Congestive heart failure acute pharmacotherapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: Acute decompensated heart failure; ADHF; flash pulmonary edema

Overview

Acute heart failure can occur in the setting of a new onset heart failure or worsening of an existing chronic heart failure (also known as acute decompensated heart failure, flash pulmonary edema, ADHF). ADHF presents with acute shortness of breath due to the development of pulmonary edema (the rapid accumulation of fluid in the lung). Other signs and symptoms of ADHF include hypotension with impaired and organ perfusion manifested by worsening renal function, altered mentation and cold clammy extremities. ADHF associated with a poor prognosis if not treated aggressively. Like chronic heart failure therapy, the goal is to improve symptoms but unlike chronic therapy the other goals are to improve oxygenation and hemodynamic stability. The mainstays of the acute medical treatment in acute decompensated congestive heart failure include oxygen to improve hypoxia, diuresis to reduce both preload and intravascular volume and vasodilators to reduce afterload. Some of the mainstays of chronic heart failure therapy are not initiated acutely (ACE inhibtors,beta blockers and digoxin).

2021 ESC Guideline for management of acute heart failure

Abbreviations: AHF: Acute heart failure; LMWH: Low-molecular-weight heparin; PaO2: Partial pressure of oxygen ; SBP: Systolic blood pressure; SpO2: Transcutaneous oxygen saturation;

Recommendations for initial treatment of acute heart failure

Oxygen, ventilation support (Class I, Level of Evidence C):

❑ Oxygen is recommended in hypoxic patients with SpO2<90% or PaO2 <60 mmHg ❑ Intubation is recommended in the presence of progressive respiratory failure in spite of oxygen administration or non-invasive ventilation

Oxygen, ventilation support (Class IIa, Level of Evidence B):

❑ In patients with respiratory distress (respiratory rate >25 breaths/min, SpO2<90%), non-invasive positive pressure ventilation is recommended to decrease respiratory distress and reduce the rate of mechanical endotracheal intubation

Diuretics :(Class I, Level of Evidence C) :

❑ Intravenous loop diuretics are considered for all admitted patients with acute heart failure presented with signs, symptoms of fluid overload

Diuretics : (Class IIa, Level of Evidence B)

❑ In patients with resistant edema who do not respond to an increase in loop diuretic doses, combination of a loop diuretic with thiazide type diuretic should be considered

Vasodilators: (Class IIb, Level of Evidence B)

❑ In order to improve symptoms and reduce congestion in patients with AHF and SBP >110 mmHg, vasodilators may be considered as initial therapy

Inotropic agents : (Class 2b, Level of Evidence C)

❑ Inotropic agents may be considered in patients with SBP <90 mmHg and evidence of hypoperfusion without response to fluid challenge, to improve peripheral perfusion and maintain end-organ function

Inotropic agents (Class III, Level of Evidence C):

❑ Routinely administration of inotropic agents are not recommended , due to safety concerns, unless the patient has symptomatic hypotension and evidence of hypoperfusion

Vasopressors: (ClassIIb, Level of Evidence B)

❑ In patients with cardiogenic shock, a vasopressor, preferably norepinephrine, may be indicated to increase blood pressure and vital organ perfusion

Anticoagulant therapy: (ClassI, Level of Evidence A)

❑ Thromboembolism prophylaxis such as LMWH is recommended in patients not already anticoagulated and no contraindication to anticoagulation, to prevent the risk of deep venous thrombosis and pulmonary embolism

Opiates: (ClassIII, Level of Evidence C)

❑ Opiates is not routinely recommended, unless in selected patients with severe, intractable pain or anxiety

The above table adopted from 2021 ESC Guideline

• In the pre-hospital setting, AHF patients should be monitored by pulse oximetry, BP, heart rate, respiratory rate, and a continuous ECG.
• Oxygen therapy may be given based on a clinical judgment unless oxygen saturation is <90% in which case it should be administered.
• Indication for non-invasive ventilation:

  Respiratory distress

  Respiratory rate >25 breaths/min

• Oxygen saturation <90%

In-hospital management

• Specific causes of AHF should be searched including ACS, hypertensive emergency, rapid arrhythmias, severe bradycardia, conduction disturbance, a

acute valve regurgitation, acute pulmonary embolism, myocarditis, tamponade.

• After exclusion of these conditions, which need to be treated, AHF should be managed according to the clinical presentations.

