Does Phosphodiesterase III Inhibition Reverse the Cardiodepressive Effects of Propofol?

Pernerstorfer, Thomas; Mayer, N.; Jilma, Bernd; Krenn, Claus G.; Bayer, G. S.; Eichler, Hans‐Georg

doi:10.1213/00000539-199710000-00003

Cited by 4 publications

(3 citation statements)

References 22 publications

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“…We demonstrate an increase in HR in healthy as well as in HF dogs. These effects are in accordance with previous preclinical studies, investigating the effect of anesthesia initiation with propofol, but are fundamentally different from observations during continuous infusion [13,19,33]. By analyzing the left ventricular pressure signal, we could not detect any changes in myocardial relaxation after propofol, whereas contractility shows a slight increase.…”

Section: Discussionsupporting

confidence: 82%

“…It can be speculated that the increase in BP is triggered by the elevated HR and consequent increase in cardiac output. From previous investigations in patients it is known, that propofol infusion over a period of 30 minutes leads to a decrease in HR by resetting the baroreceptor reflex [20,33]. We demonstrate an increase in HR in healthy as well as in HF dogs.…”

Section: Discussionsupporting

confidence: 61%

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Telemetric hemodynamic assessment during anesthesia induction with propofol in experimental heart failure

Vogel¹,

Boehme²,

Wakili³

et al. 2021

J Transl Sci

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Section: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 61%

Telemetric hemodynamic assessment during anesthesia induction with propofol in experimental heart failure

Vogel¹,

Boehme²,

Wakili³

et al. 2021

J Transl Sci

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“…One possible explanation of our result is a change in the distribution of remifentanil due to the haemodynamic effects of propofol. It is well documented that propofol causes arterial hypotension 20,21 which would be expected to lead to a reduction of circulating blood volume. This has been attributed to an increase in venous capacitance by relaxing venous smooth muscle tone 22 and a significant decrease in cardiac output 23 .…”

Section: Discussionmentioning

confidence: 99%

Remifentanil Concentration during Target-controlled Infusion of Propofol

Crankshaw

Chan

Leslie

et al. 2002

Anaesth Intensive Care

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After institutional approval and with written informed consent, eight surgical patients were infused intravenously with remifentanil at 250 ng.kg lean body mass (LBM)-1 .min-1 for 30 min. Cardiovascular and respiratory parameters were recorded and arterial blood samples were taken at regular intervals. In each patient, the same protocol was repeated 40 min later during propofol infused to a target concentration of 3.0 µg.ml-1. Blood concentrations of remifentanil and propofol were assayed using capillary gas chromatography and high performance liquid chromatography techniques respectively. The number of subjects enrolled was determined by testing the successive areas under the remifentanil time-concentration curve (AUC) for significant difference or non-difference using sequential analysis. The median measured propofol concentration was 3.5 (range: 2.6-4.5) µg.ml-1 which did not change significantly during the second remifentanil infusion. The median AUC during propofol infusion was greater than control in all subjects, although there was considerable variation of 94.

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Cardiovascular Manifestations of Sedatives and Analgesics in the Critical Care Unit

Darrouj

Karma

Arora

2009

American Journal of Therapeutics

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There are numerous sedatives and analgesics used in critical care medicine today; these medications are used on critically ill patients, many of whom have heart disease, including coronary artery disease or congestive heart failure. The purpose of this review is to recognize the effects of these medications on the heart. Studies that evaluated the effects of sedatives and analgesics on normal individuals or on those with heart disease were reviewed. Current choices for sustained sedation in the critically ill include the benzodiazepines, morphine, propofol, and etomidate. Each of these medications has their particular advantages and disadvantages. Benzodiazepines provide the greatest amnesia and cardiovascular safety but they can cause significant hypotension in the hemodynamically unstable patient. Morphine provides analgesia and cardioprotective activity after ischemia, although the large observational study CRUSADE showed increased mortality rate in those patients with non-ST segment elevation myocardial infarction who received morphine. Propofol is the most easily titratable drug with cardioprotective features, but its use must be accompanied with great attention to possible development of propofol infusion syndrome, which is a deadly disease, especially in patients with head injury and those with septic shock receiving vasopressors. Etomidate has a rapid onset effect and short period of action with great hemodynamic stability even in patients with shock and hypovolemia, but the incidence of adrenal insufficiency during infusion, not bolus doses, may cause deterioration in the circulatory stability. In conclusion, the sedatives and analgesics mentioned here have characteristics that give them a cardiovascular safety profile useful in critically ill patients. However, use of these drugs on an individual basis is dependent on each agent's safety and efficacy.

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Does Phosphodiesterase III Inhibition Reverse the Cardiodepressive Effects of Propofol?

Cited by 4 publications

References 22 publications

Telemetric hemodynamic assessment during anesthesia induction with propofol in experimental heart failure

Telemetric hemodynamic assessment during anesthesia induction with propofol in experimental heart failure

Remifentanil Concentration during Target-controlled Infusion of Propofol

Cardiovascular Manifestations of Sedatives and Analgesics in the Critical Care Unit

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