Beyond the Basics: Right vs. Left Heart Failure
Heart failure is routinely classified as either left or right ventricular failure. Left ventricular failure occurs when the left ventricle ceases to function as an adequate pump of the systemic circulation. In right ventricular failure, the right ventricle fails to adequately pump blood to the pulmonary system, thereby interfering with gas exchange in the alveoli and leading to a decreased filling volume of the left ventricle.
There are several etiologies, which may be permanent or temporary, that cause the heart to fail as a forward pump. The most common etiologies of heart failure are myocardial infarction and hypertensive cardiomyopathy. Less common causes include infectious cardiac disease processes, such as acute myocarditis or endocarditis; induced heart failure from drugs/medications (e.g., cocaine, beta-blockers, tricyclic antidepressants); traumatic mechanisms, such as a myocardial contusion; or metabolic derangements that result in cardiac dysrhythmias, such as sustained tachycardias or bradycardias.
Congestive heart failure (CHF) is a common disorder associated with various degrees of ventricular failure. Approximately 4.6 million Americans are being treated for CHF, and 550,000 new cases are diagnosed each year. The prevalence of CHF increases dramatically with age, occurring in 1%-2% of people ages 50-59 years and up to 10% of people older than 75 years. Approximately 80% of all heart failure admissions occur in patients older than 65 years of age. In fact, CHF is the leading hospital discharge diagnosis in individuals aged 65 years or older.
Despite a steady decline in the incidence of coronary artery disease and stroke, both the incidence and prevalence of CHF are on the rise. Between 1985 and 1995, the number of heart failure hospitalizations increased by 51%. Approximately 870,000 hospital discharges for CHF occurred in 1996.
Heart failure has a tremendous economic impact on the U.S. healthcare system because of direct medical costs, disability and loss of employment. Estimated treatment costs in 1994 were $38 billion, of which $23 billion were spent on hospitalizations. The cost of hospitalizations for heart failure is twice that for all forms of cancer and myocardial infarction combined.
The heart itself is comprised of specialized fibers known as cardiac muscle. Myocardial fibers are unique in that they have the ability not only to initiate an impulse that will lead to contraction, but they are able to alter the speed of the conduction as it travels between fibers. The cardiac muscle is divided into three distinct tissue layers: the endocardium, myocardium and pericardium (sometimes referred to as the epicardium).
The endocardium is the innermost layer and is constantly surrounded by the blood that flows through the heart. The myocardium is the middle layer of the heart and tends to be the thickest due to its bulky muscle mass. The myocardial muscle cells are unlike other muscles in the body, because they are very strong and possess the ability to maintain constant stretch, like skeletal muscle, while simultaneously being stimulated by self-generated electrical impulses. The overall strength of contraction comes from within the myocardial muscle. The continuous workload of the myocardium and its ability to constantly contract is largely due to the vast amount of capillary blood flow that is networked within the muscle bed. This provides the required oxygen, glucose and other nutrient delivery, and, equally important, waste removal, which is mandatory in order to sustain the ongoing workload. The pericardium is the layer commonly referred to as the "pericardial sac." It is a tough fibrous sac that surrounds the heart to provide protection and also lubrication to reduce the friction of the heart wall against the sac as it contracts.
The heart contains four distinct chambers: the left and right atria, and the left and right ventricles. The ventricles are the larger chambers that have the primary function of ejecting blood into either the pulmonary arteries that carry blood to the pulmonary circulation and the lungs, or into the aorta to the systemic circulation, which carries the blood throughout the body. The walls of the ventricles are much more muscular than the atria walls and, as a result, have the ability to generate a greater force and pressure during contraction, as compared to the atria.
