Cardioinhibitory-vasodepressor response to head-up tilt without hypoxaemia or myocardial ischaemia.
We evaluated whether hypoxaemia and/or myocardial ischaemia are of importance for development of the bradycardic hypotensive phase (cardioinhibitory-vasodepressor syncope) of central hypovolaemia. Arterial blood gas variables and a twelve-lead electrocardiogram (ECG) were followed during head-up tilt in seven men. During tilt, before presyncopal symptoms appeared, mean arterial pressure (MAP) increased (from 67 +/- 7 to 78 +/- 6 mmHg) (mean +/- SE) as did heart rate (HR) (61 +/- 4 to 99 +/- 8 beats min-1) and total peripheral resistance (TPR) (11 +/- 1 to 17 +/- 1 mmHg min l-1) (P < 0.01), while cardiac output (5.9 +/- 0.5 to 4.6 +/- 0.6 l min-1) and central venous pressure (CVP) (4.2 +/- 0.4 to 1.3 +/- 0.7 mmHg) decreased (P < 0.01). After 40 +/- 7 min of head-up tilt presyncopal symptoms appeared together with a decrease in MAP to 48 +/- 7 mmHg, HR to 71 +/- 11 beats min-1 and TPR to 9 +/- 2 mmHg min l-1 (P < 0.01). Arterial oxygen tension was not changed and there was no ST-segment depression of the ECG. The results indicate that during central hypovolaemia decreases in HR and TPR are elicited during normoxaemia and without electrocardiographic signs of myocardial ischaemia.
Department of Anaesthesia, Rigshospitalet, University of Copenhagen, Denmark.
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S
Matzen
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NH
Secher
D000328:Adult; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000502:physiology; D001808:Blood Vessels / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology; D002307:Cardiography, Impedance; D002496:Central Venous Pressure / Q000502:physiology; D004562:Electrocardiography; D006257:Head / Q000502:physiology*; D006321:Heart / Q000502:physiology*; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D017202:Myocardial Ischemia / Q000503:physiopathology*; D011187:Posture; D014655:Vascular Resistance / Q000502:physiology