CHF and Aspiration Pneumonia

The explanation takes a little time to set up so I hope it is worth the wait. This is very condensed from what usually takes a couple of hours to properly describe so I apologize in advance if it is overly simplified. There are some great textbooks that explain this stuff clearly and with good detail.



Congestive heart failure is the inability of the heart to pump blood with adequate pressure to maintain the physiologic demands of organs. It occurs when the myocardium (heart muscle) becomes weak. There are several causes of this progressive weakening of the myocardium. One is disease of the heart muscle itself (cardiomyopathy). Another is arterial hypertension which forces the left ventricle to pump blood against too much resistance for a long period of time, until the muscle itself is overcome by the excessive workload. (The heart muscle first becomes thickened or hypertrophic just as your skeletal muscles get larger when you exercise but heart exercise is good only up to a point.). Likewise, pulmonary hypertension can cause right sided heart failure because the right ventricle is pumping blood through the pulmonary circulation against excessive resistance.



It is this last example that might partially answer your question. Diseases of the lungs such as some forms of COPD (emphysema in particular) can destroy portions of the respiratory membrane which is formed by the alveolar membrane plus the pulmonary capillaries. When the capillaries are destroyed the blood flow into the lungs (to pick up oxygen and get rid of CO2) is blocked so the right ventricle is pumping some blood into a dead end, the pressure in these vessels becomes very high. The result of this pulmonary hypertension is the leakage of material from the blood (that should not leak out of the circulatory system) into the lung. This example is one way that patients develop pulmonary edema (this fluid leakage into the lung is defined as pulmonary edema caused by congestive heart failure). Similarly this heart failure causes fluid to accumulate in the pleural cavity (the space outside of the lungs between the inner and outer pleural membranes that line the lungs and chest cavity).



OK so now we have COPD as a source of CHF. Patients with COPD have reduced mucociliary clearance, reduced expiratory capacity, both of which increase the patient’s resistance to infection (i.e. pneumonia) which are some reasons that COPD patients have a higher risk of any type of pneumonia. These patients also have a different pattern of breathing/swallowing coordination than normals that disrupts the typical “swallow at the onset of exhalation” pattern that predominates in normals, and also increases the respiratory rate above a normal (12-20 or so breaths per minute) further discoordinating (I don’t know if that is a real word) swallow-breathing. Likewise COPD patients exhibit more frequent laryngeal penetration than normals (Mokhlesi, Logemann, Rademaker, Stangl, & Corbridge, 2002; Good-Fratturelli, Curlee, & Holle, 2000)



CHF itself and the associated pulmonary edema and pleural effusions, reduce respiratory surface area by restricting inflation of the lungs (effusions) or by obstructing air from the respiratory membrane (edema). The result of either is the patient has to breathe more times per minute (increased respiratory rate- see above).



There are some good studies that show the association between COPD and dysphagia, and CHF and dysphagia, (see below) but the link between these conditions and dysphagia, as well as the link to subsequent pneumonia risk, is based on the understanding of the pathophysiology of those diseases and mostly based on animal studies, though the inferences are very strong. For example, we know the above processes take place in these diseases, and we know that these patients have increased respiratory rate, swallow-respiratory coordination abnormalities, higher incidence of pneumonia, etc., so we infer that the diseases’ properties explain some if not all of the association between them and dysphagia, increased pneumonia risk, etc. (Langmore, Skarupski, Park, & Fries, 2002).



Cricopharyngeal dysfunction is also seen in some patients with COPD and this can contribute to prandial aspiration and increased likelihood of inoculating thelungs with pathogens ((Good-Fratturelli, Curlee, & Holle, 2000; Langmore, Skarupski, Park, & Fries, 2002; Mokhlesi, 2003; Mokhlesi, Logemann, Rademaker, Stangl, & Corbridge, 2002; Stein, Williams, Grossman, Weinberg, & Zuckerbraun, 1990).



Cheers,



James L. Coyle, Ph.D., CCC-SLP, BRS-S

Assistant Professor, Communication Science and Disorders

University of Pittsburgh



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Good-Fratturelli, M. D., Curlee, R. F., & Holle, J. L. (2000). Prevalence and nature of dysphagia in VA patients with COPD referred for videofluoroscopic swallow examination. Journal of Communication Disorders, 33(2), 93-110.

Langmore, S. E., Skarupski, K. A., Park, P. S., & Fries, B. E. (2002). Predictors of aspiration pneumonia in nursing home residents. Dysphagia, 17(4), 298-307.

Mokhlesi, B. (2003). Clinical implications of gastroesophageal reflux disease and swallowing dysfunction in COPD. American Journal of Respiratory Medicine, 2(2), 117-121.

Mokhlesi, B., Logemann, J. A., Rademaker, A. W., Stangl, C. A., & Corbridge, T. C. (2002). Oropharyngeal deglutition in stable COPD. Chest., 121(2), 361-369.

Stein, M., Williams, A. J., Grossman, F., Weinberg, A. S., & Zuckerbraun, L. (1990). Cricopharyngeal dysfunction in chronic obstructive pulmonary disease. Chest.97(2):347-52.