Morbid obesity is not merely an excess of body weight. It represents a chronic cardiometabolic disease state that exerts continuous stress on the cardiovascular system, leading to structural remodeling, functional impairment, and altered physiological reserve. For anesthesiologists, this distinction is critical: patients with extreme obesity and no “comorbidities” may already have advanced yet silent myocardial disease.

Echocardiography has emerged as the most comprehensive perioperative cardiovascular assessment tool in bariatric anesthesia. It does not simply identify pathology; it quantifies functional reserve, reveals preload dependence, assesses pulmonary vascular physiology, and predicts vulnerability to anesthetic stress. Unlike electrocardiography or chest radiography, echocardiography delivers dynamic insight into ventricular compliance, atrial pressure burden, right heart mechanics, and volume responsiveness—variables that directly influence anesthetic management.

This chapter applies echocardiographic interpretation to a typical bariatric surgery patient and translates imaging findings into practical anesthetic strategy.

A 50-year-old male with body mass index (BMI) of 50 kg/m² is scheduled for laparoscopic sleeve gastrectomy. He has no documented hypertension, diabetes, coronary disease, or heart failure. However, he reports poor exercise tolerance, loud snoring, and daytime somnolence suggesting undiagnosed obstructive sleep apnea.

Given his extreme obesity and reduced functional capacity, preoperative transthoracic echocardiography was obtained in anticipation of cardiopulmonary stress from general anesthesia, pneumoperitoneum, and reverse Trendelenburg positioning.

Despite the lack of overt cardiovascular disease, obesity itself imposes chronic hemodynamic stress leading to silent structural and functional cardiac remodeling.

Structural and Functional Summary

Two-dimensional measurements:

• Left ventricular end-diastolic diameter: 51 mm

• Left ventricular end-systolic diameter: 34 mm

• Interventricular septum thickness: 16 mm

• Posterior wall thickness: 16 mm

• Left atrial diameter: 49 mm

• Inferior vena cava diameter: 15 mm with respiratory collapse

Functional data:

• Ejection fraction: 60%

• Fractional shortening: 32%

• Right ventricular size: normal

Doppler parameters:

• Mitral E/A ratio ≈ 0.7

• Reduced tissue Doppler e′ velocity

• Grade I diastolic dysfunction

Valve assessment:

• Aortic sclerosis without stenosis

• Trivial mitral, tricuspid, and aortic regurgitation

Integrated Impression

Moderate concentric left ventricular hypertrophy, dilated left atrium, preserved systolic function, impaired relaxation, no pulmonary hypertension, and normal right ventricular size.

Obesity imposes a sustained high-output circulatory state through increased metabolic demand and blood volume expansion. Over time, this results in:

• Increased left ventricular wall stress

• Elevated systemic vascular resistance

• Endothelial dysfunction

• Neurohormonal activation

• Pulmonary vascular remodeling

At the cellular level, obesity leads to lipid infiltration of cardiomyocytes, interstitial fibrosis, impaired calcium cycling, and mitochondrial dysfunction. These mechanisms collectively reduce ventricular compliance and impair myocardial relaxation.

This evolution produces an obesity cardiomyopathy phenotype characterized by concentric hypertrophy, left atrial...