Heart%20failure%20-%20acute Treatment

Management should include rapid identification, stabilization of clinical and hemodynamic status together with determination and treatment of the primary pathology, precipitating factors and aggravating secondary causes

• Treatment strategy for acute heart failure is similar in patients with and without coronavirus disease 2019 (COVID-19) infection 

Goals of Treatment 

• Treat symptoms, stabilize the patient and improve hemodynamics, congestion and organ perfusion
  • Titrate supplemental oxygen (O₂) to achieve SpO₂ >95% and maintain SBP >90 mmHg and peripheral perfusion
  • Fluid challenge with saline or Ringer’s lactate is recommended in patients with cardiogenic shock if without overt signs of fluid overload
• Identify etiology and comorbid illnesses and initiate specific therapy
• Limit organ damage (cardiac, renal, hepatic, gut) and prevent thromboembolism
• Adjust therapy to control symptoms, manage congestion and hypoperfusion, and optimize blood pressure
• Initiate and assess the need to increase disease-modifying pharmacological therapy
• Minimize side effects
• Consider device therapy in appropriate patients
• Create a plan of care that includes medical and device therapy and follow-up
• Educate and initiate lifestyle modification and improve symptoms, quality of life and survival
• Prevent early readmission

Refer Patient to Cardiovascular Intensive Care Unit (ICU)

• With acute heart failure and associated shock or ACS
  • Patients at high risk for ACS may also be referred to the cardiac catheterization lab
• Vital signs include SBP <90 mmHg, heart rate <40 beats/minute (bpm) or >130 bpm, respiratory rate >25 breaths/minute, SpO₂ <90%, use of accessory respiratory muscles
• Arrhythmias
• There is a need for intubation or is already intubated
• Signs of hypoperfusion are present, eg altered mental status, cold extremities, metabolic acidosis, oliguria, lactate >2 mmol/L, SvO₂ <65%
• Poor response to non-invasive ventilation or to high fraction of inspired oxygen (FiO₂)  
• Requirement for ≥2 vasoactive drugs to maintain blood pressure, for invasive cardiac output monitoring, or for mechanical circulatory support 

Management of Patients Based on Clinical Profile in the Initial Phase

• Warm-dry: Compensated patients with adequate peripheral perfusion will have adjustment of oral therapy
• Warm-wet
  • Predominant congestive symptoms: Give diuretic, vasodilator; consider ultrafiltration if resistant to diuretic therapy
  • Predominant hypertension: Give vasodilator, diuretic
• Cold-dry: May consider fluid challenge or an inotropic agent if patient is still hypoperfused
• Cold-wet
  • If SBP <90 mmHg: Give an inotropic agent, diuretic when perfusion is corrected; in refractory cases (eg hypoperfusion and congestion), may consider giving a vasopressor
    • If unresponsive to medical therapy (eg persistent hypoperfusion or organ damage), may consider mechanical circulatory support and/or renal replacement therapy
  • If SBP >90 mmHg: Give vasodilators, diuretics; in refractory cases, may consider giving an inotropic agent

Diuretics

• Eg loop diuretics, potassium-sparing diuretics, thiazide diuretics
• Cornerstone of treatment for patients with acute heart failure
• Restore and maintain normal volume status in patients with fluid overload
  • Dose of intravenous (IV) diuretic should be based on the type of acute heart failure in patients with volume overload and titrated to reduce congestive symptoms
  • Recommended to be given either as intermittent boluses or as continuous infusion
• Provides rapid symptomatic relief in patients with pulmonary edema
• Low-dose combinations of loop diuretics with thiazides or aldosterone antagonists are often more effective and with fewer side effects than high-dose monotherapy
  • Can be used to treat resistant edema or patients with insufficient treatment response and achieve and maintain euvolemia with the lowest effective dose
  • Adjust dose after restoring the patient’s dry weight to avoid the risk of dehydration
• On admission, consider giving a higher dose of diuretic than that which patient is currently taking unless there are contraindications
  • Initial IV dose of patients receiving chronic diuretic therapy should be at least equivalent to the oral dose
  • Monitor closely symptoms, weight, renal function and electrolytes and urine output during diuresis
  • A satisfactory diuresis is a urinary sodium of ≥50-70 mEq/L after 2 hours and/or urine output of ≥100-150 mL/hr after 6 hours  
• Continue oral loop diuretics at the lowest possible dose once congestion is relieved
• Patients with hypotension, hyponatremia and acidosis are unlikely to respond to diuretic treatment