Pre-discharge phase

• Oxygen therapy, ventilatory support

• In AHF, oxygen should not be used routinely in non-hypoxaemic patients due to vasoconstriction and a reduction in cardiac output.
• Oxygen therapy is recommended in patients with AHF SpO2 <90% or PaO2 <60 mmHg to correct hypoxemia.
• In chronic obstructive pulmonary disease (COPD), hyper-oxygenation may increase ventilation-perfusion mismatch, suppress ventilation and

lead to hypercapnia.

• During oxygen therapy, acid-base balance and SpO2 should be monitored.
• Non-invasive positive pressure ventilation, either continuous positive airway pressure and pressure support, improves respiratory failure, increases oxygenation and pH, and decreases the partial pressure of carbon dioxide (pCO2) and work of breathing and reduce the rate of endotracheal intubation.
• Although
• Non-invasive positive pressure ventilation indicated to improve gas exchange and reduce the rate of endotracheal intubation in patients with:
• Respiratory distress (respiratory rate >25 breaths/min
• SpO2 <90%) he fraction of inspired oxygen

  FiO2 should be increased up to 100%, if needed, based on oxygen saturation level.

  Blood pressure should be monitored regularly during non-invasive positive pressure ventilation.

• The increase in intrathoracic pressure with non-invasive positive pressure ventilation reduces venous return and right and left ventricular preload, cardiac output and BP.
• In the setting of RV dysfunction, the increase in pulmonary vascular resistance and RV afterload may be present.
• Intubation is indicative if there is progressive respiratory failure despite oxygen administration or non-invasive ventilation.

Diuretics

• Intravenous diuretics are mainstay therapy of AHF.
• Efficacy of diuretics are due to increase renal excretion of salt and water and reduce of fluid overload and congestion.
• There was a greater relief of dyspnoea, change in weight and net fluid loss (with no prognostic role for increases in serum creatinine) in the higher-dose regimen.
• High diuretic doses may associate with greater neurohormonal activation and electrolyte disturbance and poor outcomes.
• Diuretic treatment should be started with an initial i.v. dose of furosemide, or equivalent dose of bumetanide or torasemide,

