Print Friendly, PDF & Email

Common cardiovascular examination exam questions for medical finals, OSCEs and MRCP PACES

Click on the the example questions below to reveal the answers


Question 1.

What is the JVP?

  • The internal jugular vein (IJV) connects to the right atrium without any intervening valves. The pulsation of the right atrium therefore causes the column of blood in the IJV to rise and fall – this is called the the jugular venous pulse (JVP).
  • The jugular venous pressure (also called the JVP and often used interchangeably with the jugular venous pulse) is the height of this pulsation above the atrium.
  • The jugular venous pulse therefore provides an estimate of the central venous pressure (CVP) and hence the patient’s volume status and heart function.
  • Although an important part of the cardiovascular examination, clinical assessment of CVP using the JVP has poor sensitivity.
  • The usual JVP waveform looks like this:

See below for descriptions of the waveform

Question 2.

How do you measure the JVP?

  • To measure the JVP, position the patient at 45 degrees. Ask them to turn their head to the left and extend their neck gently backwards. It may be helpful to adjust the patient’s head into the correct position.
  • First measure the height of the JVP’s highest point in centimetres. This is the vertical height above the sternal angle at which a pulsation is observed in the internal jugular vein.
  • Look for the JVP along the course of the vein which travels from the earlobe, down the neck and into the chest, between the two heads of sternocleidomastoid.


  • A JVP of greater than 4cm above the sternal angle is said to be elevated.

Question 3.

What are the waves and descents of the JVP waveform?

  • The JVP has a subtle double pulsation which follows the pattern below:

  • The waves and descents of the JVP are:
  • A wave: right Atrial contraction [presystolic]
  • X descent: right atrial relaXation
  • C wave (not seen Clinically): bulging of the tricuspid valve into the right atrium [beginning of systole]
  • V wave: maximum Venous return [late systole]
  • Y descent: Right ventricular filling [diastole]

Question 4.

How can you differentiate the JVP from the carotid pulse?

  • The JVP rises with pressure on the liver (hepatojugular reflux)
  • The JVP is easily occludable
  • The JVP is not strongly pulsatile
  • The JVP has a double waveform, the carotid pulse is single

Question 5.

What is Kussmaul’s sign?

  • Kussmaul’s sign is a paradoxical increase in the JVP with inspiration. It can occur in any condition where right ventricular filling is restricted such as constrictive pericarditis or cardiac tamponade

Question 6.

What is the usual position of the apex beat?

  • The apex beat should be situated in the fifth intercostal space along the midclavicular line.
  • If the apex beat is impalpable here, move inferiorly and laterally.
  • Displacement of the apex in this direction suggests cardiomegaly.

Question 7.

Why might the apex beat be impalpable?

  • Hyperexpanded lungs: obstructive lung disease (e.g. COPD)
  • Reduced impulse: tamponade or restrictive pericarditis
  • Obesity
  • Dextrocardia (try palpating on the right)

Question 8.

What can you to to emphasise the apex beat?

  • If you are unable to feel the apex try rolling the patient further to the left to bring the heart closer to the chest wall. If there is still no beat palpable, try feeling on the right for dextrocardia.

Question 9.

What scars are common in a cardiac examination?

  • Median sternotomy scar: Previous valve surgery or a coronary artery by-pass graft (CABG)
    • If you see a median sternotomy scar look at the lower limbs. If there are scars on either calf this implies vein harvesting and therefore previous CABG as opposed to  valve surgery.
    • Note that a lack of scar on the calf does not definitely indicate that the patient has not had a CABG: veins may be harvested from the internal mammary arteries which are not visible.
  • Lateral thoracotomy scar (in mid-axillary line): previous thoracic surgery.
  • Inferior clavicle scar (and implant): cardiac pacemaker or defibrillator (usually on left)

Question 10.

How can you describe murmurs in a cardiovascular examination?