Loop Diuretics

• Eg Bumetanide, Furosemide, Torasemide
• Considered as the diuretic class of choice for the treatment of heart failure
• Dose given is the smallest amount that can give adequate clinical response and adjusted based on prior renal function and prior dose of diuretic agents
  • Initial IV dose of Furosemide drip should be at least equivalent to the preexisting oral dose
• Higher doses of IV loop diuretics or addition of another diuretic is reasonable with inadequate diuresis

Potassium-Sparing Diuretics

• Eg Amiloride, Triamterene
• Have no direct diuretic activity
• Formulated in combination with thiazides for the treatment of hypertension
• Concomitant administration of these agents can be helpful in patients with excessive potassium losses secondary to loop diuretics

Thiazide Diuretics

• Eg Bendroflumethiazide, Hydrochlorothiazide, Indapamide, Metolazone
• May be effective as monotherapy in patients with heart failure with mild volume overload and preserved renal function
• More effective as antihypertensive agents than loop diuretics

Vasopressin Antagonists

• Eg Conivaptan, Tolvaptan
• Promote aquaresis by blocking the action of arginine vasopressin at the V₂ receptor in the renal tubules
• Used in treating patients with volume overload and resistant hyponatremia despite fluid restriction
  • Administered to patients with fluid retention unresponsive to treatment with other diuretics including loop diuretics (excluding those with hypernatremia)

Opiates

• Eg Morphine
• Induce mild venodilatation and mild arterial dilatation leading to reduction in preload, heart rate and sympathetic drive
• May be used in some patients with acute pulmonary edema to decrease anxiety and relieve distress associated with dyspnea
• Should not be routinely offered to patients with acute heart failure except for those with intractable/severe pain or anxiety

Vasodilators

• Eg Nesiritide, Nitroglycerin, Nitroprusside
• Reduces venous and arterial tone resulting in optimization of preload and reduction in afterload respectively
• Mostly used in patients with severe hypertension
  • IV therapy may be given as initial treatment when patient's SBP is >110 mmHg to reduce congestion and improve symptoms; sublingual nitrates may be considered alternatives
• May be considered as an adjunct to diuretics for rapid improvement of congestive symptoms in patients with acute decompensated heart failure without systemic hypotension or significant obstructive valvular heart disease (eg mitral or aortic stenosis)
• Slow titration with frequent blood pressure monitoring is recommended
  • Reduce dose or discontinue use if symptomatic hypotension or worsening renal function develops
  • Reintroduction in incremental doses can be done once symptomatic hypotension resolves

Nesiritide

• Recombinant B-type natriuretic peptide developed for the treatment of acute heart failure
• Causes dose-dependent decrease in filling pressure, systemic and pulmonary vascular resistance and an increase in cardiac output
• Recently shown to decrease dyspnea by a small but significant amount when added to conventional therapy such as diuretics

Nitroglycerin

• Lowers venous tone more than arterial tone; decreases pulmonary congestion by acutely decreasing left ventricular filling pressure
• May enhance coronary blood flow making it more effective in patients with acute decompensated heart failure secondary to acute ischemia or myocardial infarction, hypertension or significant mitral regurgitation

Nitroprusside

• Potent vasodilator with balanced effects on venous and arteriolar tone, ie decrease in systemic vascular resistance
• Causes immediate decrease in pulmonary capillary wedge pressure and increase in cardiac output
• Used in patients with severe congestion and hypertension, acute aortic regurgitation or left ventricular dysfunction complicated by mitral valve regurgitation
• May be used as an alternative in patients unresponsive to nitrates 
• Used with caution in patients with renal dysfunction because of possible thiocyanate toxicity

