heart%20failure%20-%20acute
HEART FAILURE - ACUTE
Heart failure is a clinical syndrome caused by cardiac dysfunction usually secondary to myocardial muscle loss or dysfunction.
It is characterized by either left ventricular hypertrophy or dilation or both.
It leads to neurohormonal and circulatory abnormalities.
Acute heart failure is the rapid onset of or change in the signs and symptoms of heart failure.
It arises as a result of deterioration in patients previously diagnosed with heart failure or may also be the first presentation of heart failure.
It is characterized by pulmonary congestion, decreased cardiac output and tissue perfusion.
It is a life-threatening condition that needs immediate medical attention.

Principles of Therapy

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

Goals of Treatment:

  • Treat symptoms, stabilize the patient and improve hemodynamics and organ perfusion
    • Maintain peripheral capillary oxygen saturation (SpO2) >90%, systolic blood pressure (SBP) >90 mmHg and peripheral perfusion
  • Minimize side effects
  • Prevent cardiac or renal damage and thromboembolism
  • Identify etiology and co-morbid illnesses and initiate specific therapy
  • Adjust therapy to control symptoms and optimize blood pressure (BP)
  • Initiate and assess the need to increase disease-modifying pharmacological therapy
  • 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 acute coronary syndrome (ACS)
    • Patients at high risk for ACS may also be referred to the cardiac catheterization lab
  • Vital signs include SBP <90 mmHg, respiratory rate (RR) >25, arterial oxygen saturation (SaO2) <90%, use of accessory respiratory muscles
  • 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%
  • Fluid challenge with saline or Ringer’s lactate is recommended in patients with cardiogenic shock if without overt signs of fluid overload

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, may consider giving a vasopressor
      • If unresponsive to medical therapy, may consider mechanical circulatory support
    • If SBP >90 mmHg: Give vasodilators, diuretics; in refractory cases, may consider giving an inotropic agent

Pharmacotherapy

Diuretics

  • Eg Loop diuretics, Potassium-sparing diuretics, Thiazide diuretics
  • Restore and maintain normal volume status in patients with fluid overload
    • Dose of intravenous diuretic should be based on the type of acute heart failure in patients with volume overload
    • 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 intravennous (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
  • 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 should be at least equivalent to the preexisting oral dose

Thiazide Diuretics

  • Eg Bendroflumethiazide, Hydrochlorothiazide, Metolazone, Indapamide
  • 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

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

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

Vasopressin Antagonists

  • Eg Tolvaptan, Conivaptan
  • Block renal water reabsorption
  • May be used in treating patients with significant cognitive symptoms due to resistant hyponatremia

Vasodilators

  • Eg Nitroglycerin, Nitroprusside, Nesiritide
  • Reduces venous and arterial tone resulting in optimization of preload and reduction in afterload respectively
  • Mostly used in patients with hypertension
    • IV therapy may be given as initial treatment 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 symptomatic 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

Nitroglycerin

  • 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 (MI), hypertension, or significant mitral regurgitation

Nitroprusside

  • Potent vasodilator with balanced effects on venous and arteriolar tone
  • Causes immediate decrease in pulmonary capillary wedge pressure and increase in cardiac output
  • Used in patients with severe congestion and hypertension or left ventricular (LV) dysfunction complicated by mitral valve regurgitation
  • Used with caution in patients with renal dysfunction because of possible thiocyanate toxicity

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

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
    • Short-term IV infusion may also be considered in patients with hypotension and/or hypoperfusion despite adequate filling status, for increasing blood pressure 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
  • 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/minute), 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/minute), it has inotropic effects which cause an increase in myocardial contractility and cardiac output
  • At higher doses (>5 mcg/kg/minute), 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, Milrinone, Enoximone
  • 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 Norepinephrine, Epinephrine
  • Agents with prominent peripheral arterial vasoconstrictor activity which increase blood pressure and redistribute cardiac output from the extremities to the vital organs
  • Reserved for use in emergencies to maintain 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 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
  • Reduces the risk of developing deep venous thrombosis and pulmonary embolism
  • Recommended in patients not anticoagulated and without contraindication to anticoagulation therapy

Drugs After Stabilization

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, coronary artery disease, stroke, diabetes mellitus, patients with another major risk factor or diabetes mellitus (DM) 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 DM 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

  • Decrease cardiac ischemia, reinfarction, and myocardial remodeling after acute MI
  • 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
  • Recommended in patients with recent decompensation of heart failure after optimization of volume status and discontinuation of IV diuretics, vasoactive agents, and inotropes
  • Discontinue beta-blockers in patients taking these medications if they have a heart rate of <50 beats/minute, 2nd- or 3rd-degree AV block, or shock

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 DM, 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%

Non-Pharmacological Therapy

Ventilation

Oxygen

  • Oxygen should be given to treat hypoxemic patients [peripheral capillary oxygen saturation (SpO2) <90% or  partial pressure of oxygen in arterial blood (PaO2) <60 mmHg] in order to maintain oxygen (O2) saturation at ≥95% [≥90% in patients with chronic obstructive pulmonary disease (COPD)]
  • Should not be used routinely in nonhypoxemic patients because it causes vasoconstriction and decreases cardiac output

