Pressure-Volume (P-V) Loops

The Basic Loop - Four Phases

Phase 1: Ventricular Filling (Diastole) - bottom limb, left to right

• Mitral valve opens; LV fills passively from the LA
• Volume rises from ~50 mL (end-systolic volume, ESV) to ~120-140 mL (end-diastolic volume, EDV)
• Pressure rises only slightly (from ~5 to ~10 mmHg) because the ventricle is highly compliant during diastole
• This low-pressure, high-volume filling segment defines the end-diastolic pressure-volume relationship (EDPVR)

Phase 2: Isovolumetric Contraction - right vertical limb, upward

• Mitral valve closes (end of diastole); all valves are now closed
• LV pressure rises sharply from ~10 to ~80 mmHg with no change in volume
• Contraction continues until LV pressure exceeds aortic diastolic pressure, when the aortic valve opens

Phase 3: Ventricular Ejection - top limb, right to left

• Aortic valve opens; blood is ejected into the aorta
• Volume falls from EDV (~120 mL) to ESV (~50-70 mL) - the difference is stroke volume (SV)
• Pressure rises to its peak (~130 mmHg at point E) then falls as ejection decelerates
• The loop touches the end-systolic pressure-volume relationship (ESPVR) at the top-left corner - this is point 3 in the Costanzo diagram

Phase 4: Isovolumetric Relaxation - left vertical limb, downward

• Aortic valve closes; all valves are closed again
• Pressure falls precipitously from ~100 mmHg to ~7 mmHg with no change in volume
• When LV pressure falls below LA pressure, the mitral valve opens and the cycle repeats

Key Boundaries: ESPVR and EDPVR

• The ESPVR is approximately linear; its slope (E_es) is the most load-independent index of myocardial contractility available in vivo
• The EDPVR is exponential; increased stiffness (lower compliance) shifts it upward and to the left
• The triangular area between ESPVR and EDPVR to the left of the loop represents potential energy remaining in the ventricle wall at end-systole

Stroke Work and Energetics

• The area enclosed by the P-V loop = stroke work (SW) - the external mechanical work done by the LV per beat (in mmHg·mL, convertible to joules)
• Total mechanical energy = SW (kinetic, the loop area) + potential energy (triangular area to the left) = pressure-volume area (PVA)
• Myocardial oxygen consumption (MVO₂) is linearly proportional to PVA: MVO₂ = α·PVA + β (Suga's model)
• The SW/PVA ratio is an index of mechanical efficiency

Effects of Loading and Contractility Changes

Increased Preload

• Loop shifts right - larger EDV, larger SV
• Peak pressure is maintained; the loop is wider
• ESPVR and afterload (aortic pressure) are unchanged

Increased Afterload

• Loop shifts upward - higher systolic pressure, but reduced SV (less ejection)
• EDV may increase slightly (Frank-Starling compensation)
• Loop becomes taller and narrower

Increased Contractility (positive inotrope)

• ESPVR rotates upward/left (steeper slope = higher E_es)
• SV increases at any given preload; the loop is taller and wider
• ESV decreases (more complete emptying)

Decreased Contractility (HFrEF)

• ESPVR rotates downward/right (shallower slope)
• LV dilates (compensatory increase in preload/EDV)
• SV may be preserved initially but at a much higher filling pressure
• The loop shifts right along a normal EDPVR

Decreased Compliance (HFpEF)

• EDPVR shifts upward - higher pressure for any given volume
• Loop height increases (more pressure required to achieve same EDV)
• EF may be preserved but filling pressures are elevated

LV-Arterial Coupling

• Optimal coupling (maximum efficiency): E_es / E_a ≈ 1
• In HFrEF: E_es/E_a < 1 (depressed contractility + vasoconstriction)
• In HFpEF: E_es/E_a > 1 (systolic stiffening predominates)
• EF is mathematically related to this ratio: EF/(1-EF) = E_es/E_a, so an EF of 50% implies ideal coupling

Indices of Contractility Derived from P-V Analysis

Clinical Applications (from Kaplan Cardiac Physiology)

• Cardiac anesthesia monitoring: Conductance catheters or real-time TEE allow P-V framework application intraoperatively
• HFrEF vs HFpEF distinction: A depressed ESPVR slope (reduced E_es) signals HFrEF; an upward-shifted EDPVR signals HFpEF. Both can coexist
• Myocardial ischemia: Regional ischemia causes the P-V loop to tilt and collapse - aneurysmal systolic lengthening appears as a rightward expansion of the loop in the ischemic zone
• Pericardial disease: Tamponade shifts the EDPVR upward (parallel shift), restricting filling
• Volatile anesthetics: Cause dose-dependent depression of E_es and reduction of SW/PVA, worsening LV-arterial coupling at higher MAC concentrations
• Vasodilators in HFrEF: Reduce E_a, restore E_es/E_a toward unity, increase SV; effective because the ESPVR slope is shallow
• Vasodilators in HFpEF: Cause marked hypotension with minimal SV gain because the steep ESPVR means the ventricle is resistant to volume unloading

Diastolic Function Assessment with P-V Loops

1. Isovolumic relaxation - quantified by the time constant τ (tau); increased τ = delayed relaxation (ischemia, hypertrophy)
2. Early filling - assessed by the rate of EDPVR traversal; impaired relaxation or reduced compliance slows this
3. Atrial systole - the "A" loop in LA P-V analysis; contributes 15-25% of LV stroke volume under normal conditions