This article originally posted at Limmer Education and is reprinted with permission.
By Chris Ebright
This initial installment of the Back to the Basics series is going to compare and contrast a common chief complaint: shortness of breath. Many etiologies provoke this, but many EMT students have a hard time differentiating a dyspneic congestive heart failure patient from one with chronic bronchitis. Both conditions present with physical similarities, coughing, wheezing, fatigue and signs of hypoxia. Even though their chief complaint is identical, these patients develop dyspnea by different means. So, let’s compare the pathophysiology of each condition and see if we can clear this up, shall we?
Congestive heart failure (CHF) is a consequence of an abnormality in cardiac structure, function, rhythm or conduction. Hypertension, infection, a massive myocardial infarction or the cumulation of smaller infarcts, disease of the atrioventricular valves and/or the semilunar valves, and diseases of the heart muscle (cardiomyopathies) are typical etiologies. Some conditions cause atrophy (diminish the size) of the ventricular wall, while others excessively enlarge (hypertrophy) the wall. Regardless, the initial insult is usually to the left ventricle, eventually causing it to become an inefficient pumping chamber.
Typically, the left ventricular wall hypertrophies as compensation from increased afterload, or by direct damage from a myocardial infarct secondary to coronary artery disease. The Frank-Starling law of the heart states that as ventricular volume increases and stretches the myocardial muscle fibers, the stroke volume increases proportionally. A hypertrophied left ventricle, though, has the consistency of concrete (so to speak) that grossly diminishes its stretching ability, thus negatively affecting output. Additionally, the hypertrophied wall expands into the ventricular chamber, dwindling the amount of available space.
The reduced filling space decreases the available blood volume wall to stretch the myocardial muscle fibers, and the inflexible, rigid wall produces insufficient pressure to force adequate volume through the aorta. The result is a decrease in cardiac output, which compromises not only systemic circulation, but also coronary circulation. The left ventricle has now failed as a forward pump.
The openings for the left and right coronary arteries are just superior to the aortic semilunar valve, which closes during ventricular diastole. When this valve closes, the blood remaining within the aorta flows back toward it, filling the coronary arteries. As CHF progresses, the associated decrease in aortic blood volume, consequently curtails coronary artery filling. Less blood and nutrients become available to the myocardium, perpetuating the heart failure.
A hormone release as a response to the decrease in cardiac output causes more problems. Activation of the renin-angiotensin system stimulates renal retention of salt and water, thus, increasing circulating blood volume. Activation of this system also initiates systemic vasoconstriction, increasing the resistance (afterload) against which the failing heart must pump.
The left ventricle becomes even less efficient as a forward pump. The excessive retained volume trying to pass through a narrow ventricle chamber, combined with an increased afterload causes a ventricular diastolic pressure increase. This pressure cannot be effectively reduced by pumping volume through the aorta, so it back-builds into the left atrium, eventually dilating and thinning the left atrial wall. Thinner in comparison to the left ventricular wall, it cannot withstand increased pressure nearly as long, and swiftly fails. The left-sided diastolic pressure continues to escalate, leading to pulmonary venous congestion.
As the venous pressure increases, pulmonary capillaries and lymphatic vessels are recruited to deal with the added volume, essentially providing extra drainage avenues to keep the pulmonary circulation pressure “normal.” However, as the pressure continues climbing, these mechanisms fail, and the patient develops pulmonary hypertension.
An acute exacerbation of left ventricular failure induces a spike in left diastolic pressure, consequently increasing pulmonary capillary pressure. The result is excessive leakage of serum fluid, proteins, and occasionally red blood cells (pulmonary edema), into the interstitial lung tissue and alveoli. Crackles, wheezing, coughing, and shortness of breath typically manifest as signs and symptoms.
A congestive heart failure patient’s hypoxia and call to EMS for shortness of breath arise from a ventilation/perfusion mismatch. Outside of infection, when a CHF exacerbation occurs, air will effectively flow through the upper and lower airways. Past this point, oxygen cannot effectively traverse into the bloodstream through the fluid-filled alveoli. Ergo, carbon dioxide is retained within the bloodstream for the same reason. Hypoxemia, hypoxia and acidosis develop, causing similar symptoms seen with chronic bronchitis.
Left-sided failure and pulmonary hypertension eventually cause the right side of the heart to fail in many CHF patients. The consequence of a similar series of events – retrograde venous blood flow, increasing back-pressure, etc., as seen with the chronic bronchitis patient is evident during the CHF patient assessment. In contrast, however, the basic CHF treatment regimen focuses on fluid removal and reduction of pulmonary and systemic afterload. This is accomplished by the application of CPAP and assisting with the administration of sublingual nitrates. Occasionally, diuretics at the advanced level of care, are administered to release additional fluid from the body.
Summing up, COPD and CHF are severe conditions that affect a patient’s breathing, but have different origins – COPD affects the lungs and CHF affects the heart. Both conditions present with physical similarities, symptoms and risk factors. However, the EMT must recognize that a thorough history and physical exam may allow an accurate differentiation, but may not always be possible, as these two conditions can exist simultaneously.
Listen for more: Serial killers: Shortness of breath
About the author
Chris Ebright is an EMS education specialist with ProMedica Air and Mobile in Toledo, Ohio, managing all aspects of internal continuing EMS education as well as for numerous EMS systems in northwest Ohio and southeast Michigan. He has been a nationally registered paramedic for 25 years, providing primary EMS response, land, and air critical care transportation. Chris has educated hundreds of first responders, EMTs, paramedics, and nurses for 24 years with his trademark whiteboard artistry sessions, including natives from the Cayman Islands and Australia. Chris’ passion for education is also currently featured as a monthly article contributor, published on the Limmer Education website. He has been a featured presenter at numerous local, state and national EMS conferences over the past 13 years, and enjoys traveling annually throughout the U.S. meeting EMS professionals from all walks of life. Chris is a self-proclaimed sports, movie and rollercoaster junkie and holds Bachelor of Education degree from the University of Toledo in Toledo, Ohio. He can be contacted via email at c.ebrightnremtp@gmail.com or through his website, www.christopherebright.com.