corresponding to 1�2 times the daily oral dose taken by the patient before admission. If the patient was not on oral diuretics, a starting dose of 20�40 mg of furosemide, or a bolus of 10�20 mg i.v. torase�mide, can be used.145,467 Furosemide can be given as 2�3 daily boluses or as a continuous infusion. Daily single bolus administrations are discouraged because of the possibility of post-dosing sodium retention.145,461 With continuous infusion, a loading dose may be used to achieve steady state earlier. Diuretic response should be evaluated shortly after start of diuretic therapy and may be assessed by performing a spot urine sodium content measurement after 2 or 6 h and/or by measuring the hourly urine output. A satisfactory diu�retic response can be defined as a urine sodium content >50�70 mEq/L at 2 h and/or by a urine output >100�150 mL/h dur�ing the first 6 h.145,468 If there is an insufficient diuretic response, the loop diuretic i.v. dose can be doubled, with a further assessment of diuretic response.145 If the diuretic response remains inadequate, e.g. <100 mL hourly diuresis despite doubling loop diuretic doseconcomitant administration of other diuretics acting at different sites, namely thiazides or metolazone or acetazolamide, may be consid�ered. However, this combination requires careful monitoring of serum electrolytes and renal function (Figure 13).145,469,470 This strat�egy, based on early and frequent assessment of diuretic response, allows starting treatment with relatively low doses of loop diuretics, with frequent dose adjustments that may be less likely to cause dehy�dration and increase in serum creatinine. The loop diuretic dose should be progressively decreased when a significant negative fluid balance has been obtained. However, it should be pointed out that this algorithm is entirely based on expert opinion, to date.145,461 Transition to oral treatment should be commenced when the patient’s clinical condition is stable. It is recommended that, after achievement of congestion relief, oral loop diuretics are continued at the lowest dose possible to avoid congestion.463,471 Care must also be taken to avoid patients being discharged from hospital with persis�tent congestion, as this is a major predictor of increased deaths and rehospitalizations.462,472 Hence, care should be taken to achieve adequate decongestion and establish an appropriate long-term diu�retic dose before discharge.427,473 11.3.4 Vasodilators Intravenous vasodilators, namely nitrates or nitroprusside (Supple�mentary Table 21), dilate venous and arterial vessels leading to a reduction in venous return to the heart, less congestion, lower after�load, increased stroke volume and consequent relief of symptoms. Nitrates act mainly on peripheral veins whereas nitroprusside is more a balanced arterial and venous dilator.474,475 Because of their mechanisms of action, i.v. vasodilators may be more effective than diuretics in those patients whose acute pulmonary oedema is caused by increased afterload and fluid redistribution to the lungs in the absence or with minimal fluid accumulation.427,476�478 However, two recent randomized trials comparing usual care with early inten�sive and sustained vasodilation failed to show a beneficial effect of i.v. vasodilators vs. high-dose diuretics.479,480 No recommendation favouring a regimen based on vasodilator treatment vs. usual care can thus be given, to date. Intravenous vasodilators may be considered to relieve AHF symp�toms when SBP is >110 mmHg. They may be started at low doses and uptitrated to achieve clinical improvement and BP control. Nitrates are generally administered with an initial bolus followed bInotropes Inotropes are still needed for treatment of patients with low cardiac output and hypotension (Table 22). They should be reserved for patients with LV systolic dysfunction, low cardiac output and low SBP (e.g. <90 mmHg) resulting in poor vital organ perfusion. However, they must be used with caution starting at low doses and uptitrating them with close monitoring.387,388 Inotropes, especially those with adrenergic mechanisms, can cause sinus tachycardia, increase ventricular rate in patients with AF, may induce myocardial ischaemia and arrhythmias, and increase mor�tality.387,388,430,478 Levosimendan or type-3-phosphodiesterase inhibitors may be preferred over dobutamine for patients on beta-blockers as they act through independent mechanisms.482,483 Excessive peripheral vasodilation and hypotension can be major limi�tations of type-3-phosphodiestaerase inhibitors or levosimendan, especially when administered at high doses and/orVasopressors Vasopressors used for the treatment of AHF are reported in Table 22. Among drugs with a prominent peripheral arterial vasoconstrictor action, norepinephrine may be preferred in patients with severe hypotension. The aim is to increase perfusion to the vital organs. However, this is at the expense of an increase in LV afterload. Therefore, a combination of norepinephrine and inotropic agents may be considered, especially in patients with advanced HF and car�diogenic shock. Some studies, though with limitations, support the use of norepi�nephrine as first choice, compared with dopamine or epinephrine. Dopamine was compared with norepinephrine as a first-line vaso�pressor therapy in patients with shock and was assocarrhythmic events and with a greater mortality in patients with car�diogenic shock but not in those with hypovolaemic or septic shock. Although the trial included 1679 patients, significance was seen only in a subgroup analysis of the 280 patients with cardiogenic shock and <10% of the patients had MI. As there were no data regarding revas�cularization, this limits the generalizability of the results.485 In another prospective randomized trial epinephrine was compared with nore�pinephrine in patients with cardiogenic shock due to acute MI.486 The trial was stopped prematurely due to a higher incidence of refractory shock with epinephrine. Epinephrine was also associated with higher heart rate and lactic acidosis. Despite limitations related to its rela�tively small sample size, short time of follow-up and lack of data regarding the maximum reached dose, the study suggests superior efficacy and safety with norepinephrine. These data are consistent with a meta-analysis including 2583 patients with cardiogenic shock showing a three-fold increase in the risk of death with epinephrine, compared with norepinephrine, in patients with cardiogenic shock.487 However, the lack of information about dose, duration oftreatment, and aetiology, makes these results partially explorativ Opiates Opiates relieve dyspnoea and anxiety. They may be used as sedative agents during non-invasive positive pressure ventilation to improve patient adaptation. Dose-dependent side effects include nausea, hypotension, bradycardia, and respiratory depression. Retroanalyses suggest that morphine administration is associated with a greater frequency of mechanical ventilation, prolonged hospitalization, more intensive care unit admissions, and increased mortality.488�491 Thus, routine use of opiates in AHF is not recommended although they may be considered in selected patients, particularly in case of severe/intractable pain or anxiety or in the setting of palliation. 11.3.8 Digoxin Digoxin should be considered in patients with AF with a rapid ven�tricular rate (>110 b.p.m.) despite beta-blockers (see also section 12.1.1).151,492,493 It can be given in boluses of 0.25�0.5 mg i.v., if not used previously. However, in patients with comorbidities (i.e. CKD) or other factors affecting digoxin metabolism (including other drugs) and/or the elderly, the maintenance dose may be difficult to estimate theoretically and measurements of serum digoxin concentrations should be performed. Digitoxin is a potential alternative to digoxin and is currently being evaluated in a randomized placebo-controlled trial (ClinicalTrials.gov Identifier: NCT0 Thromboembolism prophylaxis Thromboembolism prophylaxis with heparin (e.g. low-molecular�weight heparin) or another anticoagulant is recommended, unless contraindicated or unnecessary (because of existing treatment with oral anticoagulants).494,49

