What is the primary anesthesia goal for a patient with hypertrophic obstructive cardiomyopathy (HOCM)?

Anesthesia Goals for Hypertrophic Obstructive Cardiomyopathy

The primary anesthesia goal for patients with hypertrophic obstructive cardiomyopathy (HOCM) is to prevent worsening of left ventricular outflow tract (LVOT) obstruction by maintaining adequate preload, maintaining or increasing afterload, avoiding tachycardia, and preventing increases in myocardial contractility. 1

Core Hemodynamic Principles

The pathophysiology of HOCM centers on dynamic LVOT obstruction that worsens with decreased preload, decreased afterload, or increased contractility 1. Your anesthetic management must directly counteract these three triggers:

Maintain Adequate Preload

• Avoid hypovolemia at all costs - this is the most common precipitant of hemodynamic collapse 1
• Ensure adequate volume loading before induction 2
• Use cautious fluid administration to maintain left ventricular filling 1

Maintain or Increase Afterload

• Avoid vasodilation - this critically worsens LVOT obstruction 1
• Use alpha-agonists (phenylephrine or vasopressin) rather than beta-agonists for hypotension 1
• Phenylephrine is the preferred agent for acute hypotension 3
• Never use vasodilators including nitrates, hydralazine, or dihydropyridine calcium channel blockers 3

Control Heart Rate

• Maintain relatively slow heart rate to ensure adequate diastolic filling time 2
• Target resting heart rate of 60-65 bpm 3
• Avoid tachycardia which reduces ventricular filling and worsens obstruction 1

Minimize Contractility

• Avoid positive inotropic agents (dopamine, dobutamine, digoxin) which worsen LVOT obstruction 1, 3
• Beta-blockers are beneficial for reducing contractility and should be continued perioperatively 1

Preoperative Medication Management

Continue These Medications

• Beta-blockers must be continued without interruption in the perioperative period 1
• Non-dihydropyridine calcium channel blockers (verapamil, diltiazem) should be continued 1
• Abrupt discontinuation of beta-blockers precipitates rebound tachycardia and worsening symptoms 3

Discontinue These Medications

• Stop all vasodilators including ACE inhibitors, ARBs, and dihydropyridine calcium channel blockers as they worsen LVOT obstruction 1
• Discontinue digoxin which increases contractility 1

Intraoperative Monitoring and Assessment

• Evaluate severity of LVOT obstruction via echocardiography (resting and provoked gradients) preoperatively 1
• Transesophageal echocardiography is very useful for intraoperative assessment and management of LVOT obstruction and mitral regurgitation 2
• Monitor for systolic anterior motion (SAM) of the mitral valve, which causes LVOT obstruction and mitral regurgitation 2

Anesthetic Technique Considerations

General Anesthesia

• Avoid propofol as the sole anesthetic agent due to its vasodilatory and negative inotropic effects 2
• Balanced anesthesia is preferable 2
• Consider laryngeal mask airway to minimize hemodynamic fluctuations during induction and emergence 4

Regional Anesthesia

• Regional anesthesia can be advantageous by minimizing hemodynamic fluctuations and avoiding intubation 5
• Combined spinal-epidural anesthesia has been used successfully but requires careful titration to avoid sympathectomy-induced vasodilation 6
• Neuraxial techniques carry risk of unpredictable hemodynamic changes from sympathetic blockade 5, 7

Management of Hemodynamic Crisis

If LVOT obstruction with mitral regurgitation leads to hemodynamic collapse:

• Immediate volume loading with crystalloid or colloid 2
• Administer phenylephrine to increase afterload 1, 3
• Beta-blockers (landiolol, esmolol) decrease myocardial contraction and attenuate SAM 2, 6
• Discontinue any inotropic drugs 2
• Avoid vasodilators or inotropes like dopamine or dobutamine which worsen obstruction 3

Critical Pitfalls to Avoid

• Never combine beta-blockers with non-dihydropyridine calcium channel blockers - this causes severe bradycardia and heart block 8, 3
• Dihydropyridine calcium channel blockers (nifedipine) should never be used as vasodilation aggravates outflow obstruction 8
• Avoid hypovolemia from excessive diuresis or neuraxial sympathectomy 8
• In patients with severe outflow obstruction, elevated pulmonary artery wedge pressure, and low systemic blood pressure, calcium channel blockers may trigger increased outflow obstruction and precipitate pulmonary edema 8