Blood flow through the heart originates in the right atrium, where unoxygenated blood, which is also high in carbon dioxide, coming from the venous circulation is delivered to the heart via the superior and inferior vena cava. Once the unoxygenated blood enters the right atrium, it is ejected with the next contraction and passively flows into the right ventricle. Upon contraction of the right ventricle, the blood is pumped out into the pulmonary artery and pulmonary capillaries in the lungs, where alveolar/capillary gas exchange occurs. The oxygen diffuses across the alveolar membrane and the alveolar/capillary interface, where it enters the pulmonary capillary. Approximately 95% to 97% of the oxygen combines with an iron site on the hemoglobin molecule, while the small remaining amount dissolves in the plasma. Conversely, the carbon dioxide, which is carried as bicarbonate attached to an amino site on the hemoglobin or dissolved in plasma, crosses the pulmonary capillary membrane and the capillary/alveolar interface and into the alveoli, where it is eventually exhaled. This process leads to arterial oxygenation and carbon dioxide removal.
Upon leaving the pulmonary capillaries, the oxygenated blood enters the pulmonary veins and is transported back to the left atrium of the heart. The blood filling the left atrium generates pressure on the atrial walls, eventually causing the mitral valve to open and allowing blood to passively enter the left ventricle. Approximately 70% of the blood from the right and left atria flows passively into the right and left ventricles, respectively, as a result of gravity. The remaining 30% of the blood volume is ejected into the ventricle during atrial contraction. Upon contraction of the left ventricle, the blood is ejected through the aortic valve and into the aorta for distribution to organs and cells throughout the body. It is important to note that the left ventricle must generate enough force with each contraction to overcome the pressure at the aortic root, commonly known as afterload.
The most important vessels associated with heart failure are the coronary arteries. Although the heart's chambers may have a full blood volume, it is the coronary arteries that are responsible for delivering oxygenated blood throughout the heart muscle to provide for adequate cardiac cell oxygenation. When a patient is experiencing ischemic chest pain or a myocardial infarction, it is typically due to a compromised coronary artery blood supply. The coronary arteries originate at the base of the aorta. The root of the coronary vessels is known as the coronary sinus. The coronary sinuses provide blood flow through the left and right coronary arteries. The left coronary artery supplies the left ventricle, the intraventricular septum, part of the right ventricle and part of the heart's electrical conduction pathways. The right coronary artery supplies a portion of the right atrium and right ventricle and the other part of the heart's electrical conduction pathways. As the left ventricle contracts, the coronary vessels are occluded by the opened leaflets of the aortic valve; thus, the coronary vessels receive their blood supply at the end of diastole. When the heart relaxes during diastole, the leaflets are pulled away from the opening of the coronary sinuses and the oxygen-rich residual blood in the aorta is drawn into the coronary sinuses. Thus, the volume of blood in the left ventricle at the end of diastole is an important determinant of coronary blood flow. A reduction in left ventricular end-diastolic blood volume will lead to a reduction in coronary artery perfusion and may present as myocardial ischemia in the patient.
Two important variables play a direct role in cardiac output: preload and afterload. Cardiac output is defined as the amount of blood ejected from the ventricle in one minute. It is a determinant of the overall effective function of the heart. An explanation of preload and afterload will provide a better understanding of the complications potentially facing a patient suffering from a cardiac pump or volume-related problem.
Preload is the tension on the ventricular wall when it begins to contract. Preload is determined primarily by the pressure created in the ventricle by the volume of blood at the end of diastole (end-diastolic filling volume). Blood volume at the end of diastole is primarily determined by the venous volume and blood flow from the right side of the heart through the pulmonary vessels. An increase in preload puts the patient in danger of an overload state in the ventricle. Increased blood flow exceeds the heart's ability to effectively eject all of the volume before the next contraction, resulting in an overly stressed myocardium. The increased workload of the heart results in an increased demand for oxygen. In other words, too much preload will result in undue myocardial stress and an increase in myocardial oxygen demand, and ultimately, can lead to myocardial ischemia.
Conversely, if the preload volume is grossly diminished, the blood volume being ejected from the ventricles will also be diminished, leading to a low blood flow state that will cause the patient to experience a relative state of hypovolemia. The danger of this condition is a reduction in perfusion of the core organs, including the heart. A reduction in preload will result in a decrease in the residual volume available to the coronary vessels, leading to a decrease in coronary artery perfusion.
