MCAT topics → Integrative Organ Systems → Cardiac Cycle and Pressure-Volume Relationships

Cardiac Cycle and Pressure-Volume Relationships

MCAT trap: Reverses which valve closures produce S1 versus S2. S1 is caused by AV valve closure (mitral + tricuspid) at the start of systole, and S2 by semilunar valve closure (aortic + pulmonic) at the start of diastole.

The cardiac cycle is one of the highest-yield topics on the MCAT — and it tests whether you can track two things simultaneously: what the valves are doing and how ventricular volume is changing. One specific misconception to flag early: stroke volume is read off the volume axis (horizontal width) of a PV loop, not off the pressure axis — students who confuse these consistently pick wrong answers on data interpretation questions. The exam hits this topic at multiple levels: straightforward recall of valve states during each phase, quantitative calculation of stroke volume and cardiac output, and data interpretation from pressure-volume loops presented in passages. If you can mentally 'walk around' a PV loop and narrate the physiology at each corner, you're in good shape.

What makes this topic tricky is that students often conflate pressure changes with volume changes. During isovolumetric contraction, for example, pressure is spiking dramatically — but volume isn't moving at all because both sets of valves are shut. Students also routinely flip S1 and S2, associating the sounds with the wrong valve closures, which then cascades into wrong answers about timing and clinical findings. The MCAT loves to present a passage about a patient with a valve pathology and ask you to reason about which heart sound is altered and why — so the causal logic matters, not just the label.

The pressure-volume loop is a high-yield data interpretation target. The exam will hand you a PV loop — possibly a shifted one from a drug intervention or pathology — and ask you to extract stroke volume, identify EDV or ESV, or reason about what changed. Students who haven't practiced reading the loop often try to read stroke volume off the pressure axis (peak pressure) rather than the volume axis (horizontal width). Build the habit now: stroke volume lives on the x-axis, not the y-axis.

Common misconceptions

Common mistake
Wrong: S1 is caused by semilunar valve closure and S2 by AV valve closure.
Right: S1 is caused by AV valve closure (mitral + tricuspid) at the start of systole, and S2 by semilunar valve closure (aortic + pulmonic) at the start of diastole.
S1 and S2 are named in chronological order: S1 comes first, at the beginning of systole, and it's caused by the AV valves (mitral and tricuspid) snapping shut to prevent backflow into the atria. S2 comes at the end of systole when the ventricles start to relax and the semilunar valves (aortic and pulmonic) close to prevent backflow from the great vessels. A useful anchor: 'S1 = start of systole = AV closure; S2 = start of diastole = semilunar closure.' Reversing these will cost you points on valve pathology questions.
Common mistake
Wrong: During isovolumetric contraction, the aortic valve is open so blood pressure can build.
Right: During isovolumetric contraction, both AV and semilunar valves are closed, so pressure rises with no change in volume.
During isovolumetric contraction, the ventricle is a closed box — both the AV valves (already shut because ventricular pressure just exceeded atrial pressure) and the semilunar valves (not yet open because ventricular pressure hasn't exceeded aortic/pulmonic pressure) are closed simultaneously. This is why pressure rises steeply while volume stays flat on the PV loop. The aortic valve doesn't open until ventricular pressure exceeds aortic pressure, which happens at the end of isovolumetric contraction, not during it.
Common mistake
Wrong: Paradoxical splitting of S2 occurs because the pulmonic valve closes abnormally late.
Right: Paradoxical splitting occurs because the aortic valve closes abnormally late (e.g., in LBBB), so on inspiration the normal early pulmonic closure merges with the delayed aortic closure, narrowing rather than widening the split.
Normal S2 splitting occurs on inspiration because increased venous return delays pulmonic valve closure, widening the gap between aortic and pulmonic closure sounds. Paradoxical splitting is the opposite pattern — the split narrows on inspiration — and it happens because the aortic valve is closing abnormally late (e.g., in left bundle branch block, the left ventricle contracts late, so the aortic valve closes late). On inspiration, the pulmonic valve's normal delay moves it closer to the already-delayed aortic closure, paradoxically narrowing the split. Delayed pulmonic closure causes wide (physiologic or fixed) splitting, not paradoxical splitting.
Common mistake
Wrong: Stroke volume is read from the pressure-volume loop as the maximum pressure reached.
Right: Stroke volume is the horizontal width of the PV loop, equal to EDV minus ESV.
On a PV loop, the x-axis is volume and the y-axis is pressure. Stroke volume is the difference between end-diastolic volume (EDV, the rightmost point of the loop) and end-systolic volume (ESV, the leftmost point), so it's read as the horizontal width of the loop, entirely on the volume axis. Peak pressure is a measure of afterload and contractility, not stroke volume. If you ever catch yourself reading a value off the pressure axis to answer a stroke volume question, stop — you're on the wrong axis.
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What the exam tests

  1. Know the four phases of the cardiac cycle — isovolumetric contraction, ejection, isovolumetric relaxation, and filling — and which valves (AV vs. semilunar) are open or closed during each phase.
  2. Read a pressure-volume loop and correctly identify EDV (right edge), ESV (left edge), and stroke volume (horizontal width of the loop), even when the loop is shifted by a drug or disease state.
  3. Calculate stroke volume using SV = EDV − ESV, and calculate cardiac output using CO = SV × HR, given numerical values in a passage or question stem.
  4. Identify what causes S1 (closure of mitral and tricuspid valves at the start of systole) and S2 (closure of aortic and pulmonic valves at the start of diastole), and apply this to reason about the timing and clinical significance of each sound.

Can you avoid these mistakes?

A patient has a left bundle branch block. On auscultation, the split between A2 and P2 is narrower during inspiration than expiration. Which valve is closing abnormally late, and why does inspiration narrow rather than widen the split?
On a pressure-volume loop, a drug shifts the end-systolic pressure-volume relationship (ESPVR) line leftward and upward. EDV stays the same. Does stroke volume increase or decrease, and how do you read that off the loop?
During which phase of the cardiac cycle are both the mitral valve and the aortic valve simultaneously closed? What is happening to ventricular pressure and volume during this phase?
A patient has an EDV of 130 mL, an ESV of 50 mL, and a heart rate of 70 bpm. Calculate stroke volume and cardiac output. If contractility increases and ESV drops to 30 mL with EDV unchanged, what is the new cardiac output?

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