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Heart failure can arise from multiple causes, all resulting in decreased perfusion of body tissues. Conditions that may lead to heart failure include drug overdose, infection, myocardial infarction, and chronic hypertension. Regardless of whether the presentation is acute or chronic, the symptoms of heart failure may range from mild to life-threatening. Recognition of heart failure and its underlying cause is difficult to accomplish in the field due to the often limited availability of diagnostic tools and trained clinicians qualified to interpret testing results. Still, the priorities of emergency medical services when encountering a patient in respiratory distress in the prehospital setting include quick clinical assessment, oxygen supplementation, proper positioning, fluid overload reduction, and immediate transport to an appropriate facility. This activity for healthcare professionals is designed to enhance learners' proficiency in evaluating and managing heart failure in the field. Trainees gain a broader grasp of the condition's risk factors, pathophysiology, presentation, and best diagnostic and therapeutic practices in the prehospital setting. Greater competence enables learners to collaborate within an interprofessional team caring for patients with heart failure, improving outcomes. Objectives: Identify the signs and symptoms indicative of heart failure. Identify capnography results consistent with heart failure. Develop a clinically guided initial management strategy for suspected heart failure cases. Collaborate with the interprofessional team to educate, treat, and monitor patients with heart failure to improve health outcomes. Access free multiple choice questions on this topic.

Heart failure (HF) is a condition characterized by the heart's inability to pump effectively, leading to fluid accumulation in the lungs and body and decreased perfusion of body tissues. HF may be acute or chronic and result from various etiologies, including drug overdose, infection, myocardial infarction, and chronic hypertension. Symptom severity can range from mild dyspnea to respiratory distress and shock.[1][2][3][4] Field identification of HF can be difficult due to the limited diagnostic tools available.[5][6] Greater awareness and training can enhance recognition and treatment in prehospital settings.

HF results from cardiac system dysfunction that impairs the ventricle's ability to either pump or fill with blood.[7] This dysfunction can result from several causes, including ischemic and valvular heart disease, hypertension, inflammatory diseases, congenital anomalies, and dysrhythmias.[8] The most common etiology of HF is ischemic heart disease. These cardiac insults initially lead to a compensated state that eventually fails to sustain cardiac output, resulting in maladaptation and the onset of symptoms.

According to the American Heart Association, nearly 5.7 million people in the United States have HF, making it the cardiac disease with the fastest-growing incidence in the country.[9] The United States National Health and Nutrition Examination Survey from 2015 to 2018 found that over 6 million people older than 20 years in the US have heart failure, which is equivalent to 2.5% of the population. Prevalence rates are reported to be 3.9% in Canada and 1.5% to 3% in Europe.[10] The incidence of heart failure in the US ranges from 6.0 per 1000 person-years in people older than 45 to 21.1 per 1000 person-years in individuals older than 65. Other factors, such as genotype and ethnicity, also influence incidence.[11] Estimates indicate that over 64 million people worldwide have heart failure.[12]

HF results from initial compensatory mechanisms that ultimately fail, including the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system, and atrial natriuretic peptide (ANP).[13] Any cardiac insult may result in decreased systolic blood pressure. Hypotension triggers the release of renin, which cleaves the prohormone angiotensinogen to produce angiotensin I. Circulating angiotensin I is converted by angiotensin-converting enzyme to angiotensin II. Angiotensin II has strong vasoconstrictive properties and raises arterial pressure. Angiotensin II also acts on the kidneys to reduce salt and water excretion, increasing arterial pressure via the increase in circulating volume.[14][15] The sympathetic nervous system can rapidly regulate systolic blood pressure via baroreceptors located in the internal carotid artery and the wall of the aortic arch. A decrease in blood pressure prompts the central nervous system to constrict peripheral vessels. Meanwhile, the brainstem activates the sympathetic nervous system, triggering a release of epinephrine, primarily from the adrenal glands, and norepinephrine from sympathetic nerves near the heart. These hormones trigger positive chronotropic and inotropic effects that enhance heart rate and contractility, respectively. Another mechanism involves the release of ANP from the atria, triggered by increased atrial stretching due to decreased cardiac output. Brain natriuretic peptide (BNP) is a second type of natriuretic peptide. Both peptides promote renal water and salt loss while inhibiting the RAAS, resulting in overall fluid loss and reduced workload on the failing heart. Additionally, ANP and BNP function as sympatholytics, downregulating the SNS.[16] Failure of these mechanisms contributes to cardiac dysfunction, leading to a low cardiac output state. The release of BNP and ANP downregulates the RAAS in heart failure, resulting in increased fluid and salt retention in the kidneys, which further elevates the heart's workload.[17]

Another mechanism involves the release of ANP from the atria, triggered by increased atrial stretching due to decreased cardiac output. Brain natriuretic peptide (BNP) is a second type of natriuretic peptide. Both peptides promote renal water and salt loss while inhibiting the RAAS, resulting in overall fluid loss and reduced workload on the failing heart. Additionally, ANP and BNP function as sympatholytics, downregulating the SNS.[16] Failure of these mechanisms contributes to cardiac dysfunction, leading to a low cardiac output state. The release of BNP and ANP downregulates the RAAS in heart failure, resulting in increased fluid and salt retention in the kidneys, which further elevates the heart's workload.[17] The sympathetic nervous system promotes worsening heart failure by uncoupling β1-adrenergic receptors from cardiomyocytes. Though β2- and α1-adrenergic receptors contribute to maintaining inotropy, β1-receptors play a key role in the progression of heart failure. More specifically, as the disease progresses, β1-receptors decrease in number, and various enzymes important in cardiac contraction begin to lose function. Ultimately, the flow of blood into the right atrium slows, causing congestion in the pulmonary circulation. As blood stagnates, capillary hydrostatic pressure increases, exceeding both interstitial hydrostatic and osmotic pressures. Plasma filtration from the alveolar capillaries into the alveoli leads to alveolar fluid accumulation.[18]

