Related Experiment Video
Updated: Jul 22, 2026

Rodent Working Heart Model for the Study of Myocardial Performance and Oxygen Consumption
Published on: August 16, 2016
Haemodynamic and catecholamine response to simulated ventricular tachycardia in man: effect of baseline left
T M Kolettis1, E Psarros, Z S Kyriakides
1Department of Cardiology, University of Ioannina, Ioannina, Greece. thkolet@cc.uoi.gr
Objective:
To examine the effects of baseline left ventricular function on the haemodynamic and catecholamine responses to ventricular tachycardia.
Design:
Experimental cohort study.
Setting:
Cardiac catheterisation laboratory in tertiary referral centre.
Subjects:
24 patients (19 male, 5 female; mean (SD) age, 59 (10) years) without coronary artery disease, divided into two groups with normal or impaired left ventricular function: group A, ejection fraction > 65% (n = 10); group B, ejection fraction < 45% (n = 14). Other medical and demographic factors were similar in the two groups.
Interventions:
Ventricular tachycardia was simulated with rapid pacing at 150 beats/min for 10 minutes.
Main Outcome Measures:
Arterial blood pressure; venous plasma catecholamine concentrations.
Results:
During rapid pacing, blood pressure was lower in group B (with impaired left ventricular function) than in group A: systolic blood pressure, 102 (11) v 115 (9) mm Hg (p = 0.005); mean blood pressure, 79 (6) v 85 (6) mm Hg (p = 0.02). The ejection fraction correlated with the lowest systolic blood pressure (r = 0.64, p = 0.0006). Although the rise in adrenaline was comparable between the two groups, the rise in noradrenaline was more pronounced (p < 0.05) in patients in group B.
Conclusion:
At low rates and in selected patients, the underlying state of left ventricular function affects haemodynamic tolerance of ventricular tachycardia. Patients with impaired left ventricular function have a lower blood pressure during ventricular tachycardia, despite an exaggerated noradrenaline release.
Related Concept Videos
Pathophysiology of Cardiac Performance
Heart Failure Drugs: β-Blockers
Regulation of Heart Rates
The SNS increases heart rate through the release of norepinephrine and epinephrine, which act on beta-1 adrenergic receptors in the heart. This action increases the rate of depolarization in the sinoatrial (SA) node, the heart's...
Cardiac Output I:Effect of Heart Rate on Cardiac Output
Cardiac output (CO) refers to the total amount of blood ejected by one of the ventricles in liters per minute (L/min). In a resting adult, CO ranges from 5 to 6 L/min, adjusting according to the body's metabolic requirements.
Effect of Heart Rate on Cardiac Output
Cardiac output adapts to metabolic demands during stress, physical activity, or illness. The autonomic nervous system regulates heart rate via the sinoatrial node. The parasympathetic nervous system decreases heart rate...
Heart Failure II: Pathophysiology

