Mastering CHF

Current strategies for the prehospital care of congestive heart failure



Bryan E. Bledsoe, DO, FACEP | | Tuesday, February 24, 2009

JEMS Clinical Review Features

This clinical review feature article is presented in conjunction with the Department of Emergency Medicine Education at the University of Texas Southwestern Medical Center, Dallas Course Objectives

Learning Objectives

>>Discuss congestive heart failure and its pathophysiology.

>>Describe the assessment of the patient with heart failure.

>>Discuss updated prehospital management for the patient in heart failure.

Glossary Terms

Afterload: Peripheral vascular resistance, or the pressure in the systemic arterial system that the heart must overcome before blood moves forward.

Biventricular failure: Combination of right and left heart failure.

Cardiogenic shock: When the heart can_t meet the metabolic demands of the body.

Cardiac output: Amount of blood pumped by the heart in one minute.

Continuous positive airway pressure (CPAP): Device that transmits an increased airway pressure to patients and is effective in treating hypoxemia and pulmonary edema.

Flash pulmonary edema: Pulmonary edema that has a very rapid onset.

In extremis: Close to death.

Left heart failure: Type of heart failure where the left ventricle becomes ineffective as a forward pump and fluid accumulates in the pulmonary circulation.

Right heart failure: Type of congestive heart failure where the right ventricle becomes ineffective as a forward pump and fluid accumulates in the systemic circulation.

Stroke volume: Amount of blood pumped by the heart in a single heart beat.

Preload: Amount of blood received by the heart from the venous system.

Pulmonary edema: Accumulation of fluid in the lung tissues and alveoli.

Congestive heart failure (CHF), which occurs when the heart becomes an ineffective pump, is a frequently encountered emergency in prehospital care. Because CHF involves numerous body systems, it_s now often referred to as ˙acute heart failure syndromeÓ (AHFS). More than 3 million Americans have CHF and 400,000 new cases are identified each year.1

In CHF, although the heart can_t pump effectively, it_s still able to meet the metabolic demands of the body. When it can_t meet the body_s metabolic demands, the condition is referred to as"cardiogenic shock." The difference between these two conditions is important to understand.

CHF is often classified asright heart failure orleft heart failure, depending on the ventricle involved. With right heart failure, the right ventricle becomes ineffective as a forward pump and fluid accumulates in the systemic circulation. With left heart failure, the left ventricle becomes ineffective as a forward pump and fluid accumulates in the pulmonary circulation. In most patients, there_s a combination of right and left heart failure (known as"biventricular failure"). In fact, the most common cause of right ventricular failure is left ventricular failure.

CHF can also be classified as backward or forward heart failure. Backward failure results from elevated systemic venous pressure and involves primarily the right ventricle. Forward heart failure is due to reduced forward flow into the aorta and systemic arterial circulation.

Additionally, CHF is typically classified as either acute or chronic. Acute CHF develops relatively rapidly. Chronic CHF develops over a longer period of time. Treatment strategies differ based upon whether CHF is acute or chronic.


The heart is a highly effective pump. In a normal person, the heart beats approximately 100,000 times a dayƒthat_s 35 million times a year, or 2.5 billion times over the course of their life. The circulatory system is a closed system, which means the heart can pump out only what is delivered to it. It also means that the right ventricle and left ventricle normally pump the same amount of blood with each contraction.

The amount of blood pumped by the heart in one minute is called ˙cardiac outputÓ (CO), and it can be defined as follows:

Cardiac Output (CO) = Stroke Volume (SV) _ Pulse Rate

Thestroke volume(SV) is the amount of blood pumped by the heart with each beat. The pulse rate is the number of times the heart beats per minute. Thus, the amount of blood the heart pumps is affected by the SV and the pulse rate.

To increase CO, the body (through the brain_s command) can increase the heart rate or SV. To decrease CO, the body can decrease the heart rate or SV.

Several factors affect stroke volume. First, the heart can pump only the amount of blood it receives from the venous system. This is called the"preload". If the preload is decreased, there_s less blood for the heart to pump, and cardiac output falls. The most common reason for a decreased preload is inadequate fluid in the circulatory system (due to such causes as dehydration, blood loss, spinal injury or anaphylaxis).

The strength of the ventricular contraction varies based on several conditions. For example, the more the ventricle is stretched, the stronger the subsequent contraction. This phenomenon is referred to as Starling_s law of the heart. The most common cause of ventricular stretch is increased preload. Thus, as more blood is forced into the ventricle, and the more it_s stretched, the greater the force of the subsequent contraction.

