The Effects of Obesity on the Cardiopulmonary System: Implications for Critical Care Nursing

Kim Garrett, RN, MS, CNP; Kathy Lauer, RN, PhD; Beth-Anne Christopher, RN, MS


Prog Cardiovasc Nurs. 2004;19(4) 

In This Article

Obesity-Related Pathophysiology of the Cardiovascular System

Obesity affects the cardiovascular system in multiple ways. Obese individuals have an increased total blood volume to meet the perfusion needs of the increased adipose tissue. Increases are seen in both intracellular and extracellular fluid and are associated with increased stroke volume, although resting heart rate remains unchanged. The increased stroke volume increases resting cardiac output and left ventricular (LV) work.[14,15] Cardiac and stroke work indices remain normal in normotensive obese individuals. The increase in cardiac output is also accompanied by a decrease in systemic vascular resistance in normotensive obese individuals. Because of increased LV workload, oxygen consumption is also increased; the oxygen consumption increases linearly with the increase in body weight.[15]

The incidence of hypertension is more prevalent in the obese.[14,15] Mild to moderate hypertension is seen in 50%-60% of obese individuals, and 5%-10% of obese individuals have severe hypertension. The exact etiology is unknown but may be related in part to volume overload and resistance for blood transit in the capillaries, particularly vessels in the adipose-filled subcutaneous tissue.[17] In addition, adipocytes themselves have been recognized as a direct source of hormones, such as atrial natriuretic peptide and the renin-substrate angiotensin, which regulate fluid volume.[18] Two other common problems seen in the obese are hyperinsulinemia and insulin resistance. Hyperinsulinemia can stimulate the sympathetic nervous system, causing sodium retention; insulin resistance may be responsible for increased activity of norepinephrine and angiotensin II.[16]

Obese individuals tend to have increased values of fibrinogen, factor VII, factor VIII (von Willebrand factor), and plasminogen activator inhibitors,[19] as well as decreased levels of antithrombin III and circulating fibrinolytic activity.[15] Polycythemia may also develop as a result of chronic hypoxia.[20] These hemostatic and fibrinolytic changes, when combined with decreased mobility and venous stasis, place obese individuals at increased risk for thromboembolic disease, especially deep vein thrombosis. One recent study[15] reported that obesity is the singlemost important risk factor for pulmonary embolism.

As a result of the continuous pressure overload, increased blood viscosity, obesity-related hypertension, and concentric left ventricular hypertrophy (LVH) develop. In the absence of hypertension, the myocardium may also be damaged by the chronic fluid overload related to increased cardiac output, which may lead to LV dilatation and an eccentric LVH.[21] Concentric and eccentric LVH increase the risk of developing both systolic and diastolic ventricular dysfunction. In the obese, systolic dysfunction is most evident. Increased LV end-diastolic volume is often accompanied by decreased ejection fraction in the chronically obese, putting them at risk for congestive heart failure[15,18,21] and cardiac arrhythmias. The incidence of premature ventricular contractions is higher in individuals with concentric LVH. Because of dilatation of the atria related to increased fluid volume, the prevalence of atrial fibrillation and stroke is also higher in this population.[18,21]


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