The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes.
Cardiac Arrest Following Ketamine Administration for Rapid Sequence Intubation
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. A major limitation of the study was the use of a convenience sample to recruit subjects. Another limitation was possible effects of other medications used in the sedation. Timing of ECG obtained during sedation likely had some variability with attempt made to adhere to the one-minute post ketamine administration time frame. 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.
Figure 2. Variability of Vital Signs During Sedation.
One patient in the ischemia group had been enrolled in this study previously on a separate patient encounter. As noted previously, each patient in the study received dose as part of their procedural sedation. However, it was not a requirement for ketamine to be the sole sedating agent during the sedation. Other agents, including propofol, opioid analgesics, and anti-emetics, specifically ondansetron, were administered during the procedural sedations at the discretion of the treating provider (Figure 1). Sedation protocol was decided by the physician primarily managing patient’s care and was not influenced by the research team.
Figure 1.
We report a case of an 8-year-old girl, previously diagnosed with tetralogy of Fallot who presented for operative correction of the congenital anomaly. On the second postoperative day, and upon removal of a chest drain with the use of ketamine for sedation, the patient suffered cardiopulmonary arrest. After repeated cycles of resuscitation, the patient returned to spontaneous circulation. Three rats (30%) in the ketamine group died at day 45, 50 and 52 of drug administration, while all rats survived through the entire procedure in the other three groups. Rats in the control and metoprolol alone groups gained weight steadily, while the ketamine-treated rats appeared to have thin, brittle and dull fur.
- Recruitment occurred during hours when the three-person research team members were working clinically in the ED.
- Ketamine-treated rats co-administered metoprolol were in a better state of nutrition and more stable emotionally than those treated only with ketamine.
- We do not receive any commission or fee that is dependent upon which treatment provider a caller chooses.
Table 1. Electrocardiogram Manifestations of Acute Myocardial Ischemia.
Ketamine, an N-methyl-D-aspartate receptor antagonist, has been found to exert analgesic effects in humans and is widely used as a dissociative anaesthetic. However, in the past decade, the application of ketamine has been considered as a double-edged sword. On the one hand, it is used as an anaesthetic agent, especially in paediatric and geriatric short-lasting surgeries.
Effects of administration of ketamine (Ket) for 12-weeks on sympathetic sprouting and distribution of nerve fibres. Procedural sedation for various indications commonly takes place in the ED setting. Common dosing for ketamine when given intravenously for procedural sedation ranges from 0.25 mg/kg to 1 mg/kg, depending on if other anesthetic and/or analgesic medications are concomitantly administered. 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). 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.
Table 2. Patient Characteristics.
Adverse ReactionsKetalar-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. 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.
ECGs were reviewed for any ischemic changes from the baseline to post-ketamine ECG, with the two ECGs directly compared to one another. Patient demographics, blood pressure, heart rate, and comorbidity data were retrospectively collected from the electronic medical record. 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.
Ketamine & cardiovascular stability
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. Injection of ketamine, the rats became overexcited and dysphoretic for about 1–3 min. They suffered nystagmus, clonus, hind limb stand followed by immediate falling down.
The authors commented that the patients were septic, hypovolemic or cirrhotic and had severe stress preoperatively. It is possible that in these ill patients, adrenocortical and catecholamine stores had been depleted prior to ketamine administration. Alternatively, in the setting of prolonged preoperative stress, there may be resistance to further sympathetic and/or adrenocotical stimulation by ketamine. In either case, preoperative stress may blunt the usual physiologic responses to ketamine, setting the stage for possible adverse effects.
- In fact, I very rarely see a drop in blood pressure when I use it for RSI even in significantly shocked patients.
- It differs from other intravenous anesthetics in many respects, and produces dissociative anesthesia rather than generalised depression of the central nervous system.
- 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.
- Three rats (30%) in the ketamine group died at day 45, 50 and 52 of drug administration, while all rats survived through the entire procedure in the other three groups.
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. To our knowledge, this is the first case describing an association of ketamine with acute systolic heart failure. Primary outcome was the incidence of new changes suggestive of myocardial ischemia apparent on ECG. Ischemia was defined using the third universal criteria from the Task Force for the Universal Definition of Myocardial Infarction (Table 1) 7.
Computed tomography (CT) scan of the chest and abdomen showed bilateral pleural effusions with congestive hepatopathy and ascites. I ‘jumped ship’ from etomidate to ketamine for rapid sequence intubation does ketamine cause cardiac arrest (RSI) in sick patients about seven years ago. I’ve been one of the aggressive influences behind my prehospital service’s switch to ketamine as the standard induction agent for prehospital RSI. It’s no secret that I think propofol has no place in RSI in the critically ill.I love ketamine for its haemodynamic stability compared with other induction agents.