Various factors and substances increase the strength of the ventricular contraction, including the hormones epinephrine and norepinephrine. These hormones are released by the adrenal medulla glands in response to stress (sympathetic stimulation). In addition, it has been recently discovered that the heart secretes hormones. These hormones are referred to as ˙natriuretic peptides.Ó Thus far, two peptides have been identified: atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP).

ANP is manufactured, stored and released by atrial muscle cells in response to such actions as atrial dilation and sympathetic stimulation. It primarily causes a reduction in blood volume, resulting in decreased central venous pressure (CVP), cardiac output and blood pressure.

BNP was initially discovered in the brain, but it_s principally secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells. It also causes a reduction in blood volume, resulting in decreased CVP, cardiac output and blood pressure BNP levels are elevated in CHF and have become a marker for its presence.

BNP (marketed as nesiritide or Natrecor) can be administered as a treatment for acute decompensated CHF.

Thus, in times of increased demand, various hormones are released to stimulate increased cardiac contraction (inotropy). When the heart starts to fail, natriuretic peptides and other hormones are released to increase cardiac contractile strength and reduce blood volume.

The final factor to affect stroke volume isafterload. Afterload is the pressure in the systemic arterial system that the heart must overcome before blood moves forward. Thus, the greater the afterload, the less the stroke volume will be. In adults, preload, cardiac contractile force and afterload can impact stroke volume. Children, on the other hand, have very little capacity to change their stroke volume. Instead, they rely on changes in heart rate (chronotropy) to regulate their cardiac output.

As discussed earlier, CHF occurs when the heart becomes ineffective as a forward pump. There are various causes of this, primarily when the heart muscle itself becomes damaged through myocardial infarction. When a part of the heart is infarcted, the effected muscle dies and is replaced by scar tissue, which can_t contract. When enough of the ventricular mass is affected, CHF occurs. When a large percentage of the ventricular mass is affected (usually greater than 40%), cardiogenic shock often develops.

Other factors can adversely affect the ability of the heart to contract. Damage can occur from various chemicals, such as prolonged exposure to alcohol or cocaine. Several of the cancer chemotherapy agents (e.g., adriomycin) are also known to impair cardiac function. Although the causes of CHF can be numerous, most, in fact are due to hypertension and infarcts.

Signs & Symptoms

The presentation of CHF can range from subtle to overt. Generally, signs and symptoms suggest which side of the heart is involved. If the right ventricle fails, blood will accumulate and pressure will increase in the venous system. This causes edema of the legs and feet (pre-sacral area in bedbound patients), distension of the jugular veins, engorgement and enlargement of the liver, and weight gain (due to water gain). Typically, the pulse rate will be increased to help compensate for the fall in CO.

Failure of the left ventricle causes accumulation of fluid in the pulmonary system (pulmonary edema). Pulmonary edema is the accumulation of fluids in the spaces in the lungs outside of the blood vessels. This results in dyspnea, the inability to breathe while lying flat (orthopnea) and abnormal lung sounds (crackles or rales) from fluid accumulation. As more of the lungs are affected, hypoxemia will develop, and the patient will develop altered mental status (e.g., agitation, confusion, anxiety). If untreated, this may progress to coma and death.

CHF is often detected and treated before it becomes severe, and your patient_s medications will be clues in your assessment. Initially, a diuretic is prescribed to help promote the elimination of water through the kidneys. Usually, furosemide (Lasix) or a similar loop diuretic is used. In addition, many patients are started on digoxin (Lanoxin). Digoxin is a cardiac glycoside that increases the strength of the cardiac contraction. Most patients are also placed on a blood pressure medication to counter some of the effects on other body systems involved in the development of CHF.

Most important, patients are instructed to maintain a careful diet. An increased intake of sodium or a similar substance can worsen the patient_s condition.

Acute CHF can develop in patients who have chronic CHF or in patients who have never had it. Pulmonary edema associated with CHF can occur so quickly that it_s often called"flash pulmonary edema". With acute CHF and pulmonary edema, patients can rapidly become hypoxic and deteriorate. Thus, it_s essential for prehospital personnel to identify the problem early and provide the necessary treatment.

As noted, the signs and symptoms of CHF can vary based on which side of the heart is principally involved. Most patients will have some combination of biventricular failure and will exhibit mixed signs and symptoms. Common signs and symptoms of CHF are listed in Table 1 (See March 09JEMS,p. 61).

