is the mainstay treatment of symptomatic AS
  • Asymptomatic severe AS with EF <50% or abnormal exercise treadmill test
  • Asymptomatic severe AS in a patient undergoing other cardiac surgery.
Common Pitfalls
  • Failure to see scar particularly sub-mammary scars in females.
  • Candidate can not differentiate mitral from aortic valve prosthesis.
  • Failure of the candidate to recognize signs of IE.
Examiner Instructions
  • Examine this patient's cardiovascular system
  • Examine this patient's precordium
  • Listen to this patient's heart
This patient has a sternotomy scar and an audible metallic click heard loudest in the mitral area coinciding with S1. There are no signs of heart failure or IE. He has a metallic mitral valve, which seems to be functioning well.
Examiner: What are the different types of prosthetic heart valves?
  • Metallic:
    • Caged ball valve: For example, Starr-Edwards valve
    • Tilting disc valve: For example, Medtronic Hall valve
    • Bileaflet valves: For example, St. Jude valve
    • On-X mechanical valve (lower thrombosis rate)
  • Biological valves (Bioprosthetic).
Examiner: What are the advantages of the On-X mechanical valves over other mechanical valves?
Candidate: On-X mechanical valves are made purely of carbon which makes them having smooth surface and lower thrombosis rate. The INR target in these types of valves is therefore lower than other mechanical valves (1.5–2.0). This in turn lowers the bleeding from anticoagulation.
Examiner: What are the clinical features indicating a malfunctioning metallic valve?
  • Signs of heart failure
  • Absence of normal valve closure sound
  • Development of abnormal regurgitant murmur (normal metallic valve may be associated with systolic murmurs)
  • Signs of infective endocarditis.
Examiner: What are the complications of metallic valves?
  • Metallic valve malfunction leading to heart failure or sudden death
  • Infective endocarditis
  • Systemic embolization
  • Microangiopathic hemolysis
  • Anticoagulation-related bleeding.
Examiner: If this patient presents with anemia, name 2 possible causes?
Candidate: Warfarin-related bleeding or microangiopathic hemolysis due to destruction of red blood cells (RBCS) on the metallic valve.
Examiner: What are the advantages and disadvantages of the metallic and bioprosthetic valves?16
  • Metallic valves have a lower rate of valve dysfunction such as paravalvular leak and therefore are more durable
  • Bioprosthetic valves do not require anticoagulation
  • Survival is equal
Examiner: How long do artificial valves usually last?
  • Metallic valve: Up to 30 years
  • Bioprosthetic valve: Up to 15 years.
Examiner: In which group of patients is a bioprosthetic valve recommended?
Candidate: A bioprosthetic valve although less durable does not require anticoagulation. Therefore, it is recommended for patients aged 65-year-or above, patients at risk of bleeding from warfarin and patients who may be poorly compliant with warfarin therapy.
Examiner: How would you manage this patient?
  • Patient counseling and education
  • Complete blood count (CBC), bilirubin and urine microscopy
  • Echocardiography to assess valve function
  • Anticoagulation (warfarin is recommended)
  • IE prophylaxis: Patients with prosthetic heart valves are high risk group and should receive IE prophylaxis (see infective endocarditis section)
  • Counseling regarding pregnancy (risk of valve dysfunction, heart failure, thromboembolism and warfarin use).
Examiner: What is the target INR level in mechanical valves?
Candidate: Aortic valve INR is 2–3; mitral valve INR is 2.5–3.5.
Examiner: When would you consider the addition of Aspirin to Warfarin?
Candidate: Those patients with high risk factors such as atrial fibrillation, venous thromboembolism, left ventricular dysfunction, and a hypercoagulable state.
Examiner: How would you manage anticoagulation for major surgical procedures?
Candidate: Warfarin is stopped 5 days prior to surgery to achieve INR < 1.5 at the time of operation and bridging anticoagulation using unfractionated heparin or low molecular weight heparin is given until the day of surgery. Warfarin is started 24 hrs after surgery following confirmation of hemostasis.
Common Pitfalls
  • Failure to recognize signs of Down's syndrome
  • Misdiagnosing VSD as MR
Examiner Instructions
  • Examine this patient's cardiovascular system
  • Examine this patient's precordium
  • Listen to this patient's heart and tell me the diagnosis.
This patient has a loud harsh holosystolic murmur associated with a systolic thrill heard best in the left 4th intercostal space. There are no signs of pulmonary hypertension and no cyanosis. The patient has VSD.
