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.
Relationships between levels and effects
- In our case, the patient had elevated troponins along with an EF of 15% which improved in 2–4 weeks.
- 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.
- The study took place at an academic medical center with a level-one trauma designation that serves as a regional referral center for orthopedic injuries and other specialty care.
- One should however try to remain open to evidence that disconfirms ones biases, lest we allow science to be replaced by religion.
- It is a drug of choice for short-term procedures when muscle relaxation is not required.33 The effect of ketamine on the respiratory and circulatory systems is different from that of other anesthetics.
A similar case report to ours showed that upon administration of intravenous (IV) ketamine, a patient experienced delusions, tachycardia, hypertension, and 1 mm ST depression in V3–V6 on ECG with elevated troponins. Cardiac catheterization showed no significant coronary artery disease, and the echocardiogram showed a left ventricular EF of 45% with moderate apical hypokinesis which improved to 60% the following day14. In this ketamine-induced model of cardiac toxicity, the PARP–AIF/NF-κB pathways may contribute to structural remodelling, while β-NGF may play an important role in sympathetic remodelling. Metoprolol was effective in preventing the ketamine-induced cardiac toxicity in our experiments.
- On the other hand, there are more and more concerns regarding the increasing abuse of ketamine, particularly by young people in social settings.
- It is possible that in these ill patients adrenocortical and catechol stores had been depleted prior to ketamine administration.
- Electrocardiogram showed normal sinus rhythm and transthoracic echocardiography (TTE) showed left ventricular ejection fraction (EF) of 15%, dilated left ventricle, and severe tricuspid and mitral regurgitation.
- There were 31 ECGs included in the final evaluation, with two patients enrolled on subsequent visits.
Figure 2. Variability of Vital Signs During Sedation.
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).
Expression of apoptosis related proteins PARP-1, AIF and NF-κB after ketamine administration in rats
In our case, the patient had elevated troponins along with an EF of 15% which improved in 2–4 weeks. The transient nature of acute systolic heart failure along with ruling out other possible etiologies leaves ketamine-induced heart failure as the most plausible explanation. The data on the management of ketamine induced heart failure is sparse and is mainly driven by similar case reports. Close follow-up and monitoring are required, and steps should be taken to ensure cessation of ketamine use.
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.
Figure 3.
The sympathomimetic effect of ketamine can produce elevations in blood pressure, heart rate, and cardiac output, which are typically mild-to-moderate. Ketamine increases coronary perfusion, enhancing myocardial contraction and increasing myocardial oxygen consumption. Hence, ketamine should also be used with caution in patients with cardiac disease, especially coronary artery disease (e.g., angina). Ketamine raises pulmonary arterial pressures somewhat more than systemic pressures and may exacerbate preexisting pulmonary hypertension or congestive heart failure. In addition, cardiac monitoring may be prudent in patients with thyroid disease requiring thyroid replacement therapy.
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.
Effect of Ketamine on Cardiovascular Function During Procedural Sedation of Adults
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All sedations had a nurse present for the sedation and a physician responsible for monitoring the patient separate from the procedural physician. All patients received continuous monitoring of blood pressure, heart rate, oxygen saturation, and end-tidal CO2. Prospectively, a convenience sample of patients older than 50 years receiving ketamine for procedural sedation in the ED was used. Recruitment occurred during hours when the three-person research team members were working clinically in the ED. Patients were offered enrollment after sedation choice was made by the treating provider, and informed consent was obtained if patients agreed to enrollment.
The incidence of myocardial ischemia following ketamine administration is unknown. Ketamine is included in the American Heart Association (AHA) list of medications that may cause or exacerbate heart failure and has been reported to precipitate myocardial ischemia in the elderly 2,3. There is limited evidence of ketamine precipitating myocardial ischemia during short-term use in the emergency department (ED). The cardiovascular stimulation-inhibition balance of ketamine may be altered by severe critical illness, and the doses of any induction agent should be significantly reduced in critically ill patients. It is a drug of choice for short-term procedures when muscle relaxation is not required.33 The effect of ketamine on the respiratory and circulatory systems is different from that of other anesthetics.
Alterations in cardiac electrophysiological properties after ketamine treatment in rabbits
Secondary outcomes included changes in vital signs after ketamine administration and a case-control analysis comparison of patients with changes suggestive of ischemia to those without. Clinically significant vital sign change was defined as an increase or decrease of greater than or equal to 20% from baseline. 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 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. In our case, we suspect catecholamine is depleted as our patient suffered from major stress and that could have been worsened by the rapid bolus which was given and the body failed to compensate. In isolated rabbit and canine hearts and in intact dogs, ketamine has been demonstrated to produce myocardial depression 7. At lower, sub-anesthetic doses, it is used as a treatment for pain and treatment-resistant depression. Metoprolol prevented the cardiotoxicity of ketamine, indicating a promising new therapeutic strategy.
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 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 does ketamine cause cardiac arrest 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.
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.
