Volume I:
First Thirty Minutes
- Section 1
  Acute Care Algorithm/ Treatment Plans/ Acronyms
- Section 2
  Universal Approach
  - CALS Universal Approach To Emergency Advanced Life Support
- Section 3
  Steps 1-6
- Section 4
  Preliminary Impression/Focused Clinical Pathways
Volume II:
Resuscitation Procedures
Volume III:
Definitive Care

Cardiovascular 12: Acute Heart Failure Portal

Acute heart failure may appear as severe pulmonary congestion (with associated tachypnea, labored breathing, rales, and jugular venous distention) and/or manifest the signs and symptoms of reduced cardiac output (such as pallor, weak pulses, and hypotension). Non-cardiac disorders must be ruled out as causes for a patient's distress. In hemodynamically compromised patients, rapid intervention is necessary and must be instigated after only a minimal number of basic diagnostic tests. Diagnostic tests are necessary only to exclude specific causes of heart failure that require specific therapeutic interventions. Examples of causes for acute heart failure that need to be identified early include myocardial injury or infarction, symptomatic tachycardia (VT or SVT), pulmonary embolus, malignant hypertension, and high-grade AV block. If these causes are not apparent from the initial evaluation, aggressive treatment of the patient's heart failure takes precedence over further diagnostic testing.

Heart Failure: General Considerations

Assessing the presence and severity of heart failure may require the evaluation of many parameters that include¹:

The fluid status of the patient judged by a change in the patient’s weight, the degree of jugular venous distension, the presence of congestion in the lungs and liver, and the degree of edema.
The two-dimensional echocardiogram coupled with Doppler flow studies is the single most useful diagnostic test in evaluating a patient with heart failure.¹ The most valuable piece of information gained from an echocardiogram is the measurement of the left ventricular ejection fraction. A patient with an ejection fraction of <40% is considered to have systolic dysfunction.¹
A chest x-ray helps to detect pulmonary congestion, cardiomegaly, and pulmonary disease.
Coronary arteriography may be useful in assessing the potential value of revascularization in some appropriately selected patients with heart failure.²
Invasive hemodynamic and electrophysiologic testing is not routinely justified in patients with heart failure, except those who do not respond to treatment or those who have life-threatening pump failure or arrhythmias.²
B–type natriuretic peptide (BNP) is a cardiac neurohormone that is secreted from the membrane granules of the heart ventricles in response to ventricular pressure overload and volume expansion. BNP levels have been shown to elevate in patients with left ventricular dysfunction and be useful in both diagnosing and staging CHF.³ There is a significant direct correlation between the level of the pulmonary wedge pressure and the height of the BNP level,⁴ and an inverse relationship between the BNP level and the ejection fraction of the left ventricle.⁵ In patients with decompensated CHF, the higher the level of the BNP value the poorer the prognosis. Falling BNP levels with treatment reflect benefit from treatment.³ Since BNP has a short half-life (22 minutes) the level will rapidly fall as the patient’s wedge pressure falls in successfully treated CHF patients.4 BNP levels of <100 pg/mL or NT pro-BNP levels of <300 pg/mL are highly sensitive and specific in excluding CHF; likewise BNP levels of > 400 to 500 pg/mL or NT pro-BNP levels of >900 pg/mL are more than 90% sensitive and specific for heart failure. Therefore, BNP or NT ProBNP levels can be a sensitive and specific test to help diagnosis or exclude CHF.^6,7

Evaluation and Treatment of Acute Heart Failure Syndromes (Including Pulmonary Edema and Cardiogenic Shock)

Recently, the concept of acute heart failure syndromes has replaced the older classification of congestive heart failure, pulmonary edema, and cardiogenic shock. An understanding of pathophysiology of acute decompensated heart failure is useful in directing evaluation and management.

Heart failure is often classified as systolic heart failure, in which the left ventricular ejection fraction is decreased (generally less than 40%), and diastolic heart failure, in which the left ventricular filling pressures are elevated but the LV ejection fraction is preserved. Patients with decompensated diastolic heart failure may present with hypertension, rapid onset of symptoms (ie, hours), and relatively little fluid overload. Patients with systolic heart failure may present after a longer prodrome and be quite fluid overloaded. Hypotensive patients may, in fact, have intravascular volume depletion and actually require fluids.

