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Cardiac factors in orthostatic hypotension
H Lollgen1, P Dirschedl, K Koppenhagen
1Med. Dept., Div. Cardiol., Univ. of Bochum.
Insights
Low body pressure (LBNP) simulates orthostatic stress, decreasing cardiac output. Echocardiography reliably assesses these hemodynamic changes, differentiating early from late fainters.
Area of Science:
- Cardiovascular Physiology
- Hemodynamics
- Non-invasive Cardiology
Background:
- Orthostatic stress causes footward blood shift, compensated by increased afterload.
- Lower body negative pressure (LBNP) is a model for orthostatic stress.
- Invasive and non-invasive methods show similar cardiac responses to LBNP.
Purpose of the Study:
- To analyze cardiac and hemodynamic changes during LBNP.
- To compare invasive and non-invasive assessment methods.
- To evaluate LBNP's utility in orthostatic stress testing.
Main Methods:
- Graded lower body negative pressure (LBNP) applied.
- Invasive (right heart catheterization) and non-invasive (echocardiography) measurements.
- Assessment of cardiac output, stroke volume, ejection fraction, and Vcf.
Main Results:
- LBNP decreased preload, increased afterload and heart rate, and reduced stroke volume and cardiac output.
- Contractile state remained normal, indicated by unchanged ejection fraction and Vcf.
- Echocardiography correlated closely with invasive methods for cardiac output and stroke volume.
- Reduced arterial oxygen partial pressure suggests impaired ventilation/perfusion ratio.
- Dihydroergotamine effectively countermeasured LBNP-induced changes.
Conclusions:
- Echocardiography is a reliable non-invasive tool for LBNP and orthostatic stress.
- LBNP-induced changes mimic hypovolemia but maintain normal contractility.
- Findings aid in identifying orthostatic intolerance and differentiating fainter types.
Abstract:
Cardiac function is determined by preload, afterload, heart rate and contractility. During orthostatic stress, the footward blood shift is compensated for by an increase of afterload. LBNP is widely used to analyze effects of volume displacement during orthostatic stress. Comparisons of invasive (right heart catheterization) and non-invasive approach (echocardiography) yielded similar changes. Preload and afterload change with graded LBNP, heart rate increases, and stroke volume and cardiac output decrease. Thus, the working point on the left ventricular function curve is shifted to the left and downward, similar to hypovolemia. However, position on the Frank-Starling curve, the unchanged ejection fraction, and the constant Vcf indicate a normal contractile state during LBNP. A decrease of arterial oxygen partial pressure during LBNP shows impaired ventilation/ perfusion ratio. Finally, LBNP induced cardiac and hemodynamic changes can be effectively countermeasured by dihydroergotamine, a potent venoconstrictor. Comparison of floating catheter data with that of echocardiography resulted in close correlation for cardiac output and stroke volume. In addition, cardiac dimensions changed in a similar way during LBNP. From our findings, echocardiography as a non-invasive procedure can reliably used in LBNP and orthostatic stress tests. Some information can be obtained on borderline values indicating collapse or orthostatic syncope. Early fainters can be differentiated from late fainters by stroke volume changes.