Non-invasive Ventilation

  • Continuous positive airway pressure (CPAP) and non-invasive positive pressure ventilation (NIPPV) relieve dyspnea and improve oxygen 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 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; contraindicated in patients with vomiting, possible pneumothorax, and altered sensorium

Endotracheal Intubation and Invasive Ventilation

  • Indicated in patients with respiratory failure, which may lead to hypoxemia, hypercapnia, and acidosis, that cannot be managed through non-invasive measures
  • Also considered in patients with physical exhaustion, decreased consciousness, and inability to maintain the airway

Monitoring

Non-invasive Monitoring

  • Monitoring the temperature, respiratory rate (RR), heart rate (HR) and rhythm (ECG), blood pressure (BP), oxygenation, urine output, and peripheral perfusion is mandatory
  • Evaluate patient’s signs and symptoms for correction of fluid overload
  • Pulse oximeter should be used continuously in any unstable patient who is on oxygen therapy
  • Transcutaneous arterial oxygen saturation monitoring is recommended for patients on oxygen therapy and ventilatory support
  • Acid-base balance should also be checked on admission in cases of acute pulmonary edema or prior history of COPD
  • While admitted in the hospital, patient monitoring should also include daily measurement of weight, renal function and electrolytes

Invasive Monitoring

Intra-arterial Line

  • Insertion of an intra-arterial line should only considered in patients with low systolic blood pressure and persistent heart failure despite treatment (eg cardiogenic shock)

Central Venous Line

  • Useful for fluids and drugs administration and monitoring of central venous pressure and venous oxygen saturation which provides an estimate of the body oxygen consumption/delivery ratio

Pulmonary Artery Catheterization

  • Measures the cardiac output and superior vena, right atrium, right ventricle, and pulmonary artery pressures
  • Can be used to distinguish between a cardiogenic and non-cardiogenic mechanism in patients with concurrent cardiac and pulmonary disease
  • Should only be considered in patients who are refractory to pharmacological therapy, persistently hypotensive, have uncertain left ventricular filling pressure, or being considered for surgery

Interventional Therapy

Mechanical Assist Devices

  • Temporary mechanical circulatory assistance may be indicated in patients with acute heart failure who have potential for myocardial recovery but unresponsive to conventional treatment
  • Also used as a bridge to heart transplantation or interventions that may lead to significant recovery of the heart function
  • Mechanical circulatory support used in the short term may be considered in patients with refractory cardiogenic shock depending on patient’s age, presence of comorbidities, and neurological function

Intra-aortic Balloon Pump Counterpulsation (IABP)

  • Standard component of therapy in cardiogenic shock or severe acute left heart failure in patients who:
    • Do not respond rapidly to fluid administration, vasodilatation, and inotropic support
    • Are complicated by significant mitral regurgitation or rupture of the interventricular septum
    • Have severe myocardial ischemia in preparation for coronary angiography and revascularization
  • Should only be used in patients who may recover spontaneously or whose underlying condition may be corrected by coronary revascularization, valve replacement, or heart transplant
  • Contraindicated in patients with aortic dissection, significant aortic insufficiency, severe peripheral vascular disease, uncorrectable causes of heart failure, or multi-organ failure

Ventricular Assist Devices

  • Mechanical pumps that partially replace the mechanical work of the ventricle
  • Decrease myocardial work and pump blood into the arterial system thus increasing peripheral and end-organ flow
  • Considered in patients with >2 months of severe symptoms despite optimal medical and device treatment who have >1 of the following conditions:
    • Left ventricular ejection fraction (LVEF) <25% and peak maximum oxygen consumption <12 mL/kg/minute
    • ≥3 heart failure hospitalizations in the last 12 months with no known precipitating cause
    • Dependence on intravenous (IV) inotropes
    • Progressive end-organ dysfunction from reduced perfusion
    • Without deteriorating right ventricular function
  • Complications include thromboembolism, bleeding, infection, and device malfunction

Ultrafiltration

  • Venovenous isolated ultrafiltration is sometimes used to remove fluid in patients with heart failure who are not responsive to diuretics

Coronary Revascularization

  • Can be considered in patients with heart failure and suitable coronary anatomy for relief of refractory angina or acute coronary syndrome

Valvular Surgery

  • May be indicated in patients with valvular heart disease as the etiology of heart failure or as an important aggravating factor for heart failure
  • Performed after stabilization and optimal medical management of heart failure and co-morbid conditions
  • Emergency surgery should be avoided if possible

Heart Transplantation

  • Can be considered in patients with end-stage heart failure, severe acute myocarditis, postpuerperal cardiomyopathy, major myocardial infarction (MI) within an initially poor outcome after revascularization, and no alternative treatment options
  • Significantly increases survival, exercise capacity, quality of life, and return to work compared with conventional therapy
  • Can only be performed until the patient’s condition has been stabilized
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