The Cardiovascular Effects of Halothane in Man during Spontaneous Ventilation

Bahlman, Steven H.; Eger, E. I.; Halsey, Michael J.; Stevens, WC; Shakespeare, Thomas F.; Smith, N. Ty; Cromwell, Thomas H.; Fourcade, Henry E.

doi:10.1097/00000542-197205000-00017

Cited by 42 publications

(9 citation statements)

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“…[1][2][3][4][5][6][7] Briefly, studies were made on healthy volunteers between 21 and 30 years of age. Blood and voided urine specimens were obtained immediately prior to anaesthesia.…”

Section: Methodsmentioning

confidence: 99%

Comparative toxicity of isoflurane, halothane, fluroxene and diethyl ether in human volunteers

Stevens

Eger

Joas

et al. 1973

Canad. Anaesth. Soc. J.

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“…[1][2][3][4][5][6][7] Briefly, studies were made on healthy volunteers between 21 and 30 years of age. Blood and voided urine specimens were obtained immediately prior to anaesthesia.…”

Section: Methodsmentioning

confidence: 99%

Comparative toxicity of isoflurane, halothane, fluroxene and diethyl ether in human volunteers

Stevens

Eger

Joas

et al. 1973

Canad. Anaesth. Soc. J.

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“…This controversy has resulted in part because the response to halothane appears to depend on the drug's concentration (1)(2)(3)(4), the duration of its administration (1)(2)(3)(4)(5), and the precision and extent to which ventilation is controlled (3,4). Moreover, many earlier studies of the drug's effects have been conducted in isolated muscle (4,(6)(7)(8)(9) or in previously anesthetized preparations (10)(11)(12)(13)(14)(15)(16) in which the control state has been altered by the general anesthetic's effects on the cardiovascular system.…”

mentioning

confidence: 99%

Effects of Halothane on Left Ventricular Function and Distribution of Regional Blood Flow in Dogs and Primates

Vatner

Smith

1974

Circulation Research

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Left ventricular and regional vascular effects of halothane were assessed in dogs and primates in which coronary, mesenteric, renal, and iliac blood flows, arterial blood pressure, left ventricular diameter and pressure, dD/dt (i.e., the velocity of myocardial fiber shortening), and dP/dt were continuously measured in the control resting state, while the conscious animals were breathing O 2 , and during halothane-O 2 anesthesia maintained at 1% or at 2% for 90 minutes (separate experimental days). Halothane caused a concentration-dependent depression of myocardial contractility: (dP/dt)/P fell 68 ± 5% during 2% halothane anesthesia and left ventricular end-diastolic diameter rose. Halothane also caused a redistribution of regional blood flows. At a concentration of 1% halothane, the most intense vasodilatation occurred in the renal bed (renal resistance fell 46 ± 5%), but mesenteric resistance rose (42 ± 15%). With 1% halothane regional vascular resistances tended to rise with time, but with 2% halothane regional blood flows rose with time. A direct vasodilating action of halothane was observed following direct intra-arterial injection of the drug. Probably this action was responsible for the renal and iliac vasodilatations and for the opposition to the metabolically induced vasoconstriction in the coronary bed. Thus, the administration of the most commonly employed potent inhalation anesthetic, halothane, substantially alters myocardial contractility and regional blood flows and resistances. These effects are, in many instances, a function of the concentration of the anesthetic and the duration of its administration. KEY WORDSanesthesia renal flow mesenteric flow iliac flow myocardial contractility baboon chimpanzee

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“…These data support other studies of anaesthetized man, where reliable circulatory responses required Pro2 increments of 2.0 kPa (15 torr) or more. [4][5][6] We emphasize that these results probably relate only to the conditions specified, l~r liminary work in our laboratory comparing responscs during anaesthesia with and without concurrent surgical stimulation indicate that the factor of surgery may greatly modify rate and rhythm responses to carbon dioxide.…”

Section: Disc Usstonmentioning

confidence: 81%

Cardiovascular signs of acute hypoxaemia and hypercarbia during enflurane and halothane anaesthesia in man

Manninen

Knill

1979

Canad. Anaesth. Soc. J.

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HYPOXIA AND HYPERCARBIA are always potential complications of anaesthesia. How can they be recognized quickly? Signs frequently sought in the anaesthetized patient are changes in heart rate and rhythm and blood pressure. In awake man, acute hypoxaemia accelerates heart rate obviously, while increasing blood pressure only slightlyJ'2; acute hypercarbia augments both) ,4 The cardiovascular responses to steady states of hypercarbia during anaesthesia have been previously described s,6 and are well known; however, there is no information on the human response to hypoxia during anaesthesia.We have studied changes in heart rate and blood pressure brought about by brief periods of controlled hypoxaemia (Po~ approximately 6.0 kPa [45 torr]) in human subjects awake and when anaesthetized with enflurane or halothane. We have also recorded their responses to a mild carbon dioxide stimulus (Pco2 increment of 1.3 kPa [ 10 torr]). Our results indicate that during anaesthesia with these drugs, neither blood pressure nor heart rate is a reliable indicator of acute moderate hypoxaemia or of mild hypercarbia. METHODSWe studied 13 young healthy subjects. Their mean age, weight and height (-I-S.D.) were respectively 22 _ 5 years, 66 --. 14 kg and 170 4-9 centimetres. All were patients scheduled for elective dental surgical procedures, usually multiple odontectomy. Each was informed of the protocol and risks involved and signed a written consent form which had been approved by the University Human Research Committee. We Canad. Anaesth. Soc. J., vol. 26, no. 4, July 1979 studied each subject twice, first while anaesthetized with either enflu rane (n = 8) or halothane (n == 5) and subsequently while conscious.Anaesthesia studies were conducted during a 45-minute period of anaesthesia before the operation. The subjects were not premedicated. We induced anaesthesia with thiopentone 3 to 5 rag" kg -I and, after producing neuromuscular paralysis with succinylcholine I mg. kg -~ we intubated the trachea with an 8 or 9 mm cuffed tube. The subject inhaled a mixture of oxygen and either enflurane or halothane from a nonrebreathing circuit for a period of at least 30 minutes. The concentration of inspired vapour was set to achieve a steady end-tidal concentration equivalent to I.l MAC. Intravenous fluid (5 per cent dextrose in 0,2 percent saline) was infused in amounts up to one litre to maintain systolic blood pressure above 70 per cent of the awake vatue. Nasopharyngeal temperature was monitored and remained above 36 degrees Celsius in all subjects. When the end-tidal vapour concentration had been steady for ten minutes, we induced periods of hypoxaemia and hypercarbia individually and recorded heart rate and blood pressure responses.We conducted conscious studies in a quiet laboratory approximately one week after the operation. Each subject sat in a comfortable chair breathing through a mouthpiece with a nose-clip in place. We induced hypoxaemia and hypercarbia by the same methods employed during anaesthesia and recorded the responses fo...

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The Cardiovascular Effects of Halothane in Man during Spontaneous Ventilation

Cited by 42 publications

References 0 publications

Comparative toxicity of isoflurane, halothane, fluroxene and diethyl ether in human volunteers

Comparative toxicity of isoflurane, halothane, fluroxene and diethyl ether in human volunteers

Effects of Halothane on Left Ventricular Function and Distribution of Regional Blood Flow in Dogs and Primates

Cardiovascular signs of acute hypoxaemia and hypercarbia during enflurane and halothane anaesthesia in man

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