Management of acute heart failure

Cardiogenic shock, respiratory failure

NO

Yes

Identifying acute causes

Pharmacologic therapy Ventilatory support Mechanical circulatory support

Acute Coronary syndrome Hypertension emergency Arrhythmia Mechanical causea Pulmonary embolism Infections Tamponade

Yes

NO

Immediate initiation of specific treatment

Further treatment

The above algorithm adopted from 2021 ESC Guideline

2021 ESC Guideline for management of pulmonary edema

Management of patients with pulmonary edema

Oxygen (Class I) or ventilatory support (Class IIa)

Systolic blood pressure ≥110 mmHg

Yes

NO

Loop diuretics (Class I) and/or vasodilators (Class IIb)

Signs of hypoperfusion

Yes

NO

Loop diuretics (Class I) and inotropes/vasopressors(Class IIb)

Loop diuretics (Class I)

Congestion relief

Yes

NO

Optimized medical therapy

Renal replacement therapy Mechanical circulatory support Palliative therapy

The above algorithm adopted from 2021 ESC Guideline

2021 ESC Guideline for management of cardiogenic shock

Management of patients with cardiogenic shock

Acute coronary syndrome (ACS), mechanical complications

Yes

NO

Emergency PCI or surgical treatment

Identifying and treatment of other specific causes

Oxygen therapy (Class I) or ventilatory support (Class IIa) Inotropes, vasopressors (Class IIb) Short-term mechanical circulatory support (Class IIa)

Improvement of hypoperfusion and organ dysfunction

Yes

NO

Weaning from inotropes/vasopressors and/or mechanical circulatory support Treatment of underlying etiology and medical therapy optimization (Class I )

Mechanical circulatory support(Class IIa) Renal replacement therapy (Class IIa) Palliative care

The above algorithm adopted from 2021 ESC Guideline

Hospitalization

Hospitalization is required for the management of the patient with ADHF with the following signs, symptoms and laboratory abnormalities:

• Hypotension and/or cardiogenic shock
• Evidence of poor end organ perfusion such as worsening renal function, cold clammy extremities, altered mental status
• Hypoxemia with an oxygen saturation under 90%
• Atrial fibrillation with a rapid ventricular response resulting in hypotension
• The possible presence of an acute coronary syndrome and ongoing myocardial ischemia

Telemetry and Monitoring

The patient should be admitted to a level of care that allows for constant electrocardiographic monitoring given the risk of arrhythmias and frequent vital signs.

• The heart rhythm and oxygen saturation should be monitored continuously.
• Is and Os (intake and output) should be monitored carefully. A daily target should be established (for example the patient should be one liter negative for the day) and diuretic dosing should be adjusted to achieve this target.
• Daily weights should be obtained using the same scale at the same time of the day, usually before the patient has eaten, and after they have first voided in the morning. Often times Is and Os measurements will underestimate insensible losses that occur through the lungs.
• The BUN and creatinine, serum sodium (to detect hyponatremia which carries a poor prognosis), chloride, bicarbonate (to detect contraction alkalosis) and serum potassium (to detect hypokalemia as a result of diuresis and which can precipitate arrhythmias) should be monitored daily. Potassium and magnesium should be repeated as needed following diuresis.
• If the patient is hyponatremic this does not suggest an inadequate intake of salt, but excess free water ingestion and retention. In these patients, access to free water should be restricted to <2 li/day if the Na is < 130 meq/li, and < 1 li/day or more if the Na is < 125 meq/li. It should be borne in mind that juices are essentially free water with sugar. In the hyponatremia patient, drips should not be in D5W. Patients with congestive heart failure should be on a <2 g per day sodium diet.

Oxygen

Oxygen improves the patient's status if hypoxemia is present, and the goal is to keep the oxygen saturation above 90%. Continuous positive airway pressure may be applied using a face mask; this has been shown to improve symptoms more quickly than oxygen therapy alone, and has been shown to reduce the risk of death. Severe respiratory failure requires treatment with endotracheal intubation and mechanical ventilation.

