The relationship between cardiac output and dynamic cerebral autoregulation in humans.
Summary of "The relationship between cardiac output and dynamic cerebral autoregulation in humans."
Cerebral autoregulation adjusts cerebrovascular resistance in the face of changing perfusion pressures to maintain relatively constant flow. Results from several studies suggest that cardiac output may also play a role. We tested the hypothesis that cerebral blood flow would autoregulate independent of changes in cardiac output. Transient systemic hypotension was induced by thigh cuff deflation in 19 healthy volunteers (7 females) in both supine and seated positions. Mean arterial pressure (Finapres), cerebral blood flow (TCD) in the anterior (ACA) and middle cerebral artery (MCA), beat-by-beat cardiac output (echocardiography) and end-tidal CO2 were measured. Autoregulation was assessed using the Autoregulatory Index (ARI) defined by Tiecks et al. Cerebral autoregulation was better in the supine position in both the ACA (Supine
5.0 +/- 0.21 (mean+/-SEM), Seated
3.9 +/- 0.4, p=0.01) and MCA (Supine
5.0 +/- 0.2, Seated
3.8 +/- 0.3, p=0.004). In contrast, cardiac output responses were not different between positions and did not correlate with cerebral blood flow autoregulatory indices. In addition, females had better autoregulation in the ACA (p=0.046) but not the MCA, despite having the same cardiac output response. These data demonstrate cardiac output does not appear to affect the dynamic cerebral autoregulatory response to sudden hypotension in healthy controls, regardless of posture. These results also highlight the importance of considering gender when studying cerebral autoregulation.
1National University of Ireland, Galway.
This article was published in the following journal.
Name: Journal of applied physiology (Bethesda, Md. : 1985)
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/20689094
- DOI: http://dx.doi.org/10.1152/japplphysiol.01262.2009
Medical and Biotech [MESH] Definitions
Cardiac Output, High
A state of elevated cardiac output due to conditions of either increased hemodynamic demand or reduced cardiac oxygen output. These conditions may include ANEMIA; ARTERIOVENOUS FISTULA; THYROTOXICOSIS; PREGNANCY; EXERCISE; FEVER; and ANOXIA. In time, compensatory changes of the heart can lead to pathological form of high cardiac output and eventual HEART FAILURE.
Cardiac Output, Low
A state of subnormal or depressed cardiac output at rest or during stress. It is a characteristic of CARDIOVASCULAR DISEASES, including congenital, valvular, rheumatic, hypertensive, coronary, and cardiomyopathic. The serious form of low cardiac output is characterized by marked reduction in STROKE VOLUME, and systemic vasoconstriction resulting in cold, pale, and sometimes cyanotic extremities.
A condition of fainting spells caused by heart block, often an atrioventricular block, that leads to BRADYCARDIA and drop in CARDIAC OUTPUT. When the cardiac output becomes too low, the patient faints (SYNCOPE). In some cases, the syncope attacks are transient and in others cases repetitive and persistent.
A potent vasoactive agent that dilates cerebral and coronary arteries, but slightly constricts femoral arteries, without any effects on heart rate, blood pressure or cardiac output.
Brain dysfunction or damage resulting from sustained MALIGNANT HYPERTENSION. When BLOOD PRESSURE exceeds the limits of cerebral autoregulation, cerebral blood flow is impaired (BRAIN ISCHEMIA). Clinical manifestations include HEADACHE; NAUSEA; VOMITING; SEIZURES; altered mental status (in some cases progressing to COMA); PAPILLEDEMA; and RETINAL HEMORRHAGE.
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