The Wiggers Diagram: A Comprehensive Guide to the Cardiac Cycle
The Wiggers Diagram is the standard clinical and physiological model used to map the synchronized mechanical, electrical, and acoustic events of a single mammalian cardiac cycle. Named after its creator, Dr. Carl Wiggers, this diagram aligns changing pressures, volumes, and electrical states over time, providing a clear window into how the heart functions as a coordinated pump.
Understanding the overlapping curves of the Wiggers Diagram is essential for mastering cardiac hemodynamics, heart murmurs, and valvular pathology.
Core Components of the Diagram
The Wiggers Diagram synchronizes multiple physiological tracings along a single timeline, tracking the left side of the heart (where pressures are highest):
1. Pressure Curves
Aortic Pressure: Tracks the fluctuating pressure within the aorta. It remains relatively high even during diastole due to the elastic recoil of the aortic wall, dropping to a baseline of around 80 mmHg. It reaches its peak at approximately 120 mmHg during ventricular ejection. A characteristic dip, the dicrotic notch (incisura), marks the abrupt closure of the aortic valve.
Left Ventricular Pressure: Displays the most dramatic shifts. During diastole, ventricular pressure drops close to 0 mmHg as the chamber fills. During systole, it skyrockets to match and briefly exceed aortic pressure (reaching 120 mmHg) to force blood out of the heart.
Left Atrial Pressure: Maintains low baseline pressures (typically between 2 and 12 mmHg). Its wave features three distinct positive deflections:
a wave: Caused by active atrial contraction.
c wave: Caused by the bulging of the mitral valve back into the atrium as the ventricle begins to contract rigidly.
v wave: Caused by passive atrial filling from the pulmonary veins while the mitral valve remains closed during ventricular systole.
2. Left Ventricular Volume
Tracks the absolute volume of blood within the left ventricle:
End-Diastolic Volume (EDV): The maximum volume achieved at the end of ventricular filling (typically around 120 to 130 mL).
End-Systolic Volume (ESV): The residual volume of blood left in the chamber at the end of contraction (typically around 50 to 60 mL).
Stroke Volume: The total volume of blood ejected during a single beat, represented by the net drop from EDV to ESV.
3. Electrocardiogram (ECG)
The electrical trigger that precedes every mechanical action:
P wave: Reflects atrial depolarization, which triggers the mechanical atrial contraction (the "a" wave).
QRS complex: Reflects ventricular depolarization, triggering the immediate mechanical contraction of the ventricles.
T wave: Reflects ventricular repolarization, initiating ventricular relaxation.
4. Phonocardiogram (Heart Sounds)
The acoustic recording of structural closures:
First Heart Sound (S1): The classic "lub" sound, caused by the closure and vibrations of the AV valves (mitral and tricuspid) at the absolute start of ventricular systole.
Second Heart Sound (S2): The classic "dub" sound, caused by the closure of the semilunar valves (aortic and pulmonary) at the start of ventricular diastole.
Phases of the Cardiac Cycle
The Wiggers Diagram is divided chronologically into distinct mechanical phases based on whether the muscle is contracting or relaxing, and whether the valves are open or closed:
Phase 1: Atrial Contraction (Active Filling)
Triggered by the P wave of the ECG, the left atrium contracts, forcing the remaining blood through the open mitral valve into the left ventricle. This registers as the "a" wave on the atrial pressure curve and causes a slight final rise in ventricular volume.
Phase 2: Isovolumetric Contraction
The QRS complex triggers ventricular depolarization. The left ventricle contracts sharply, causing ventricular pressure to climb rapidly. As soon as ventricular pressure exceeds atrial pressure, the mitral valve snaps shut, generating the S1 heart sound. For a brief moment, ventricular pressure is higher than atrial pressure but lower than aortic pressure. Because all four valves are completely closed, the ventricle contracts without any change in volume, causing the pressure curve to rise almost vertically.
Phase 3: Rapid Ventricular Ejection
As ventricular pressure rises, it surpasses the resting pressure in the aorta (around 80 mmHg). This pressure differential forces the aortic valve open. Blood rushes out of the ventricle into the systemic circulation, causing a sharp drop in ventricular volume and a parallel rise in both ventricular and aortic pressures to their systolic peak.
Phase 4: Reduced Ventricular Ejection
Ventricular repolarization begins (represented by the T wave). The strength of the ventricular contraction begins to wane, and the rate of blood flow into the aorta slows down. Ventricular volume continues to decline toward its lowest point (ESV), while pressure curves begin to slope downward.
Phase 5: Isovolumetric Relaxation
The ventricle relaxes, and its internal pressure drops rapidly below aortic pressure. The backward momentum of blood forces the aortic valve to snap shut, creating the dicrotic notch on the aortic pressure curve and generating the S2 heart sound. Because ventricular pressure is still higher than atrial pressure, the mitral valve remains closed. The ventricle relaxes with all valves shut, dropping pressure vertically while maintaining a constant volume (ESV).
Phase 6: Rapid Ventricular Filling (Passive)
As the ventricle continues to relax, its internal pressure drops below left atrial pressure. This pressure drop forces the mitral valve to open. Blood that had been accumulating in the atrium (the "v" wave) pours rapidly into the ventricle, causing a steep, early rise in ventricular volume.
Phase 7: Reduced Ventricular Filling (Diastasis)
As the ventricle fills and expands, the pressure gradient between the atrium and ventricle flattens out. The flow of blood slows down significantly, relying on passive systemic venous return until the next P wave triggers active atrial contraction, restarting the cycle.
Wiggers Diagram References
Wiggers, C. J. (1915). Modern Aspects of the Circulation in Health and Disease. Philadelphia: Lea & Febiger.
Hall, J. E., & Hall, M. E. (2020). Guyton and Hall Textbook of Medical Physiology (14th ed.). Philadelphia: Elsevier.
Mohrman, D. E., & Heller, L. J. (2018). Cardiovascular Physiology (9th ed.). New York: McGraw-Hill Education.
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