Heart Failure and Fluid Overload

Introduction

What Is Heart Failure?

Congestive heart failure (CHF) is a condition in which the heart is unable to pump enough blood to adequately meet the body’s needs. It can develop when a disorder interferes with normal ventricular filling, normal ventricular contraction, or the heart’s ability to move blood effectively into the circulation.

When the heart cannot keep up with circulatory demands, blood and fluid may begin to back up. This can lead to edema, or abnormal fluid accumulation, in the lungs, legs, abdomen, and other areas of the body.

Heart failure affects millions of people worldwide and is an important cause of chronic illness, hospitalization, and cardiovascular death.

Major Types of Heart Failure

Certain lifestyle factors can contribute to cardiovascular disease and increase the likelihood of developing heart failure, including:

Medical conditions that may increase the risk of CHF include:

CHF is usually a chronic condition requiring ongoing medical management. Although treatment may not completely reverse advanced heart failure, medications, lifestyle changes, procedures, and other therapies can improve symptoms, function, and quality of life.

Common Effects of CHF

Patients living with heart failure may experience symptoms that interfere with normal daily activities, including:

EMS and Heart Failure

EMS may be requested for several different complaints related to worsening heart failure. A patient may call because of:

CHF emergencies can range from relatively mild worsening of symptoms to severe respiratory distress, pulmonary edema, poor perfusion, or cardiac compromise.

A complete assessment is important because patients with heart failure may have problems involving the airway, breathing, circulation, hemodynamic status, and cardiovascular system. EMTs should identify immediate life threats, support oxygenation and ventilation when needed, and recognize when rapid transport or ALS assistance is appropriate.

Heart Failure Foundations

Basic Cardiac Anatomy

The Heart

The heart is responsible for circulating oxygen-rich blood throughout the body. Adequate circulation allows tissues to receive the oxygen and nutrients required for normal cellular function.

When the myocardium is damaged or weakened, the heart may lose its ability to fill or pump effectively. This can contribute to the development or worsening of heart failure.

Major Heart Structures

Layers of the Heart

The heart wall is composed of multiple tissue layers that provide protection, muscular strength, and a smooth internal surface for blood flow.

From outermost to innermost:

The heart lies within the pericardial sac, where a small amount of lubricating fluid normally helps reduce friction as the heart beats.

Coronary Circulation and Cardiac Blood Supply

Coronary Vessels

The coronary circulation provides oxygen-rich blood directly to the heart muscle. Coronary arteries originate near the beginning of the ascending aorta and supply the myocardium with the oxygen and nutrients required for continuous contraction. After oxygen is used by the cardiac tissue, coronary veins return deoxygenated blood toward the right atrium.

Adequate coronary blood flow is essential for normal heart function. Narrowing, obstruction, or damage to a coronary artery can decrease oxygen delivery to the myocardium. If blood flow is significantly reduced or completely blocked, myocardial ischemia or infarction may occur, weakening the heart and decreasing its ability to pump effectively.

Major Coronary Blood Vessels

Coronary veins collect deoxygenated blood from the myocardium and return most of it through the coronary sinus into the right atrium.

Cardiac Electrical Conduction

The heart has the ability to generate electrical impulses automatically through specialized cardiac cells. This property is known as automaticity.

Electrical impulses travel through an organized conduction pathway that causes the atria and ventricles to contract in a coordinated sequence. Proper timing allows the atria to empty blood into the ventricles before ventricular contraction begins.

Electrical Conduction Pathway

Sinoatrial Node (SA Node):
The SA node is normally the heart’s primary pacemaker. It is located high in the right atrium and initiates an electrical impulse that spreads across both atria, causing atrial depolarization and contraction.

Atrioventricular Node (AV Node):
The AV node is located near the lower portion of the right atrium. It briefly delays the electrical impulse before transmitting it into the ventricles. This short delay allows the ventricles additional time to fill following atrial contraction.

Bundle of His:
Also called the atrioventricular bundle, the Bundle of His receives the impulse from the AV node and conducts it into the interventricular septum.

Right and Left Bundle Branches:
The electrical impulse divides into right and left pathways that carry the signal toward the corresponding ventricles.

Purkinje Fibers:
Purkinje fibers distribute the electrical impulse throughout the ventricular myocardium, resulting in coordinated ventricular depolarization and contraction.

The normal sequence can be remembered as:

SA node → AV node → Bundle of His → right and left bundle branches → Purkinje fibers

Understanding the ECG

An electrocardiogram (ECG or EKG) records the electrical activity produced as impulses travel through the heart’s conduction system.

