Anesthesia and the Contractile Force of the Heart

Brown, Joe R.

doi:10.1213/00000539-196011000-00010

Cited by 18 publications

(13 citation statements)

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“…4), before the administration of the glycoside. This is not surprising since barbiturates (21)(22)(23)(24) and other anesthetics, such as halothane (21,24,48) have been reported to cause myocardial depression, and digitalis has been shown to be protective in anesthetic-induced myocardial depression by these agents (49,50).…”

Section: Discussionmentioning

confidence: 99%

“…Thus the majority of evidence indicates that cardiac glycosides stimulate the contractility of the nonfailing heart. However, the previous studies utilizing isolated cardiac muscle or anesthetized open chest preparations (12)(13)(14)(15)(16)(17)20) may have been biased to the extent that anesthesia or surgical manipulations alter the myocardial contractile state (21)(22)(23)(24) while the studies in conscious man utilized indirect means of evaluating the contractile state (18,19,25).…”

Section: Introductionmentioning

confidence: 99%

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Effects of cardiac depression and of anesthesia on the myocardial action of a cardiac glycoside

Vatner¹,

Higgins²,

Patrick³

et al. 1971

J. Clin. Invest.

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A B S T R A C T The effects of ouabain (G-strophanthin) 20 /Ag/kg, on left ventricular (LV) pressure (P), diameter (D), velocity of contraction (dD/dt), and dP/dt were studied in conscious dogs instrumented with ultrasonic diameter gauges and miniature pressure gauges. The effects of ouabain were compared on separate occasions in the same dogs after cardiac depression with propranolol, 3.0 mg/kg, and also after general anesthesia with Na pentobarbital, 30 mg/kg. Maximal pressor effects were observed in the first 10 min, but maximal effects on the contractile state occurred at 30 min after ouabain. At this time, in conscious dogs, ouabain had increased LV isolength systolic pressure by 5%, LV isolength velocity by only 9%, and LV (dP/dt)/P by 21%, while end systolic diameter (ESD) decreased slightly and end diastolic diameter (EDD) and heart rate (HR) were unchanged. After anesthesia, ouabain increased LV systolic pressure by 8%, velocity 32%, (dP/dt)/P by 47%, and ESD decreased by 1.2 mm while EDD rose slightly and HR fell by 26 beats/min. Returning HR to control with atrial pacing decreased EDD 0.9 mm below control. After cardiac depression with propranolol, ouabain caused responses similar to those observed in the anesthetized dogs. Thus, the cardiac glycoside was found to exert only minor inotropic effects on the nonfailing heart of conscious dogs but far more striking inotropic responses in the anesthetized state.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of cardiac depression and of anesthesia on the myocardial action of a cardiac glycoside

Vatner¹,

Higgins²,

Patrick³

et al. 1971

J. Clin. Invest.

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“…Actual reduction of cardiac contractile force by thiopental was demonstrated by Brown. 25 Other barbiturates seem to have similar effects. 26 The clinical application of barbiturates in the setting of circulatory collapse may, therefore, be hazardous.…”

Section: Discussionmentioning

confidence: 98%

Failure of thiopental to modify global anoxic injury.

Snyder¹,

Ramírez-Lassepas²,

Sukhum³

et al. 1979

Stroke

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SUMMARY To corroborate thiopental protection from cerebral anoxia after cardiopulmonary arrest, 23 sedated, curarized, adult dogs were asphyxiated by plugging the endotracheal tube. Cardiopulmonary resuscitation (CPR) was started 7 minutes after electrocortical silence. Twelve animals received no other treatment (controls), 10 regained consciousness and spontaneous respirations, but remained decerebrate, blind, unable to drink or feed. Two dogs returned to a normal neurologic state. Ten dogs were treated with thiopental after CPR, 7 received 15 mg/kg the first minute, followed by 23 mg/kg over 1 hour; 3 received 60 mg/kg in the first 3 minutes, followed by 30 mg/kg over 1 hour. Except for 1 dog in the low-dose group that recovered neurologically, thiopental-treated dogs showed no neurological or survival improvement over the controls.Stroke, Vo! 10, No 2, 1979LABORATORY DEMONSTRATION of central nervous system recovery after prolonged ischemic anoxic injury 1 has resulted in renewed interest in the treatment of post-anoxic states.Several studies have demonstrated the effectiveness of barbiturate anesthetics in ameliorating the effects of focal ischemic injury.2 Clinically, patients may do surprisingly well after deep barbiturate coma and anoxia.3 Several laboratories have reported beneficial effects of barbiturates in models of global anoxic injury. 49 We attempted to demonstrate a similar benefit in a model closely paralleling the clinical situation of hypoxic cardiac arrest. MethodsTwenty-two, 8 to 16 kg adult mongrel dogs were fasted for 12 hours prior to the experiment. They were anesthetized with a combination of fentanyl and droperidol (Innovar-Vet), 0.1 cc/kg body weight and paralyzed with pancuronium bromide, 0.1 mg/kg. They were then intubated and placed on a piston ventilator with an in-line CO 2 meter (Godart Capnograph). Tidal volume and respiratory rate were adjusted to achieve an expired CO 2 content of 3.5 to 4.5% throughout the experiment. Biparietal scalp EEG leads, ECG electrodes, and a rectal temperature probe were attached. Intravenous dextrose 5% in water, 60 cc per hour, was given throughout the experiment (approximately 5 hours). Normal saline with 1000 U heparin/1 was used as a flushing solution. Through an inguinal incision, a Swan-Ganz catheter was passed via the femoral vein and placed in the right atrium as confirmed by pressure tracings. A femoral arterial line was inserted into the aorta and attached to a Statham strain gauge. Arterial blood pressure (AP), heart rate, and EEG were monitored throughout the experiment.The animals were allowed to emerge from anesthesia to the point of regaining a pedal withdrawal reflex and minimal respiratory efforts. At this time, pancuronium was re-administered and the endotracheal tube plugged after emptying the chest by compression. The EEG was observed until it became isoelectric. This state was maintained for 7 minutes. At that time, standard cardiopulmonary resuscitation was begun with Ambu bag ventilation with 100% oxygen and closed chest card...

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“…Hypotension is an important potential h a z a r d . d u r i n g experimental a n d t h e r a p e u t i c a d m i n i s t r a t i o n o f barbiturates, and in drug overdose (Esten and Li 1955, Brown 1960, Price 1975, Bleyaert et a/. 1978, Breivik et a/.…”

Section: Physical Properties and Side-effects Of Barbituratesmentioning

confidence: 99%

Barbiturate Therapy in the Management of Cerebral Ischaemia

Steer

1982

Develop Med Child Neuro

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Anesthesia and the Contractile Force of the Heart

Cited by 18 publications

References 0 publications

Effects of cardiac depression and of anesthesia on the myocardial action of a cardiac glycoside

Effects of cardiac depression and of anesthesia on the myocardial action of a cardiac glycoside

Failure of thiopental to modify global anoxic injury.

Barbiturate Therapy in the Management of Cerebral Ischaemia

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