Sedatives are described as a variety of therapeutic substances that decrease cerebral function and can produce a continuum of cognitive states, from minimal sedation to general anaesthesia. Analgesics have pain relief activity and work on the physiological mechanisms of pain. There are many classes of analgesics, but opioid analgesics, acting through opioid receptors, remain the mainstay of therapy for alleviating pain in critically ill patients. In 2014, Yan and Jiang109 reviewed preclinical and clinical data, suggesting the neurotoxic and neuroprotective effects of ketamine may depend on dose, exposure frequency, and the presence or absence of noxious stimuli. does ketamine cause cardiac arrest This was highlighted by Brown and colleagues110 in 2015, who found that lower doses (5 mg kg−1) prevented apoptosis, whereas higher doses (20 mg kg−1) induced apoptosis.

For example, in 2004, Porter54 published a case series of 32 pre-hospital adult and paediatric trauma patients treated by the British Association of Immediate Care Scheme (BASICS). Porter54 described ketamine as safe and effective for analgesia and anaesthesia in a mixed cohort of pre-hospital trauma patients, with no significant adverse airway effects and maintained blood pressure in patients with hypotension. Results indicated a decrease in neurocognitive functioning compared to baseline in seven patients in the ketamine group versus 21 patients in the placebo group.

  • Given its side-effects and potential for abuse, the exact role of ketamine as an analgesic, particularly in the outpatient or community setting is still unclear.
  • In 2024, Shafique and colleagues94 published a comprehensive review of the literature comparing S-ketamine and R-ketamine in depression.
  • MO was responsible for conducting the literature search alongside research librarians, reviewing relevant sources, writing the manuscript, and referencing the works cited.
  • 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.
  • 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).

Cardiac arrest following ketamine administration for rapid sequence intubation

In either case, preoperative stress may blunt the usual physiologic responses to ketamine, setting the stage for possible adverse effects. The authors propose that the administration of ketamine following ROSC in CA patients may result in improved neurologic outcomes. However, evidence from the literature is indirect, based on in vitro or other neurological models, and thus should be interpreted cautiously.

Metabolic Risk Factors and Cardiovascular Safety in Ketamine Use for Treatment Resistant Depression

  • Physical examination showed basal crackles on lung auscultation and 2+ bilateral lower extremity oedema.
  • Although ketamine use disorder is increasing, data on long-term side effects is minimal.
  • Respiratory System Ketamine is a potent bronchodilator suitable for anesthetizing patients at high risk for bronchospasm.
  • Despite increasing recreational use, there are very few statistics available on ketamine-related deaths.
  • This is especially true in patients who are hemodynamically unstable or in other “low flow” low cardiac output states.

This medicine will add to the effects of alcohol and other CNS depressants (medicines that make you drowsy or less alert). Some examples of CNS depressants are barbiturates or medicine for seizures or other anesthetics, including some dental anesthetics. Check with your medical doctor or dentist before taking any of the above while you are receiving this medicine. The tumour-suppressing properties of ketamine may also relate to immune modulation.

Ketamine is also being used off-label to manage pain and multiple studies have reported it to be safe and effective2. Major side effects include nausea, vomiting, tachycardia, tachypnea, convulsion, temporary paralysis, and hallucinations3. Effects of administration of ketamine (Ket) for 12-weeks on sympathetic sprouting and distribution of nerve fibres. In the study by Aya et al. ketamine induced a concentration-dependent lengthening of the RR interval and slowed ventricular conduction and prolonged refractoriness without changing anisotropy or increasing dispersion of refractoriness. However, no arrhythmia could be induced by ketamine, regardless of its concentration. There is evidence that ketamine cardiovascular effects enhances the dysrhythmogenicity of epinephrine.

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does ketamine cause cardiac arrest

Clinical Pharmacology12 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.

