emDOCs Podcast – Episode 50: Acute Heart Failure Management Misconceptions

Welcome back to emDOCs cast with Brit Long, MD (@long_brit). Today we focus on management, but first a bit of an introduction on the types of heart failure, including Sympathetic Crashing Acute Pulmonary Edema (SCAPE).

Episode 50: Acute Heart Failure Management Misconceptions

Introduction

• To best understand treatment, understanding the type of acute heart failure (AHF) is essential.
• Sympathetic Crashing Acute Pulmonary Edema (SCAPE): sudden/excessive afterload resulting in pulmonary edema, flash/sudden pulmonary edema, hypertensive, hypoxic, occurs rapidly, critically ill, varied volume status (may be euvolemic, hypovolemic, hypervolemic), systemic congestion may be absent, lungs with crackles.
• Fluid Overload, subacute: gradual onset over days, usually not critically ill, systemic fluid overload/hypervolemic (ascites and peripheral edema with pulmonary congestion). Treatment focuses on removing excess volume through diuresis.
• Cardiogenic shock: poor perfusion, hypotensive, volume status varies (wet vs. dry). Treatment focuses on improving systemic perfusion, inotropy, and correcting underlying cause (reperfusion for MI, valvular repair, etc.)
• These may occur concomitantly (not mutually exclusive).
• However, differentiating the forms is important clinically important, as the treatment is different.

SCAPE Treatment:

• Airway: NIPPV with CPAP or BPAP are effective. Reduces mortality and intubation.
• Nitroglycerin: Can provide bolus for loading. Studies have evaluated boluses of 1,000-2,000 mcg over ~2 minutes (e.g., 400-800 mcg/min for 2.5 min). Then infusion 100-300 mcg/minute after.
  • With normotension and patient improvement, reduce infusion rate.
  • If patient remains hypertensive despite nitroglycerin, can provide clevidipine or nicardipine. Fentanyl can be used for patient comfort and to reduce air hunger. Enalaprilat may also be used.

Misconception #1: Diuretics are the mainstay of therapy in all cases of AHF

• Diuretics are a key component of therapy in acute decompensation and chronic therapy, and they are a part of the guidelines.
• AHA/ACC state diuretics are first line, with an IV dose that is equal or greater than the patient’s daily dose.
• ACEP Level B recommendations: “Treat patients with moderate-to-severe pulmonary edema resulting from acute heart failure with furosemide in combination with nitrate therapy”, followed by a Level C recommendation that “(1) Aggressive diuretic monotherapy is unlikely to prevent the need for endotracheal intubation compared with aggressive nitrate monotherapy. (2) Diuretics should be administered judiciously, given the potential association between diuretics, worsening renal function, and the known association between worsening renal function at index hospitalization and long-term mortality.”
• The most common diuretics include furosemide, torsemide, and bumetanide.
• IV administration in AHF is the recommended route, as this route possesses greater bioavailability, allowing for diuresis to begin within 30-60 minutes.
• However, as we discussed, AHF is a heterogeneous syndrome and not one distinct entity, with patients demonstrating differences in hemodynamic status (including systolic blood pressure (SBP)) and degree of systemic versus pulmonary congestion.
• In patients with SBP ranging from 100-140 mm Hg and systemic fluid overload, diuretics improve systemic congestion.

Pearl #1: In SCAPE, nitroglycerin and noninvasive positive pressure ventilation should be first-line therapies before diuresis.

• In acute pulmonary edema (APE), over 50% of patients do not have true volume overload, but rather volume distribution, with movement of fluid into the lungs.
• Fluid shifts from other body compartments such as the splanchnic circulation into the pulmonary circulation may result in pulmonary edema.
• Studies suggest no to little significant increase in dry weight in patients who present with APE and hypertension (SCAPE).
• Patients with APE who receive furosemide first may experience decreased LV function, increased LV filling pressures, and increased systemic vascular resistance. The medication can also decrease GFR, potentially even further decreasing diuresis.
• Diuretics are beneficial in patients with systemic congestion from true volume overload, which includes signs and symptoms such as ascites and extensive peripheral edema accumulating over an extended period of time.
• In patients with APE with AHF and little to no evidence of systemic congestion, nitroglycerin and NIPPV are first line. These improve work of breathing, decrease preload, and can decrease afterload.

Pearl #2: Several diuretic strategies can be used in patients with systemic congestion, and ultrafiltration may improve diuresis in patients refractory to IV diuretics.

• AHA/ACCF Heart Failure Guidelines recommend an initial IV dose equivalent or greater than the home dose given bolus or continuously. If this does not improve symptoms, a repeat bolus at a higher dose can be given, or a second diuretic added (thiazide).
• Bolus versus continuous infusion of diuretic is controversial.
• Literature suggests high-dose loop diuretics may improve symptoms but increase serum creatinine (Cr), while continuous versus intermittent boluses do not clinically differ.
• If diuresis with IV loop diuretics fails, ultrafiltration (UF) is another method to remove further congestion in hypervolemia (greater reduction in net weight and fluid loss, but no no change in mortality).

