Question 7(p.2)

College Answer

The main points expected were the determinants of myocardial oxygen supply. These include
arterial oxygen content and coronary blood flow. Coronary blood flow depends on coronary
perfusion pressure and coronary vascular resistance and that most left coronary blood flow
occurs in diastole. Tachycardia reduces diastolic time and hence left coronary blood flow. In
comparison blood flow in the right coronary artery is continuous both in systole and diastole
and is little affected by heart rate. A correctly labelled diagram of left and right coronary
blood flow attracted extra marks. Unfortunately most diagrams were inaccurate, not labelled
and had no units on the axes. Systolic compression particularly reduces blood supply to the
left ventricular subendocardium which is most susceptible to ischaemia. Extra marks were
given for describing metabolic autoregulation, the high oxygen extraction, explaining that
oxygen supply cannot be increased by increasing oxygen extraction in the coronary
circulation and describing the driving pressure differences in both coronary arteries in
systole and diastole.

A description of the determinants of myocardial oxygen demand was also required (e.g. left
ventricular, preload, contractility, afterload and tachycardia This part of the question was
particularly poorly answered.

Discussion

When thinking about the effects of tachycardia, one does not immediately think of coronary artery anatomy. And if "the main points expected were the determinants of myocardial oxygen supply",  a better question would have asked directly, "describe the determinants of myocardial oxygen supply". Those minor gripes aside, the question "how does myocardial oxygen consumption change with increased workload" sounds like something a CICM trainee should have a good grasp of.

A helpful way of creating headings for this answer would have been to separate the question into supply and demand, list the factors determining each, and then briefly mentioning how they are affected by tachycardia. What follows was devised as an exhaustive list, for trainees to check their own written answers agains. It is not a "model answer", as nobody could be expected to reproduce all of the points over the time allotted to each SAQ in the written paper. This also demonstrates the limitations of the question: one cannot simply ask "explain human cardiac physiology in ten minutes" and then complain that it was "poorly answered". 

• Myocardial oxygen consumption is:
  • Calculated as (coronary blood flow × arteriovenous O₂ difference)
  • Expressed as the oxygen extraction ratio (which is usually 75%, i.e. high)
  • The  implication of this is that the myocardium cannot achieve an increase in oxygen delivery by increasing the extraction ratio, and instead needs to increase blood flow to meet increasing demand.
• Myocardial oxygen consumption  is determined by:
  • Heart rate is the main determinant
  • Preload is a minor contributor (decreases during tachycardia)
  • Contractility is a major contributor (may increase during tachycardia)
  • Afterload is a major contributor:
    • (may increase in tachycardia if it is accompanied by other autonomic phenomena
  • Cost of electrical conduction:  thought to be a minimal contributor, but this will also increase during tachycardia
  • Basal cost of cardiac metabolism, and the factors which affect it, which are:
    • Temperature (which may increase cardiac oxygen consumption if it is associated with an increased heart rate, eg. when the patient is febrile)
    • Drugs, some of which may cause tachycardia as well as an alteration in cardiac metabolism
  • Thus, overall, the effect of tachycardia is to increase myocardial oxygen demand, and the most important determinant is the heart rate 
• Myocardial oxygen supply is determined by:
  • Oxygen content of the blood, which is not affected by tachycardia in a normal individual
  • Coronary blood flow, which is determined by:
    • Coronary perfusion pressure: difference between aortic and ventricular pressure 
      • This is higher in the right ventricle than in the left;
      • i.e. right coronary perfusion pressure will be greater because the right ventricular chamber pressure is lower
    • Coronary vascular resistance, which is affected by:
      • Metabolic autoregulatory activity eg.  in reponse to ischaemia and hypoxia 
      • Autonomic control eg. sympathetic vasoconstriction
      • Systolic compression: compression by contracting LV
      • Pharmacological agents: eg. GTN and dipyridamole 

The "correctly labelled diagram of left and right coronary blood flow" would have probably expected something like this, reproduced from the  6th edition of Barash's Clinical Anesthesia. An alternative to this official image is also offered.

An important feature to point out is that the upper half (where the aortic waveform is) represents pressure over time, whereas the lower half represents flow. That could be a costly labelling mistake.  Also, the x-axis on the non-canonical diagram is labelled with events of the cardiac cycle rather than with seconds, and there is solid rationale for this. No matter which time intervals you decide to memorise, they will likely be inaccurate (as the values depend considerably on the heart rate and which textbook the examiners have been reading) and pointless (because the exact numbers don't really reveal any additonal understanding of the physiological concepts, whereas the events of cardiac cycle do). Thus, the time scale values should probably be omitted from the trainee's exam diagrams, as it would be inadviseable to reproduce something in the exam which you know is both inaccurate and pointless. 

Duncker, Dirk J., and Robert J. Bache. "Regulation of coronary blood flow during exercise." Physiological reviews 88.3 (2008): 1009-1086.

MJ Kern MJ and MJ Lim, “Chapter 24: Evaluation of Myocardial and Coronary Blood Flow and Metabolism,” in Grossman & Baim's Cardiac Catheterization, Angiography, and Interventions, pp. 505–544, 8th edition (2013)

Spieckermann, P. G., and H. M. Piper. "Oxygen demand of calcium-tolerant adult cardiac myocytes." Basic research in cardiology 80 (1985): 71.

Engelman, Richard M., et al. "The metabolic consequences of blood and crystalloid cardioplegia." Circulation 64.2 Pt 2 (1981): II67-74.

Mayr, A., W. Pajk, and W. Hasibeder. "Oxygen Supply and Consumption in Tissues." Sepsis and Organ Dysfunction. Springer, Milano, 2000. 43-48.