Abnormalities Seen on Wiggers Diagram During Ventricular Systole
Pathological Conditions Affecting Ventricular Systole
The most clinically significant abnormalities visible during ventricular systole on the Wiggers diagram include dynamic left ventricular outflow tract obstruction (as seen in hypertrophic cardiomyopathy), valvular stenosis or regurgitation, and ventricular systolic dysfunction—each producing characteristic alterations in pressure tracings, valve timing, and flow patterns. 1, 2
Dynamic Left Ventricular Outflow Tract Obstruction
Hypertrophic obstructive cardiomyopathy produces distinctive systolic abnormalities:
Mid-systolic pressure gradient: The left ventricular pressure tracing shows a characteristic spike-and-dome configuration, with LV pressure rising above aortic pressure during mid-to-late systole due to systolic anterior motion (SAM) of the mitral valve creating dynamic obstruction 2
Abnormal aortic pressure contour: The aortic pressure waveform demonstrates a bifid or "spike-and-dome" pattern, with an initial rapid rise followed by a mid-systolic dip and secondary rise, reflecting the dynamic nature of obstruction 2
Rapid early systolic flow: LVOT velocities exceed 2.7 m/s (corresponding to gradients ≥30 mmHg), with peak instantaneous gradients ≥50 mmHg in severe cases requiring intervention 2
Prolonged ejection time: The duration of ventricular systole extends abnormally due to continued ejection through the partially obstructed outflow tract 2
Mitral Regurgitation During Systole
Mitral valve incompetence creates specific systolic abnormalities 1:
Abnormally high LV emptying: The left ventricular pressure tracing shows rapid pressure decay during systole as blood ejects through both the low-impedance mitral valve (retrograde into left atrium) and the higher-impedance aortic valve 1
Low LV end-systolic volumes: Despite adequate total stroke volume, the ventricle empties excessively due to the dual ejection pathways 1
Elevated left atrial pressure during systole: The left atrial pressure tracing shows abnormally high v-waves during ventricular systole, reflecting regurgitant flow 1
Supranormal ejection fraction: The LVEF appears falsely elevated due to the low-impedance ejection pathway, making assessment of true myocardial contractility difficult 1
Aortic Stenosis
Fixed outflow obstruction produces characteristic changes 1:
Elevated LV systolic pressure: The left ventricular pressure tracing shows markedly increased peak systolic pressure (often >200 mmHg in severe cases) while aortic pressure remains relatively low, creating a large systolic gradient 1
Delayed and diminished aortic pressure rise: The aortic pressure waveform shows pulsus parvus et tardus—a slow upstroke with reduced peak pressure 1
Prolonged ejection time: The duration from aortic valve opening to closure extends significantly as blood flows slowly through the stenotic valve 1
Reduced aortic flow velocity: Despite high LV pressure, actual flow through the stenotic valve is diminished 1
Ventricular Systolic Dysfunction
Impaired contractility manifests as 3:
Reduced rate of LV pressure rise: The peak positive dP/dt is diminished, reflecting impaired contractile function 4
Lower peak LV systolic pressure: Maximum left ventricular pressure during systole fails to reach normal values 4
Reduced LVOT time-velocity integral: Values <15 cm indicate the heart ejects less volume per beat than normal, regardless of ejection fraction 3
Prolonged time to peak pressure: The interval from onset of contraction to peak LV pressure extends abnormally 4
Cardiac Tamponade
Pericardial effusion with hemodynamic compromise shows 1:
Equalization of diastolic pressures: While primarily a diastolic phenomenon, this affects the subsequent systolic phase by reducing ventricular filling and preload 1
Reduced LV systolic pressure: Peak left ventricular pressure is diminished due to inadequate filling 1
Pulsus paradoxus: Systolic blood pressure drops >10 mmHg during inspiration, visible as exaggerated respiratory variation in the arterial pressure tracing 1
Timing Abnormalities of Isovolumic Contraction
Abnormal isovolumic contraction period indicates dysfunction 5:
Prolonged isovolumic contraction time: The interval between mitral valve closure and aortic valve opening extends beyond normal (typically >40-50 ms), reflecting impaired contractility 5
Reduced rate of pressure rise during isovolumic contraction: The slope of LV pressure increase before aortic valve opening is diminished in systolic dysfunction 5
Delayed aortic valve opening: The point at which LV pressure exceeds aortic pressure occurs later than normal 6
Aortic Regurgitation Effects on Systole
Aortic valve incompetence creates 1:
Elevated LV systolic pressure: The ventricle must generate higher pressures to compensate for regurgitant volume 1
Wide pulse pressure: The difference between systolic and diastolic aortic pressure increases markedly, with elevated systolic and reduced diastolic pressures 1
Rapid aortic pressure decay: Following peak systole, aortic pressure falls precipitously due to retrograde flow into the ventricle 1
Common Pitfalls in Interpretation
Confusing peak instantaneous gradient with mean gradient: Always use peak instantaneous LVOT gradient when assessing obstruction severity, as this determines clinical management 2
Missing dynamic obstruction: LVOT gradients can be normal at rest but markedly elevated with provocation (Valsalva, exercise, standing)—resting measurements alone may miss obstructive physiology 2
Misinterpreting supranormal ejection fraction: In mitral regurgitation, an elevated EF does not indicate hyperdynamic function but rather reflects the low-impedance ejection pathway 1
Overlooking loading conditions: Systolic function parameters are highly dependent on preload and afterload—abnormalities may reflect altered loading rather than intrinsic myocardial dysfunction 1, 4