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The influence of ectopic beats and tachyarrhythmias on stroke volume and cardiac output
Insights
Premature ventricular contractions significantly decrease stroke volume by impairing diastolic filling. Postextrasystolic beats offer only minor augmentation, suggesting arrhythmias substantially reduce cardiac output.
Area of Science:
- Cardiology
- Cardiac Electrophysiology
Background:
- Cardiac rhythm disturbances, including premature ectopic beats and tachyarrhythmias, can impact cardiac performance.
- Left ventricular end-diastolic volume is a primary determinant of stroke volume.
Purpose of the Study:
- To investigate the influence of premature ectopic beats and tachyarrhythmias on cardiac performance.
- To assess echocardiographic left ventricular stroke volume in patients with cardiac rhythm disturbances.
Main Methods:
- Echocardiographic assessment of beat-to-beat left ventricular stroke volume in 21 patients.
- Analysis of stroke volume variations in relation to end-diastolic volume during various arrhythmias.
Main Results:
- Premature ventricular contractions reduced stroke volume by 71% compared to sinus beats.
- Postextrasystolic beats increased stroke volume by only 18% over sinus beats, indicating a minor role for potentiation.
- Ventricular bigeminy, trigeminy, and quadrigeminy lowered cardiac output by 1.3, 0.9, and 0.7 L/min, respectively.
- Tachyarrhythmias often led to continuously changing end-diastolic and stroke volumes.
Conclusions:
- Premature contractions decrease stroke volume primarily by infringing on diastolic filling.
- Left ventricular end-diastolic volume is the principal determinant of stroke volume in arrhythmias.
- The frequency and prematurity of ectopic beats significantly influence the reduction in cardiac output.
Abstract:
The potentially adverse influence of premature ectopic beats or tachyarrhythmias on cardiac performance was studied by assessing the echocardiographic left ventricular stroke volume in 21 patients with cardiac rhythm disturbances. The beat to beat stroke volume correlated closely with end-diastolic volume in each patient (average R = .9). Premature ventricular contractions decreased stroke volume by an average of 48 +/- 8 ml (-71%) compared with sinus beats; whereas the postextrasystolic beats, although preceded by a pause and higher end-diastolic volume, increased stroke volume by only 16 +/- 7 ml (18%) over the sinus beats. Those postextrasystolic beats with equivalent timing and end-diastolic volume to the sinus beats had a mean stroke volume only 8 ml higher, suggesting that postextrasystolic potentiation plays only a minor role in augmenting stroke volume. Transient aberrant ventricular conduction of intermittent left bundle branch block, ectopic beats or atrial fibrillation failed to alter stroke volume. Ventricular bigeminy, trigeminy and quadrigeminy lowered cardiac output by 1.3, .9 and .7 l/min. The onset of tachyarrhythmias was oftentimes associated with a continuously changing end-diastolic volume and stroke volume, with either alternation or progressive increment of these variables. It is apparent that premature contractions decrease stroke volume by virtue of their infringement on diastolic filing, the principle beat to be determinant of stroke volume in arrhythmias being left ventricular end-diastolic volume. Since premature beats decrease stroke volume to an extent greater than postextrasystolic beats increase it, they may reduce cardiac output by a substantial degree, depending on their frequency of occurrence and degree of prematurity.