The various findings seen in congestive heart failure all point to failure of the heart as an effective forward pump. As CHF worsens, oxygen delivery to essential tissues, such as the brain, declines and the patient becomes symptomatic, exhibiting confusion, malaise and agitation. When oxygen delivery begins to fall, the condition is emergent. Prehospital treatment strategies should be directed at correcting hypoxemia and then administering medications to improve cardiac output.

Prehospital Treatment

During the past few years, the treatments for CHF and acute pulmonary edema have undergone significant changes.1 For years, the mainstays of CHF and acute pulmonary edema were morphine and diuretics. Now, these agents are contraindicated. For example, in a Cleveland study, the administration of morphine to patients with acute decompensated CHF resulted in an increased need for mechanical ventilation, longer hospitalization, more ICU admissions and higher mortality.2

Furosemide (Lasix), a potent diuretic, has been widely used in the treatment of CHF and acute pulmonary edema despite limited studies on its effectiveness.3 Studies have associated diuretic therapy for acute CHF with short-term adverse clinical outcomes, particularly at high doses, raising concerns for its toxicity.4 Some harmful effects of furosemide have been identified. Further, most CHF patients are already taking furosemide and bolus administration seems to have little effect.5

Current strategies in the prehospital treatment of CHF and acute pulmonary edema include correction of hypoxemia and administration of medications to improve cardiac output. As soon as patient contact is made, EMS personnel should immediately begin the administration of 100% oxygen via a non-rebreather mask. This will maximize oxygen concentration and fully saturate circulating hemoglobin.

After the mask is placed, monitors should be applied (e.g., 12-lead ECG, pulse oximetry, capnography, noninvasive blood pressure). A saline lock should be started. If IV access is not readily attainable, and the patient isin extremis, consider placing an intraosseous (IO) needle.

For patients who have moderate to severe pulmonary edema, noninvasive ventilations should be started. In the prehospital setting, this is best performed withcontinuous positive airway pressure(CPAP). CPAP increases airway pressures and is effective in treating hypoxemia and pulmonary edema.

CPAP is probably the single most important change in CHF treatment developed in the past few decades. It decreases the need for endotracheal intubation and is highly effective.6 CPAP is easy to administer and can be performed by EMT-basics with appropriate training.7

The pharmacologic treatment of CHF and acute pulmonary edema primarily involves the use of nitrates. Nitrates, the most common of which is nitroglycerin (NTG), are vasodilatorsƒprimarily venous. NTG reduces myocardial work. Current strategies in the management of CHF call for more aggressive dosing of NTG. In fact, hypertensive patients with CHF (systolic blood pressure, or SBP, > 180 mm Hg) should generally receive three tablets or sprays of 0.4 mg NTG initially. CHF patients with an SBP between140 and 180 mmHg should receive two tablets or sprays of 0.4 mg NTG initially.

Normotensive patients (systolic blood pressure between 90 and 140 mmHg) should receive one tablet or spray of 0.4 mg NTG. Nitroglycerin should be repeated every three to five minutes if the SBP remains greater than 100 mmHg. ALS personnel should consider using intravenous NTG if allowed by local protocols. IV NTG is more predictable and effective. Topical NTG should be used only as a last resort (when a patient on CPAP does not tolerate sublingual NTG). Absorption of NTG in the paste form is often unreliable and unpredictable in the emergency setting.

Nitrates should not be used in patients who have taken any erectile dysfunction drugs. Generally, you should avoid the administration of NTG if the patient has taken sudenafil (Viagra) or vardenafil (Levitra) in the prior 24 hours or tadalafil (Cialis) in the prior 48 hours. Fatal hypotension has been reported when NTG has been administered to patients taking these medications.

Following aggressive NTG therapy, a second vasodilator is often added. The most commonly used are the angiotensin-converting enzyme (ACE) inhibitors. These include enalopril (Vasotec) and captopril (Capoten). Enalopril can be given intravenously. There_s probably still a limited role for the loop diuretics, such as furosemide (Lasix), in patients who have normotensive CHF and are already taking oral diuretics.

The administration of a BNP (nesiritide) can help improve cardiac output. Although commonly used in the hospital setting, it_s not frequently used in the prehospital setting. Studies on it_s effectiveness are mixedƒbut certain patients seem to benefit from administration.8,9

For a long time, morphine sulfate has been a mainstay for acute CHF treatment. However, recent studies have shown morphine to be of little benefit in CHF.10 The primary effect of morphine appears to be a reduction in anxiety. Most anxiety in CHF is due to hypoxemia and usually resolves once this has been corrected.

