The Cardiac Cycle: Filling, Contraction and the Wiggers Diagram

Pressure-volume loops, valve timing, heart sounds S1–S4, preload, afterload, and contractility explained with the Wiggers diagram — plus clinical correlations to heart failure in dogs and cats.

Introduction: The Heart as a Sequential Pump

The cardiac cycle is the sequence of mechanical and electrical events that occurs from the beginning of one heartbeat to the beginning of the next. It is a story of precise timing: valves must open and close at exactly the right moments; pressure gradients must reverse in milliseconds; and the atria and ventricles must alternate between contraction and relaxation with metronomic regularity. When this choreography fails — when a valve leaks, when the myocardium stiffens, when the conduction system misfires — heart failure ensues.

This article walks you through the seven phases of the cardiac cycle using the Wiggers diagram — the most information-dense graph in cardiovascular physiology — and the pressure-volume loop, which distils ventricular performance into a single closed curve. We then connect these concepts to clinical practice: what the heart sounds mean, how preload and afterload determine stroke volume, and what happens when the system fails.

The Seven Phases of the Cardiac Cycle

Phase 1: Atrial Systole — The 'Atrial Kick'

The cardiac cycle begins with atrial depolarisation (the P wave on ECG). Approximately 0.1 seconds later, the atria contract, generating a small pressure rise — the 'a' wave on the atrial pressure tracing. Atrial contraction pushes the final 15–25% of ventricular filling volume into the ventricles. In normal dogs, this 'atrial kick' is modest; but in animals with impaired ventricular relaxation (diastolic dysfunction), the atrial contribution can rise to 30–40% of end-diastolic volume — explaining why cats with hypertrophic cardiomyopathy (HCM) decompensate catastrophically when they fibrillate and lose atrial transport.

Phase 2: Isovolumetric Contraction

Ventricular systole begins. As the ventricles contract, intraventricular pressure rises rapidly. When LV pressure exceeds LA pressure, the mitral valve closes → S1 (first heart sound — 'lub'). For a brief period (~30–50 ms), ALL valves are closed: the mitral valve is shut (ventricular pressure > atrial pressure) but the aortic valve has not yet opened (ventricular pressure < aortic pressure). The ventricle contracts against a closed chamber — volume is constant but pressure rises steeply. This is isovolumetric contraction.

Phase 3: Rapid Ejection

When LV pressure exceeds aortic diastolic pressure (~80 mmHg in a normotensive dog), the aortic valve opens. Blood is ejected rapidly into the aorta — approximately 70% of the stroke volume is ejected in the first third of systole. Aortic pressure rises to its peak (systolic pressure). Ventricular volume decreases rapidly.

Phase 4: Reduced Ejection

As systole continues, the pressure gradient between the ventricle and aorta narrows, and ejection slows. Ventricular repolarisation begins (the T wave on ECG). The aortic pressure tracing shows a gradual decline. At the end of ejection, the volume remaining in the ventricle is the end-systolic volume (ESV) — normally ~30–40% of end-diastolic volume.

Phase 5: Isovolumetric Relaxation

Ventricular repolarisation is complete. The ventricle begins to relax. When LV pressure falls below aortic pressure, the aortic valve closes → S2 (second heart sound — 'dub'). The brief backflow of blood against the closed aortic valve cusps creates the dicrotic notch (incisura) on the aortic pressure tracing. For a brief period, ALL valves are again closed: the aortic valve is shut (aortic pressure > ventricular pressure) but the mitral valve has not yet opened (ventricular pressure > atrial pressure). The ventricle relaxes against a closed chamber — isovolumetric relaxation.

Phase 6: Rapid Filling

When LV pressure falls below LA pressure, the mitral valve opens. Blood that accumulated in the atria during ventricular systole rushes into the ventricles. In normal hearts, this rapid filling phase accounts for 70–80% of ventricular filling. An audible third heart sound (S3) during this phase indicates rapid filling into a non-compliant ventricle — pathological in small animals.

