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Acute Congestive Heart Failure

Camilo Mohar, DO


Over 1 million hospitalizations occur each year as a result of acute congestive heart failure (CHF). With the ever increasing age of the US population, the prevalence of CHF is becoming more and more common. For this reason, it is important to understand the physiology and adequate management of congestive heart failure for healthcare providers in the emergency department.

Think of the heart as a two cycle pump that pushes blood through the pulmonary and
systemic vascular system. During one cycle (diastole) the pump is filling. During in the other cycle, the pump is pushing blood out (systole). Acute congestive heart failure occurs when the pump cannot adequately fill with blood during diastole or pump enough blood out during systole. Thus you have diastolic versus systolic heart failure. Although the pathophysiology may be different, it is not distinguishable at the bedside unless performing a bedside transthoracic echo. From a clinical perspective, the management for either condition is the same.

Acute Congestive Heart Failure

Clinical Findings of Acute Congestive Heart Failure

Heart failure is primarily a clinical syndrome. It is a constellation of findings and symptoms that point to a failing pump in which the heart functions. Common symptoms include dyspnea, lower extremity edema, rapid weight gain, and fatigue. A failing heart causes pulmonary edema and fluid third spacing. These are the primary reasons for symptoms. Physical exam findings that support such a syndrome include jugular venous distension, pitting edema of the lower extremities, crackles or rales on pulmonary auscultation, and S3 gallop if there is systolic heart failure. Despite the delineation of diastolic versus systolic heart failure, in the ED, the treatment for acute heart failure is the same. Common interchangeable terms include decompensated or symptomatic heart failure.

The differential diagnosis for dyspnea with pulmonary adventitious lung sounds is broad. Brain natriuretic peptide (BNP) can be helpful to make the diagnosis. However, some clinical conditions can falsely elevate the BNP. The pathophysiology of heart failure is complex and involves neurohormonal activation as well as sodium and water retention. Increased systemic vascular resistance worsens fluid retention. The cardiovascular system often promotes perfusion for a short period but unless addressed, can lead to increasing work for the heart. Likewise, this may lead to further complications like further decompensation, heart remodeling, and/or ischemia.

Causes of Congestive Heart Failure

It is important to investigate precipitating factors that lead to heart failure. Therefore, the goal of treatment is to address the underlying cause. The ultimate goal for acute management is to blunt neurohormonal activation and water retention. This is critical to adequately resuscitate the patient in the emergency department. Understanding the types and causes of congestive heart failure can help to guide management.

Heart failure is further classified as high and low output states. High output cardiac failure is less common. This type of failure is also associated with warm extremities and pulmonary congestion. High output cardiac failure is the result of the pump failing the demands of the body more so than the pump itself failing. High output failure is often accompanied by increased metabolism or decreased systemic vascular resistance. These include Illnesses like beriberi, thyrotoxicosis, anemia, and AV fistula formations. These conditions are rarely encountered but should be considered in the presence of pulmonary edema. This Is especially true in patients with tachycardia, and warm extremities.

Literature also describes heart failure as right versus left heart failure. However, for the sake of relevance we will describe the most common presentation of heart failure in the ED – acute on chronic decompensated heart failure. The most common type of heart failure is acute on chronic heart failure. This variant may present with high, normal or low blood pressure. A patient may have a history of diastolic or systolic heart failure upon presentation which may aid in the diagnosis.

Diagnosing Acute Congestive Heart Failure

There are no single physical exam findings, historical markers or lab results that confirm the diagnosis of CHF. In these cases, a constellation of findings and clinical gestalt helps to make the diagnosis.

Chest radiographs often reveal pulmonary congestion, edema and/or cardiomegaly but a normal study does not exclude the diagnosis. An ECG can detect underlying ischemia or dysrhythmia. Commonly found ECG abnormalities include left bundle branch block, left ventricular hypertrophy or new inverted T waves. Point of care ultrasound is growing in popularity in the ED. Associated findings include B lines (ring down artifacts that arise from the interface of the visceral and parietal pleura when there is congestion). However, B lines can be seen with other conditions such as pulmonary contusion, fibrosis, and pneumonia. Biomarkers such as B-NP are useful if there is clinical uncertainty however factors such as body habitus, sepsis, and acute kidney injury may cause false elevation.