Management Considerations

The patient's therapy must be tailored to:

• Whether the patient has acute diastolic or systolic heart failure
• The patient's intravascular volume status
• The patient's hemodynamic status
• The precipitant of the decompensation

Systolic Versus Diastolic Heart Failure

The management of the patient with acute decompensated heart failure depends upon whether the patient has acute decompensated systolic heart failure or acute decompensated diastolic heart failure. Both forms of acute decompensated heart failure are treated with oxygen and vasodilator therapy and diuresis. Importantly, inotropic agents that increase contractility are not indicated in the patient with acute decompensated diastolic heart failure while they are important for the patient with acute decompensated systolic heart failure. While beta blocker initiation is relatively contraindicated in acute decompensated systolic heart failure, control of tachycardia is very useful in the patient with diastolic heart failure to prolong left ventricular filling time. While the initiation of ACE inhibitors may not be recommended in acute decompensated systolic heart failure, ACE inhibition may be of benefit in acute decompensated diastolic heart failure.

Intravascular Volume Status

The aggressiveness of diuresis depends upon the patient's volume status. If the patient is total body and intravascular volume overloaded in normotensive, then diuresis alone should be undertaken. If the patient is volume overloaded but hypotensive, then inotropes must be administered in addition to diuretics. Vasodilators cannot be administered to these patients.

Identification of and Treatment of Underlying Cause of Decompensation

Identification of and treatment of precipitants of acute decompensation is a mainstay of therapy. Please see the accompanying chapters for detailed management strategies.

• Hypertension: Vasodilators should be administered
• Acute coronary syndrome: Antiplatelets, antithrombin, vasodilators, PCI, intra-aortic balloon pump placement should be used to reverse myocardial ischemia
• Valvular heart disease: For mitral regurgitation vasodilator therapy should be administered, for mitral stenosis heart rate slowed to prolonged left ventricular filling, for aortic stenosis either balloon vavlotomy, TAVR or valve replacement may be necessary
• Atrial fibrillation can cause acute decompensation of heart failure due to an increase in heart rate and oxygen demands, and conversely acute decompensation of heart failure can precipitate atrial fibrillation due to left atrial dilation and increased wall stress. Thus, atrial fibrillation and acute decompensated heart failure are often intimately related, and the successful management of atrial fibrillation is often critical to the success of reversing the acute decompensation.

In the patient with acute decompensated heart failure, rate control of atrial fibrillation is the mainstay of arrhythmia therapy. Obviously agents that have a negative inotropic effect such as beta blockers and non-dihydropyridine calcium channel blockers are relatively contraindicated in the management of acute decompensated systolic heart failure. Intravenous diltiazem does not have a negative inotropic effect and is often used for rate control. Short acting esmolol is sometimes used. Digoxin has a very narrow therapeutic/toxic window, it's onset of action is relatively delayed, and it is often not used.

If a patient is in cardiogenic shock, then cardioversion can be considered in the patient with atrial fibrillation, however in the absence of severe hemodynamic compromise it should be noted that atrial fibrillation will often recur in this setting. Thus, cardioversion is not particularly helpful in the absence of profound hemodynamic compromise. Cardioversion can also be undertaken if new onset atrial fibrillation is the clear precipitant of the hemodynamic decompensation. If the patient is going to be cardioverted, unfractionated heparin should be administered.

• Ventricular Arrhythmias: The development of either ventricular tachycardia or ventricular fibrillation are life-threatening complications and must be treated promptly with the cardioversion. Many antiarrhythmic's can be pro-arrhythmic in the patient with heart failure and are contraindicated. Amiodarone is the antiarrhythmic of choice for the management of ventricular arrhythmias in the patient with heart failure. Underlying precipitants of ventricular arrhythmias such as hypokalemia and hypomagnesemia should be corrected. It should also be noted that inotropic agents can be proarrhythmic, and for this reason as low a dose as possible should be used, and they should be tapered as soon as possible.