An ECG displays electrical activity; it does not directly prove that the heart is producing an effective mechanical contraction or pulse. For example, organized electrical activity may be present during pulseless electrical activity (PEA) even though there is no palpable pulse.

Basic ECG Components

For EMT-level study, remember that electrical depolarization occurs immediately before the corresponding mechanical contraction.

Blood and the Circulatory System

The circulatory system transports blood throughout the body so cells can receive oxygen and essential nutrients. It also carries carbon dioxide, metabolic waste, hormones, and other substances to locations where they can be processed or eliminated.

Whole blood contains several important components, including red blood cells, white blood cells, platelets, and plasma.

Red Blood Cells

Red blood cells (RBCs), or erythrocytes, are primarily responsible for transporting oxygen.

White Blood Cells

White blood cells (WBCs), or leukocytes, are part of the body’s immune defense system.

Plasma

Plasma is the liquid portion of blood and makes up approximately 55% of whole blood volume.

It is composed mostly of water and also carries:

Plasma helps transport blood cells and substances throughout the circulatory system while also contributing to blood volume and normal physiologic balance.

Blood Components, Circulation, and Gas Exchange

Plasma and Platelets

Plasma serves as the liquid transport medium of the blood. In addition to carrying blood cells, it helps move nutrients, metabolic waste, antibodies, hormones, proteins, electrolytes, and other substances throughout the cardiovascular system.

Platelets, also called thrombocytes, are small cell fragments that play an essential role in blood clot formation and control of bleeding.

Blood vessels form the transportation network that delivers oxygen and nutrients to tissues. They also return carbon dioxide and other metabolic waste products toward organs that remove or process them. Deoxygenated blood is eventually returned to the heart and then sent to the lungs, where carbon dioxide is released and oxygen is added.

Major Types of Blood Vessels

Arteries carry blood away from the heart. Their walls contain relatively large amounts of smooth muscle and elastic tissue because they must tolerate the higher pressures generated by cardiac contraction.

Capillaries are extremely small, thin-walled vessels located throughout tissues. Their thin walls permit the exchange of oxygen, nutrients, carbon dioxide, waste products, and fluid between the blood and surrounding cells.

Veins return blood toward the heart. Because pressure within the venous system is lower than in the arterial system, veins generally have thinner walls. Many veins contain valves that help prevent backward flow and reduce pooling of blood.

Normal Vessel Pathway

Blood generally moves through the circulation in the following order:

Layers of a Blood Vessel

Most larger blood vessels contain three primary wall layers.

Tunica externa (adventitia):
The outermost layer. It provides structural strength, protection, and support to the vessel.

Tunica media:
The middle layer, containing smooth muscle and elastic tissue. Contraction and relaxation of this layer change the vessel’s internal diameter and therefore influence vascular resistance and blood pressure.

Tunica intima:
The innermost layer. It contains a smooth endothelial lining that reduces friction and allows blood to move efficiently through the vessel.

Systemic Blood Flow

Systemic circulation carries oxygenated blood from the heart to tissues throughout the body and returns deoxygenated blood back to the heart.

Blood leaves the left ventricle through the aorta and travels through progressively smaller arteries and arterioles before reaching the capillaries. At the capillary level, oxygen and nutrients are delivered to cells while carbon dioxide and metabolic wastes enter the bloodstream.

The blood then travels through venules and veins, eventually entering the superior and inferior vena cava and returning to the right atrium.

Systemic circulation supplies organs and tissues such as the brain, heart, abdominal organs, skeletal muscles, skin, and extremities.

Pulmonary Blood Flow

Pulmonary circulation carries deoxygenated blood from the right side of the heart to the lungs for gas exchange and then returns oxygenated blood to the left side of the heart.

Blood leaves the right ventricle through the pulmonary artery. The pulmonary artery divides into right and left branches that carry blood toward each lung.

As these vessels become smaller, they eventually form pulmonary capillaries surrounding the alveoli. At this level:

Oxygenated blood then travels through the pulmonary veins and enters the left atrium, where it can continue into systemic circulation.

Respiratory Effects of Heart Failure

Congestive heart failure can significantly affect the respiratory system. A weakened heart may cause pressure to increase within the pulmonary circulation, allowing fluid to move into the lung tissues and potentially into the alveoli.

This accumulation of fluid can interfere with normal gas exchange and contribute to pulmonary edema, dyspnea, hypoxemia, and respiratory distress.

Heart failure can also produce fluid accumulation outside the lungs, including:

Understanding normal gas exchange and movement of fluid between blood vessels and tissues helps explain why patients with CHF can develop these findings.