Management of Acute Congestive Heart Failure

Supplemental Oxygen


The level of severity determines the treatment of acute CHF. Always prioritize airway, breathing and circulation. Often hypoxia requires supplemental oxygen. Non-invasive positive pressure ventilation (NIPPV) such as CPAP or BIPAP may also be used. These methods decrease the work of breathing. These also decrease pulmonary congestion by reducing preload (the volume of blood returning to the heart). NIPPV should be avoided if the patient is altered or cannot tolerate the mask. Likewise, consider intubation if the patient is hypoxic or severely encephalopathic.

Nitroglycerin

If a patient presents hypertensive, begin with reduction of systemic vascular resistance. There are a few ways to accomplish this. Sublingual or Intravenous nitroglycerin are popular options and recommended. They are short acting, and reduce systemic vascular resistance (afterload). They also decrease preload through this mechanism, which leads to decreased pulmonary vascular congestion. Nitroprusside is an alternative to nitroglycerin.

Avoid nitroglycerin or nitroprusside in preload-dependent states. These states include right ventricular infarction, aortic stenosis, hypertrophic obstructive cardiomyopathy, or volume depletion states seen with hypotension.

Diuretics

Loop diuretics such as lasix or bumex reduce the overall volume of the patient for diuresis. These should be given with care. These drugs are not as reversible as nitroglycerin. Use these medications sparingly in patients who are have not taken these medications previously. Their effect is measured by urine output. Diuresis should begin within one hour of administration.

In a normotensive patient presenting with heart failure, loop diuretics are first line agents
used to aid in the improvement of symptoms that have resulted in pulmonary congestion. The
DOSE trial suggests a one time dose of the daily diuretic as an IV push. Diuretics however may
worsen renal function. Monitor electrolytes for this reason. The dose can be doubled if there is no urine output in thirty to sixty minutes. Consider a vasodilator such as nitroglycerin if there is worsening pulmonary congestion.

Avoid loop diuretics if the patient is hypovolemic, or oliguric. Diuresis usually occurs after there is improvement in blood pressure and respiratory status. For this reason, these medications should be given with care.

Vasopressors


Patients that present with low blood pressure have high morbidity and mortality and
often have end stage heart failure. Vasopressors are often needed to maintain perfusion for a short period. This allows other causes of hypotension to be investigated. These can include acute coronary syndrome requiring catheterization, or other processes such as sepsis.

After Acute Management

If there is no underlying correctable process for significant heart failure with hypotension, the ultimate treatment would be heart transplant. A small subset of patients may qualify for artificial heart implantation.

Comorbidities also contribute to the development of heart failure. These conditions are managed by a multispecialty team. A Cardiologist should direct care. Overall, heart failure carries a poor prognosis with 50% of patients dying within 5 years of initial diagnosis. Hospitalized patients have a higher mortality than outpatients.

Disposition

Although CHF is a common reason for ED presentation and hospitalization, there are no decision risk stratification tools to determine disposition. Disposition should be on a case by
case basis. Outpatient management decisions should consider such things as patient capacity to sel-administer drugs, measure their weight, assess urine output, and their access to follow up. Many patients with CHF can be managed in the ED observation unit. Time for diuresis and symptom improvement may take just a few hours. Good discharge candidates include those who have follow up within 7 days, do not need a repeat echo, have unlimited activities of daily living, and are able to obtain their medications. Encourage a shared decision making model. Likewise, discussion with the patient’s cardiologist can ensure follow up and medication adjustments will take place.

Summary

The ED management of CHF can be straightforward or quite complicated depending on the situation. A good understanding of the underlying process and its approach is a step forward in helping patients with their illness. Providing stabilizing care is only the start of a life-long continuum of maintenance, and knowing that the condition is likely to worsen over time. Like with all long-term and severe conditions that we manage, knowing your patient, and proving a safety net for outpatient management is the best management option.

References


Tintinalli’s Emergency Medicine A Comprehensive Study Guide 8th Edition Chapter 53 Acute
Heart Failure


EB Medicine Acute Decompensated Heart Failure: New Strategies for Improving Outcomes

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