In acute heart failure syndromes, this pathophysiology is reflected in the degree of pulmonary congestion and in the systemic blood pressure. Therefore, attempt to determine the patient’s pathophysiology—based on past medical history, bedside physical exam, and lab imaging studies—to guide treatment. The following assessments and interventions represent a selective amalgamation of evidence-based approaches published by several leading professional organizations.^6-11

Evaluation

Focused history: Determine if onset of symptoms was rapid (hours) or slow (days). If slow, fluid overload is more likely.
Patient’s medical records: Review for previous diagnosis, echocardiograms, and prior heart failure evaluations.
Physical examination: Pay special attention to jugular venous distention and peripheral edema as index of volume status. (Caution: this may not be entirely reliable.). The presence of S3 is highly specific for LV dysfunction.
Obtain the following:
- 12-lead ECG. (Institute continuous ECG monitoring.)
- Blood studies (CBC, electrolytes, BUN, creatinine, cardiac enzyme levels, and BNP or NT-pro BNP).
- Chest x-ray. Central congestion with peripheral sparing and Kerley’s B-lines are quite specific for cardiogenic pulmonary edema.⁷
- Pulse oximetry and/or ABGs
Transthoracic Doppler/two-dimensional echocardiography (if needed and available). Trained non-cardiologists have been successful in estimating ejection fraction using bedside cardiac ultrasound.¹²
Institute arterial blood pressure monitoring (if available) for hypotensive patients.
In refractory acute pulmonary edema or if acute intervention is needed for MI, cardiac catheterization/coronary angiography may be necessary.

Treatment: (For details on each treatment item, see discussion in the following section.)

Administer supplemental oxygen as required to maintain O₂ saturations as appropriate for the individual patient (typically > 90%) or as guided by relief of patient’s dyspnea.
Vasodilators are important in most patients with decompensated heart failure, but most important in hypertensive patients.
- Nitroglycerin SL/IV may be the most practical. Current use of phosphodiesterase inhibitors (eg, sildenafil [Viagra]) is a contraindication.
- Sodium nitroprusside and neseritide are also options.
- An ACE inhibitor (enalaprilat [Vasotec IV]) may also be used, but be aware of the potential for hypotension.
- If the BP is < 90 mm Hg systolic, defer vasodilators and see numbers 3 and 4 below.

Pressors or inotropes (dopamine, norepinephrine, milrinone) may be needed to support blood pressure at the level required for nitroglycerine or other vasodilator therapy.
- If signs and symptoms of shock are present, use dopamine IV.
- If BP is between 70 to 100 mm Hg systolic without signs and symptoms of shock, consider dobutamine infusion.
- If BP is < 70 mm Hg systolic, norepinephrine (Levophed) infusion may be required. However, consider volume expansion first (see number 4 below).
- Inamrinone and milrinone are inotropic/vasodilating agents that may be considered when the more conventional agents (dopamine, dobutamine, norepinephrine) are ineffective.
f the patient is hypotensive, decompensation has occurred rapidly (within hours), and no other signs of fluid overload are present, give a fluid challenge of 500 cc NS with careful attention to patient’s response.
Consider non-invasive positive pressure ventilation (CPAP or BiPAP) for all patients alert enough to protect their airways. CPAP has the potential for reducing cardiac output; BiPAP has been associated with increased mortality when used in the setting of acute MI. See non-invasive positive pressure ventilation (CPAP and BiPAP).
Intubation and mechanical ventilation may be required for severe hypoxia and respiratory acidosis when a patient is not responding rapidly to treatment and/or when CPAP or BiPAP are unavailable or ineffective.
Consider loop diuretics (furosemide 40 to 80 mg IV) for most patients, unless hypovolemia is suspected.

Other Treatments

Morphine sulfate 2 to 5 mg IV has been used in the past. Its role is uncertain, and the potential adverse reactions of hypotension and oversedation may outweigh its benefits.

Special Circumstances

Thrombolytic therapy or urgent revascularization (angioplasty or coronary artery bypass surgery) may be indicated for acute myocardial infarction.
Intra-aortic balloon counterpulsation may be indicated for patients with severe acute heart failure and cardiogenic shock not responding to initial treatment.
Definitive correction of underlying cause (mitral valve replacement, repair of acute ventricular septal defect) may be needed.
Treatment of arrhythmias significant enough to lead to decompensation (eg, ventricular tachycardia, extreme bradycardias, atrial fibrillation with rapid response) may be required.