Misconception #2: The safest way of providing nitroglycerin IV is to begin with small doses and titrate to relief of symptoms to ensure patient safety in those with pulmonary edema.

• Nitrates cause venous and arterial vasodilation, reducing biventricular filling pressures, systemic arterial blood pressure, and pulmonary vascular resistance. Nitroglycerin improves coronary blood flow and reduces myocardial ischemia.
• The greatest benefit is in those with pulmonary edema due to systemic improvements in preload and fluid redistribution.
• Current guidelines from the AHA recommend vasodilator use in addition to diuretics in those who fail to respond to diuretics alone, or in patients with severe fluid overload without hypotension. ACEP’s clinical guidelines provide a Level B recommendation to “administer intravenous nitrate therapy to patients with acute heart failure syndromes and associated dyspnea.”
• Nitroglycerin is contraindicated in hypotension, obstruction of the LV outflow tract, recent use of phosphodiesterase inhibitors, and conditions similar to AHF where vasodilation is not beneficial (COPD).

Pearl #3: Nitroglycerin IV in high bolus doses is safe and effective in SCAPE.

• Several studies have evaluated nitrates IV at higher doses (including nitroglycerin IV), whether bolus or infusion
  • Studies have found doses 500-2000 mcg as a bolus can be used safely, with reduction in intubation and ICU admission.
• Hypotension with high dose nitroglycerin in SCAPE is rare.
• Currently, administering nitroglycerin more aggressively at higher doses in SCAPE, whether bolus or infusion, is safe and may be associated with reduced need for intubation and need for ICU admission, compared with lower infusion rates. Patients with hypovolemia and SCAPE may become hypotensive and require small bolus of IV fluid.
• After nitroglycerin bolus, start infusion at 100-300 mcg/min and titrate to patient improvement. Repeat boluses may be required.
• If the patient remains hypertensive despite high infusion doses (> 500 mcg/min), ensure NIPPV is maximized. Consider adding nicardipine or clevidipine, fentanyl, or enalaprilat.
• Carefully monitor patient respiratory and hemodynamic status. Once patient improves and becomes normotensive, reduce infusion. Patients typically improve rapidly with NIPPV and nitroglycerin.
• Sublingual nitroglycerin can be used if IV nitroglycerin cannot be used and the patient experiences SCAPE. Patient requires transfer to location where IV administration can be provided. Can start with several nitroglycerin sublingual tables every 5 minutes.

Misconception #3: Morphine is safe in AHF and should be administered in AHF.

• Morphine was traditionally a key component of therapy in cardiac conditions including heart failure. It supposedly reduces preload and heart rate while providing anxiolysis. This may reduce myocardial oxygen demand.
• Initial studies evaluated dogs, cats, and patients with mild pulmonary edema and acute MI.
• Guidelines vary in recommendations concerning morphine.
  • The ESC supports the use of opioids in heart failure, stating morphine 4-8 mg should be considered if the patient has severe anxiety with pulmonary edema, but the HFSA does not include morphine in its 2010 recommendations and states the medication should be used with caution if provided.

Pearl #4: Morphine may be associated with harm in AHF based on observational data.

• Morphine can cause myocardial depression with decreased heart rate and cardiac output, as well as respiratory depression. This is primarily dose-dependent, with opioids decreasing tidal volume and respiratory rate.
• Observational evidence suggests morphine is associated with worse outcomes when compared to patients not receiving opioids.
  • The predominant literature consists of observational, retrospective studies, which suffer from confounding factors.
• Though there are confounders, physicians have many other options to improve preload and afterload in pulmonary edema and AHF (NIPPV and nitroglycerin).
• Fentanyl may be used in several special circumstances in combination with NIPPV and other therapies.
  • Fentanyl has rapid onset of action and does not cause histamine release.
  • Indications: unable to tolerate NIPPV mask or extreme dyspnea/anxiety (fentanyl can reduce air hunger and promote comfort).

Misconception #4: In patients with cardiogenic shock and SBP <100 mmHg, dopamine is the best agent to improve cardiac output and perfusion.

• Prior recommendations advised dopamine for SBP 70-100 mm Hg, with norepinephrine reserved for those with SBP < 70 mm Hg.
• Dopamine doses greater than 10 mcg/kg/min are associated with more alpha-adrenergic effects.
• Recent literature suggests dopamine may be associated with greater risk of adverse events.
  • SOAP II trial found reduced mortality and dysrhythmias with norepinephrine compared to dopamine

Pearl #5 : Norepinephrine should be used instead of dopamine in cardiogenic shock with hypotension.

• Current guidelines recommend for systemic perfusion in cardiogenic shock. Dopamine is limited by its increased risk of dysrhythmias and vasoconstriction at higher doses, which may decrease end organ perfusion.
• Evidence suggests norepinephrine is associated with improved outcomes including lower mortality and lower risk of dysrhythmia when compared with dopamine.

References and Further Reading:

• emDOCs Heart Failure Management Misconceptions
• Long B, Koyfman A, Chin EJ. Misconceptions in acute heart failure diagnosis and Management in the Emergency Department. Am J Emerg Med. 2018 Sep;36(9):1666-1673.