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The cardiac cycle

Seven phases, the pressure–volume loop, the heart sounds and the CVP waveform — all lined up against the ECG that triggers them.

What each ECG feature triggers

The ECG is the electrical cause; everything mechanical follows it. Fix this mapping first.

ECG	Electrical event	Mechanical consequence
P wave	Atrial depolarisation	Atrial contraction — the "atrial kick"
PR interval	AV nodal delay	Allows ventricular filling to complete before systole
QRS	Ventricular depolarisation	Ventricular contraction begins → S1 at the end of QRS
ST segment	Plateau (phase 2), ventricles fully depolarised	Ejection
T wave	Ventricular repolarisation	Relaxation → S2 at the end of the T wave

The two heart sounds

S1 — beginning of systole. Ventricular pressure exceeds atrial pressure, so the AV valves (mitral + tricuspid) close. Coincides with the end of the QRS. It marks the start of isovolumetric contraction.
S2 — end of systole. Aortic and pulmonary valves close at the end of the T wave. It marks the start of isovolumetric relaxation and therefore the beginning of diastole.
So: S1 → IVC, S2 → IVR. Systole is the interval between them.

The phases, in order

Lettered to match the pressure–volume loop below: A mitral closure, B aortic opening, C aortic closure, D mitral opening.

1

Late diastole — passive filling (D → A)

AV valves open, semilunar valves closed. About 80% of ventricular filling is passive. The P wave then triggers atrial contraction — the atrial kick — supplying the last portion and completing EDV ≈ 120–130 ml.
2

Isovolumetric contraction (IVC) (A → B)

Triggered by the QRS. All four valves are shut, so volume is constant while pressure rises steeply. Begins as LV pressure exceeds LA pressure, closing the mitral valve (S1). Ends at about 80 mmHg, when the aortic valve opens. Produces the c wave of the CVP trace.
3

Rapid ejection (B → C)

Aortic and pulmonary valves open. Corresponds to the ST segment. Peak LV pressure about 120 mmHg; roughly 70% of the stroke volume is ejected in this early phase, the remainder during reduced ejection.
4

Point C — end of ejection

The T wave (repolarisation) is underway. ESV ≈ 50 ml, so SV = EDV − ESV ≈ 70 ml.
5

Isovolumetric relaxation (IVR) (C → D)

Ventricle relaxes, pressure falls, all valves shut again. Aortic valve closure gives S2 and the dicrotic notch on the arterial trace. Ends when LV pressure falls below atrial pressure — the mitral valve opens and diastole proper begins. Ends with the v wave of the CVP trace.
6

Rapid then reduced filling (D onward)

Mitral and tricuspid open, ventricles fill rapidly down the pressure gradient, then more slowly (diastasis).
7

Atrial systole — the last third

Contributes about 10% of filling at rest, but up to 40% at high heart rates when diastole is short. This is why losing the atrial kick (AF) is so poorly tolerated in stiff ventricles — AS, HCM, diastolic dysfunction.

The pressure–volume loop

Read it anticlockwise from A. The four corners are the four valve events.

Point	Valve event	Marks
A	Mitral closes (LV pressure > LA)	S1 · start of IVC · end of diastole
B	Aortic opens (LV > aortic, ~80 mmHg)	Start of ejection
C	Aortic closes (LV < aortic)	S2 · dicrotic notch · start of IVR · ESV ≈ 50 ml
D	Mitral opens (LA > LV)	Start of filling

120–130 ml

EDV

50 ml

ESV

~70 ml

stroke volume

55–70%

ejection fraction

How the loop changes

↑ Preload — loop widens to the right, SV rises (Frank–Starling).
↑ Afterload — loop gets taller and narrower; ESV rises, SV falls.
↑ Contractility — the end-systolic pressure–volume relationship steepens; ESV falls, SV rises.
The area inside the loop is stroke work.