Phase 7: Reduced Filling (Diastasis)

The pressure gradient between atria and ventricles equilibrates, and filling slows to a trickle. In animals with slow heart rates (horses, large-breed dogs), diastasis is prolonged and accounts for a significant fraction of diastole. At fast heart rates (cats, small dogs), diastasis is abbreviated or absent. The cycle then repeats with the next atrial systole.

The Wiggers Diagram: Everything on One Page

Carl Wiggers' 1915 diagram is the most information-dense graph in cardiovascular physiology. On a shared time axis (typically 0.8 seconds for a dog at 75 bpm), it plots:

• Left ventricular pressure (scale: 0–120 mmHg) — the dominant waveform.
• Left atrial pressure (scale: 0–15 mmHg) — showing a, c, and v waves.
• Aortic pressure (scale: 0–120 mmHg) — showing systolic peak, dicrotic notch, and diastolic run-off.
• Left ventricular volume (scale: ~60–140 mL for a 25 kg dog) — showing filling and ejection.
• Electrocardiogram (lead II) — showing P wave, QRS complex, and T wave.
• Phonocardiogram — showing S1, S2, and pathological S3/S4.

The Atrial Pressure Waves: a, c, v

• 'a' wave = Atrial contraction — pressure rises as the atrium contracts against the closed AV valve.
• 'c' wave = AV valve closure — the closed AV valve bulges back into the atrium as ventricular pressure rises (isovolumetric contraction).
• 'v' wave = Venous return during ventricular systole — blood continues to enter the atria from the great veins while the AV valves are closed, gradually raising atrial pressure.

In mitral regurgitation, the 'v' wave is dramatically amplified — a large volume of blood is ejected backward into the left atrium during ventricular systole, producing a giant 'v' wave (sometimes called 'cv' or 'regurgitant' wave) that can reach 50–60 mmHg in severe cases. This is readily visible on a pulmonary artery wedge pressure tracing and is a hallmark of severe mitral regurgitation.

Heart Sounds: Listening to the Cycle

In horses, an S3 and even an S4 can be normal findings in fit, athletic animals with large, compliant ventricles. The large stroke volume of the equine heart (~800–1000 mL) produces audible filling sounds that would be pathological in a dog or cat. Always interpret heart sounds in a species-specific context.

The Pressure-Volume Loop: Ventricular Performance in One Curve

Constructing the PV Loop

A pressure-volume (PV) loop is a closed curve that plots left ventricular pressure (y-axis) against left ventricular volume (x-axis) throughout one cardiac cycle. Time is implicit — the loop is traced counterclockwise: filling (bottom), isovolumetric contraction (right side), ejection (top), isovolumetric relaxation (left side).

Preload, Afterload, Contractility — The Three Determinants of Stroke Volume

The PV loop framework allows us to visualise the three factors that determine stroke volume:

• Preload (EDV): An increase in preload (e.g., volume loading, venoconstriction) shifts the right side of the loop rightward → EDV increases → SV increases (Frank-Starling mechanism).
• Afterload (aortic pressure): An increase in afterload (e.g., systemic hypertension) shifts the top of the loop upward → the ventricle must generate higher pressure before the aortic valve opens → ejection shortens → SV decreases.
• Contractility: An increase in contractility (e.g., sympathetic stimulation, dobutamine) shifts the ESPVR line (end-systolic pressure-volume relationship) upward and leftward → for any given EDV, the ventricle ejects to a smaller ESV → SV increases.

Clinical Correlations: Heart Failure through the PV Loop Lens

Systolic Heart Failure (HFrEF) — Dilated Cardiomyopathy in Dogs

In dilated cardiomyopathy (DCM), the ventricle is large, thin-walled, and poorly contractile. The PV loop shifts RIGHTWARD (dilated ventricle) and has REDUCED WIDTH (decreased stroke volume) and REDUCED HEIGHT (lower developed pressure). The ESPVR line is depressed (reduced contractility). The EDV is massive but the ESV is also large — ejection fraction falls below 30–40%. Clinically: weak pulses, S3 gallop, systolic murmur (secondary mitral regurgitation from annular dilation), and signs of low cardiac output.