  • Murmurs should be described in terms of timing, site of greatest intensity, character, loudness, and radiation
  • The intensity of a murmur does not necessarily help in assessing the severity of the valve lesion, but a change in intensity can be important.

Question 11.

How is the loudness (intensity) of murmurs graded?

  • Grade 1: Heard by an expert in optimum conditions
  • Grade 2: Heard by a non-expert in optimum conditions
  • Grade 3: Easily heard, no thrill
  • Grade 4: Loud murmur, palpable thrill
  • Grade 5: Very loud murmur, often heard over a wide area, palpable thrill
  • Grade 6: Extremely loud, heard without a stethoscope

Question 12.

What is a third heart sound and what causes it?

  • A third sound is caused by passive filling of ventricles in systole
  • It happens in any condition where the artia are more full than they should be:
    • Volume overload
    • Mitral regurgitation
    • Aortic regurgitation
  • NB. An opening snap or myxoma polyp can be confused for a third sound

Question 13.

What is a fourth heart sound?

  • The fourth heart sound is caused by atrial contraction against a stiff left ventricle. Causes include:
    • Fibrosis (e.g. post-MI)
    • Hypertension
    • Aortic stenosis
    • HOCM

Question 14.

What does the splitting of heart sounds mean?

  • The second heart sound (S2) is composed of aortic and pulmonary valve closure (A2 and P2)
  • A2 usually occurs just before P2 as the aortic pressure is higher than pulmonary pressure so the valve snaps closed quicker. This difference in timings is referred to as splitting.
  • S2 is therefore physiologically slightly split
  • A2 gets closer to P2 during expiration
  • The loudness of P2 is a measure of pulmonary vascular resistance

Question 15.

What is wide or pathological splitting of heart sounds

  • Pathological splitting is when the physiological splitting (A2 before P2) is exaggerated. It can happen either if A2 occurs early or if P2 occurs late.
  • A2 earlier: (i.e. if blood leaves the left ventricle by other means, giving a very quick reduction in LV pressure)
    • Mitral regurgitation
    • VSD
  • P2 later: (i.e. high volume load or delay for mechanical reasons)
    • RBBB
    • Pulmonary stenosis
    • ASD

Question 16.

What is reverse splitting of the heart sounds?

  • Reverse splitting is when the aortic sound occurs AFTER the pulmonary sound. It can happen either if A2 occurs late or if P2 occurs early:
    • A2 later (delay LV contraction)
      • Aortic stenosis
      • HOCM
      • LBBB
      • RV pacing
    • P2 early (occurs if blood leaves the right ventricle by other means, giving a very quick reduction in RV pressure)
      • TR
      • PDA

Note that in modern medicine, splitting of heart sounds is rarely clinically relevant. Sadly it still appears in exams.

Question 17.

What are the cardiac causes of clubbing?

  • Congenital cyanotic heart disease
  • Atrial myxoma
  • Infective endocarditis

Question 18.

What are the risk factors for endocarditis?

  • Previous cardiac valve surgery
  • Previous infective endocarditis
  • Mitral valve prolapse with valve leakage
  • Abnormal valves (e.g. rheumatic fever and degenerative conditions)
  • Congenital heart disease

Question 19.

What are the signs of endocarditis?

  • Eyes: Roth spots
  • Hands: Osler’s nodes, Janeway lesions
  • Nails: splinter haemorrhages
  • Kidneys: haematuria
  • Abscess formation systemically from septic emboli

Question 20.


  • Observations
    • Wide pulse pressure
  • Palpation
    • Collapsing pulse
    • Displaced apex beat that is forceful in character (volume-loaded)
  • Auscultation
    • High-pitched early-diastolic murmur at LLSE loudest with patient leant forward
    • Commonly ejection systolic flow murmur due to large stroke volume
    • Occasionally an Austin-Flint murmur
      • Mid-diastolic murmur caused by regurgitant jet impinging on anterior mitral cusp
  • Eponymous signs of aortic regurgitation
    • Quinke’s sign: nail bed capillary pulsation
    • De Musset’s sign: Head nodding
    • Corrigan’s sign: Visible carotid pulsation
    • Duroziez’s sign: To-and-fro femoral artery bruit
    • Traub’s sign: Pistol-shot femorals

Question 21.