The numbers

Chamber / event	Pressure	Note
Atrial pressure during atrial contraction	0–5 mmHg	Left atrial slightly higher than right
Aortic valve opens	~80 mmHg	i.e. at the aortic diastolic pressure
Peak LV systolic pressure	~120 mmHg	Maximum LV pressure the ventricle can generate is far higher (~300 mmHg)
Peak RV systolic pressure	20–25 mmHg	Pulmonary circulation is a low-pressure system
LV end-diastolic pressure	5–12 mmHg	Rises in failure and in stiff ventricles

One figure to be careful with

Your page lists "max LV pressure 300 mmHg" next to "peak LV systolic 120 mmHg". Both are right but they are different quantities: 120 mmHg is the normal working peak, while ~300 mmHg is the theoretical maximum isovolumetric pressure the LV can develop against a closed outflow. Only the 120 figure is the one to quote for a normal cycle.

The CVP / JVP waveform

Three positive waves (a, c, v) and two descents (x, y). Each maps onto a phase above.

Wave	Cause	Abnormalities
a wave	Atrial contraction	Absent in AF. Cannon a waves in complete heart block / AV dissociation. Large a waves in tricuspid stenosis, pulmonary hypertension
c wave	Tricuspid bulging into the atrium during isovolumetric contraction	—
x descent	Atrial relaxation in mid-systole, with downward pull of the valve ring	Exaggerated in constrictive pericarditis and tamponade. Reduced or absent in tricuspid regurgitation and RV dysfunction
v wave	Rapid atrial filling against a closed tricuspid, ending as IVR finishes	Giant v waves in tricuspid regurgitation
y descent	Early ventricular filling once the tricuspid opens	Exaggerated in constrictive pericarditis. Blunted in tamponade

Your sticky-note summary, in one block

v = rapid filling of the right atrium against a closed tricuspid valve. ↑ v = tricuspid regurgitation (giant v waves).
x descent = right atrial relaxation, in mid-systole. ↑ x = constrictive pericarditis. ↓ or absent x = tricuspid regurgitation / RV dysfunction — hence "x is absent in tricuspid incompetence".
y descent = early ventricular filling. ↑ y = constrictive pericarditis. ↓ y = cardiac tamponade.
Sequence against the ECG: a follows P, c follows R, v follows T.

The classic discriminator

Constrictive pericarditis: prominent x AND y descents — the "M" or "W" pattern.
Tamponade: prominent x descent but blunted y — filling is impeded throughout diastole, so early filling cannot occur.
Tricuspid regurgitation: the x descent is lost and replaced by a giant fused c-v wave.

Preload, afterload & contractility

Three independent levers on stroke volume. Each moves the PV loop in its own characteristic way.

	Definition	Effect of increasing it
Preload	Ventricular fibre stretch at end-diastole — clinically related to EDV / EDP	↑ EDV → ↑ SV via Frank–Starling, within physiological limits
Afterload	The load the ventricle ejects against — for the LV, aortic pressure and SVR	↑ ESV → ↓ SV
Contractility	Intrinsic force generation, independent of loading	↓ ESV → ↑ SV and ↑ EF

	Systolic failure	Diastolic failure
Primary problem	↓ contractility, impaired ejection	Impaired relaxation, ↓ compliance
Ejection fraction	↓	Preserved / normal
LV end-systolic volume	↑	Normal or ↓
Filling pressure	↑	↑↑ despite impaired filling

What changes during exercise

Heart rate ↑↑ and contractility ↑ — the dominant contributors.
Stroke volume ↑, LVESV ↓, LVEDV maintained at a higher filling level.
Cardiac output ↑↑, approaching ~20 L/min in strenuous exercise (higher still in trained athletes).
Oxygen consumption ↑ substantially — and because the myocardium already extracts ~70% of delivered oxygen at rest, the extra demand must be met almost entirely by increased coronary flow.

One arithmetic check

Your page records SV as about 80 mL, but with EDV 120 and ESV 50 the arithmetic gives 70 mL. EF is then 70/120 ≈ 58%. All three figures are approximate normals, so quote EDV 120 · ESV 50 · SV 70 · EF 55–70% as an internally consistent set.

Built from handwritten pages IMG_0982–0985, plus the cardiovascular add-on from Lung_Volumes_and_Cardio_EDAIC_Updated.pdf.