Question 1

Relate the surface ECG to the events of the cardiac cycle (60% of mark).

Describe how the PR, QRS and QT intervals may be prolonged by the action of drugs.

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College Answer

The first part of the question is best answered by a labelled and annotated diagram of the
ECG with the pressure events of the cardiac cycle. Common errors included mistiming of the
ECG with the pressure waveform. The second part of the question could be answered in a
tabular format such as:
 

Interval Drug Mechanism
PR Digoxin

Increases refractory period
of AV node probably by
increased vagal activity

QRS

Tricyclic antidepressants

Quinidine like effect,
decreasing sodium influx
into cells

     


References:
Power and Kam 2nd edition p129 – 131
Stoelting and Hillier 4th edition p403, 409, 415

Discussion 

"A labelled and annotated diagram of the ECG with the pressure events of the cardiac cycle"  could  probably look like a bit like this. Even though theoretically one could actually draw the pressure waveforms here, a careful reading of the question will reveal that events is what they were interested in, i.e. the highlights only.  

relationship of the surface ECG to the events of the cardiac cycle

If one needed to expand on this:

  • The SA node fires well into late diastole, and this is not represented on the surface ECG, nor is the propagation of signal along the internodal tracts.
  • The P wave is produced as the atrial muscle depolarises. The right atrium contracts first.
  • At the end of the P wave, the left atrium finally contracts. The end of diastole occurs during the PR interval.
  • The R wave is generated by ventricular depolarisation, and its peak corresponds to the beginning of systole (specifically, of isovolumetric contraction). 
  • The T-wave represents ventricular repolarisation, and corresponds to the phase of decreased contraction (slow ejection).  The peak of the T-wave correlates reasonably well with the onset of diastole, i.e the closure of the aortic valve.

Describe how the PR, QRS and QT intervals may be prolonged by the action of drugs:

Note that prolonged was all the examiners were interested in. Thus:

Interval Drug Mechanism
PR β-blockers Increase refractory period of AV node by decreasing sympathetic stimulus
Digoxin Increases refractory period
of AV node probably by increased vagal activity
QRS Flecainide, lignocaine, phenytoin, tricyclic antidepressants Blockade of the fast voltage-gated sodium channels; slowed Phase 0 with a diminished magnitude
QT Amiodarone, sotalol Prolonged Phase 3 by acting as potassium channel antagonists 

References

Yates, Christopher, and Alex F Manini. "Utility of the electrocardiogram in drug overdose and poisoning: theoretical considerations and clinical implications." Current cardiology reviews 8.2 (2012): 137-151.

Antoni, H. "Electrophysiology of the heart at the single cell level and cardiac rhythmogenesis.Comprehensive Human Physiology. Springer, Berlin, Heidelberg, 1996. 1825-1842.

Pinnell, Jeremy, Simon Turner, and Simon Howell. "Cardiac muscle physiology." Continuing Education in Anaesthesia, Critical Care and Pain 7.3 (2007): 85-88.

Harley, Alexander, C. Frank Starmer, and Joseph C. Greenfield. "Pressure-flow studies in man. An evaluation of the duration of the phases of systole.The Journal of clinical investigation 48.5 (1969): 895-905.

Braunwald, Eugene, ALFRED P. FISHMAN, and AndrÉ Cournand. "Time relationship of dynamic events in the cardiac chambers, pulmonary artery and aorta in man." Circulation research 4.1 (1956): 100-107.