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. Ketamine’s effect on the cardiovascular system has been mentioned in the literature on multiple occasions.
Ketamine’s clinical and antidepressant effects can be influenced by co-administration of other drugs, though these interactions are variable and not yet fully understood. A 28-year-old female with a history of ketamine use disorder with multiple genitourinary complications presented with progressive bilateral lower extremity oedema that started 3 months prior. She also reported shortness of breath, orthopnoea, chronic cough, and decreased exercise tolerance. She reported using ketamine twice weekly along with smoking half a pack of cigarettes daily.
Links to NCBI Databases
On the other hand, there are more and more concerns regarding the increasing abuse of ketamine, particularly by young people in social settings. Reports have indicated that ketamine, or ‘Special K’ as it is also known, is being used recreationally in the UK, Sweden, Australia, USA and many other parts of the world (Dillon et al., 2003). This rapidly spreading misuse could result in perceptual distortions, thought disorders, emotional withdrawal and ‘melting into the surrounding’. Severe addictive practices induced by ketamine abuse are difficult to control and incite abusers to progressively increase ketamine doses. More importantly, long-term use of ketamine may damage the cardiovascular system and increase the risk of sudden death (Weiner et al., 2000). Echocardiography under ketamine–xylazine anaesthesia revealed an increased left ventricular (LV) wall thickness and a decreased LV lumen diameter (Kamphoven et al., 2001).
Does Ketamine Cause Cardiac Arrest?
Major side effects include nausea, vomiting, tachycardia, tachypnea, convulsion, temporary paralysis, and hallucinations3. Ketamine’s effects on the heart can have long-term consequences for people who use this drug on a regular basis. According to the Journal of Advances in Clinical Toxicology, the brain’s inability to communicate with the cardiovascular system as normal takes a toll on the heart over time.
Ketamine is an agent commonly used in emergency department procedural sedations due to its anesthetic and analgesic properties and respectable safety profile. Mild to moderate transient increases in blood pressure, heart rate, and cardiac output are common due to ketamine’s increase in sympathetic activity. Often this is a desirable effect of ketamine that may help to avoid peri-procedural hypotension. However, there is a concern that these physiological changes could result in an increased myocardial oxygen demand that may exacerbate underlying cardiac disease. Avoidance is recommended for patients with known coronary artery disease, older adults with risk factors for coronary artery disease, or those who are already hypertensive or tachycardic 1. ECGs were obtained prior to sedation and during the sedation approximately one minute after administration of ketamine.
Adverse effects
- Unlike other types of hallucinogen drugs, the brain develops a tolerance for ketamine at a rapid rate.
- Follow-up transthoracic echocardiogram showing left ventricular ejection fraction of 54% using the biplane Simpson method with normal left ventricular size.
- A rough epicardium and notable grey areas were found on the gross view of the hearts in ketamine-treated rats and rabbits.
- Tao et al. described a case of chronic ketamine poising and myocardial fibrosis with hyaline degeneration of small arteries in a 34-year-old woman6.
- The authors commented that the patients were septic, hypovolemic or cirrhotic and had severe stress preoperatively.
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.
- 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.
- Ketamine’s clinical and antidepressant effects can be influenced by co-administration of other drugs, though these interactions are variable and not yet fully understood.
- Myocardial ischemia has been reported for ketamine 2,8; however, it is unclear how soon after medication administration that this could result, namely in the immediate, post-administration timeframe (specifically one minute post administration).
- Intubation was difficult to perform due to laryngospasm, and the endotracheal tube was stuck on the vocal cords but finally inserted and resuscitation was successful.
So ketamine misapplication is not only a drug abuse problem, but could also cause long-term disruption of the cardiovascular system. However, there have been few experimental studies performed to investigate ketamine-induced toxic effects on the cardiovascular system and a corresponding pharmacological therapeutic strategy. Secondly, we assessed the protective effects of metoprolol against ketamine-induced cardiac toxicity. 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.
Cardiac Arrest Following Ketamine Administration for Rapid Sequence Intubation
In our study, AIF was up-regulated after ketamine, indicating that PARP-1–AIF pathway may play an important role in this process. NF-κB is a family of inducible transcription factors that plays an anti-apoptotic role in cell cycling by regulating the expression of genes involved in apoptosis and cell proliferation. NF-κB induces the synthesis of important anti-apoptotic proteins that regulate caspase-8 activation and also limit the duration of JNK activity via several mechanisms (Salaun et al., 2010). Recent evidence supports a role for PARP-1 as a transcriptional co-regulator in the control of NF-κB (Kraus and Lis, 2003).
Ketamine’s effects develop out of changes in the brain’s glutamate neurotransmitter levels. Glutamate chemical levels work to maintain a normal level of activity between the brain’s cells. This process enables the brain and body to communicate with one another on a continuous basis. Ketamine’s ability to interfere with cardiovascular functions does come with considerable risks, one of which being cardiac arrest. We would like to express our gratitude to the patient for allowing us to share her clinical history in this case report.
The patients..were septic, hypovolemic, or cirrhotic, and had severe stress preoperatively. It is possible that in these ill patients adrenocortical and catechol stores had been depleted prior to ketamine administration. Although these reactions can be quickly treated with a benzodiazepine, hypertension and tachycardia are often seen during these episodes, along with hallucinations and panic. This can cause an increase in oxygen consumption, as well, that could attribute to observed cardiac effects, specifically in patients with underlying cardiac disease 4-6.
Ketamine & cardiovascular stability
Although ketamine use disorder is increasing, data on long-term side effects is minimal. Screening for ketamine use disorders should be considered in patients presenting with acute systolic heart failure. Long-term studies are needed to evaluate the benefits of adding ketamine screening does ketamine cause cardiac arrest to standard urine toxicology.
PARP is a protein involved with a series of cellular processes including DNA repair and programmed cell death, cardiac hypertrophy and fibrosis. We observed that after chronic treatment with ketamine, PARP-1 expression was significantly elevated, suggesting its role in ketamine-induced apoptosis and fibrosis. AIF is involved in a caspase-independent pathway of apoptosis by translocating to the nucleus and causing large-scale DNA fragmentation and chromatin condensation. Translocation of AIF from mitochondria to the nucleus is required for PARP-1-mediated cell death (Kang et al., 2004).
Table 1. Electrocardiogram Manifestations of Acute Myocardial Ischemia.
After 15–25 min, they recovered completely without any treatment, but looked tired. These reactions lasted for 1–3 min after injection, and full recovery required 15–25 min. With chronic ketamine abuse, one or more of the above symptoms can escalate to the point where cardiac arrest occurs. Due to its hemodynamic stability, ketamine is a commonly used anesthetic agent for sedation during small procedures in the critical care unit.
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