Specific Therapies

Diuretics

• Usually, but not always, patients with decompensated systolic heart failure are total body and intravascular volume overload and intravenous diuretics are often required in the acute setting. Even in the absence of volume overload (decompensation due to hypertension or valvular heart disease) diuresis may help the symptoms of congestive heart failure because "dry lungs work better than wet lungs". These drugs also cause venodilation in the lung vasculature that also relieves shortness of breath. While contractility of the heart increases with increasing volumes, this relationship is not preserved past a certain volume. By reducing volume overload, these drugs optimize the heart's contractility (they keep the patient from falling off the end of the Starling curve). Reducing the heart's volume also reduces functional mitral regurgitation and tricuspid regurgitation.
• Diuretics reduce preload and reduce intravascular volume.
• Intravenous preparations are preferred because of more predictable absorption. When a patient is extremely fluid overloaded, they can develop intestinal edema as well, which can affect enteral absorption of medications.
• The traditional starting dose of Lasix or furosemide is 40 mg intravenously. If this does not work, the dose is doubled. There is insufficient data to suggest a Lasix drip is superior to boluses of Lasix. A useful rule of thumb is that the IV dose should be 2.5 times the usual oral dose based upon the trend for superiority of high doses over low doses in the DOSE trial . Usually an effect is seen in 30 minutes.
• Torsemide is another alternative and it's dose is 10 to 20 mg intravenously.
• If high doses of furosemide are inadequate, boluses or continuous infusions of bumetanide (1 mg intravenously) may be preferred.
• These loop diuretics may be combined with thiazide diuretics such as oral metolazone, hydrochlorothiazide (25 to 50 mg twice daily) or intravenous chlorothiazide (500 to 1000 mg/day) for a synergistic effect.
• Hypotension may result from diuresis if mobilization of fluid from the extra vascular space does not keep pace with fluid leaving the intravascular space through diuresis. Patients with diastolic dysfunction and restrictive physiology are also prone to hypotension due to reductions in preload.
• Typically the BUN and Cr will rise during diuresis (hopefully the Cr only slightly). If the rise in creatinine is minimal, and the patient remains fluid overloaded, then diuresis can continue with careful attention to the renal function. If the creatinine rises significantly before the patient is euvolemic, this suggests that there is reduced perfusion to the kidney, and this is associated with a poorer prognosis. If the creatinine rises significantly, other nephrotoxic drugs should be discontinued, and the dosing of the diuretic may need to be reduced. Despite a rise in the creatinine, continued diuresis is sometimes required if severe pulmonary edema persists and consideration should be given to the addition of an inotropic agent.
• If further efforts to induce diuresis are failing and the patient remains volume overloaded, then ultrafiltration or dialysis should be considered.
• In patients who have sustained a myocardial infarction and have heart failure, an aldosterone antagonist such as spironolactone or eplerenone can be added instead of a thiazide diuretic. Given the risk of hyperkalemia these agent should only be added if the renal function and serum potassium can be carefully monitored.

Vasodilator Therapy

In the absence of hypotension, the intravenous administration of vasodilators such as nitroglycerin, nitroprusside and nesiritide can reduce both preload and afterload and can rapidly improve symptoms. These benefits are observed when the drugs are administered in addition to diuretics or when there is a poor response to diuretics.

Nitroglycerin

• Nitroglycerine reduces afterload and reduces preload. Nitroglycerine is helpful in improving symptoms of dyspnea. At higher doses, nitroglycerin also reduces afterload.
• Unfortunately tolerance or tachyphylaxis can develop within hours of continuous administration of high-dose nitroglycerin.
• The initial dose of intravenous nitroglycerin is 5 to 10 µg per minute and this dose is increased every 3-5 minutes in 5 to 10 µg increments to a maximum dose of 10 to to 200 µg per minute.

Nitroprusside

• Like nitroglycerin, nitroprusside is both a venodilator and arterial vasodilator, but nitroprusside provides a greater degree of afterload reduction compared with nitroglycerin. Thus, clinical scenarios where rapid and potent arterial dilation are acquired may benefit from nitroprusside as opposed to nitroglycerin, and these include a hypertensive emergency, acute mitral regurgitation, ventricular septal rupture, and aortic insufficiency.
• The initial dose of nitroprusside is 5 to 10 µg per minute and this dose is titrated up every five minutes to a maximum dosing of 5 to 400 pg per minute two maintain a mean arterial pressure (MAP) of 65 mm Hg or a systolic blood pressure of 90 mm Hg.
• While patients administered intravenous nitroglycerin can develop tachyphylaxis, patients administered nitroprusside can develop an accumulation of metabolites including cyanide or thiocyanate which can be toxic and even fatal. Thus, the duration of a nitroprusside infusion is usually only 24 to 48 hours.

