Ketamine Use allows Noninvasive Ventilation in Distressed Patients with Acute Decompensated Heart Failure

Design

Case presentation

A 71-year-old female with a history of diabetes, hypertension, dilated cardiomyopathy, and permanent pacemaker implantation presented to the emergency department (ED) with severe respiratory distress and altered mental status. On arrival, she exhibited significant tachypnea, hypertension, hypoxia (oxygen saturation 75%), and bilateral lung crepitations. Despite oxygen therapy via reservoir mask, intravenous furosemide, and nitroglycerin infusion, her condition failed to improve, prompting initiation of bilevel positive airway pressure (BiPAP) ventilation.

Due to agitation and intolerance to BiPAP, sedation with an intravenous bolus of 30 mg ketamine was administered, enabling compliance and successful initiation of noninvasive ventilation. After approximately 30 minutes, an additional bolus of 15 mg ketamine was given to maintain sedation. Over the subsequent four hours, her respiratory parameters markedly improved, and she was weaned off BiPAP, maintaining stable vitals on minimal supplemental oxygen. Following further conservative management, she was discharged in stable condition after three days.

Study Author Conclusions

We believe that ketamine induced a dissociative state in the patient with acute decompensated heart failure (ADHF), facilitating noninvasive positive pressure ventilation (NIPPV) management in an otherwise uncooperative patient and allowing NIPPV to take effect. This led to the avoidance of an impending intubation. The patient had an uneventful stay in the hospital which could be attributed to the acute management in the ED. As emergency physicians, it should be our goal to avoid intubating patients and putting them on mechanical ventilation when other options may be attempted. Large series and trials would be required to establish the use of ketamine induced sedation in agitated, uncooperative patients of HF to allow compliance with NIPPV. Until then, we suggest it be used with caution in this subset of patients.

Ketamine-induced acute systolic heart failure

Design

Case presentation

A 28-year-old female with a 14-year history of ketamine use disorder who developed acute systolic heart failure reported progressive bilateral lower extremity edema, dyspnea, orthopnea, chronic cough, and reduced exercise tolerance over a three-month period. Physical examination revealed tachycardia at 118 bpm, bilateral lower extremity edema, and pulmonary crackles. Laboratory findings included an elevated troponin level of 0.07 ng/ml and a B-type natriuretic peptide (BNP) level of 2511 pg/ml. Transthoracic echocardiography (TTE) demonstrated a severely reduced left ventricular ejection fraction (LVEF) of 15%, a dilated left ventricle, and severe mitral and tricuspid regurgitation. Computed tomography (CT) imaging identified bilateral pleural effusions, congestive hepatopathy, and ascites.

Given the absence of ischemic disease and negative autoimmune markers, ketamine-induced cardiotoxicity was considered the most plausible etiology. Initial treatment included intravenous furosemide, metoprolol, and sacubitril/valsartan, which resulted in symptomatic improvement. A follow-up TTE performed two weeks later showed an increase in LVEF to 25% with moderate tricuspid regurgitation. After four months of guideline-directed medical therapy (GDMT) and cessation of ketamine use, repeat echocardiography revealed normalization of left ventricular function with an LVEF of 54% and resolution of chamber dilation.

Study Author Conclusions

Ketamine use disorder is becoming a major concern in the United States, and very little long-term data on its cardiovascular side effects are available. Ketamine has direct negative inotropic effects, central sympathetic stimulation effects, and neuronal catecholamine uptake inhibition effects. In patients with left ventricular dysfunction, sympathetic stimulation may not be adequate to overcome the negative inotropic effects, leading to decreased cardiac performance. Individuals should be counseled on these potential side effects, and screening should be considered in patients with a history of ketamine use presenting with acute systolic heart failure. Largescale studies are required to establish this association and formulate management strategies.

Ketamine’s love story with the heart: A Takotsubo twist

Design

Case presentation

A 49-year-old female who developed Takotsubo cardiomyopathy following procedural sedation with ketamine for a distal radius fracture reduction presented to a Level I trauma center after a motor vehicle collision with initial hemodynamic stability and an unremarkable cardiac ultrasound. Procedural sedation was achieved with intravenous diazepam followed by a total of 100 mg of ketamine, titrated to dissociation. Shortly after administration, the patient's systolic blood pressure spiked to 194 mmHg, peaking at 236 mmHg within 20 minutes. She subsequently experienced intermittent apnea, profound agitation, and cyanosis, leading to emergent airway management with bag-valve-mask ventilation. A bedside echocardiogram revealed diminished ejection fraction, and chest radiography demonstrated bilateral pulmonary edema. Electrocardiographic findings included new-onset conduction delay, T-wave inversions in leads I and aVL, and minimal ST elevations. Due to persistent hypoxia and agitation, clinicians proceeded with intubation. Hospital evaluation confirmed a diagnosis of Takotsubo cardiomyopathy with high-sensitivity troponin elevation to 3155 ng/L and an echocardiogram demonstrating severe left ventricular dysfunction with apical akinesis.

Cardiac catheterization on hospital day four ruled out obstructive coronary disease and revealed an improved ejection fraction of 55–60%. Standard treatment with diuresis and supportive care facilitated her rapid recovery, allowing extubation on hospital day one and discharge on day nine following orthopedic surgical fixation of her wrist fracture. Outpatient cardiology follow-up was unremarkable, though no echocardiogram was performed to confirm complete resolution.

Study Author Conclusions

The authors acknowledged previous studies that suggest that ketamine’s sympathomimetic activity may lead to increased myocardial oxygen demand and ischemia. One small study reported that 9.7% of patients developed myocardial ischemia, confirmed through an electrocardiogram, after ketamine. This report corroborates these findings, extending ketamine’s sympathomimetic effects further as a potential trigger for Takotsubo cardiomyopathy in susceptible patients, underscoring the need for clinicians to remain vigilant for stress-induced cardiac dysfunction even in cases where ketamine is traditionally considered safe.