Discussion of Treatment of Acute Cardiogenic Pulmonary Edema

Nitroglycerin is an effective initial treatment agent for acute pulmonary edema due to ischemic and non-ischemic causes. If systemic BP is > 95 to 100 mm Hg and the patient does not have signs and symptoms of shock, administer nitroglycerin 0.4 to 0.6 mg SL every 5 minutes up to 4 doses followed by nitroglycerin 10 to 20 µg/min IV to decrease preload and afterload of the heart.^13,14
Potent diuretics like furosemide (Lasix) inhibit reabsorption of sodium primarily in the loop of Henle.¹⁵ Give Furosemide 40 to 80 mg IV early in the treatment. Higher doses may be necessary for patients with massive fluid retention or renal insufficiency. An association between higher diuretic doses (>200 mg) and poorer outcome has been reported,¹⁶ particularly in the subset of hypertensive patients with rapid onset pulmonary edema, but convincing evidence of causation is lacking. Place a urinary catheter early in the treatment to monitor urine output. Limit the furosemide dose to that necessary to achieve the desired diuresis. In most cases, the dose is no more than 2 mg/kg. The initial effect is to decrease preload by a direct venodilating effect. This occurs within 5 minutes.¹⁷ Peak diuresis occurs in 30 to 60 minutes. The newer loop diuretics have side effects and actions similar to furosemide. They include torsemide (Demadex), which has a relative potency of 1:40 compared to furosemide.¹⁷ Loop diuretics maintain their efficacy down to a creatinine clearance < 5 mL/min.¹ Some patients will not respond to high dose loop diuretics alone but will respond when the loop diuretic is combined with diuretic agents that act in the distal renal tubules like thiazides, metolazone (Zaroxolyn), and potassium sparing agents.^15,17 Thiazides lose their effectiveness in patients with moderate renal impairment with creatinine clearance < 30 mL/min.¹
Morphine sulfate 2 to 5 mg IV decreases preload and afterload of the heart and therefore improves symptoms in acute pulmonary edema. With morphine sulfate, there is a potential for oversedation as well as respiratory depression and hypotension. These factors—along with the development of more effective agents—have resulted in decreased utilization. Do not give morphine if the systolic BP is < 100 mm Hg. Use morphine with caution for patients with chronic pulmonary insufficiency or respiratory or metabolic acidosis with suppressed ventilatory drive.¹³
Sodium nitroprusside 0.1 to 5 µg/kg/min IV is especially helpful with severe acute pulmonary edema associated with hypertensive emergencies.14 It may also be used when ischemia is not a prominent feature and nitroglycerin IV is not effective. The dose may be increased until the patient improves or systolic BP is diminished to 85 to 90 mm Hg.¹³
Dopamine infusion 2 to 20 µg/kg/min IV is useful for patients with acute pulmonary edema with signs and symptoms of shock with initial systolic BP of 70 to 100 mm Hg.^13,18 In doses of 5 to 10 µg/kg/min, the beta-1 and beta-2 inotropic or cardiac-stimulating effects predominate, but in doses of 10 to 20 µg/kg/min, the alpha-receptor effects become prominent with systemic and splanchnic arteriolar vasoconstriction resulting in increased cardiac work.¹⁷
Dobutamine 2 to 20 µg/kg/min IV may be used for acute pulmonary edema for patients with initial systolic BP between 70 to 100 mm Hg if there are no signs or symptoms of shock or if systolic BP is > 90 to 100 mm Hg.¹⁷Dobutamine is primarily a beta-receptor stimulator that increases the myocardial contractility and decreases left ventricular filling pressures. In doses > 20 µg/kg/min, dobutamine causes an increase in heart rate that may induce myocardial ischemia.¹⁷
Norepinephrine is a potent vasoconstrictor. In acute heart failure syndromes, its use should be limited to instances in which the systolic BP remains < 70 mm Hg, despite use of fluids and inotropes. Typical doses of norepinephrine are 0.5 to 12 µg/min administered as an infusion.
Inamrinone (loading dose of 0.75 mg/kg IV over 2 to 3 minutes, followed by infusion of 5 to 15 µg/kg/min IV) has inotropic and vasodilatory effects similar to dobutamine. Milrinone has similar properties to inamrinone and is administered as a slow loading dose of 50 µg/kg IV over 10 minutes followed by an IV infusion at a rate of 0.375 to 0.75 µg/kg/min.¹⁷ The inotropic and vasodilator properties of these drugs increase cardiac output and reduce both systemic vascular resistance and pulmonary capillary wedge pressure without significantly increasing myocardial oxygen consumption.¹⁹ Nevertheless, due to the lack of benefit in reducing hospital mortality or readmission, the use of Milrinone for the treatment of the acute exacerbation of chronic heart failure cannot be routinely recommended.¹⁹
Nesiritide is a recombinant human brain, or B-type, natriuretic peptide. When combined with standard therapy of digoxin, diuretics, and ACE inhibitors in patients with acute decompensation of CHF and given in a dose of 2 µg/kg IV bolus followed by a 0.01 µg/kg/min IV infusion, nesiritide resulted in an improvement of the symptoms in patients with CHF that is greater than observed with the use of nitroglycerin IV.²⁰ However, recent studies have suggested an increased 30-day mortality in patients treated with nesiritide versus standard vasodilators.²¹ Nesiritide has arterial, venous, and coronary vasodilatory effects that reduce preload and afterload and thus increases cardiac output without a direct inotropic effect on the heart.²⁰ Nesiritide also increases the glomerular filtration rate, suppresses the renin-angiotensin-aldosterone axis, and causes a natriuresis in patients with decompensated CHF.²² The primary adverse effects include hypotension (that was usually mild to moderate and either resolved spontaneously or with an IV volume challenge of 250 mL or less) and headache.²⁰ In summary, nesiritide should be reserved for patients not responding to more conventional therapy with vasodilators and diuretics. Compared to dobutamine, it may require less intense monitoring and carry less risk of arrhythmia.
ACE Inhibitors: Activation of the neurohormonal (renin-angiotensin) system is thought to play a major role in decompensated heart failure; therefore, ACE inhibitors would seem to be a rational choice for treatment.¹⁰ Use of ACE inhibitors is becoming more common, although the evidence base supporting their efficacy is not large.²³ Currently, there is no standard regimen for this indication; however, conservative initial doses include enalaprilat (Vasotec IV) 0.625 mg over 5 minutes or captopril (Capoten) 6.25 mg SL. Hypotension has been associated with an initial dose of these agents.⁸
Non-invasive positive pressure ventilation (CPAP and BiPAP) may be very helpful to improve gas exchange by preventing alveolar collapse. In an alert nonintubated patient, CPAP may be delivered by a special tight-fitting face mask with a CPAP valve attached to wall O₂ or with a BiPAP machine. Typical initial setting for CPAP is 5 cm H₂O increasing by 2 cm H₂O as needed to a max of 10 to 15 cm H₂O. CPAP may decrease cardiac output, so monitor blood pressure carefully. Non-invasive positive-pressure ventilation has been found to improve outcomes in acute heart failure syndromes overall²⁴; however, BiPAP specifically has been associated with an increased incidence of acute MI, and may be best avoided in the setting of acute ischemia.²⁵(Vol II—AIR SKILLS 8 Intubating Laryngeal Mask Airway)
Intubation and mechanical ventilation are essential for patients with severe hypoxia and respiratory acidosis who are not responding rapidly to therapy. If a patient's PaO₂ cannot be maintained > 60 mm Hg with 100% oxygen and the patient is showing signs of cerebral hypoxia, increasing respiratory acidosis, and increasing PaCO₂, intubation and mechanical ventilation is necessary.
Pulmonary artery balloon catheter for measuring pulmonary wedge pressure is usually not required for cardiogenic pulmonary edema, unless the patient does not respond to initial therapy or the pulmonary edema is complicated by hypotension of shock.¹³
Intra-aortic balloon counterpulsation may be indicated for patients with severe acute heart failure not responding to initial treatment. It is particularly useful as a bridge until the patient may undergo urgent cardiac catheterization and definitive corrective therapy.¹³