Diastolic Heart Failure (HFpEF) — Hypertrophic Cardiomyopathy in Cats

In hypertrophic cardiomyopathy (HCM), the ventricle is thick-walled, stiff, and poorly compliant. The PV loop is NARROWER (small ventricular cavity) but has NORMAL HEIGHT and NORMAL WIDTH — ejection fraction is preserved (>50%). However, the filling portion of the loop (bottom, D→A) is shifted UPWARD — the ventricle fills at higher pressures because of reduced compliance. The end-diastolic pressure-volume relationship (EDPVR) is steeper. Clinically: normal systolic function on echo, but elevated left atrial pressure → pulmonary oedema → respiratory distress. The atrium dilates in response to chronically elevated filling pressures, providing the substrate for atrial thrombosis and arterial thromboembolism (ATE, the 'saddle thrombus').

Mitral Regurgitation — Volume Overload

In mitral regurgitation, blood leaks backward into the LA during systole. The PV loop LOSES its isovolumetric phases — as soon as ventricular pressure rises above LA pressure, blood flows backward through the incompetent valve. There is NO true isovolumetric contraction (the mitral valve does not fully close) and NO true isovolumetric relaxation. The loop becomes more rectangular with less distinct corners. The left ventricle faces a dual afterload — ejecting forward into the aorta AND backward into the LA — which increases stroke work dramatically. Over time, compensatory eccentric hypertrophy → progressive annular dilation → progressively worsening regurgitation (the 'mitral regurgitation begets mitral regurgitation' cycle).

Pressure-Volume Loop Analysis in Common Cardiac Diseases

Aortic Stenosis — Pressure Overload (Afterload Increase)

In aortic (subvalvular) stenosis — the commonest congenital heart defect in large-breed dogs (Boxers, Golden Retrievers, Newfoundlands) — the left ventricle must generate supranormal systolic pressure to overcome the stenotic orifice. The PV loop: TALLER (higher peak systolic pressure — sometimes >250 mmHg vs. normal 120 mmHg), NARROWER (slightly reduced stroke volume), and shifted RIGHTWARD (concentric hypertrophy → reduced chamber compliance → elevated filling pressures). The ESPVR line is normal (contractility is initially preserved) but the ventricle works against massively increased afterload. The area inside the loop (stroke work) is markedly increased → concentric hypertrophy (sarcomeres added in parallel) → eventually decompensation to systolic failure.

Mitral Regurgitation — Volume Overload (Preload Increase)

In chronic mitral valve disease (Cavaliers, small-breed dogs), the incompetent mitral valve allows regurgitation during systole → the left atrium receives blood from BOTH the pulmonary veins AND the regurgitant jet. The LA dilates to accommodate the volume. The LV faces a REDUCED afterload because the regurgitant pathway offers a low-resistance 'escape' from the high-pressure chamber. The PV loop: there is NO TRUE isovolumetric contraction (as soon as LV pressure > LA pressure, regurgitation begins) and NO TRUE isovolumetric relaxation. The loop is distorted — more rectangular, with the isovolumetric corners rounded. The ventricle ejects a large TOTAL stroke volume (forward + regurgitant) but the FORWARD stroke volume may be normal for years. Eventually the chronic volume overload → eccentric hypertrophy → progressive annular dilation → worsening regurgitation → congestive heart failure.

Restrictive Cardiomyopathy — Stiff Walls, Small Space

Restrictive cardiomyopathy (seen in cats, occasional in dogs) is characterised by severe diastolic dysfunction with relatively preserved systolic function. The ventricular walls are infiltrated with fibrous tissue → massively reduced compliance → the EDPVR line is dramatically STEEP → a small increase in volume produces a large increase in pressure. The PV loop is NARROW (small chamber) and TALL (normal systolic pressure) but shifted UPWARD — the filling pressures are elevated from the start. Clinically: severe diastolic heart failure → giant left atrium → arterial thromboembolism. Differentiate from HCM by echocardiography — normal wall thickness in restrictive disease.

Echocardiographic Correlates of the Cardiac Cycle

Echocardiography allows REAL-TIME visualisation of the cardiac cycle — you can watch the mitral valve open and close, the ventricle fill and empty, and the myocardium thicken and thin. Understanding the echo correlates of each phase of the cardiac cycle dramatically accelerates your ability to interpret echo studies.

