What are the cardiovascular concerns with using ketamine as an induction agent for Rapid Sequence Intubation (RSI) in a Chronic Obstructive Pulmonary Disease (COPD) patient?

Cardiovascular Concerns with Ketamine for RSI in COPD Patients

Ketamine is the preferred induction agent for COPD patients requiring RSI due to its bronchodilation benefits, but paradoxical hypotension is the primary cardiovascular concern—particularly in patients with depleted catecholamine stores from chronic hypoxemia, cor pulmonale, or concurrent sepsis. 1

Primary Cardiovascular Risk: Paradoxical Hypotension

Despite ketamine's well-known sympathomimetic properties, critically ill COPD patients may experience paradoxical hypotension and even cardiovascular collapse when their endogenous catecholamine stores are depleted from:

• Prolonged respiratory distress 1
• Chronic hypoxemia 1
• Concurrent sepsis 1
• Chronic cor pulmonale 1

This paradoxical effect occurs because ketamine's cardiovascular stability depends on intact sympathetic nervous system reserves and adequate catecholamine stores. 2 When these are exhausted, ketamine's direct myocardial depressant effects predominate, leading to hypotension rather than the expected hemodynamic stability. 3

Evidence on Hemodynamic Instability

• Recent meta-analysis demonstrates ketamine is associated with higher post-induction hypotension compared to etomidate (RR 1.30,95% CI: 1.03-1.64), though this did not translate to mortality differences. 4
• Observational air medical data showed ketamine was associated with higher rates of both hypotension and cardiopulmonary arrest (18.3% vs 12.4% with etomidate), likely reflecting selection bias toward more unstable patients. 5
• The 2023 Society of Critical Care Medicine guidelines found mixed results regarding peri-intubation hemodynamics between ketamine and etomidate, with no difference in vasopressor duration or mortality. 6

Right Ventricular Dysfunction Considerations

COPD patients with cor pulmonale present unique cardiovascular vulnerability during RSI. While historical concerns existed about ketamine increasing pulmonary vascular resistance and worsening right ventricular function, a case report demonstrated hemodynamic stability was maintained in a patient with severe COPD, cor pulmonale, and CO₂ retention, with no clinically observed deleterious effects on right ventricular afterload. 7

Dosing Algorithm to Minimize Cardiovascular Risk

Use the lower end of ketamine dosing (1 mg/kg IV) in COPD patients with any of the following high-risk features: 1

• Hemodynamic compromise or hypotension
• Chronic cor pulmonale
• Signs of right ventricular dysfunction
• Concurrent sepsis
• Prolonged respiratory distress with suspected catecholamine depletion

Administer ketamine slowly over 60 seconds, as rapid administration results in respiratory depression and enhanced vasopressor response. 8

Essential Preparation to Mitigate Cardiovascular Collapse

• Have vasopressors immediately available at the bedside before administering ketamine, as post-intubation hypotension is common and associated with increased mortality. 9, 2
• Ensure adequate preoxygenation with high-flow nasal oxygen (HFNO) when laryngoscopy is expected to be challenging, or noninvasive positive pressure ventilation (NIPPV) if PaO₂/FiO₂ < 150. 6
• COPD patients have reduced functional residual capacity and desaturate rapidly despite ketamine's theoretical preservation of respiratory drive. 1

Additional Cardiovascular Considerations Specific to COPD

Administer anticholinergic premedication (glycopyrrolate 0.2 mg or atropine 0.5 mg) 3-5 minutes before ketamine to prevent secretion-related complications, as ketamine significantly increases upper airway secretions in COPD patients. 1 While this addresses airway concerns, the anticholinergic may provide modest cardiovascular support through vagolytic effects.

Critical Pitfall to Avoid

Never assume ketamine's sympathomimetic properties guarantee hemodynamic stability in critically ill COPD patients. 1 The traditional teaching that ketamine maintains blood pressure does not apply when catecholamine stores are exhausted—a common scenario in COPD patients with chronic hypoxemia, acute exacerbations, or concurrent sepsis. 2 This misconception can lead to inadequate preparation for cardiovascular collapse.

Comparative Context: Why Ketamine Remains Preferred Despite Cardiovascular Concerns

Despite the hypotension risk, ketamine remains superior to alternatives in COPD patients because:

• Propofol causes profound myocardial depression and vasodilation, making it unsuitable for hemodynamically compromised patients. 1
• Thiopental can cause severe bronchoconstriction in reactive airway disease. 1
• Etomidate offers hemodynamic neutrality but provides no bronchodilation benefit, which is critical in baseline airflow obstruction. 1
• No mortality difference exists between ketamine and etomidate (OR 0.95; 95% CI: 0.72-1.25), making the decision hinge on disease-specific advantages rather than survival outcomes. 1, 4

The bronchodilation benefit of ketamine in COPD outweighs the cardiovascular risk when proper precautions are taken (lower dosing, vasopressor availability, and recognition of high-risk features). 1