Even with high-quality chest compressions, only a fraction of cardiac output may be achieved 8. Thus, inevitably, after restoration of circulation, ischemia–reperfusion brain injury ensues. To mitigate its effects on neuronal and glial cells, various interventions are employed with the intention of decreasing the cerebral metabolic rate. It is included in the 2021 does ketamine cause cardiac arrest revision of the European Resuscitation Council (ERC) guidelines for post-resuscitation care by Nolan et al.
Is Ketamine safe for TBI patients?
In 2024, Shafique and colleagues94 published a comprehensive review of the literature comparing S-ketamine and R-ketamine in depression. This review highlights the potential of R-ketamine to provide more potent and longer-lasting antidepressant effects compared with S-ketamine. Although there are promising animal and preclinical studies, the authors caution that overall data on R-ketamine in humans are limited. Ketamine has gained popularity as an anaesthetic agent owing to its favourable cardiovascular effects in haemodynamically compromised patients.
Figure 2. Variability of Vital Signs During Sedation.
Individuals should be counselled on these potential side effects and screening should be considered in patients with a history of ketamine use presenting with acute systolic heart failure. Large-scale studies are required to establish this association and formulate management strategies. Chronic treatment with ketamine caused significant ventricular myocardial apoptosis, fibrosis and sympathetic sprouting, which altered the electrophysiological properties of the heart and increased its susceptibility to malignant arrhythmia that may lead to sudden cardiac death.
1. Study Design, Setting, and Ethical Considerations
She reported using ketamine twice weekly along with smoking half a pack of cigarettes daily. She denied any family history of cardiac diseases and never experienced similar symptoms previously. Physical examination showed basal crackles on lung auscultation and 2+ bilateral lower extremity oedema. She had a troponin level of 0.07 ng/ml and a B-type natriuretic peptide (BNP) level of 2511 pg/ml. Electrocardiogram was normal sinus rhythm (Fig. 1) and transthoracic echocardiography (TTE) showed left ventricular ejection fraction (EF) of 15%, dilated left ventricle, and severe tricuspid and mitral regurgitation (Fig. 2 and Fig. 3).
- Prospectively, a convenience sample of patients older than 50 years receiving ketamine for procedural sedation in the ED was used.
- Arrhythmia (arrhythmia exacerbation) has also been reported in patients receiving ketalar.
- Ketamine, the NMDA antagonist, acts on the sympathetic nervous system causing haemodynamic effects, i.e., tachycardia and hypertension, potentially facilitating recovery of systemic blood pressure during CPR.
Ketamine and increased intracranial pressure
- The purpose of this paper is to investigate the relationship between cardiovascular measures and psychometric outcomes in the course of intravenous ketamine treatment in treatment refractory inpatients with MDD and BP.
- The cardiovascular stimulation-inhibition balance of ketamine may be altered by severe critical illness, and doses of any induction agent should be significantly reduced in critically ill patients.
- 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.
- She had a troponin level of 0.07 ng/ml and a B-type natriuretic peptide (BNP) level of 2511 pg/ml.
- Check with your medical doctor or dentist before taking any of the above while you are receiving this medicine.
A rough epicardium and notable grey areas were found on the gross view of the hearts in ketamine-treated rats and rabbits. The epicardium in the ketamine plus metoprolol-treated animals showed no obvious grey and rough areas. As demonstrated in Figure 4A–C, the normal cardiomyocytes contained compactly arranged fibres with no intercellular space under the light microscopy in the control group, while in the ketamine group, cardiomyocytes were hypertrophic, oedematous and severely degenerated. In the ischemia group, the median dose was higher than the milligram per kilogram dosing of the non-ischemia group (0.84 vs. 0.56).
Systemic blood pressure, heart rate, cardiac output, cardiac work, and myocardial oxygen requirements all are increased after IV administration of ketamine cardiovascular effects . The cardiovascular-stimulating effects are blunted or prevented by prior administration of benzodiazepines or concomitant administration of inhaled anesthetics, including nitrous oxide. Given their relative hemodynamic stability, ketamine and etomidate are commonly chosen anesthetic agents for sedation during the endotracheal intubation of critically ill patients. As the use of etomidate has come into question particularly in patients with sepsis, due to its effect of adrenal suppression, there has been a shift in practice with more reliance on ketamine. However, as ketamine relies on a secondary sympathomimetic effect for its cardiovascular stability, cardiovascular and hemodynamic compromise may occur in patients who are catecholamine depleted.
Those left with significant neurological deficits may become reliant on the healthcare system for additional support for years following their CA. The purpose of this scoping review is to explore the utility of ketamine in post‐CA management to improve neurological outcomes of CA survivors. Cardiorespiratory effects of ketamine and Althesin were measured in two groups of premedicated patients with cardiac disease. The drugs were given in clinically equivalent doses with a second dose administered about 10 min after induction. The first dose of ketamine caused a marked increase in systemic and pulmonary arterial pressure, heart rate, and central venous and wedge pressures and cardiac index. The first dose of Althesin caused a decrease in systemic arterial pressure, central venous pressure, cardiac index and heart work, but little change in heart rate.
Structural and functional alterations after ketamine treatment in rabbits
ECGs were obtained prior to sedation and during the sedation approximately one minute after administration of ketamine. One minute was chosen as evaluation time, given the onset of intravenous ketamine being estimated at 30 seconds. ECGs were only obtained for the purpose of the study and were not standard of care at this institution for patients undergoing a procedural sedation. ECGs were obtained on Mortara ELI 350 and ELI 380 machines (Mortara Instrument Inc., Milwaukee, WI). ECGs were reviewed by the physician performing the sedation during acute care for any abnormal findings.
In addition, levels of CRP were found to be lower across all subjects in the ketamine group compared to the control.34 Further information is summarized in Table 1. One opportunity for clinical intervention to attenuate damage caused by excitotoxicity is the administration of ketamine. If ketamine is administered following CA upon hospital admission for sedation, it may be effective in inhibiting the above‐mentioned apoptotic cascades, thus resulting in improved neurologic outcomes. Ketamine exhibits antidepressant properties in treatment-resistant depression (TRD) with some concern over its cardiovascular safety and tolerability issues. This paper reports on the cardiovascular safety in short-term intravenous ketamine treatment in TRD inpatients with major depressive disorder (MDD) and bipolar disorder (BP).
Cardiovascular adverse events
It differs from other intravenous anesthetics in many respects, and produces dissociative anesthesia rather than generalised depression of the central nervous system. Ketamine has bronchodilating effects, and protective airway reflexes are preserved to some extent. Because of the sparing of these reflexes, an increase in secretions, coughing, hiccup and laryngospasm are more prevalent than with thiopental 1. Ketamine has direct negative inotropic and vasodilating activity, but these effects usually are overwhelmed by the indirect sympathomimetic action of the drug 2. Flow chart of the medical record review process for nontraumatic adult patients admitted to the emergency department due to sudden cardiac arrest.
Interest in using ketamine to treat numerous psychiatric conditions has gained traction over recent years. These include major depressive disorder (MDD), posttraumatic stress disorder (PTSD), and substance misuse. Ketamine in this application has the additional benefits of few to no life-threatening adverse effects of accidental intravenous or intrathecal administration. All authors have met authorship requirements, and the final manuscript was approved by all authors. This manuscript has not been published elsewhere and is not under consideration by another journal.
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