Inotropic Agents

• Eg Dobutamine, Dopamine, Levosimendan, phosphodiesterase inhibitors, Norepinephrine, Epinephrine
• Considered in patients with advanced heart failure or low output syndrome or unresponsive to or intolerant of IV vasodilators; not indicated in heart failure patients with preserved systolic function presenting with hypotension
• May be considered in patients with hypotension (SBP <90 mmHg) and hypoperfusion (ie cardiogenic shock), who are unresponsive to standard treatment including fluid challenge, for increasing BP and cardiac output, improvement of peripheral perfusion and maintenance of end-organ function
• If hypotension with subsequent hypoperfusion is deemed to be from beta-blocker therapy, consider giving Levosimendan or a phosphodiesterase inhibitor (eg Milrinone)
• Continuous blood pressure and cardiac rhythm monitoring are recommended because inotropes and vasopressors may induce myocardial ischemia, arrhythmia and hypotension

Dobutamine

• Positive inotropic agent which stimulates beta₁ and beta₂ receptors
• At low doses, Dobutamine induces mild arterial vasodilatation which augments stroke volume by decreasing afterload while at higher doses, it causes vasoconstriction
• Increases cardiac output in patients with cardiogenic shock

Dopamine

• Endogenous catecholamine which involves dopaminergic, beta-adrenergic and alpha-adrenergic receptors
• At low doses (<3 mcg/kg/min), causes selective vasodilation in the renal, splanchnic, coronary and cerebral vascular beds causing increase renal blood flow, with an increased response to diuretics
• At intermediate doses (3-5 mcg/kg/min), it has inotropic effects which cause an increase in myocardial contractility and cardiac output
• At higher doses (>5 mcg/kg/min), it has vasoconstrictor activity causing an increase in peripheral vascular resistance

Levosimendan

• Calcium sensitizer which improves cardiac contractility by binding to troponin-C in cardiomyocytes
• Increases cardiac output and stroke volume, decreases pulmonary wedge pressure, systemic vascular resistance and pulmonary vascular resistance, and slightly increases heart rate and decreases blood pressure
• Alternative for patients on beta-blockers because its inotropic effect is independent of beta-adrenergic stimulation

Phosphodiesterase Inhibitors

• Eg Amrinone, Enoximone, Milrinone
• Have significant inotropic, lusitropic and peripheral vasodilating effects
• Indicated in patients with peripheral hypoperfusion with or without congestion who are resistant to diuretics and vasodilators and preserved systemic blood pressure
• May be preferred than Dobutamine in patients on concomitant beta-blocker and/or with inadequate response to dobutamine

Vasopressors

• Eg Epinephrine, Norepinephrine
• Agents with prominent peripheral arterial vasoconstrictor activity which increase blood pressure and redistribute cardiac output from the extremities to the vital organs
• Cardiac-stimulant effect is more pronounced at low doses and vasoconstrictor effect at high doses
• Reserved for use in emergencies to maintain end-organ perfusion in life-threatening persistent hypotension in spite of adequate filling status
• Should be used with caution and only transiently because it may increase left ventricular afterload and decrease cardiac output which may further decrease end-organ perfusion
• If vasopressors are needed in patients with cardiogenic shock, Norepinephrine is recommended over Dopamine

Prophylaxis for Thromboembolism

• Eg low-molecular-weight Heparin, unfractionated Heparin, Fondaparinux, direct oral anticoagulant (DOAC)
• Reduces the risk of developing deep venous thrombosis and pulmonary embolism
• Recommended in patients not anticoagulated and without contraindication to anticoagulation therapy
  • If with contraindication, may consider using a mechanical device (eg intermittent pneumatic compression device) for venous thromboembolism prophylaxis

Drugs After Stabilization

• Oral disease-modifying therapy for heart failure should be continued during acute heart failure episodes except in patients who are hemodynamically unstable or with biochemical adverse reactions
• Evaluate the effects of the components of long-term therapies on renal function
• Evidence-based oral medical treatment is recommended to be given prior to discharge