Examiner: What are the types of VSD?
  • Perimembranous: Most common type
  • Supracristal: May be associated with AR
  • Muscular
  • Posterior.
Examiner: How does the size of a VSD correlate with the murmur?
Candidate: The smaller the size of VSD, the louder the murmur.
Examiner: What are the complications of VSD?
  • Pulmonary hypertension
  • Polycythemia
  • Eisenmenger complex.
Examiner: How would you manage this patient?
  • Serial echocardiography
  • Cardiac catheterization to quantify the net shunt
  • IE prophylaxis is not indicated if no cyanosis and no previous IE
  • Diuretic therapy and ACEI
  • Surgery.
Examiner: What are the indications of surgical repair in VSD?
  • The ratio of total pulmonary blood flow to total systemic blood flow QP/QS > 2
  • Prior history of infective endocarditis
  • Left ventricular volume overload
  • QP/QS >1.5 with PAP < two-third of systemic pressure
  • Presence of VSD and AR
Examiner: What does it mean if the murmur disappears in a patient with VSD?
Candidate: It means either the VSD closed (very rare after the age of 4 years) or the patient has developed Eisenmenger complex.18
Examiner: What are the clinical manifestations of Eisenmenger complex?
  • The holosystolic murmur disappears
  • Signs of pulmonary hypertensions and right heart failure
  • Cyanosis
  • Finger clubbing (Figure 1.6)
  • Polycythemia
Examiner: What is the treatment of choice of Eisenmenger complex develops?
Candidate: Heart-Lung transplantation
Common Pitfalls
  • Candidates miss the wide fixed splitting of S2
  • Candidates think that the cause of the ejection systolic murmur in ASD is the flow across the ASD shunt.
Examiner Instructions
  • This patient complains of exertional dyspnea, please listen to his heart
  • Examine this patient's heart.
Examiner: What are the types of ASD?
  • Ostium secondum: The most common type of ASD
  • Ostium primum: The second most common type of ASD. Usually associated with mitral valve abnormalities.
  • Sinus venosus: The least common.
Examiner: What are the auscultatory findings in ASD?
Candidate: An ejection systolic murmur in the pulmonary area and fixed wide splitting of S2.
Examiner: What causes the ejection systolic murmur in ASD?
Candidate: The systolic murmur heard in ASD is due to the increased flow across the pulmonary valve (functional stenosis) and not as a result of blood flow across the ASD shunt itself.
Examiner: Which murmur mimics that heard in ASD and how would you differentiate the two?
Candidate: Pulmonary stenosis also gives an ESM at the pulmonary area. However, fixed wide splitting of S2 occurs in ASD but not in PS.19
Examiner: If in addition to the ASD murmur, you hear a mid-diastolic murmur in this patient, what is the explanation?
Candidate: If a mid-diastolic murmur is heard in the tricuspid area, it is due to increased blood flow across the tricuspid valve because of a large ASD. If a mid-diastolic murmur is heard in the mitral area (mitral stenosis murmur) this is called “Lutembacher syndrome” which is a combination of ASD and mitral stenosis.
Examiner: What are the complications of ASD?
  • Pulmonary hypertension
  • Eisenmenger syndrome
Examiner: How would you manage this patient?
  • Echocardiography to assess the size of the shunt and the presence of pulmonary hypertension
  • Spontaneous closure in adults is unlikely (commonly happen in childhood)
  • Surgical closure is indicated in patients with significant shunts and patients who develop pulmonary hypertension and right ventricular overload.
Common Pitfalls
  • Failure to auscultate over the right chest when candidates cannot hear heart sounds on the left
  • Failure to recognize associated features of Kartagener's syndrome such as clubbing due to bronchiectasis
  • Examiner instructions
  • Examine this patient's cardiovascular system
  • Examine this patient's precordium
  • Listen to this patient's heart.
This patient has dextrocardia evidenced by an absent apex beat and heart sounds over the left side of the chest, which can be heard clearly over the right side. He also has finger clubbing, so I would like to examine the chest and ask him a few questions to confirm the diagnosis of Kartagener's syndrome.
Examiner: What conditions are associated with dextrocardia in adults?
  • Kartagener's syndrome: Characterized by the triad of situs inversus, paranasal sinusitis, and bronchiectasis
  • Congenitally corrected transposition of the great arteries (TGA)
  • The heterotaxy syndromes of asplenia and polysplenia20
Examiner: How would you manage this patient?
