Congestive heart failure (CHF) can arise from multiple causes, all resulting in decreased perfusion of body tissues. CHF may result from a drug overdose, infection of the myocardium, myocardial infarction, chronic hypertension, and numerous other causes. It may also be acute or chronic. Regardless of either the acute or chronic nature of CHF, it can range from mild symptoms to a serious emergency.
The beginning of CHF arises from failing compensatory mechanisms. To understand the pathophysiology of CHF, one must first look at the mechanisms used in patients to maintain cardiac output in the failing heart.
Nearly 5.7 million people in the United States suffer from CHF and is the fastest growing cardiac disease in the United States, according to the American Heart Association. Though the body has multiple compensatory strategies to maintain cardiac output (CO) and end-organ perfusion, they may fail. These compensatory mechanisms consist primarily of neurohormonal systems.
One such mechanism is the renin-angiotensin-aldosterone system. Initial insult to the heart via any one of the mechanisms listed in the previous section may result in a decreased systolic blood pressure. Hypotension acts to release renin in the kidney, which cleaves the prohormone angiotensinogen, producing angiotensin I. This protein is released into circulation, where it is converted by angiotensin-converting enzyme (ACE) to angiotensin II. Angiotensin II has strong vasoconstrictive properties, raising arterial pressure. Angiotensin II acts on the kidney to reduce the excretion of salt and water, increasing arterial pressure further. This mechanism occurs over a span of approximately 20 minutes.
Another mechanism is the sympathetic nervous system (SNS), whereby systolic blood pressure is rapidly regulated. The sympathetic nervous system measures systolic blood pressure via baroreceptors located in large systemic arteries, specifically in the internal carotid artery and the wall of the aortic arch. When this occurs, the central nervous system acts to constrict peripheral vessels. Regarding the heart, a specific region of the brain stem transmits sympathetic nervous system impulses to the heart, increasing heart rate and contractility (positive chronotropic and inotropic effects). These effects are accomplished primarily via the release of epinephrine (from adrenal glands) and norepinephrine (released from sympathetic nerves near the heart).
Another mechanism is the release of atrial natriuretic peptides (ANPs) from the atria. As heart failure produces increased atrial stretching via decreased cardiac output, Atrial natriuretic peptides are released from the atria. The second type of natriuretic peptide is known as brain natriuretic peptide (BNP). These peptides act to promote water and salt loss in the kidneys, as well as inhibit the renin-angiotensin-aldosterone system, promoting overall fluid loss, and decreasing the work of the failing heart. Additionally, both atrial natriuretic peptides and brain natriuretic peptide serve as a sympatholytic, promoting a downregulation of the sympathetic nervous system.
Each of the above mechanisms fails or undergo changes in heart failure, resulting in a low cardiac output state.
As mentioned previously, the renin-angiotensin-aldosterone system is down-regulated when brain natriuretic peptides and atrial natriuretic peptides are released in heart failure. Overall, this promotes more fluid and salt retention in the kidneys, increasing the workload of the heart.
The means by which the sympathetic nervous system acts to promote heart failure is through the uncoupling of beta-1 adrenergic receptors from actual cardiomyocytes. Though beta-2 adrenergic receptors and alpha-1 adrenergic receptors do function to maintain inotropy, it is the beta-1 receptors that play a key role in the progression of heart failure. More specifically, as the disease progresses, beta-1 receptors decrease in number, and various enzymes important in cardiac contraction begin to decrease in function.
Ultimately, blood return to the right atrium is slowed. As blood return slows, this results in a damming up of blood in the pulmonic circulation. As blood remains stagnant, capillary hydrostatic pressure increases, becoming greater than both the interstitial hydrostatic and interstitial osmotic pressures. This produces filtration of plasma out of the alveolar capillaries and into the alveoli themselves, filling them with fluid.
Certain hallmarks for CHF include jugular venous distention (JVD), dyspnea/tachypnea, tachycardia, crackles in the lungs, and pitting pedal edema. JVD is due to decreased venous return to the heart via the right atrium. As blood continues to back up in the system circuit, the superficial vessels of the neck may become swollen with blood. Dyspnea arises from the decreased gas exchange at alveoli flooded with fluid. Tachypnea is a compensatory mechanism by which the body attempts to exhale excess carbon dioxide, and tachycardia acts to return blood to the lungs as quickly as possible to accomplish gas exchange. As plasma is filtered into the alveoli, crackles begin to be heard bilaterally. These crackles often are first noticed in the lower lung fields, as filtered plasma is affected by gravity. Waveform capnography may show normal end-tidal carbon dioxide levels and waveform, as opposed to elevated carbon dioxide and abnormal waveform found in bronchospasm.
Field evaluation involves careful history and physical exam. Further testing in the field is not available.
Reducing the workload of the failing heart is the primary goal of treating CHF. This goal is accomplished by increasing oxygenation through supplemental oxygen, increasing airway pressures, and decreasing pre-load. A nasal cannula, a non-rebreather, or (preferably and if tolerated) by continuous positive airway pressure or CPAP may deliver supplemental oxygen may. CPAP acts to provide continuous pressure to the alveoli, thereby opening any alveoli that have collapsed (a condition known as atelectasis), and increasing the pressure within the alveoli, forcing fluid back into the alveolar vasculature. Additional medications like nitroglycerin or other vasodilators act to dilate blood vessels. Vasodilation promotes a decrease in capillary hydrostatic pressure, which allows the increased alveolar pressure of CPAP to force the filtrate (essentially blood plasma) from the alveolar sac back into pulmonic circulation. Both vasodilators and CPAP should be judiciously used, if not withheld entirely, in the patient with low systolic blood pressure (usually considered less than 90 mmHg to 100 mmHg) and/or recent erectile dysfunction drugs. Follow local protocol or contact medical direction if any question about CPAP or nitroglycerin use exists.
Another important tool in monitoring the efficacy of CHF treatment is waveform capnography. In the case of determining CHF, asthma, or chronic obstructive pulmonary disease (COPD) as a cause of a patient’s respiratory distress, capnography is extremely useful. Both the pulmonary edema associated with CHF and the bronchospasm from asthma may produce wheezing in patients, the actual end-tidal carbon dioxide waveforms are different. A normal capnograph is rectangular in nature, indicating normal exhalation of carbon dioxide. As carbon dioxide is soluble in water, CHF patients will have a normal capnograph, even if they present to emergency medical services providers with wheezing. This is different from the shark fin appearance of a bronchospastic waveform.
The management of acute CHF is with an interprofessional team that includes an emergency department physician, cardiologist, internist, and intensivist. In the field, EMS can assess the patient and initiate treatment but cannot confirm the diagnosis of CHF. The key is to keep the patient upright, provide oxygen, and limit IV fluids. These patients need immediate transport to a medical facility. The role of EMS is to recognize the signs of severe heart failure, initiate prehospital treatments, and safely transport the patient without delay.
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