Cardiac PhysiologyMarch 28, 20265 min read

Q-Bank Breakdown: Cardiac cycle (pressure-volume loops) — Why Every Answer Choice Matters

Clinical vignette on Cardiac cycle (pressure-volume loops). Explain correct answer, then systematically address each distractor. Tag: Cardiovascular > Cardiac Physiology.

You’re going to see pressure–volume (PV) loops in a lot of disguises on Step 1 and Step 2: murmurs, shock, inotropes, valves, afterload/preload changes, and “what happens to stroke volume?” questions. The trick isn’t memorizing one loop—it’s learning how to interrogate every answer choice using the same few rules.

Tag: Cardiovascular > Cardiac Physiology


The Clinical Vignette (Q-bank style)

A 68-year-old man with long-standing hypertension presents with acute crushing chest pain and diaphoresis. ECG shows ST-segment elevations in the anterior leads. He becomes hypotensive. A bedside echocardiogram shows new left ventricular systolic dysfunction.

Which of the following changes is most likely present on the patient’s left ventricular pressure–volume loop?

A. Increased end-systolic volume and decreased ejection fraction
B. Decreased end-systolic volume due to increased contractility
C. Increased end-diastolic volume due to decreased afterload
D. Increased stroke volume due to increased preload
E. Increased left ventricular end-diastolic pressure due to improved lusitropy

Correct Answer: A. Increased end-systolic volume and decreased ejection fraction

Acute MI → decreased contractility (negative inotropy).

On the PV loop, decreased contractility:

  • Decreases slope of ESPVR (end-systolic pressure–volume relationship; the “contractility line”)
  • Causes the ventricle to generate less pressure at any given volume
  • Leads to less ejection → higher end-systolic volume (ESV)
  • Therefore stroke volume decreases and ejection fraction decreases

High-yield definitions

  • Stroke volume (SV): SV=EDVESVSV = EDV - ESV
  • Ejection fraction (EF): EF=SVEDV=EDVESVEDVEF = \frac{SV}{EDV} = \frac{EDV-ESV}{EDV}

So if contractility drops, ESV rises, SV falls, and EF falls—exactly answer A.


PV Loop Basics You Must Be Able to “Read” Quickly

The 4 phases (counterclockwise)

  1. Ventricular filling (mitral valve open): volume increases at low pressure
  2. Isovolumetric contraction (both valves closed): pressure increases at constant volume
  3. Ejection (aortic valve open): volume decreases while pressure first rises then falls
  4. Isovolumetric relaxation (both valves closed): pressure drops at constant volume

Anchors that show up in answer choices

  • EDV (rightmost point): end of filling (preload proxy)
  • ESV (leftmost point): what’s left after ejection (strongly affected by afterload & contractility)
  • ESPVR slope: contractility
  • Loop width: stroke volume
  • Area inside loop: stroke work

Why Each Distractor Is Wrong (and what it’s testing)

B. Decreased end-systolic volume due to increased contractility

This describes increased contractility, the opposite of an acute anterior MI.

If contractility increases:

  • ESPVR slope increases (steeper line)
  • ESV decreases (more complete emptying)
  • SV and EF increase

Classic causes: dobutamine, digoxin, exercise, sympathetic stimulation.

Exam tip: If they mention MI with cardiogenic shock, think down-and-right shift of the end-systolic point (higher ESV, lower systolic pressure).


C. Increased end-diastolic volume due to decreased afterload

This is internally inconsistent physiology and a common trap.

  • Decreased afterload (e.g., vasodilators) usually allows more ejection, so ESV decreases, SV increases.
  • It does not directly cause EDV to increase. EDV is more about preload (venous return) and filling time/compliance.

What can happen indirectly: if SV rises, the next beat’s EDV might change depending on venous return and reflexes—but PV loop questions nearly always treat EDV as preload-driven.

Key association:

  • ↓ afterload → leftward shift of end-systolic point (↓ ESV) and wider loop (↑ SV)

D. Increased stroke volume due to increased preload

Increasing preload can increase stroke volume (Frank–Starling), but it doesn’t match this patient.

In acute systolic failure, the ventricle is weak:

  • For a given preload increase, the SV rise is blunted
  • And in cardiogenic shock, you’re not “helpfully” increasing preload; you’re failing to eject.

Also, PV-loop-wise, increased preload primarily:

  • Increases EDV (rightward shift of the loop’s right border)
  • Often increases SV (wider loop), unless contractility is impaired enough that ESV rises disproportionately.

How to think on test day:
If the stem screams “pump failure,” the primary PV change is ↓ contractility → ↑ ESV, ↓ SV, not “preload went up and fixed it.”


E. Increased LV end-diastolic pressure due to improved lusitropy

This is a double wrong turn.

  • Improved lusitropy means better relaxation (diastolic function improves).
  • Better relaxation/compliance tends to lower LVEDP for a given volume (or allow more filling with less pressure).

In MI (especially ischemia), you can actually get worse lusitropy:

  • Impaired relaxation → higher LVEDP and pulmonary congestion
  • But that would be due to worsened, not improved, lusitropy.

High-yield link:

  • Diastolic dysfunction (↓ compliance) shifts the EDPVR up/left → higher diastolic pressures at smaller volumes.

The “PV Loop Rulebook” (What each intervention does)

ChangeEDVESVSV (width)ESPVR slopeClassic examples
↑ Preload~no changefluids, venoconstriction
↓ Preload~no changehemorrhage, nitrates
↑ Afterload~no changeHTN, aortic stenosis, phenylephrine
↓ Afterload~no changeACE inhibitors, hydralazine
↑ Contractility~dobutamine, exercise
↓ Contractility~MI, HFrEF, beta-blockers (acute)

~ means “no primary change” in the simplified PV-loop model.


Rapid-Fire Classic Patterns (USMLE favorites)

1) Aortic stenosis (AS): “Afterload problem”

  • ↑ afterload↑ ESV, ↓ SV
  • Often ↑ LV systolic pressure markedly
  • Murmur: systolic crescendo–decrescendo radiating to carotids

2) Mitral regurgitation (MR): “No true isovolumetric phases”

  • Regurg begins when pressure rises → blood can move into LA
  • Isovolumetric contraction and relaxation are blunted/absent
  • Often ↑ EDV (volume overload), ↓ effective forward SV

3) Aortic regurgitation (AR): “Big EDV, wide pulse pressure”

  • ↑ EDV (volume returns during diastole)
  • No true isovolumetric relaxation (leak during diastole)
  • Bounding pulses, wide pulse pressure

4) HFrEF (systolic failure): “Contractility line down”

  • ↓ contractility↑ ESV, ↓ SV, often ↑ EDV over time (compensation)

Step-Style Takeaways (What to say out loud to yourself)

  • Contractility changes tilt ESPVR. MI → less tiltESV up.
  • Afterload changes move the end-systolic point. Afterload up → ESV up.
  • Preload changes move the right border. Preload up → EDV up.
  • If an answer claims improved relaxation raises LVEDP, it’s backwards.

Mini Self-Check (10 seconds)

In acute anterior MI:

  • Contractility: down
  • ESPVR slope: down
  • ESV: up
  • SV and EF: down

If an answer choice says those words in that order, it’s almost certainly correct.