  • Take a history of cardiac symptoms, chronic cough or cardiac surgery in early life.
  • Chest X-ray
  • Echocardiography.
Common Pitfalls
  • Missing the presence of AF
  • Missing the features of hyperthyroidism as the cause of AF
  • Confusion regarding differentiating AF from multiple ventricular ectopic beats.
Examiner Instructions
  • Perform a general examination
  • Examine the heart
  • Examine this patient's pulse.
Examiner: What are the causes of AF?
  • M : Mitral stenosis
  • A : Alcohol
  • T : Thyrotoxicosis
  • C : CAD
  • H : Hypertension
Examiner: What simple bedside test differentiates AF from ventricular premature beats?
Candidate: Ask the patient to perform some exercise. Ventricular premature beats will reduce in frequency with exercise but AF will not.
Examiner: What do you mean by paroxysmal AF, persistent AF, permanent AF and lone AF?
  • Paroxysmal AF: Self-terminating
  • Persistent AF: AF that fails to terminate within 7 days
  • Permanent AF: AF that lasts for more than one year and failed cardioversion or not attempted
  • Lone AF: AF occurring in the absence of structural heart disease21
Examiner: How would you manage this patient?
  • Treat the underlying cause, e.g. thyrotoxicosis, mitral stenosis, alcohol
  • Rate control: Beta-blockers, diltiazem, digoxin, amiodarone
  • Rhythm control: Amiodarone, flecainide
  • Anticoagulation: Warfarin or the new oral anticoagulants: Dabigatran, rivaroxaban, apixaban.
  • AF ablation: Antrum pulmonary vein ablation, pulmonary vein antrum isolation, circumferential ablation.
  • Cardioversion: If AF < 48 hours and low risk for stroke
Examiner: What is the risk of stroke in nonvalvular AF?
Candidate: Around 5% per year.
Examiner: How do you assess (predict) the risk of stroke in nonvalvular AF?
Candidate: Using the CHA2 DS2-Vasc score
C (CHF points 1), H (hypertension points 1), A2 (age > 75 points 2), D (Diabetes points 1), S (stroke/TIA points 2), V (vascular disease “CAD, PVD” points 1), A (age 65–74 points 1), Sc (sex category female point 1)
Patients with AF and a score of 2 or more should be anticoagulated. Many patients with a score of 1 should be considered for oral anticoagulation. Aspirin can be used if anticoagulation is declined.
Common Pitfalls
  • Missing the signs of IE in patients with valvular lesions.
  • Failure to recognize the presence of stroke in a patient with IE.
Examiner Instructions
  • Examine the cardiovascular system.
  • Have a look at this patient's hands and then examine the heart.
Examiner: What are the signs of IE? And what are the mechanisms behind them?
  • Splinter hemorrhages (vascular phenomenon “septic emboli”)
  • Janeway lesions (vascular phenomenon “septic emboli”)
  • Roth spots (immune complex phenomenon)
  • Osler's nodes (immune complex phenomenon)
  • Finger clubbing (Figure 1.1)
Examiner: What organisms cause IE?
  • Streptococcus viridans
  • Staphylococcus aureus22
  • Staphylococcus epidermidis
  • Enterococcus
  • HACEK group (Hemophilus parainfluenzae and aphrophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella)
Examiner: What are the causes of culture negative endocarditis?
  • Certain organisms:
    • HACEK group
    • Bartonella
    • Coxiella
    • Chlamydia
    • Legionella
    • Brucella
  • Prior antibiotic use
  • Fungal endocarditis
Examiner: What is the significance of growing Streptococcus bovis in a blood culture?
Candidate: There is a significant association between the presence of Streptococcus bovis endocarditis and colonic neoplasia.
Examiner: How do you collect blood cultures in suspected endocarditis?
  • They should be collected prior to antibiotic use unless the patient is severely ill
  • Use strict sterile technique
  • Minimum number of cultures 3
  • Minimum amount of blood for each culture is 10 mL
  • Should be from separate veins
  • Should be at different times
  • Not necessarily during the fever.
Examiner: What criteria are used to diagnose IE?
Candidate: The modified Duke criteria: Two major and five minor criteria. The major criteria depend on the blood culture findings and evidence of endocardial involvement. The minor criteria involve the presence of a predisposing heart condition, fever, vascular phenomenon, immunological phenomena or a positive culture that does not meet major criteria.
  • Definite IE: 2 major, 1 major and 3 minor or 5 minor.
  • Possible IE: 1 major and 1 minor or 3 minor criteria.
