In fact, I very rarely see a drop in blood pressure when I use it for RSI even in significantly shocked patients. One should however try to remain open to evidence that disconfirms ones biases, lest we allow science to be replaced by religion. I therefore was interested to read a report of two cases of cardiac arrest following the administration of ketamine for rapid sequence intubation (RSI)(1).
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 does ketamine cause cardiac arrest oxygen consumption, as well, that could attribute to observed cardiac effects, specifically in patients with underlying cardiac disease 4-6.
- Additionally, we appreciate the guidance and expertise provided by the cardiology department throughout the diagnostic process and treatment of this complex case.
- On the second postoperative day, and upon removal of a chest drain with the use of ketamine for sedation, the patient suffered cardiopulmonary arrest.
- The unauthorized non-medical use of ketamine has increased in the United States over the past two decades.
- As noted previously, each patient in the study received dose as part of their procedural sedation.
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).
Figure 3.
Heart failure in young adults is uncommon and known etiologies include familial cardiomyopathy, peripartum cardiomyopathy, and tachycardia-induced cardiomyopathy. Less frequently heart failure can be seen in spontaneous coronary artery dissection, malignant hypertension, or illicit drug use such as cocaine use disorder8. We report a case of acute systolic heart failure likely secondary to street ketamine use disorder. 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).
- Although these reactions can be quickly treated with a benzodiazepine, hypertension and tachycardia are often seen during these episodes, along with hallucinations and panic.
- The second dose of Althesin caused changes similar to those following the first dose, but less marked.
- In spite of it’s reputation as a “date rape” drug, ketamine actually offers certain medical benefits as an surgical anesthetic agent.
- Another limitation was possible effects of other medications used in the sedation.
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.
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 to standard urine toxicology.
Cardiac sympathetic remodelling and β-NGF expression after ketamine treatment in rats
We present 2 critically ill patients who experienced cardiac arrest following the administration of ketamine for rapid sequence intubation (RSI). The literature regarding the use of etomidate and ketamine for RSI in critically ill patients is reviewed and options for sedation during endotracheal intubation in this population are discussed. In a 2012 case report by Dewhirst et al. 4, two critically ill patients suffered from cardiovascular arrest following ketamine administration for rapid sequence intubation.
Treatment Considerations
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).
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.
Terminal deoxynucleootidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining
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.
Pain
The patient was discharged on GDMT and a follow-up echocardiogram showed an improvement in EF to 50%. 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. The patient was controlled under mechanical ventilation for 24 hours with synchronised intermittent mandatory ventilation mode pressure support then weaned gradually and extubated on the third postoperative day. She recovered well and was transferred to the Surgical Ward where she completed her recovery and was subsequently discharged a week later without further complications.
Ketamine is 2-(0-Chlorophenyl)-2-(methylamino)-cyclo-hexanone hydrochloride, a phencyclidine derivative that was introduced in 1965. 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.
Figure 3. Baseline ECG on Second Visit.
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.
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.
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