Congestive heart failure acute pharmacotherapy
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Synonyms and keywords: acute decompensated heart failure, ADHF, flash pulmonary edema
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).
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 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.
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
- 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 slightly will rise during diuresis. If the rise in creatinine is minimal, at 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 post MI patients with 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.
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.
- 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.
- 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.
- 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.
- 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
- 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 results in persistent hypotension in the setting of aggressive diuresis.
- 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 are associated with hypotension following the administration of an ACE inhibitor.
- 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.
- 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 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.
- ↑ Lindenfeld J, Albert NM, Boehmer JP, Collins SP, Ezekowitz JA, Givertz MM, Katz SD, Klapholz M, Moser DK, Rogers JG, Starling RC, Stevenson WG, Tang WH, Teerlink JR, Walsh MN (June 2010). "HFSA 2010 Comprehensive Heart Failure Practice Guideline". Journal of Cardiac Failure 16 (6): e1–194. doi:10.1016/j.cardfail.2010.04.004. PMID 20610207. Retrieved on 2013-04-29.
- ↑ Gray A, Goodacre S, Newby DE, Masson M, Sampson F, Nicholl J (July 2008). "Noninvasive ventilation in acute cardiogenic pulmonary edema". N. Engl. J. Med. 359 (2): 142–51. doi:10.1056/NEJMoa0707992. PMID 18614781.
- ↑ Peter JV, Moran JL, Phillips-Hughes J, Graham P, Bersten AD (April 2006). "Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis". Lancet 367 (9517): 1155–63. doi:10.1016/S0140-6736(06)68506-1. PMID 16616558.
- ↑ Weng CL (May 2010). "Meta-analysis: Noninvasive ventilation in acute cardiogenic pulmonary edema". Ann. Intern. Med. 152 (9): 590–600. doi:10.1059/0003-4819-152-9-201005040-00009. PMID 20439577.
- ↑ Salvador DR, Rey NR, Ramos GC, Punzalan FE (2005). "Continuous infusion versus bolus injection of loop diuretics in congestive heart failure". Cochrane Database of Systematic Reviews (Online) (3): CD003178. doi:10.1002/14651858.CD003178.pub3. PMID 16034890. Retrieved on 2013-04-30.
- ↑ Felker GM, Lee KL, Bull DA, Redfield MM, Stevenson LW, Goldsmith SR, LeWinter MM, Deswal A, Rouleau JL, Ofili EO, Anstrom KJ, Hernandez AF, McNulty SE, Velazquez EJ, Kfoury AG, Chen HH, Givertz MM, Semigran MJ, Bart BA, Mascette AM, Braunwald E, O'Connor CM (March 2011). "Diuretic strategies in patients with acute decompensated heart failure". The New England Journal of Medicine 364 (9): 797–805. doi:10.1056/NEJMoa1005419. PMID 21366472. Retrieved on 2013-04-30.
- ↑ Sigurdsson A, Swedberg K (May 1994). "Left ventricular remodelling, neurohormonal activation and early treatment with enalapril (CONSENSUS II) following myocardial infarction". European Heart Journal 15 Suppl B: 14–9; discussion 26–30. PMID 8076657. Retrieved on 2013-04-30.
- ↑ Butler J, Young JB, Abraham WT, Bourge RC, Adams KF, Clare R, O'Connor C (June 2006). "Beta-blocker use and outcomes among hospitalized heart failure patients". Journal of the American College of Cardiology 47 (12): 2462–9. doi:10.1016/j.jacc.2006.03.030. PMID 16781374. Retrieved on 2013-04-30.
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