How Obesity Impacts Patient Health and EMS

There are many explanations for why obesity is rising. Our diets are filled with fats and sugars, people are more sedentary, and extended work and school hours are limiting time for calorie burning activities. Regardless of how this epidemic has arisen, there are real consequences that directly affect EMS systems and providers through both increased call volume and serious logistical issues.

Physiological Effects

Obesity is a risk factor for many diseases and illnesses, including:

• Coronary artery disease

• Type 2 diabetes

• Cancer (endometrial, breast, colon)

• Hypertension

• Stroke

• Liver and gallbladder disease

• Sleep apnea

• Osteoarthritis

• Gynecological problems

• Kidney disease

• Psychological issues.

As an individual becomes overweight, their body stores excess fat as adipose tissue. Most commonly this adipose tissue is stored across the abdomen, around the liver and surrounding muscles. Adipose tissue has also been found to release a large number of cytokines. Cytokines are molecules that signal cells to carry out (or not carry out) specific functions and can be comprised of proteins, peptides or glycoproteins. Some cytokines are immunomodulating agents, which affect the immune system, while others affect different organ systems. While the specific function of each cytokine is beyond the scope of this article, several of these will be mentioned throughout the article.

Effects on pulmonary health

Even in the absence of pulmonary diseases, obesity causes a decrease in pulmonary residual volume and total lung capacity. Fatty deposits across the abdomen and the chest inhibit lung compliance by stiffening the chest wall and limiting diaphragm contraction.³ Obesity hypoventilation syndrome (OHS) can develop, which causes hypercapnia and is suspected to be caused by a combination of a reduced respiratory drive and the above-described reduced respiratory mechanics. As hypercapnia worsens, respiratory acidosis develops. Because this happens over time there is some degree of metabolic compensation. The respiratory drive is thought to be reduced in obese patients because adipose tissues release the aforementioned cytokines that impairs the central nervous system’s control over respiration.

The symptoms of obesity hypoventilation syndrome include obstructive sleep apnea (OSA), exertional shortness of breath, daytime sleepiness, hypercapnia, polycythemia and chronic hypoxia. The polycythemia is secondary to the chronic hypoxia experienced by these patients, which in turn is from the increased oxygen demand of excessive body mass and the heart’s excessive workload. Up to 10% of all morbidly obese patients experience OHS.⁴

As a result of these physiological changes obese patients often present with tachypnea and become short of breath easily. All tissue, including adipose tissue, requires oxygen and as a result of obesity the body’s oxygen demand rises exponentially. This requires the heart to circulate blood faster to accommodate increased distribution and the individual to breathe more rapidly to increase the rate of gas exchange. However, when combined with decreased total lung capacity, many patients struggle to keep up with oxygen demands and as a result have very limited oxygen reserves.

This limited oxygen reserve was well illustrated in a study performed on patients undergoing rapid sequence intubation in the operating room. Obese patients receiving the same amount of preoxygenation desaturated more than twice as fast as healthy adults (Figure 2).⁵ This is exacerbated by an increased airway resistance found in obesity which makes proper ventilation difficult in even the best of circumstances.⁶

Effects on cardiovascular health

For every 10 kg increase in body weight, there is a measurable 3.0 mmHg increase in systolic and 2.3 mmHg increase in diastolic blood pressure.⁷ Not surprisingly, nearly 75% of the incidence of hypertension is related to obesity. When certain cytokines are released by adipose tissue they act on the renal system and on the sympathetic nervous system. In the kidneys they activate the renin-angiotensin-aldosterone (RAA) axis, which increases sodium absorption. With the RAA axis activated, sodium reabsorption increases water retention. Blood pressure increases from both water retention and the stimulation of the sympathetic nervous system. This cardiovascular stress can cause long-term damage to the renal system by stretching the renal blood vessels, stressing glomerular filtration rates and compressing the renal medulla.