Inotropic Therapy

• Ionotropes may be administered if the cardiac output and the systolic blood pressure are low, if there is evidence of end organ hypoperfusion (e.g. a rising creatinine), and if there is evidence of elevated filling pressures (an elevated pulmonary capillary wedge pressure or an elevated jugular venous pressure) which limit diuresis and/or vasodilator therapy.
• Milrinone increases contractility and reduces afterload
• Dobutamine increases contractility in reduces afterload
• Dopamine increases blood pressure and increases renal perfusion at low doses
• There is ongoing concern that inotropes, by increasing heart rate and contractility, may damage hibernating but viable myocardium. These agents are also proarrhythmic. Consistent with these concerns, the randomized OPTIME-CHF trial demonstrated that randomization to Milrinone versus placebo was associated with an increased incidence of hypotension, atrial arrhythmias as well as a non-significant increase in mortality.
• In so far as Milrinone does not exert its effects through beta receptors, it may be more effective in those patients on a beta blocker.
• The starting dose of dobutamine is 2.5 µg/kg/min and the dosing can be gradually titrated up to 15 µg/kg/min.
• The loading dose of Milrinone is 50 µg/kg over 10 minutes. The initial maintenance dose is 0.375 µg/kg/min and the maximum dose is 0.750 µg/kg/min.

Vasopressor Support

• In the presence of severe hypotension and impaired end organ perfusion despite optimal left ventricular filling pressures on invasive monitoring, either intravenous norepinephrine, vasopressin or dopamine at a dose > 5 µg/kilogram/minute can be administered.
• Vasopressors increase afterload and may decrease cardiac output and should only be used transiently if possible.

Prophylaxis for Venous Thromboembolism

In the absence of contraindications, either low-dose unfractionated heparin, fondaparinux or a low molecular weight heparin are recommended as DVT prophylaxis in the patient with acute decompensated heart failure.

ACE Inhibition

Continuation of Chronic ACE Inhibition

• ACE inhibition can be continued in the setting of acute decompensated congestive heart failure if the patient is hemodynamically stable without a rising creatinine or hyperkalemia. An exception is the patient who chronically has a systolic blood pressure below 90 mm Hg who may tolerate the continued administration of an ACE inhibitor in the decompensated setting. The half-life of an ACE inhibitor is relatively long, and this could result in persistent hypotension in the setting of aggressive diuresis.

Initiation of Acute ACE Inhibition

• An ACE inhibitor should not be initiated within the first 12 to 24 hours of acute decompensation of heart failure as these agents may result in prolonged hypotension and impaired end organ perfusion. In particular, intravenous enalaprilat has been associated with poor outcomes among patients with acute MI and heart failure.
• Hyponatremia and a low systolic blood pressure are markers of increased activation of the renin angiotensin system, and may be associated with hypotension following the administration of an ACE inhibitor.

Beta Blockers

• While beta blockers may play a role in the management of chronic heart failure, beta blockade should not be initiated dring acute decompensated heart failure.
• If the patient is chronically administered a beta blocker, the beta blocker can be continued in the absence of hypotension. Withdrawal of beta blockers in the setting of acute decompensated heart failure can be associated with higher mortality. If the patient becomes hemodynamically unstable, the beta blocker dosing can be reduced.
• If inotropic agents are required, then the beta blocker should be discontinued.

Aldosterone Antagonism

• If the patient is chronically being administered an aldosterone antagonist prior to the episode of decompensated congestive heart failure, the agent may be continued in the absence of hypotension, hyperkalemia, and impaired renal function.
• If the patient meets the criteria for initiation of an aldosterone antagonist for the management of chronic heart failure, this can be initiated prior to hospital discharge.

Morphine

• Morphine reduces preload, reduces catecholamines, and reduces the stimulation by stretch receptors in the lung thereby improving symptoms of dyspnea.
• Nonrandomized observational studies have demonstrated that in the setting of acute decompensated heart failure morphine is associated with an increase in-hospital mortality, increased mechanical ventilation and longer hospital admissions despite adjustment of covariates in multivariate models.
• Given the potential hazard identified in these non-randomized observational studies, morphine administration is generally not recommended in the setting of acute decompensated heart failure.

Contraindicated medications

Congestive heart failure is considered an absolute contraindication to the use of the following medications:

• Mannitol