Increased Stroke Volume via Frank-Starling Mechanism
Increased stroke volume via the Frank-Starling mechanism means that greater ventricular filling (end-diastolic volume) leads to stronger cardiac contraction and more blood ejected per heartbeat, without requiring changes in contractility. This fundamental cardiac principle allows the heart to automatically adjust output based on venous return 1.
Physiological Basis
The Frank-Starling mechanism operates through:
Sarcomere Length-Tension Relationship: When the ventricle fills with more blood:
Preload Dependence:
- Preload refers to the ventricular end-diastolic volume/pressure
- Increased preload stretches the ventricular wall
- This stretching directly increases contractile force 3
Clinical Significance
The Frank-Starling mechanism is crucial for:
Matching Right and Left Ventricular Output:
- Ensures balanced cardiac output between ventricles
- Prevents pulmonary congestion or systemic venous pooling 2
Exercise Response:
Postural Changes:
- When moving from standing to supine position, venous return increases
- Stroke volume automatically increases via Frank-Starling 5
Pathophysiological Implications
In heart failure:
Impaired Frank-Starling Response:
Compensatory Mechanisms:
- Heart failure patients rely more on increased heart rate than stroke volume
- Stroke volume may only increase to 50-65 mL vs. 100 mL in healthy individuals 3
Diagnostic and Therapeutic Relevance
Fluid Responsiveness Assessment:
Pharmacological Interventions:
The Frank-Starling mechanism represents the heart's intrinsic ability to adapt to changing hemodynamic conditions, providing a crucial autoregulatory function that maintains cardiovascular homeostasis across various physiological and pathological states.