Gas Exchange and Diffusion

The respiratory system provides oxygen for cellular metabolism while removing carbon dioxide produced by the body.

Gas exchange occurs primarily through diffusion, which is the movement of molecules from an area of higher concentration or partial pressure toward an area of lower concentration or partial pressure.

Within the lungs:

The alveolar and capillary walls are extremely thin, allowing oxygen and carbon dioxide to move efficiently across the alveolar-capillary membrane.

When fluid collects around or within the alveoli, as can occur with pulmonary edema from heart failure, the distance across which gases must move increases. This can significantly impair oxygen transfer.

Capillary Pressure and Fluid Movement

At the capillary level, thin vessel walls permit movement of gases, nutrients, waste products, and fluid between the circulation and surrounding tissues.

Fluid movement depends on several pressure forces that normally remain balanced. When that balance is disrupted, excessive fluid may move out of the vessels and accumulate in surrounding tissues.

Hydrostatic Pressure

Hydrostatic pressure is the pressure exerted by fluid against the walls of a container or blood vessel.

Within the capillary system:

In congestive heart failure, increased vascular pressure can promote excessive movement of fluid out of the circulation. Depending on which side of the heart is failing, this may contribute to pulmonary edema, peripheral edema, or other forms of fluid congestion.

Osmotic pressure is created largely by differences in protein concentration between the blood and surrounding interstitial tissues. Blood normally contains more proteins, especially albumin, than the interstitial space. These proteins help draw water back toward the vascular system.

At the arterial end of a capillary, hydrostatic pressure tends to push fluid outward into the surrounding tissues. As blood moves through the capillary, hydrostatic pressure gradually decreases. Toward the venous end, plasma proteins help favor movement of fluid back toward the circulation.

Not all filtered fluid returns directly to the capillaries. The lymphatic system normally collects excess interstitial fluid and eventually returns it to the bloodstream.

When this balance is disrupted, more fluid may remain within the tissues, producing edema.

Factors That Can Promote Edema

Why CHF Causes Fluid Accumulation

In congestive heart failure, one or both ventricles may be unable to pump blood forward efficiently. Reduced forward flow causes blood to accumulate behind the affected ventricle, increasing vascular hydrostatic pressure.

When pressure within the circulation rises, more fluid is forced out of capillaries and into surrounding tissues. The result may be peripheral edema, ascites, or pulmonary edema, depending on which side of the heart is primarily affected.

Right-sided failure commonly causes congestion within the systemic venous circulation, producing swelling in dependent areas such as the feet, ankles, and lower legs. Fluid may also accumulate in the abdomen.

Left-sided failure causes blood to back up into the pulmonary circulation. Increasing pressure in the pulmonary capillaries can force fluid into the lung interstitial tissue and, in severe cases, into the alveoli.

When alveoli become filled or surrounded by fluid, oxygen must travel through a greater barrier to enter the bloodstream. This reduces effective gas exchange and may lead to hypoxemia and significant respiratory distress.

In some patients, fluid accumulation within the lungs develops very rapidly. This is often called acute or flash pulmonary edema and may quickly progress to severe hypoxia, respiratory failure, or cardiac arrest if not treated promptly.

How Congestive Heart Failure Develops

Heart failure may result from structural or functional damage that interferes with normal cardiac filling or pumping.

Conditions that can contribute to heart failure include:

As cardiac function worsens, the body activates compensatory mechanisms in an effort to maintain cardiac output and adequate perfusion.

The sympathetic nervous system releases catecholamines such as epinephrine and norepinephrine. These hormones increase heart rate, contractility, and vascular tone. Initially, these responses may support circulation, but over time they can increase myocardial workload and oxygen demand.

Decreased cardiac output may also activate the renin-angiotensin-aldosterone system (RAAS). This system promotes sodium and water retention and causes vasoconstriction.

Although these mechanisms are intended to support blood pressure and perfusion, chronic activation may worsen heart failure by:

As the heart works harder against increased resistance and volume, additional myocardial damage may develop, creating a cycle of worsening cardiac function.

Functional Severity of Heart Failure

Heart failure may be described according to how much the patient’s symptoms interfere with physical activity. The severity of symptoms does not always perfectly match the amount of structural heart disease.

Class I

The patient has no meaningful limitation of ordinary physical activity.

Normal daily activity does not typically produce significant fatigue, palpitations, or dyspnea.

Class II

The patient has a mild limitation of physical activity.

