F is for Failure

      "134 Main Street for a patient experiencing trouble breathing," the radio squawks. You and your partner look at each other and say, "Daniel O'Shea!" You know Daniel well, and he generally only calls when he is truly sick.

   Daniel is a 57-year-old male who lives with his wife in an area of the country known for deep-fried foods. He has a history of hyperlipidemia, coronary artery disease (CAD), hypertension, atrial fibrillation and emphysema, with a 45-pack/year smoking history. Last year, he suffered an acute myocardial infarction (AMI) that involved the anterolateral wall, and he has not been his active self since.

   A look inside Daniel would show left ventricular damage from the AMI; however, the damage occurred long before that event. For years, Daniel's hypertension went untreated, causing the left ventricle to pump harder to overcome afterload and expel blood into the systemic circulation to maintain stroke volume. As pressure overload continued, the ventricle wall became thicker and more muscular (hypertrophic), at the same time becoming stiff and rigid and decreasing in elasticity and overall volume. As cardiac output fell and the baroreceptors recognized a state of low pressure, the adrenal gland released norepinephrine and epinephrine to increase cardiac output by increasing stroke volume and heart rate. Prolonged activation of the sympathetic nervous system, or a sensed drop in renal perfusion pressure, activated the renin-angiotensin-aldosterone system (RAAS). Not only did the RAAS release additional norepinephrine, it also promoted a greater preload and afterload through increasing venous and arterial tone by converting angiotensin I into angiotensin II using angiotensin-converting enzyme (ACE). This vasoconstriction increased preload back to the heart, creating increased stretching of the ventricular walls and a greater contraction (Frank-Starling law). Over time, the ventricle walls became overstretched and weak, like a balloon that is repetitively overinflated and deflated. The overstretching caused excessive myocardial dilation that eventually diminished contractility and stroke volume, as well as the ejection fraction. The increased stress finally took its toll on Daniel last year in the form of an AMI. As the infarct progressed, the heart muscle cells, or cardiomyocytes, lengthened and began to thin. An inflammatory response ensued, the necrotic dead tissue was absorbed and scar tissue formed. The ventricle soon dilated, reshaping itself from elliptical to more spherical and changing its mass, composition, volume and cardiac function. This ventricular remodeling further injured the ventricle, decreased the ejection fraction and lowered the amount of blood available to the system.

   Daniel's body again responded to decreased cardiac output by engaging the sympathetic nervous system and RAAS, placing more stress upon his already damaged heart that was now expelling less blood. With a greater amount of blood remaining in the ventricle, hydrostatic pressures increased, leading to venous bed congestion in the tissues and organs located near the affected ventricle. As cardiac output continued to diminish, Daniel's heart rate increased to compensate for decreasing coronary filling times, leading to additional hypoxia and ischemia. This increased workload caused the heart to enlarge even further and increase its oxygen demand, worsened by decreased coronary filling times. Essentially, his body's attempt to compensate for decreased cardiac output was worsening his condition by causing the damaged heart to work harder. It was this repetitive downward spiral of injury, compensation, injury that led to Daniel's current state.

   Although it would be nice to have this much information about your patients prior to arriving, that is not always possible. Therefore, when a patient presents with a complaint of "trouble breathing," it is imperative to review the potential causes, or differential diagnoses, which include heart failure, COPD, pneumonia, pulmonary emboli, pneumothorax, anaphylaxis, aspiration and any number of cardiac etiologies like myocardial infarction.