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Effects of systole-specific pericardial pressure increases on coronary flow
C Hassapoyannes1, J F Harper, L M Stuck
1Department of Physiology, University of South Carolina School of Medicine, Columbia 29201.
Insights
Increased intrathoracic pressure may impair cardiac function. Systole-specific pericardial pressure increases (SSPPI) initially preserved coronary flow, but higher levels may directly affect coronary sinus flow (CSF) in heart failure.
Area of Science:
- Cardiology
- Physiology
- Hemodynamics
Background:
- Intrathoracic pressure changes can affect cardiac function and coronary blood flow.
- The relationship between altered cardiac function and coronary flow during increased intrathoracic pressure is not fully understood.
Purpose of the Study:
- To investigate whether increased intrathoracic pressure, specifically systole-specific pericardial pressure increases (SSPPI), alters cardiac function and coronary flow in a canine model of heart failure.
- To determine if coronary flow changes are a cause or a result of altered cardiac function under these conditions.
Main Methods:
- Used 14 anesthetized dogs with propranolol-induced heart failure.
- Induced systole-specific pericardial pressure increases (SSPPI) via thoracoabdominal binding, synchronized ventilation, and cardiac pacing.
- Measured left atrial transmural pressure, cardiac output, left ventricular end-systolic transmural pressure, myocardial O2 consumption, coronary sinus flow (CSF), and coronary arteriovenous O2 gradient.
Main Results:
- SSPPI of 15 and 30 mmHg decreased left atrial transmural pressure and increased cardiac output.
- Decreases in left ventricular end-systolic transmural pressure and myocardial O2 consumption were directly related.
- At 15 mmHg SSPPI, decreased CSF and unchanged coronary arteriovenous O2 gradient indicated autoregulation.
- At 30 mmHg SSPPI, CSF decreased further, but the arteriovenous O2 gradient remained unaltered, suggesting a potential limit to autoregulation.
Conclusions:
- Systole-specific pericardial pressure increases can alter cardiac function and myocardial oxygen consumption in heart failure.
- Coronary autoregulation is present at moderate SSPPI but may be compromised at higher levels, potentially due to decreased diastolic aortic pressure.
- A limit exists for increasing SSPPI beyond which coronary sinus flow may be directly impaired.
Abstract:
It has been postulated that intrathoracic pressure increases may impair cardiac function by decreasing coronary flow. To determine whether altered coronary flow causes or results from change in cardiac function, we used 14 anesthetized dogs in propranolol-induced heart failure following atrioventricular node ablation. After thoracoabdominal binding, the animals were paced and ventilated at the same frequency, and inspiration was synchronized with cardiac systole, resulting in systole-specific pericardial pressure increases (SSPPI). At SSPPI magnitudes of 15 and 30 mmHg, left atrial transmural pressure decreased and cardiac output increased, whereas decreases in left ventricular end-systolic transmural pressure and myocardial O2 consumption were directly related. Concurrent decreases in coronary sinus flow (CSF) and coronary arteriovenous O2 gradient with SSPPI 15 mmHg indicate autoregulation. However, the arteriovenous O2 gradient remained unaltered with SSPPI 30 mmHg, despite further decrease in CSF. Because the absolute diastolic aortic pressure decreased, a limit may exist for increasing SSPPI above which CSF may be directly affected.