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AI-Generated response:

What are the cardiovascular effects of Ketamine?

Answer generated on June 4, 2024

The AI-generated responses are for illustration purposes only and should not be used for medical purposes.

Ketamine can cause dose-dependent increases in blood pressure, heart rate, and cardiac output, and may lead to hypertension, tachycardia, and arrhythmias; it should be used cautiously in patients with cardiovascular risks such as hypertension or cardiac disease.[1-4]

  • Ketamine's cardiovascular stimulation is primarily mediated by the indirect sympathomimetic effects due to increased endogenous catecholamines, leading to elevated blood pressure and heart rate.[2-4]

  • Despite its sympathomimetic properties, ketamine also has direct negative inotropic effects, which can cause hypotension and bradycardia, especially in patients with diminished myocardial contractility.[1-2]

  • The cardiovascular effects of ketamine, such as increased blood pressure and heart rate, typically peak within a few minutes after administration and generally return to baseline within 15 minutes.[2-4]

  • Use of ketamine is contraindicated in patients where significant elevation of blood pressure would pose a serious hazard, such as those with uncontrolled hypertension, aneurysm, or history of stroke.[2]

  • Ketamine can exacerbate pulmonary hypertension and should be used with caution in patients with preexisting pulmonary hypertension or congestive heart failure.[2]

Additional info

Ketamine's cardiovascular effects are complex due to its dual action of indirect sympathomimetic stimulation and direct negative inotropic effects. The initial increase in blood pressure and heart rate is beneficial in some clinical scenarios, such as induction of anesthesia in patients at risk of hypotension. However, these effects can be detrimental in patients with preexisting cardiovascular conditions, necessitating careful monitoring and consideration of alternative agents. The transient nature of these effects should be considered in the timing of monitoring and intervention. Additionally, the potential for arrhythmias and exacerbation of pulmonary hypertension requires careful patient selection and monitoring during ketamine administration. The use of adjunctive medications like benzodiazepines, barbiturates, or synthetic opioids can help mitigate some of the adverse cardiovascular effects of ketamine.[2]

References

Reference 1

1.

Elsevier ClinicalKey Clinical Overview

Special Considerations Ketamine causes elevations in blood pressure, cardiac output, and heart rate, potentially creating an acute risk in people with hypertension, cardiac disease, baseline elevated risk of stroke, or elevated intracranial pressure Ketamine's direct negative inotropic effects are typically masked by its indirect sympathomimetic effects, but hypotension and cardiac arrest may still occur in cases of diminished myocardial contractility

Reference 2

2.

Elsevier ClinicalKey Drug Monograph

Content last updated: March 4, 2024.

Adverse Reactions Ketamine-induced hypertension and sinus tachycardia are dose-dependent and mediated through the sympathetic nervous system with the release of endogenous catecholamines. Elevation of blood pressure begins shortly after ketamine injection, reaches maximum levels within a few minutes, and usually returns to preanesthetic levels within 15 minutes of injection. In the majority of cases, the systolic and diastolic blood pressure peaks from 10% to 50% above baseline shortly after induction, but the elevation can be higher and longer in some patients. Ketamine-induced hypertension and tachycardia can be attenuated with the administration of a benzodiazepine, a barbiturate, or a synthetic opioid. In general, ketamine's indirect sympathomimetic effects compensate for its direct negative inotropic properties; however, hypotension, bradycardia, and even cardiac arrest may occur in patients with diminished myocardial contractility. Arrhythmia (arrhythmia exacerbation) has also been reported in patients receiving ketamine.

Mechanism Of Action Indirect sympathomimetic activation and an increase in endogenous catecholamines stimulate the cardiovascular system by producing a dose-related increase in blood pressure, heart rate, and cardiac output. In general, indirect sympathomimetic effects compensate for ketamine's direct negative inotropic effect. However, direct negative inotropic effects may predominate in patients with exhausted catecholamine stores or maximal sympathetic stimulation (e.g., critically ill patients, those with diminished myocardial contractility) and hypotension may occur. Stimulation of cholinergic receptors mediates cerebral vasodilation, increased systemic perfusion pressures, and elevated intracranial pressure. Cholinergic stimulation is also responsible for increased salivary and bronchial gland secretions.

Contraindications And Precautions Ketamine is contraindicated in patients for whom a significant elevation of blood pressure would constitute a serious hazard , such as those with uncontrolled hypertension, aneurysm, thyrotoxicosis, or a history of stroke. Monitor patients with increased intracranial pressure in a setting with frequent neurologic assessments. Use ketamine with great caution in any patient with the potential for increased intracranial pressure, including those with head trauma, intracranial mass lesions or abnormalities, intracranial bleeding, and hydrocephalus. Alternative agents may be preferable in patients with known structural barriers to normal cerebrospinal fluid flow. Similarly, use ketamine with caution in patients with increased intraocular pressure (e.g., glaucoma), ocular trauma, or those undergoing ocular surgery. Ketamine can have direct negative inotropic properties and should be titrated cautiously in patients with poor ventricular function. The sympathomimetic effect of ketamine can produce elevations in blood pressure, heart rate, and cardiac output, which are typically mild-to-moderate. Ketamine increases coronary perfusion, enhancing myocardial contraction and increasing myocardial oxygen consumption. Hence, ketamine should also be used with caution in patients with cardiac disease, especially coronary artery disease (e.g., angina). Ketamine raises pulmonary arterial pressures somewhat more than systemic pressures and may exacerbate preexisting pulmonary hypertension or congestive heart failure. Monitor vital signs and cardiac function during ketamine administration. In addition, cardiac monitoring may be prudent in patients with thyroid disease requiring thyroid replacement therapy. Ketamine-induced hypertension and tachycardia can be attenuated with the administration of a benzodiazepine, a barbiturate, or a synthetic opioid.

