CVS Changes with Obesity
Describe the cardiovascular changes that occur with morbid obesity
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
- Normal: BMI < 25
- Overweight: BMI 25 - 30
- Obese: BMI > 30
- Morbidly Obese:
- Obesity related disease and a BMI > 35
- BMI > 40
Characteristics of obesity include:
- Complex genetic and environmental causes
- Increased caloric intake
- Increased metabolic rate (normal for BSA)
The effect of obesity on the cardiovascular system is complex, and can be classified into:
- Hormonal changes
Abdominal visceral fat is responsible for secreting a large number of hormones which affect cardiovascular parameters:- Increased leptin
Contributes to cardiac remodelling and LVH. - Angiotensinogen
Leads to systemic hypertension and LV remodelling.- Small amounts are produced in adipocytes, which increases as fat volume increases
- Plasminogen activator inhibitor-1
Reduces fibrinolysis and predisposes to VTE. - Inflammatory adipokines
Impair endothelial function, leading to increased SVR. - Catecholamines
Increased contractility, SVR, and worsen endothelial function.- Released with:
- Hypoxia
- Hypercapnea
- Negative intrathoracic pressure
- Fragmented sleep
Due to OSA.
- Released with:
- Increased leptin
- Changes in key cardiovascular parameters
- Increased VO2
Due to increased LBM and fat mass. - Increased Blood Volume
Due to increased angiotensin II and aldosterone. - Increased Stroke Volume
Due to:- Increased preload (major factor)
- Increased contractility (minor factor)
Due to increased circulating adrenal hormones.
- Increased Cardiac Output
To maintain DO2.- Initially with preserved ejection fraction
- Increased VO2
- Cardiac changes
- Diastolic dysfunction
Due to myocardial fibrosis impairing relaxation. - Fatty infiltration of myocardium and conducting system
- Predisposes to arrhythmias
Risk is worsened by change in myocardial architecture, hypoxia, and increased circulating catecholamines.
- Predisposes to arrhythmias
- Biventricular hypertrophy as a response to increased afterload
- LV afterload increased due to systemic hypertension
LVH is much more common than RVH.- Eccentric hypertrophy due to volume overload
- Concentric hypertrophy due to pressure overload or hormonal changes
- RV hypertrophy due to:
- LV diastolic failure
- Increased PVR
- Hypoxia
Due to:- Effects of OSA
- Increased shunt through collapsed lung bases
- Acidosis
- Hypoxia
- LV afterload increased due to systemic hypertension
- Diastolic dysfunction
References
- Alvarez A, Brodsky J, Lemmens H, Morton J. Morbid Obesity: Peri-operative Management. Cambridge: Cambridge University Press. 2010.
- Lotia S, Bellamy MC. Anaesthesia and morbid obesity. Contin Educ Anaesth Crit Care Pain 2008; 8 (5): 151-156.