M-Mode: Time on the X-Axis, Depth on the Y-Axis

M-mode echocardiography places a single ultrasound beam through the heart and graphs tissue depth against time — producing a tracing that bears a remarkable resemblance to the Wiggers diagram. At the standard right parasternal short-axis view at the level of the chordae tendinae, the M-mode trace shows: right ventricular free wall (thin, anterior), interventricular septum, left ventricular chamber, and left ventricular free wall (thick, posterior). KEY MEASUREMENTS: (1) LV internal diameter in diastole (LVIDd) and systole (LVIDs) — the difference is an estimate of stroke volume. (2) Fractional shortening (FS) = (LVIDd − LVIDs) / LVIDd × 100 — normal 28–44% in dogs. (3) E-point to septal separation (EPSS) — the distance between the anterior mitral valve leaflet at its maximal opening (E-point) and the interventricular septum. EPSS >7 mm in a dog suggests poor systolic function (the mitral valve doesn't open fully because the LV is dilated). (4) Septal and LV free-wall thickening fraction — reduced in myocardial disease.

Pulsed-Wave Doppler: The Haemodynamic Correlate

Pulsed-wave Doppler at the mitral valve tips (left apical 4-chamber view) shows the transmitral flow pattern. TWO WAVES: the E wave (early diastolic filling — passive, corresponds to rapid filling phase) and the A wave (atrial contraction — the 'atrial kick'). The E:A ratio changes with diastolic function: (1) Normal young adult dog: E > A (E:A ~1.5). (2) Impaired relaxation (early diastolic dysfunction, e.g., early HCM): E < A (reversal of the normal ratio — 'pseudonormalisation' may mask this). (3) Restrictive filling (severe diastolic dysfunction): E >> A (E:A >2.0) — the atrium is pumping against high LV pressures, and early filling is driven by high LA pressure, producing a tall, narrow E wave with rapid deceleration. Tissue Doppler imaging (TDI) of the mitral annulus distinguishes true normal from pseudonormal.

The Coronary Circulation: Perfusing the Pump

The heart is the only organ that perfuses itself — and it does so with unique haemodynamic constraints. Understanding coronary blood flow completes the picture of the cardiac cycle.

Coronary Blood Flow Is Phasic

Unlike most vascular beds, coronary blood flow is HIGHEST during DIASTOLE and LOWEST during SYSTOLE. This is because the contracting myocardium compresses the intramyocardial coronary vessels during systole, increasing coronary vascular resistance. The effect is most pronounced in the LEFT ventricle (which generates systolic pressures of 120 mmHg) and minimal in the RIGHT ventricle (systolic pressure ~25 mmHg). At a heart rate of 70 bpm, approximately 70–80% of left coronary flow occurs during diastole. Tachycardia is therefore doubly dangerous — it increases myocardial O₂ demand WHILE reducing the diastolic perfusion time (both the absolute duration and the fraction of the cardiac cycle spent in diastole decrease). This is why aortic stenosis (increased myocardial O₂ demand + reduced coronary perfusion pressure distal to the stenosis) and tachycardia together are a lethal combination.

Myocardial Oxygen Extraction Is Near-Maximal at Rest

The heart extracts ~70–75% of the oxygen from coronary blood AT REST — the highest extraction ratio of any organ (compare: kidney ~10%, brain ~35%, skeletal muscle ~25% at rest). This means the heart CANNOT significantly increase O₂ extraction to meet increased demand — it is entirely dependent on INCREASED CORONARY BLOOD FLOW. Coronary flow can increase 4–6× during maximal exercise (coronary vasodilation mediated by local metabolites — adenosine, NO, K⁺, and hypoxia). When coronary flow reserve is exhausted (e.g., in hypertrophic cardiomyopathy, where capillary density relative to myocyte mass is reduced), any further increase in demand produces myocardial ischaemia.

Frequently asked questions

Self-check quiz

Test yourself. Answers are below each question — cover them first if you are studying.