Patients who remain anxious after the correction of hypoxemia might benefit from a small dose of a benzodiazepine, such as diazepam (Valium), midazolam (Versed) or lorazepam (Ativan). These drugs are anxiolytics and are more effective on anxiety than morphine and don_t have the adverse vascular effects.

Patients with cardiogenic shock (SBP < 90 mmHg) should receive pressor support (dobutamine or dopamine) and transport. Remember that these patients may also be suffering acute coronary syndrome (ACS). They should receive aspirin and be transported, if possible, to a hospital with invasive cardiology capabilities. See Figure 1(See March 09JEMS, p. 64) for a sample algorithm.

Future Strategies

As we better understand the pathophysiology of CHF, we will develop strategies and treatments to help correct the problem. As mentioned, one new treatment is CPAP, which has allowed many patients to be managed without being intubated and placed on a ventilator. Many states and medical directors have started to allow basic EMTs, with additional training, to use CPAP and nitrates. Because CHF treatment is time-dependent, starting appropriate treatment early can save lives.

Unfortunately, many hospitals don_t have simple CPAP devices (although ventilators can be used in a CPAP mode). The transition to CPAP is best performed as a system (EMS and hospitals acquiring and introducing the device at the same time). A collaborative effort will ensure patients started on CPAP in the field can continue the same care in the hospital.


This overview of the current treatment of CHF shows the significant shift in strategy regard ing the management of CHF and pulmonary edema. Morphine should not be used, and furosemide (Lasix) should be used judiciously. The mainstay of therapy should be nitrates and CPAP. These interventions can be supplemented with other vasodilators, such as ACE inhibitors.11 EMS personnel should always follow local protocols in regard to actual patient care issues.

Bryan Bledsoe, DO, FACEP, is a board-certified emergency physician and an author. A former EMT, paramedic and paramedic instructor, Dr. Bledsoe has written numerous EMS textbooks, including Brady_s paramedic textbook series. He_s a frequent contributor to JEMS and regular speaker at EMS conferences worldwide. Contact him atbbledsoe@me.comor find him

Learn more from Dr. Bledsoe at the EMS TodayConference & Expo, March 2Ï6 in Baltimore.


  1. Mosesso VN Jr, Dunford J, Blackwell T, et al: ˙Prehospital therapy for acute congestive heart failure: State of the art.ÓPrehospital Emergency Care.7(1):13Ï23, 2003.
  2. Peacock WF, Hollander JE, Diercks DB, et al: ˙Morphine and outcomes in acute decompensated heart failure: An ADHERE analysis.ÓEmergency Medicine Journal. 25(4):205Ï209, 2008.
  3. Tang WH: ˙Pharmacologic therapy for acute heart failure.ÓCardiology Clinics. 25(4):539Ï551, 2007.
  4. Cotter G, Metzkor E, Kaluski E, et al: ˙Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema.ÓLancet.351(9100):389Ï393, 1998.
  5. Hoffman JR, Reynolds S: ˙Comparison of nitroglycerin, morphine and furosemide in treatment of presumed pre-hospital pulmonary edema.ÓChest. 92(4):586Ï593, 1987.
  6. Hubble MW, Richards, ME, Jarvis R, et al: ˙Effectiveness of preshospital continuous positive airway pressure in the management of acute pulmonary edema.ÓPrehospital Emergency Care.10(4):430Ï439, 2006.
  7. Wesley K: ˙The Âbasic_ skill of CPAP: Adding CPAP to the EMT-B scope of practice.ÓJEMS. 32(10 Supp):21Ï33, 2007.
  8. Korinek J, Boerrigter G, Mohammed SF, et al: ˙Insights into natriuretic peptides in heart failure: An update.ÓCurrent Heart Failure Reports. 5(2):97Ï104, 2008.
  9. Hiestand B, Abraham WT: ˙Safety and efficacy of nesiritide for acute decompensated heart failure: Recent literature and upcoming trials.ÓCurrent Cardiology Reports. 9(3):182Ï186, 2007.
  10. Mattu A, Martinez JP, Kelly BS: ˙Modern management of cardiogenic pulmonary edema.ÓEmergencyMedicine Clinics of North America. 23(4):1105Ï1125, 2005.
  11. Bledsoe BE, Porter RS, Cherry RA: Paramedic Care:Principles and Practices, Third Edition. Brady/Pearson Education: Upper Saddle River, N.J., 2009.

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Related Topics: Cardiac and Circulation, Medical Emergencies

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