References

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Cheng V, Kazanagra R, Garcia A, et al. A rapid bedside test for B-Type peptide predicts treatment outcomes in patients admitted for decompensated heart failure: a pilot study. J Am Coll Cardiol. 2001:37:386-391.
Kazanegra R, Cheng V, Garcia A, et al. A rapid test for B-Type natriuretic peptide correlates with falling wedge pressures in patients treated for decompensated heart failure: a pilot study. J Card Fail. 2001:7:21-29.
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Cuffe MS, Califf RM, Adama KF Jr, et al. Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA. 2002:287:1541-1547.
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Sackner-Bernstein JD, Kowalski M, Fox M, Aaronson K. Short-term risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled trials. JAMA. 2005;293:1900-1905.
Hobbs RE, Mills RM. Therapeutic potential of nesiritide (recombinant b-type natriuretic peptide) in the treatment of heart failure. Expert Opin Investig Drugs. 1999:8:1063-1072.
Annane D, Bellissant E, Pussard E, Asmar R, Lacombe F, Lanata E, Madonna O, Safar M, Giudicelli, JF, Gajdos P. Placebo-controlled, randomized, double-blind study of intravenous enalaprilat efficacy and safety in acute cardiogenic pulmonary edema. Circulation. 1996;94:1316-1324.
Collins SP, Mielniczuk LM, Whittingham HA, Boseley ME, Schramm DR, Storrow AB. The use of noninvasive ventilation in emergency department patients with acute cardiogenic pulmonary edema: a systematic review. Ann Emerg Med. 2006;48:260-269.
Mehta S, Jay GD, Woolard RH, et al. Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema. Crit Care Med. 1997;25:620–628.

Cardiovascular 12: Acute Heart Failure Portal

References

Edition 13-October 2011