Examiner: What are the complications of IE?
  • Local complications:
    • Valve abscess23
    • Heart failure
    • Valve dysfunction and destruction
  • Systemic complications:
    • Systemic embolization leading to stroke, cerebral abscesses, septic pulmonary emboli, disseminated abscesses in other organs and mycotic aneurysms
    • Immune complex phenomena: Glomerulonephritis, Osler's nodes and Roth spots
    • Severe sepsis or septic shock.
Examiner: What do you mean by mycotic aneurysms?
Candidate: Mycotic aneurysms result from septic embolization into the wall of the blood vessels. It can occur anywhere in the body but intracranial vessels are the most frequently involved with a poor prognosis.
Examiner: What is the sensitivity of transthoracic and transesophageal echocardiography in diagnosing IE?
  • Sensitivity of TTE is about 60%
  • Sensitivity of TEE > 90%
Examiner: What are the poor prognostic factors in IE?
  • Old age
  • Diabetes
  • Prosthetic valve IE
  • Presence of complications from IE
  • Staphylococcal IE
  • Fungal IE
  • Large vegetation's on echo
Examiner: What is the usual duration of therapy in IE?
Candidate: 4–6 weeks.
Examiner: What are the indications for surgery in IE?
  • Refractory heart failure or cardiogenic shock
  • Uncontrolled infection such as abscess formation, fistula or enlarging vegetation despite treatment
  • Prosthetic valve IE
  • Fungal IE
  • Multidrug resistant organism
  • Persistent fever and positive blood culture after 7–10 days
  • Large vegetation > 10 mm with systemic embolization
  • Very large vegetation > 15 mm24
Examiner: Can endocarditis occur due to noninfectious causes?
Candidate: Yes, vegetations on valves can occur due to other noninfectious conditions. This is called Nonbacterial thrombotic endocarditis or Marantic endocarditis. The causes are:
  • Malignancies
  • Libman Sack's endocarditis of SLE
  • Hypercoagulable states
Examiner: What features differentiate Marantic endocarditis from IE?
Candidate: Absence of fever and leukocytosis, absence of heart murmur, small size of the vegetation's on echocardiography
Examiner: How would you manage this patient?
  • CBC, C-reactive protein (CRP) erythrocyte sedimentation rate (ESR), rational functional tester (RFT)
  • Blood cultures (minimum 3)
  • Echocardiography (TEE better than TTE)
  • IV antibiotics (initially empiric combination, e.g. ampicillin and gentamicin or vancomycin, gentamicin and ciprofloxacin and then guided by culture result)
  • Surgery as mentioned above
  • Colonoscopy if blood culture grows Streptococcus bovis.
Examiner: What are the indications for antibiotic prophylaxis against infective endocarditis in patients with valvular heart disease?
Candidate: Indications of antibiotic prophylaxis depend on the type of valvular heart disease and the type of surgical procedure.
High-risk patients that need prophylaxis are:
  • Patients with prosthetic heart valves
  • Patients with previous IE
  • Cardiac transplant recipients with abnormal valve
  • Certain patients with congenital heart disease: Who have unrepaired cyanotic congenital heart disease or repaired congenital heart disease with residual defects adjacent to the prosthetic device or repaired congenital heart defect with prosthetic material placed during surgery (only for the first 6 months after surgery).
Procedures that require prophylaxis in the high-risk patients are:
  • Dental procedures requiring manipulation of the gingival, periapical region or perforation of the mucosa
  • Respiratory procedures that involve incision and biopsy of mucosa: Such as tonsillectomy, adenoidectomy, empyema drainage and bronchoscopy with biopsy (American but not European guidelines).
  • Skin surgery (American but not European guidelines).25
Examiner: Is prophylaxis needed before gastrointestinal tract (GIT) or genitourinary (GU) procedures?
Candidate: No.
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  1. Krishnan S, Eslick GD Streptococcus bovis infection and colorectal neoplasia: a meta-analysis. Colorectal Dis. 2014;16(9):672–80.
  1. Vahanian A, Alfieri O, Andreotti F, et al. Guidelines on the management of valvular heart disease (version 2012). Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC); European Association for Cardio Thoracic Surgery (EACTS), Eur Heart J. 2012;33(19):2451–96.
  1. Warnes CA, Williams RG, Bashore TM, et al. ACC/AHA 2008 Guidelines for the Management of Adults with Congenital Heart Disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2008;118(23):e714–833.
  1. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007;116(15):1736–54.