Angiotensin-Converting Enzyme (ACE) Inhibitors 

• Recommended for prevention of heart failure in patients at high risk of this syndrome (eg those with peripheral vascular disease, CAD, stroke, diabetes mellitus, patients with another major risk factor or diabetes mellitus patients who smoke or have microalbuminuria)
• Recommended in patients with left ventricular ejection fraction (LVEF) ≤40%, after stabilization of acute heart failure, to decrease the risk of premature death, recurrent MI and hospitalization for heart failure

Angiotensin Receptor Blockers (ARB)/Angiotensin II Antagonists

• Alternative agents in patients with decreased LVEF, symptomatic atherosclerotic cardiovascular disease or diabetes mellitus and another risk factor, who cannot tolerate the side effects of ACE inhibitors
• Also reduce the risk of premature death, recurrent MI and hospitalization for heart failure

Beta-Blockers

• Recommended in patients with recent decompensation of heart failure after optimization of volume status and discontinuation of IV diuretics, vasoactive agents and inotropes 
• Should be given in a "start low, go slow" approach until maximum tolerable doses and patient's clinical status, blood pressure and heart rate are reassessed after each dose titration
• Used in patients with symptomatic heart failure, LVEF <40% or left ventricular systolic dysfunction after MI and patients with atrial fibrillation for acute control of ventricular rate
  • Use cautiously if patient is hypotensive
  • Consider Digoxin in patients with atrial fibrillation with rapid ventricular rate despite beta-blocker therapy
• Decrease cardiac ischemia, reinfarction and myocardial remodeling after acute MI
• Should be and can be safely continued in patients with acute heart failure except in cardiogenic shock
  • Discontinue beta-blockers in patients taking these medications if they have a heart rate of <50 bpm, 2nd- or 3rd-degree AV block or shock

Mineralocorticoid Receptor Antagonists (MRA)/Aldosterone Antagonists

• May be given after stabilization since it has minimal effect on blood pressure
• Recommended in patients following an acute MI, with clinical heart failure manifestations or history of diabetes mellitus and LVEF <40%, while receiving standard therapy
• Offered as an alternative if ACE inhibitor or ARB is not tolerated

Cardiac Glycosides

• Positive inotropic effect of cardiac glycosides does not change in heart failure
• Produce a small increase in cardiac output and reduction of filling pressures
• Indicated in patients with acute heart failure secondary to atrial fibrillation with insufficient rate control
• May be used in patients with sinus rhythm with symptomatic heart failure and LVEF ≤40%

• Elevate back rest to position of comfort and limit total fluid intake to <1-1.5 L/day 
• Restrict sodium to <2 g/day in patients with symptomatic heart failure

Ventilation

Oxygen

• Should be given to treat hypoxemic patients (SpO₂ <90% or PaO₂ <60 mmHg) in order to maintain O₂ saturation at ≥95% (≥90% in patients with COPD)
• Should not be used routinely in nonhypoxemic patients because it causes vasoconstriction and decreases cardiac output

High-Flow Nasal Cannula

• Studies show it to be non-inferior to non-invasive positive pressure ventilation (NIPPV) and more effective than conventional O₂ therapy

Non-invasive Ventilation (NIV)

• Continuous positive airway pressure (CPAP), bilevel positive airway pressure (BIPAP) and NIPPV relieve dyspnea and improve O₂ saturation in patients with acute pulmonary edema
• Adjunctive therapy to relieve symptoms in patients with pulmonary edema and severe respiratory distress who are not responsive to O₂ or pharmacological therapy
• Considered in patients with conditions complicated by respiratory failure, decreased consciousness or physical exhaustion
• Initiated as soon as possible to reduce respiratory distress and decrease the rate of endotracheal intubation
• Use with caution in hypotensive patients and those with reduced preload reserve; contraindicated in patients with vomiting, possible pneumothorax and altered sensorium

Endotracheal Intubation and Invasive Ventilation

• Indicated in patients with progressive respiratory failure, which may lead to hypoxemia, hypercapnia and acidosis, that cannot be managed through non-invasive measures, or who are intolerant of or have contraindications to NIV
• Also considered in patients with physical exhaustion, decreased consciousness, inability to maintain the airway, and persistent hemodynamic instability