What are the causes of mitral regurgitation?

  • Chronic
    • Structural
      • Degenerative
      • Rheumatic heart disease
      • Congential: Marfans and Ehlers-Danloss
    • Functional
      • Dilated cardiomyapathy
      • Secondary to aortic valve disease
    • Mitral prolapse (mid-systolic click and late systolic murmur)
      • Happens in 4% population. Click moves earlier with valsalva.
      • Common in women, thyroid, E-D, Marfans, pseudoxanthoma elasticum.
      • Endocarditis prophylaxis not indicated (PT 2012)
  • Acute
    • MI: papillary muscle or chordate tendineae rupture
    • Endocarditis

Question 22.

What are the causes of aortic stenosis?

  • Calcific valve disease
    • Most common – inflammatory calcification of the valve in the elderly
  • Congenital bicuspid valve
    • 1-2% (familial 9% but sporadic). 1-2% of these need surgery
  • Rheumatic fever
  • Supravalvular aortic stenosis

Question 23.

How can you grade the severity of aortic stenosis?

  • Clinical signs of severity of aortic stenosis:
    • Small volume pulse
    • Slow-rising pulse
    • Narrow pulse pressure
    • Prolonged murmur blocking out the second heart sound
      • No other signs correlate with severity, in particular loudness of murmur is NOT correlated with severity of AS
  • Echocardiographic signs of severity of aortic stenosis are in the table below:
Degree of aortic stenosis Mean gradient  – from Gorlin formula (mmHg) Aortic valve area
(normal 3-4 cm2)
Mild <25 >1.5
Moderate 25 – 50 1.0 – 1.5
Severe >50 < 1.0
Critical >70 < 0.6

Question 24.

When is a valve replacement indicated in aortic stenosis?

  • Symptomatic patients with severe AS (gradient>50)
  • Asymptomatic with:
    • Need for CABG
    • LV dysfunction (EF<40%)
    • Abnormal BP in response to exercise
    • VT
    • Valve area <0.6cm

Question 25.

What are the indications for a pacemaker?

  • Persisting symptomatic bradycardia
  • Certain heart blocks:
    • Complete AV block
    • Mobitz type II AV block
    • Persistent AV block post anterior myocardial infarction.
  • Suppression of resistant tachyarrhythmias
  • Improving synchronisation and therefore heart function in some cardiomyopathies including HOCM

Question 26.

What are the different types of pacemaker?

  • Unipolar pacemakers
    • Permanent leads are either unipolar (where a single contact is made with the heart) or bipolar.
    • Unipolar systems (ventricular) are used in cases where AV conduction is likely to return.
    • When there is normal AV conduction and a sinoatrial (SA) disorder then the pacing wire is situated in the right atrium.
  • Dual-chamber pacemakers
    • Electrodes are in both the right atrium and the right ventricle.
    • Maintains a more physiological relationship between atrial and ventricular contraction Allows the paced heart to follow the increase in sinus rate that occurs during exercise.
  • Dual-site atrial pacing
    • Some pacing systems have two atrial leads, one in the right atrial appendage and the other either at or in the coronary sinus
    • The ventricular lead is in the right ventricle.
  • Biventricular pacemakers
    • Pacemaker leads are placed in the right atrium, right ventricle and left ventricle.
    • Used in severe heart failure where there is abnormal intraventricular conduction (most often evident as left bundle branch block) which causes deranged ventricular contraction or dyssynchrony.
  • Implantable cardioverter defibrillators
    • Treat a cardiac tachyarrhythmia directly.
    • The device senses a ventricular rate that exceeds the programmed cut-off rate and the ICD can then either:
      • Performs cardioversion/defibrillation, or…
      • Pace rapidly for a number of pulses, usually around 10, to attempt pace-termination of a ventricular tachycardia.