Adverse Reactions Ketalar-induced hypertension and sinus tachycardia are dose-dependent and mediated through the sympathetic nervous system with the release of endogenous catecholamines. Elevation of blood pressure begins shortly after ketalar injection, reaches maximum levels within a few minutes, and usually returns to preanesthetic levels within 15 minutes of injection. In the majority of cases, the systolic and diastolic blood pressure peaks from 10% to 50% above baseline shortly after induction, but the elevation can be higher and longer in some patients. Ketalar-induced hypertension and tachycardia can be attenuated with the administration of a benzodiazepine, a barbiturate, or a synthetic opioid. In general, ketalar's indirect sympathomimetic effects compensate for its direct negative inotropic properties; however, hypotension, bradycardia, and even cardiac arrest may occur in patients with diminished myocardial contractility. Arrhythmia (arrhythmia exacerbation) has also been reported in patients receiving ketalar.

Reference 3

3.

Food and Drug Administration (DailyMed).

Publish date: May 5, 2024.

Pharmacodynamics 12.2 Pharmacodynamics Nervous System Ketamine is a rapidly-acting general anesthetic producing a dissociative anesthetic state characterized by profound analgesia, normal pharyngeal-laryngeal reflexes, normal or slightly enhanced skeletal muscle tone, cardiovascular and respiratory stimulation, and occasionally a transient and minimal respiratory depression. The mechanism of action is primarily due to antagonism of N-methyl-D-aspartate (NMDA receptors) in the central nervous system. Ketamine can produce nystagmus with pupillary dilation, salivation, lacrimation, and spontaneous limb movements with increased muscle tone through indirect sympathomimetic activity. Ketamine produces analgesia. Ketamine-induced emergence delirium can be reduced with benzodiazepines. Cardiovascular System Ketamine increases blood pressure, heart rate, and cardiac output. Cardiovascular effects of ketamine are indirect and believed to be mediated by inhibition of both central and peripheral catecholamine reuptake. Elevation of blood pressure reaches a maximum within a few minutes of injection and usually returns to preanesthetic values within 15 minutes. In the majority of cases, the systolic and diastolic blood pressure peaks from 10% to 50% above preanesthetic levels shortly after induction of anesthesia, but the elevation can be higher or longer in individual cases. Respiratory System Ketamine is a potent bronchodilator suitable for anesthetizing patients at high risk for bronchospasm.

Reference 4

4.

Food and Drug Administration (DailyMed).

Publish date: June 5, 2023.

Pharmacodynamics 12.2 Pharmacodynamics Nervous System Ketamine is a rapidly-acting general anesthetic producing a dissociative anesthetic state characterized by profound analgesia, normal pharyngeal-laryngeal reflexes, normal or slightly enhanced skeletal muscle tone, cardiovascular and respiratory stimulation, and occasionally a transient and minimal respiratory depression. The mechanism of action is primarily due to antagonism of N-methyl-D-aspartate (NMDA receptors) in the central nervous system. Ketamine can produce nystagmus with pupillary dilation, salivation, lacrimation, and spontaneous limb movements with increased muscle tone through indirect sympathomimetic activity. Ketamine produces analgesia. Ketamine-induced emergence delirium can be reduced with benzodiazepines. Cardiovascular System Ketamine increases blood pressure, heart rate, and cardiac output. Cardiovascular effects of ketamine are indirect and believed to be mediated by inhibition of both central and peripheral catecholamine reuptake. Elevation of blood pressure reaches a maximum within a few minutes of injection and usually returns to preanesthetic values within 15 minutes. In the majority of cases, the systolic and diastolic blood pressure peaks from 10% to 50% above preanesthetic levels shortly after induction of anesthesia, but the elevation can be higher or longer in individual cases. Respiratory System Ketamine is a potent bronchodilator suitable for anesthetizing patients at high risk for bronchospasm.

Clinical Pharmacology 12 CLINICAL PHARMACOLOGY 12.1 Mechanism of Action Ketalar (ketamine hydrochloride), a racemic mixture of ketamine, is a non-selective, non-competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor, an ionotropic glutamate receptor. The major circulating metabolite of ketamine (norketamine) demonstrated activity at the same receptor with less affinity. Norketamine is about 1/3 as active as ketamine in reducing halothane requirements (MAC) of the rat. 12.2 Pharmacodynamics Nervous System Ketamine is a rapidly-acting general anesthetic producing a dissociative anesthetic state characterized by profound analgesia, normal pharyngeal-laryngeal reflexes, normal or slightly enhanced skeletal muscle tone, cardiovascular and respiratory stimulation, and occasionally a transient and minimal respiratory depression. The mechanism of action is primarily due to antagonism of N-methyl-D-aspartate (NMDA receptors) in the central nervous system. Ketamine can produce nystagmus with pupillary dilation, salivation, lacrimation, and spontaneous limb movements with increased muscle tone through indirect sympathomimetic activity. Ketamine produces analgesia. Ketamine-induced emergence delirium can be reduced with benzodiazepines. Cardiovascular System Ketamine increases blood pressure, heart rate, and cardiac output. Cardiovascular effects of ketamine are indirect and believed to be mediated by inhibition of both central and peripheral catecholamine reuptake. Elevation of blood pressure reaches a maximum within a few minutes of injection and usually returns to preanesthetic values within 15 minutes. In the majority of cases, the systolic and diastolic blood pressure peaks from 10% to 50% above preanesthetic levels shortly after induction of anesthesia, but the elevation can be higher or longer in individual cases. Respiratory System Ketamine is a potent bronchodilator suitable for anesthetizing patients at high risk for bronchospasm.

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