Individuals with heart failure primarily complain of dyspnea or difficulty breathing. Patients describe dyspnea on exertion and, in more severe cases, report it with minimal activity or at rest. Patients also often report orthopnea (difficulty breathing when lying down) and paroxysmal nocturnal dyspnea (nighttime shortness of breath). Patients may also have chest pain, dizziness, and leg swelling.[19] The physical evaluation of a patient with an acute exacerbation or severe heart failure may reveal tachypnea, tachycarda, and, in severe cases, hypoxia. Hypertension is a common finding, but patients may also be hypotensive due to cardiogenic shock. Pitting pedal or lower extremity edema may be evident. Some patients may also develop edema in other parts of the body, such as the abdomen or scrotum.[20] Lung auscultation may be notable for rales or diminished breath sounds. These findings arise from plasma filtering into the alveoli of the lungs. Crackles are often first noticed in the lower lung fields, as filtered plasma is affected by gravity. Dyspnea arises from reduced gas exchange in fluid-filled alveoli. Tachypnea is a compensatory mechanism that allows the body to eliminate excess carbon dioxide, while tachycardia facilitates rapid blood return to the lungs for gas exchange. Waveform capnography may display normal end-tidal carbon dioxide levels and waveforms, unlike the elevated carbon dioxide and abnormal waveform seen in bronchospasm. In some cases, patients may exhibit wheezing, often referred to as "cardiac asthma," which can lead to misdiagnosis of bronchospasm.[21] Another examination finding is jugular venous distension or engorgement of the neck's superficial vessels resulting from atrial congestion and decreased venous return to the heart.

Field evaluation typically requires careful history taking and physical examination. Beyond clinical assessment, only a few tools can help with HF recognition and management in the field. One vital tool is waveform capnography, which is useful in distinguishing HF from asthma or chronic obstructive pulmonary disease (COPD) as causes of a patient’s respiratory distress. Both the pulmonary edema associated with HF and bronchospasm from asthma or COPD may produce wheezing in patients. These conditions can be differentiated using end-tidal carbon dioxide waveforms. A normal capnograph appears rectangular, indicating normal exhalation of carbon dioxide. Since carbon dioxide is soluble in water, patients with HF may have a normal capnograph even if they present to emergency medical services (EMS) with wheezing. This pattern differs from the shark fin appearance of a bronchospastic waveform.[22] Technological advancements have made point-of-care ultrasound more portable and accessible. Observational evidence suggests feasibility, particularly in the setting of undifferentiated dyspnea.[23][24][25][26][27] B-lines may help differentiate HF from bronchospastic etiologies. However, the benefits of point-of-care ultrasound in diagnosis and patient outcomes have not been fully determined.[28][29]

Reducing the workload of the failing heart is the primary goal of treating HF. This goal is accomplished by increasing oxygenation through supplemental oxygen, increasing airway pressures, and decreasing preload.[30] Supplemental oxygen may be provided through a nasal cannula, nonrebreather mask, or continuous positive airway pressure (CPAP). Of these methods, CPAP is preferred if a patient can tolerate it. CPAP provides continuous pressure to the alveoli, opening collapsed (atelectatic) alveoli, increasing intraalveolar pressure, and forcing fluid back into the alveolar vasculature. Additional medications like nitroglycerin or other vasodilators act to dilate blood vessels. Vasodilation reduces capillary hydrostatic pressure, enabling the increased alveolar pressure from CPAP to push filtrate from the alveolar sacs back into the pulmonary circulation.[31] Nitroglycerin is converted to nitric oxide, which promotes vasodilation. This medication may be administered as a sublingual tablet, spray, or intravenous injection, either as a bolus or continuous infusion.[32] Nitroglycerin reduces preload and afterload, decreasing the heart's workload. Prehospital initiation of nitroglycerin for HF may improve mortality and time to discharge.[33][34] Both vasodilators and CPAP should be judiciously used, if not withheld entirely, in patients with low systolic blood pressure (less than 90-100 mm Hg). Caution should be exercised when administering nitroglycerin in patients taking sildenafil or other erectile dysfunction medications, as combining these drugs may cause severe hypotension.[35] EMS personnel should follow local protocol or contact online medical command if they have any questions about CPAP or nitroglycerin use.

Conditions that may resemble HF include: Acute respiratory distress syndrome Bacterial pneumonia Bronchial asthma exacerbation Cardiogenic pulmonary edema COPD Cirrhosis Community-acquired pneumonia Emphysema Goodpasture syndrome Idiopathic pulmonary fibrosis Myocardial infarction However, diagnosis is difficult in the prehospital setting, where advanced diagnostic tools and clinicians trained to interpret testing results are often unavailable. EMS should thus prioritize oxygen supplementation, placing the patient in an upright position, coordination with the nearest medical facility, and rapid transport.

Heart failure can become a chronic condition that progressively decreases a person's exercise capacity and ability to perform daily activities. Follow-up consultations with the primary care clinician and cardiologist are crucial. Proper management of HF can slow progression and help maintain quality of life.[36]

HF management requires the coordinated efforts of an interprofessional team, which should include an emergency department physician, cardiologist, internist, and intensivist. In the prehospital setting, EMS personnel can assess patients in respiratory distress and initiate treatment but are not tasked to confirm the diagnosis of HF. Key measures include keeping the patient upright, providing oxygen, and limiting intravenous fluid administration. Patients need immediate transport to a medical facility. The roles of EMS are to recognize the signs of severe heart failure, initiate prehospital treatments, and safely transport the patient without delay.[37][38]