Question 27.

What do pacemaker letters and codes mean?

  • Most pacemakers have three letter denominations only (e.g. “VVI”) though modern pacemaker can have up to five letters:
  • Letter 1: chamber that is PACED (A = atria, V = ventricles, D = dual-chamber).
  • Letter 2: chamber that is SENSED (A = atria, V = ventricles, D = dual-chamber, 0 = none).
  • Letter 3: the pacemaker’s RESPONSE to a sensed event (T = triggered, I = inhibited, D = dual – T and I, R = reverse).
  • Letter 4: rate-responsive features; an activity sensor (eg, an accelerometer in the pulse generator) in single or dual-chamber pacemakers detects bodily movement and increases the pacing rate according to a programmable algorithm (R = rate-responsive pacemaker).
  • Letter 5: anti-tachycardia facilities

Example: A pacemaker in VVI mode denotes that it paces and senses the ventricle and is inhibited by a sensed ventricular event. The DDD mode denotes that both chambers are capable of being sensed and paced.

Question 28.

What are the causes of heart failure

  • Cardiac
    • Preload issues
      • Fluid overload
    • Pump failure
      • Muscle
        • Myocerdial infarction
        • Myoarditis
        • Cadiomyopathy
      • Restriction
        • Undilated cardiomyopathy (e.g. Hypertrophic)
        • Constrictive pericarditis
        • Cardiac tamponade
      • Acute arrhythmia
      • Valve lesion
      • Congenital (e.g. ASD/VSD giving L-to-R shunt)
    • Afterload issues
      • Severe hypertension
      • Pulmonary embolus
      • Dissection
    • High output
      • Anaemia, thyrotoxicosis, haemochromatosis, Paget’s, septic shock
  • Non-cardiac
    • ARDS (essentially increased afterload)
    • PE
    • Pulmonary hypertension from any lung pathology (cor pulmonale)
    • Renal failure and renal artery stenosis

Question 29.

How do you treat heart failure?

  • Conservative
    • Lose weight
    • Restrict salt
    • Fluid restrict
    • Bed rest for exacerbations (reduced demand on heart), but encourage low-level endurance (20-30 mins waling or cycling) 3-5 times per week
  • Medication
    • To improve prognosis:
      • ACE-1
      • Beta-block
      • Aspirin
      • Statin
      • Spironalactone (if severe)
    • In addition
      • Digoxin can help prevent hospitalisations but increases risk of arrhythmia
      • Diuretics decrease oedema but have no effect on mortality

Question 30.

What medications improve prognosis in left ventricular failure?

  • Ramipril
    • Improves prognosis in LVF (as does enalipril – CONSENSUS trial)
    • Reduces mortality by 20%
      • NB ATII are the same as ACE-I
      • And ATII (candesartan) prevents readmission in people with an LVEF of >40% (CHARM study)
    • Also improves morbidity and mortality in high risk patients with normal LV function. (CAD, CVD, PVD, DM)
      • Rise in creatinine of 20% is reasonable
  • Bisoprolol or carvedilol
    • Improves symptoms, exercise tolerance, time in hospital and reduces mortality in heart failure of any cause
      • MERIT and CIBIS 2 (used metoprolol, Bisoprolol and carvedilol)
      • Basically no difference between them (BMJ 2013)
    • Can give acutely
    • Good especially in NYHA 1-2 failure, less in 3-4
  • Spironolactone
    • Reduces mortality in end-stage cardiac failure and prevents sudden cardiac death (if NYHA II-IV) e.g. if EF<35%
    • From RALES trial: RR reduction 0.7 (at 25mg)
  • Aspirin
  • Statin

Note that none of the other treatments (e.g. diuretics and digoxin) have been shown to improve mortality.

Further questions about the cardiovascular exam


Click here for all the clinical examinations: how to examine, what to look for and how to present your findings