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Cardiac examination

  • Inspection
  • Palpation
  • (Percussion is not a routine in CVS exam)
  • Auscultation
  • Peripheral then central

Exposure and Positioning

  • Proper positioning and exposure
  • Sit up at 45 degrees
  • Relaxed (both you and the patient)
  • Stand back and look at the patient - resist the temptation to touch them
    • Scars - midstenotomy scars most common (e.g. CABG); thoracotomy rare
    • Most valve replacements are done by midline
    • Left thoracotomy = valvotomy, ligation of patent ductus arteriosis, descending aorta
    • Pacemaker scars


  • General state
  • Cyanosis
  • Respiratory rate and effort
  • Drips, cardiac monitor
  • Abnormal pulsations
    • Neck Praecordium Abdomen Neck, Praecordium, Abdomen
  • Scars
    • Mid sternotomy, pacemaker, defibrillator, thoracotomy

Peripheral examination

– Do not spend too much time on it

  • Head
    • Pallor
    • Cyanosis
    • Low cardiac output state
  • Upper limbs
    • Clubbing - congenital cyanotic heart disease (note LR shunt doesn't cause clubbing - but Eisenmenger's syndrome on top of VSD does - you get RL shunt because of pulmonary hypertension)
      • Clubbing only in toes without fingers (Differential clubbing: patent ductus arteriosus with Eisenmenger's; because the ductus arteriosus connects to the aorta distal to the subclavian artery, so you don't get cyanosis/clubbing in the fingers, only in toes)
  • Cyanosis
  • Lower limbs
    • Oedema

-The 3 things that you need to spend time on…

  • Pulse
    • Radial pulse
    • Radial femoral delay
    • Pulse rate
    • Regularity
    • Pulse character
      • Important
      • Assess in large arteries
        • Carotid, brachial
      • Volume
        • Anacrotic pulse
          • slow rise, low volume, often caused by aortic stenosis
        • Collapsing pulse
          • rapid downstroke, often due to aortic regurgitation (is severe if you can detect via pulse) - blood falls back into the ventricle, rapid downstroke
      • Upstroke and down stroke
      • Single peak or double peak
        • Bisferiens pulse - bifid, double-peak pulse; mixed aortic valve disease (stenosis + regurgitation)
  • Jugular venous pressure
  • Blood pressure
    • Important
    • Ask for it


  • Look at both sides
  • Vertical distance to angle of Louis
  • Determine character
  • Should be visible, but unable to feel pulsation (compared
    • See double flicker
    • Fills up from above if pressure applied
    • Changes with respiration
      • Increased in expiration

Note: two peaks per a wave JVP1.PNG

  • a= atrial contraction (corresponds to P wave)
  • c = tricuspid valve closure
  • x = atrial relaxation (while ventricles are undergoing systole - systolic pressure not transmitted through AV valve until end of ventricular systole). Between x and v = atrial filling, pressure rises
  • v = ventricular contraction
  • y = ventricular relaxation (v-y = ventricular filling) y = rapid ventricular filling in early ventricular diastole

Overall, this explains the bifid pulsation in the

3 phases of diastole: early rapid ventricular filling, diastasis - not much flow across mitral valve (AV valve partially close), late diastole and atrial contraction (mitral valve opens again as pressure gradient returns with atrial contraction)

  • dominant a wave
    • tricuspid stenosis
    • pulmonary stenosis
    • pulmonary hypertension
  • dominant v wave
    • tricuspid regurgitation
  • cannon a wave
    • complete heart block
    • VT with retrograde atrial conduction or AV dissociation
    • Paroxysmal nodal tachycardia with retrograde atrial conduction

Blood Pressure

  • Magnitude
  • pulse pressure
    • Wide pulse pressure = AR


  • Palpation
  • Whole hand on the chest wall
  • Apex
  • Parasternal edge
  • Base of the heart

What are you feeling for

  • Apex beat
    • Character
    • Volume loaded
    • Pressure loaded
      • increased pressure load = mitral/aortic regurg.
    • Diffuse
  • Thrills
    • Indicative of murmurs
  • Palpable heart sounds
  • Parasternal heave


  • High pitch (diapgragm) and low pitch sounds (bell)
  • Pitch depends on velocity of blood flow
  • High pitch sounds
    • Diaphragm
  • 1st and 2nd heart sounds
  • AS, MR, valve clicks, AR, TR
  • Low pitch sounds
    • Bell
    • 3rd and 4th heart sounds (gallop rhythm)
    • Mitral stenosis murmur
      • At apex with bell
  • Time murmurs with carotid pulse to tell if diastolic or systolic
    • louder or softer can give list of DDx
    • Ejection systolic murmur should radiate to carotid bruit

  • Aortic and mitral regurgitation are high pitched (pressure gradient determines velocity and hence pitch)
  • Blood speed out of heart = 1m/s. Pressure gradient determined by what chambers the valve separates
  • Mitral regurgitation speed = 5.5 m/s (work it out from first principles below) = high velocity, use diaphragm
    • Systole, pressure gradient 120mmHg, divide by 4, then square it (using formula below)
  • Aortic regurgitation velocity is also diaphragm - very fast
  • Mitral stenosis - pressure gradient of 10 is VERY high for mitral stenosis, therefore use bell
    • Cutoff for low vs high velocity = 3 m/s
  • ∂P = 4v^2