The patient is comfortable at rest, but ordinary activity may cause fatigue, palpitations, or shortness of breath.

Class III

There is a marked limitation of physical activity.

The patient may remain comfortable at rest, but activity below the level of normal daily exertion produces symptoms.

Class IV

The patient has severe functional limitation.

Symptoms of heart failure may occur even while resting, and any physical activity may significantly increase discomfort.

Ejection Fraction and Heart Failure

Ejection fraction (EF) is the percentage of blood within a ventricle that is pumped out during each contraction. In heart failure, the left ventricular ejection fraction (LVEF) is frequently used to help evaluate left ventricular function.

A normal or near-normal ejection fraction is generally around 50% or greater, although exact interpretation depends on clinical guidelines and the individual patient.

Common categories include:

Ejection fraction is only one measurement of cardiac function. A patient may have significant heart failure symptoms even when the ejection fraction is relatively preserved.

As CHF progresses, decreased circulation and fluid congestion may affect many body systems, including the lungs, kidneys, liver, abdomen, and lower extremities.

Recognizing a CHF Exacerbation

Many patients live with chronic heart failure and experience periods when their symptoms worsen. These episodes are often referred to as acute exacerbations or decompensated heart failure.

Factors that may contribute to worsening CHF include:

Acute heart failure may appear suddenly or may represent a gradual worsening of previously stable disease. EMTs should consider other serious causes of the patient’s symptoms rather than assuming every episode is simply chronic CHF.

Signs and Symptoms of Worsening Heart Failure

Clinical presentation depends on how severely cardiac function has deteriorated and which side of the heart is most affected.

Possible findings include:

Not every CHF patient will have obvious crackles or severe edema. Some may present only with mild dyspnea, fatigue, or reduced exercise tolerance.

CHF may also coexist with asthma, COPD, pneumonia, myocardial infarction, or other respiratory and cardiovascular conditions, making a complete assessment essential.

EMT Assessment Focus

During the physical examination, look for findings throughout the body rather than focusing only on the lungs.

Important findings may include:

Patients with significant pulmonary edema or severe respiratory distress may require aggressive airway and breathing support according to EMT scope and local protocol, including appropriate oxygen therapy and CPAP when indicated and tolerated.

A detailed history can help identify what triggered the episode, determine whether the symptoms are typical for the patient, and guide appropriate prehospital care.

Important History Questions

When evaluating a patient with possible CHF exacerbation, useful questions may include:

Conditions That Can Mimic CHF

Many illnesses can produce dyspnea, chest discomfort, abnormal lung sounds, or hypoxia. EMTs should avoid assuming that every patient with a history of CHF is experiencing another CHF exacerbation.

Possible alternative or concurrent conditions include:

The goal in the field is not necessarily to establish a definitive diagnosis but to recognize immediate life threats, identify the most likely causes, and provide appropriate supportive treatment.

Findings That Support a CHF Exacerbation

A combination of the following findings may increase suspicion for worsening heart failure:

These findings should be considered together with the patient’s vital signs, medical history, physical examination, and overall appearance.

Assessment and Initial Management

Scene and Response Considerations

Begin with scene safety and standard precautions. Determine whether additional resources are needed based on the severity of the patient’s condition.

Severe heart failure may be associated with acute coronary syndrome or another serious cardiac problem. Consider the capabilities of the receiving hospitals in your area and follow local destination protocols.

General Impression

A large amount of useful information can be obtained immediately when approaching the patient.

Look for:

A severely ill CHF patient may appear critically distressed before a formal examination begins.

Primary Assessment

Level of Consciousness

Assess mental status early.

Patients with mild or moderate disease may remain alert but have difficulty speaking because of dyspnea. They may answer with short sentences, single words, or head movements.

Altered mental status in a patient with severe respiratory distress is particularly concerning and may suggest:

Consider other causes of altered mental status as appropriate.

Airway

The airway is often patent when the patient is awake and speaking. However, declining mental status, severe fatigue, or loss of consciousness may threaten airway patency.

Assess for:

Provide suction and basic airway adjuncts when indicated.

Breathing

Breathing problems are often the most prominent concern during an acute CHF exacerbation.

Assess:

Provide oxygen when indicated for hypoxemia or significant respiratory distress according to local protocol. Oxygen therapy should be adjusted to the patient’s clinical needs rather than automatically given to every CHF patient.

Patients who remain awake, can protect their airway, and are experiencing moderate to severe respiratory distress from suspected cardiogenic pulmonary edema may benefit from CPAP when authorized by protocol.