Despite the uncertainty over the neurotoxic or neuroprotective properties of NMDA antagonists, their benefits in specific diseases have been explored. In the 1980s, Olney and colleagues107 identified intracellular vacuolation and mitochondrial lysis, or ‘Olney’s lesions’, relating to high-dose NMDA antagonist exposure. Olney and colleagues108 also noted that the immature human brain (from 6 months of gestation through to several years after birth) is especially vulnerable to apoptosis and neuronal death from NMDA antagonist or GABA-like exposure. In the UK, there are fortunately few natural disasters resulting in the need for surgical procedures to be performed in austere environments. However, pre-hospital medicine has become a well-established practice, with ketamine being a useful agent for pre-hospital practitioners.

Associated Data

The best way to provide your battalion medical providers with the information they need is to know it yourself. For many PAs and Doctors, the use of ketamine in battlefield medicine is a relatively new and unknown concept. Although ketamine has been used in hospitals throughout the world for several decades, there are still many myths and misconceptions surrounding it. Ketamine is an excellent analgesic because it is highly effective and has a very wide therapeutic window. The goal of this page is to give the medic a resource for engaging with their battalion PA or Surgeon regarding the use of ketamine.

does ketamine cause cardiac arrest

Rats in the control and metoprolol alone groups gained weight steadily, while the ketamine-treated rats appeared to have thin, brittle and dull fur. In addition, they were emotionally unstable, more aggressive and easily became anxious. Ketamine-treated rats co-administered metoprolol were in a better state of nutrition and more stable emotionally than those treated only with ketamine. Growing evidence suggests that long-term abuse of ketamine does harm the heart and increases the risk of sudden death. The present study was performed to explore the cardiotoxicity of ketamine and the protective effects of metoprolol.

The subjects were removed due to a change in sedation medication or the decision to forego procedural sedation. There were 31 ECGs included in the final evaluation, with two patients enrolled on subsequent visits. The overall study cohort had a median age of 63 years, with orthopedic manipulation as the most common indication for sedation (Table 2). Post-ketamine vital signs showed a notable change in 29% (9/31) of initial readings and 71% (22/31) of readings at any point during the sedation.

Ketamine Cardiovascular Effects

Ketamine has been reported to cause apnea and respiratory depression with rapid IV push. Apnea can be avoided through conscientious administration by slow IV push and by consideration of factors such as known airway anatomical issues or instability. In summary, ketamine was discovered in 1962 and is primarily known as an NMDA receptor antagonist that provides dose-dependent analgesic, sedative, and anaesthetic effects. Ketamine exerts effects on NMDA, dopaminergic, serotonergic, adrenergic, cholinergic, opioid, and sigma receptors resulting in diverse and potentially beneficial properties in a variety of clinical settings. A total of 73 articles were retrieved based on the results of the second search and 71 during the last search. All three sets of results revealed no clinical trials that have directly investigated the application of ketamine as sedation to improve neurological outcomes.

Clinically, the myocardial depressant properties of ketamine are overridden by its sympathetic nervous system stimulating properties. When systemic catecholamine has been depleted or when the patient is under deep anesthesia, the myocardial depressant properties of ketamine may predominate 7. In Sudan and when there is a lack of anesthetist and equipment, ketamine should be administered with caution and with standard monitoring as guided by the Association of Anaesthetist of Great Britain and Ireland, and resuscitation kit prepared. Due to its hemodynamic stability, ketamine is a commonly used anesthetic agent for sedation during small procedures in the critical care unit.

We sought to discover if patients greater than 50 years of age who received ketamine during routine procedural sedation would have changes suggestive of cardiovascular ischemia seen on an ECG performed during the sedation. Strict monitoring protocols are standard practice during ketamine administration. Before treatment begins, a thorough screening process is conducted to identify any pre-existing heart conditions that could elevate risk. This assessment helps ensure that only suitable candidates receive the medication. In effect, ketamine’s mechanism of action within the brain can cause real problems when taken in large amounts, so cardiac arrest is definitely possible.