Auscultation - hints

  • Bell and diaphragm at apex and lower left sternal border
  • Diaphragm at base of heart
  • Do not be distracted by the most abnormal sounding noise
  • Approach systemically
  • Timing utmost importance
  • Students usually getting timing wrong
  • Diastolic murmur most difficult
  • Concentrate on 1st and 2nd
    • Each heart sound - is it split/normal?
  • Get your timing right
  • Feel the pulse to time yourself
  • Is the 1st heart sound normal?
  • Is the 2nd heart sound normal?
  • Is the second heart sound normally split
  • Is there any added heart sounds or clicks?
  • Is there any systolic murmur?
  • Characteristics of systolic murmur
  • Pansystolic
  • Mid or late systolic
  • Ejection systolic
  • Radiation
  • Is there diastolic murmur?
  • Early diastolic
  • Mid diastolic
  • High or low pitch
  • The location of the loudest intensity is a poor guide to the anatomical defect
  • Carotid bruit
    • Bell
  • Chest
  • Abdomen
    • Also look for pulsatile masses and ascites
  • Put your findings into a consistent and coherent analysis
  • Practice makes perfect

When he listens to a student presenting, he can tell they're wrong because they're contradicting each other

Ankle Oedema

  • Ankle oedema is a sign
  • Ankle swelling is a symptom
  • Ankle oedema does not equal heart failure
  • Ankle oedema does not always need diuretics therapy
  • Sometimes diuretics may make things worse!


  • Why do people get ankle oedema?
  • How do people get ankle oedema?
  • Think of the balance between the forces that push fluid out into the interstitial space and the forces that keep them in
  • Humans are destined to develop ankle oedema at some stage !!!
  • We are fighting a losing battle all the time!
  • Systemic Causes
  • Do not forget local causes

Congestive Heart Failure

  • Pathophysiological state in which the heart is unable to pump blood at a rate commensurate with the requirements of the metabolising tissues.
  • Causes:
  • Systolic dysfunction
  • Normal systolic function - diastolic dysfunction
  • Arrhythmias
  • Valvular heart disease
  • Ischaemic heart disease
  • Hypertension
  • Extra-cardiac diseases

Squeezing of the pump is a necessary but not sufficient condition for the pump to work. Also need good filling, good rate/timing, good valves. Most common cause is systolic dysfunction - poor squeeze.

Adaptive Mechanisms

When there is an insult to the heart, it will first try to make up for the loss. The patient doesn't develop failure straight away unless overwhelming insult (in which case cardiogenic shock). Ways to compensate:

  • Frank Starling Mechanism - Increased preload helps sustain cardiac performance - with a curve that flattens at the top (moving the preload to the right, the contractility increases). Increase preload = help sustain systolic performance
  • Myocardial hypertrophy ± cardiac chamber dilatation � augments mass of contractile tissue
  • Activation of neurohumoral systems-esp adrenergic and renin-angiotensin-aldosterone systems
    • These two systems are the key to heart failure

Compensatory mechanisms

  • Chamber dilatation
    • LaPlace's law: the pressure/tension on the wall is proportional to the wall of the heart; hence the demand for oxygen/nutrients is higher, therefore more afterload that needs to be dealt with by the heart
  • Chamber hypertrophy
    • More mouths to feed in ischaemic heart disease
  • Increased heart rate (more sympathetic tone)
    • Increased demand for nutrients
  • Increased contractility (sympathetic, and Frank-Starling)
    • Flogging a tired horse -- causes it to die quicker. Responsible for heart failure deaths
  • Increased blood volume (RAS)
    • Congestion, workload on heart, ankle swelling, pulmonary oedema
  • These are all counter productive in the long run.


  • More complex than a simple pump problem.
    • Includes activation of neurohumoral system, vasoconstriction, increases afterload on the heart, feeding back, causing more dysfunction, which eventually causes arrhythmia and sudden death
  • Positive ionotropes = increas
  • ACEI, ARB, Diuretics, Aldosterone inhibitors good to treat heartfailure because unflogging dead horse
    • In the past: used contractility agents, but this results in more deaths

Conceptualising heart failure

  • Cardiac cycle is a complete cycle, to be sustainable
  • Blood flowing in one direction with the heart as a pump with valves located at important points
  • Blood flows down pressure gradients. No pressure gradient = death.
    • If downstream pressure is high, then upstream has to be still higher for flow to happen
  • Pressure falls everywhere in the cycle except in RV and LV where the pumps are. No pump = no circulation.
  • Mitral stenosis
    • LV doesn't fill properly, dries up
    • LA pressure rises, dilates
    • Then the pressure in lungs must be higher, transmits all the way back the line: LA dilatation, pulmonary congestion, right ventricular dysfunction

Approach to heart failure

  • Heart failure is a syndrome
  • Not a diagnosis - need the cause so you can manage it
  • Need to find out the cause
  • Treatment
    • Directed to the primary cause
    • General treatment of heart failure
  • Aims of treatment
    • Primary cause
    • Symptomatic treatment
    • Improve prognosis
    • Treat precipitating factors
      • Anaemia
      • Renal failure
      • Sleep disordered breathing
      • Obesity