Patients who develop inadequate respirations, severe altered mental status, or respiratory arrest require positive-pressure ventilation with a bag-mask device and appropriate airway management.

Lung Sounds

Auscultate both lungs and continue to reassess.

Possible findings include:

Crackles are not unique to CHF. Pneumonia and other pulmonary disorders may produce similar findings.

Extensive pulmonary edema may cause diffuse crackles throughout both lungs, while severe fluid accumulation or poor air movement may make breath sounds more difficult to hear.

Circulation

Assess:

Many patients with acute pulmonary edema may initially be tachycardic and hypertensive. Others, particularly those with advanced pump failure, may become hypotensive.

The development of worsening hypotension, bradycardia, altered mental status, or weak pulses may indicate severe deterioration and possible impending cardiac arrest.

Treat external bleeding if present and manage shock according to protocol.

Disability

Evaluate mental status and identify possible causes of altered consciousness.

When available and appropriate, consider assessment of:

Exposure and Physical Examination

Perform an appropriate physical examination while maintaining the patient’s dignity and preventing unnecessary heat loss.

Look for:

Vital Signs and Ongoing Assessment

Obtain and trend a complete set of vital signs, including:

Repeat assessments frequently in any patient who appears unstable.

When available within the responding service’s scope, cardiac monitoring may help identify dysrhythmias or ischemic changes. Advanced ECG interpretation and 12-lead acquisition may be performed by appropriately trained personnel according to local systems.

Acute Decompensated Heart Failure

Acute decompensated heart failure occurs when cardiac function deteriorates enough to produce new or worsening symptoms that require urgent treatment.

It may occur in two general settings:

Possible triggers include:

Many patients with decompensated CHF develop both pulmonary congestion and systemic fluid retention.

Sympathetic Crashing Acute Pulmonary Edema

Sympathetic Crashing Acute Pulmonary Edema (SCAPE) describes a particularly severe form of acute pulmonary edema associated with a rapid increase in sympathetic activity.

The sudden catecholamine surge can produce intense vasoconstriction and a marked rise in blood pressure. The left ventricle must then pump against substantially increased resistance, causing pulmonary vascular pressures to rise rapidly.

Fluid can move into the lung tissues and alveoli within a short period of time, producing severe respiratory distress.

Typical Presentation

SCAPE may develop over minutes to hours and commonly includes:

These patients can deteriorate rapidly and require immediate airway and breathing support.

Treatment of Acute CHF

Management depends on the patient’s respiratory status, blood pressure, mental status, and local EMS protocols.

General EMT Care

CPAP

For an alert patient with significant respiratory distress and suspected cardiogenic pulmonary edema, CPAP may be highly beneficial when permitted by local protocol.

CPAP can:

Monitor blood pressure closely because positive airway pressure can decrease preload and may worsen hypotension.

CPAP should not be used when the patient cannot protect the airway, cannot cooperate, is vomiting, has severely impaired consciousness, or has another contraindication identified by protocol.

Nitroglycerin

Nitroglycerin may help reduce cardiac workload and vascular congestion in selected patients with acute pulmonary edema or associated ischemic chest discomfort.

At the EMT level, this generally involves assisting with the patient’s prescribed nitroglycerin when authorized by local protocol and when blood pressure and other criteria are appropriate.

Do not administer or assist with nitroglycerin when contraindications are present.

Respiratory Failure

If the patient becomes unable to ventilate adequately:

When a patient with severe heart failure continues to deteriorate despite basic airway and breathing support, more advanced interventions may be required depending on provider level, local protocol, and available resources.

Advanced Airway Considerations

Additional Cardiac Considerations

If acute coronary syndrome (ACS) or myocardial infarction is suspected, treatment should also address the underlying cardiac emergency.

Transport Considerations

Patients with severe or decompensated heart failure may require services that are not available at every receiving hospital. Destination choice should therefore take into account the patient’s condition, transport time, local protocols, and the capabilities of available facilities.

A critically ill patient may require:

When a patient is unstable, transport to the closest appropriate facility may be necessary for immediate stabilization. In other situations, local protocols may support transport to a hospital capable of providing a higher level of cardiac or critical care.

If an acute myocardial infarction, particularly STEMI, is suspected or confirmed by appropriately trained providers, early notification and transport to a facility with PCI/cardiac catheterization capability may be important when consistent with the local EMS system.

Patients who require intubation and mechanical ventilation may need prolonged critical care before they are ready to breathe independently again. Those with severe underlying heart or lung disease may have greater difficulty recovering from respiratory failure and may require extended ventilator support.

Transport Priorities