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Heart failure results from a structural or functional cardiac abnormality that leads to impaired ventricular filling or cardiac output. Chronic heart failure is typically caused by myocardial ischemia, cardiomyopathy, longstanding uncontrolled hypertension, or underlying valvular heart disease. A common way to classify heart failure is based on systolic function. Patients with impaired cardiac filling are classified as having heart failure with preserved ejection fraction, whereas those with poor cardiac output are classified as having heart failure with reduced ejection fraction [46]. It is estimated that more than 6.5 million adults are living with heart failure in the United States, although the number may be higher [47, 48]. The disease has major social and economic effects [49].

During an ADHF exacerbation, a stressor (e.g., acute MI, dysrhythmia, infection, dietary changes, or medication noncompliance) leads to an acute myocardial functional decline that overwhelms the body’s compensatory mechanisms. Symptoms of an acute exacerbation include increased shortness of breath, orthopnea, generalized weakness, and chest discomfort. Patients who are volume overloaded will often report increased bilateral lower extremity edema and weight gain. In some cases, patients will be hypotensive due to profoundly low cardiac output leading to cardiogenic shock. Clinical assessment classically reveals rales on auscultation of the lungs, which can help differentiate ADHF from a COPD exacerbation. The examination may also show jugular venous distension and edema (sacral, abdominal, lower extremity).

SCAPE occurs when a heart failure patient rapidly develops a sympathetic overdrive and acute pulmonary edema. Contrary to ADHF, which develops over days to weeks, symptoms of SCAPE develop rapidly, typically over minutes to hours. Patients suffering from SCAPE may not be volume overloaded. Consequently, clinical examination may not show the classic signs of heart failure, such as pedal edema and jugular venous distension. Additional examination clues that can aid in a patient’s volume status assessment are listed in Box 5.2.

Ultrasound may aid in the prehospital diagnosis of both ADHF exacerbation and SCAPE. B‐lines, vertical lines extending from the pleural line to the bottom of the ultrasound image, are indicative of interstitial fluid that can be seen with both ADHF and SCAPE (Figure 5.3) [9]. The presence of a pleural effusion on a prehospital chest ultrasound may be a novel prehospital marker for ADHF [50].

Figure 5.3 Ultrasound image depicting B‐lines, which may be seen in ADHF and SCAPE.

Prehospital management consists of positioning the patient in an upright posture, particularly if there is a concern for volume overload. This allows pleural effusions and edema to localize at the lung bases and venous blood to pool in the lower extremities, thereby reducing cardiac preload. Patients presenting with hypotension should prompt EMS clinicians to consider causes such as acute MI, in addition to other causes of shock (e.g., hypovolemic, distributive, or obstructive). If the cause of shock is due to low cardiac output, specific prehospital treatment might include inotropic and vasopressor medications such as epinephrine and norepinephrine. Patients may receive additional hemodynamic support from dobutamine and milrinone in the hospital.

NIPPV should be used in patients in severe respiratory distress, assuming no contraindications exist (e.g., no spontaneous respirations, vomiting). Studies have demonstrated improvement of oxygenation and hemodynamics, decreased intubation rates, and decreased mortality [51–53]. Continuous pressure at a level of 5‐10 cmH₂O improves oxygenation by recruiting atelectatic and fluid‐filled alveoli and decreasing the work of breathing. The increase in intrathoracic pressure also alters hemodynamics by decreasing the transmural wall tension of the heart [54].

Nitrates are the mainstay pharmacologic treatment for patients who present with acute respiratory distress and pulmonary edema and who have adequate or elevated blood pressure. Nitroglycerin acts rapidly to dilate veins, allowing blood to distribute to the periphery, thereby decreasing cardiac preload. At higher doses, typically above 150‐250 μg/min, nitroglycerin also acts as an arterial vasodilator, decreasing cardiac afterload [55]. Studies of nitroglycerin use have shown relatively low rates of serious adverse effects ranging from 0.3% to 3.6% [56]. EMS clinicians must be cognizant of the potential interaction with all antierectile dysfunction phosphodiesterase‐inhibiting drugs (e.g., sildenafil), which are contraindications to the use of nitroglycerin. Caution is also advised if there is concern for an underlying right ventricular MI. This may be suspected if there is ST‐elevation in the inferior limb leads (II, III, aVF), especially when the elevation in lead III is greater than in lead II.

A dose of 400 μg administered sublingually, given every 5 minutes, with frequent reassessment to ensure the maintenance of a systolic blood pressure of at least 100 mmHg, is often effective. Sublingual nitroglycerin also has the advantage of a rapid time to peak effect of 5 to 15 minutes and duration of action of less than 1 hour and can be used concurrently with NIPPV. Transdermal nitroglycerin paste is not recommended since its effectiveness is limited by slow absorption, which is further worsened by the presence of decreased skin perfusion during ADHF. Intravenous access should ideally be obtained before administering SL nitroglycerin, as it has the rare potential to produce hypotension and bradycardia [56]. However, the inability to obtain IV access should not preclude or delay its use.

Intravenous bolus of high‐dose nitroglycerin is gaining traction as a treatment option in the emergency department and prehospital settings and may be of particular benefit in patients with SCAPE [57–59]. Intravenous administration facilitates a more rapid decline in afterload as compared to SL formulations. A case series demonstrated the feasibility and safety of IV bolus nitroglycerin when administered by paramedics and revealed improvements in systolic blood pressure and oxygen saturation upon emergency department arrival [59]. One of the main indications for this therapy in this study was a systolic blood pressure >160 mmHg to avoid potential adverse events (e.g., hypotension). While studies have reported safety with bolus doses up to 2 mg for SCAPE, a reasonable starting dose is a 1 mg bolus with a repeat dose in 5 minutes if the blood pressure remains above 160 mmHg [57–60].

Loop diuretics (e.g., furosemide) are used primarily for patients with ADHF who are hypervolemic. Determining the appropriate patient to receive this treatment can be challenging prior to hospital arrival [6]. The time to peak drug response is about 30 minutes, with a prolonged duration of action. Diuretics also influence plasma electrolytes, which typically are not assessed in the field. Consequently, given the delayed onset of peak effect, protracted duration of action, and side effect profile, diuretics are rarely indicated in the prehospital setting [61]. The other treatment options (e.g., nitroglycerin and NIPPV) likely provide more benefit to the patient.

Morphine, once a staple of therapy for ADHF and SCAPE, has also been largely supplanted by the other therapies. A review of the large ADHERE database found a significant association between receiving morphine and death, as well as several other adverse outcomes [62]. One explanation may be that as morphine causes hypotension, it takes away the therapeutic room available for the use of other medications that could be used to reduce preload and afterload, such as nitroglycerin. In addition, as a respiratory depressant, morphine may decrease the respiratory drive of an already struggling patient and worsen hypoxemic respiratory failure [63].