Afterload is pressure in the aorta that the force of ventricular contraction must overcome to eject the blood. Blood circulates through the body by means of pressure created within the vessels known as systemic vascular resistance. The pressure is greatest in the arterial system. One of the most significant concerns of an elevated arterial pressure is at the site of the aorta. If the overall pressure within the aorta is higher than normal, the ventricle must work harder to overcome the higher pressure to eject the blood, thus creating an increase in afterload. Because an increase in afterload requires a greater contractile force to eject the blood out of the ventricle, it creates an increase in myocardial workload, which, again, translates into an increase in myocardial oxygen demand and consumption. A common cause of increased aortic root pressure is an elevated diastolic blood pressure, which is a direct measure of the arterial vessel resistance found between myocardial contractions. An increased diastolic blood pressure would increase the aortic pressure and require an increased force of contraction to effectively eject blood from the left ventricle. This increase in resistance not only requires an increase in myocardial workload, but also an increase in oxygen demand by the myocardial cells and delivery of blood through the coronary arteries. Chronic elevation in aortic pressure from increased resistance over time can lead to weakening and hypertrophy of the left ventricle, which results in congestive heart failure. As an analogy of this principle, give a person a one-pound weight to lift with his right arm and a 10-pound weight to lift with his left arm. Obviously, the 10-pound weight provides more resistance to lifting; thus, the muscles in the left arm require a greater workload and blood supply. If this person were to continuously lift the weight, the left arm muscles lifting the larger weight with greater resistance would fatigue and fail faster than the right arm muscles lifting against a lesser resistance. This same principle can apply to the heart muscle when a chronic elevated resistance is present.
If there is a drastic reduction in arterial pressure, afterload is reduced, since it will take less force to overcome the pressure in the aorta. If the arterial pressure is decreased, the heart may have to compensate by increasing the rate and strength of contractions to generate an adequate arterial pressure and maintain adequate circulation. An increase in myocardial rate and contractile force will lead to an increase in oxygen demand and consumption. If a patient has significant coronary artery disease, the ability of the coronary arteries to supply an increased amount of blood to the heart may be limited and unable to meet the metabolic demands of the myocardial cells, potentially further exacerbating an already ischemic heart.
Pathophysiology of Right Heart Failure
A common cause of right ventricular failure is left ventricular failure. Other causes of right ventricular failure include right ventricle infarction, massive pulmonary embolism, pulmonary hypertension and chronic obstructive pulmonary disease (COPD). When the right heart fails as a forward pump, cardiac output falls, resulting in backward dumping and leading to the common reference of "backward failure." If the right ventricle cannot pump effectively, the volume of blood in the veins increases, leading to congestion. Venous congestion in the form of edema is often easy to see in dependent areas of the body like the lower legs and hands if the patient is in a standing or seated position where the extremities are lower than the level of the heart. If the patient is supine for long periods of time, putting the legs level with the heart, edema may be seen in the area of the sacrum. Edema is due to a reduction in the ability of the lymphatic system to drain effectively into an already congested venous system. The patient may also present with engorged veins in the hands and feet due to gravitational pull on the excessive fluid. It appears as if a venous tourniquet has been applied to the extremities.
Pathophysiology of Left Heart Failure
Left heart failure is also commonly referred to as congestive heart failure. The pathophysiology of heart failure involves changes in:
- cardiac function
- neurohumoral status (neural refers to autonomic and humoral refers to circulating)
- systemic vascular function
- blood volume
Changes in Cardiac Function
The common denominator in heart failure is decreased cardiac output, which is directly influenced by systolic dysfunction, diastolic dysfunction or a combination of both. Systolic dysfunction results from compromise of the contractile properties of the heart, which is most frequently related to changes in the chemical processes within the heart. Global systolic dysfunction can also result from death or damage of myocardial cells following an acute myocardial infarction. Diastolic dysfunction occurs when the ventricle becomes less compliant, jeopardizing ventricular filling. Both systolic and diastolic dysfunctions result in elevated left ventricular end-diastolic pressure (LVEDP). Elevated LVEDP is dependent on the Frank-Starling mechanism to control stroke volume. The Frank-Starling mechanism is the relationship between the volume of blood and the stretch of myocardial fibers in the ventricle and the force of contraction needed to eject the blood. As the left ventricular end-diastolic filling volume (LVEDFV) increases, the myocardial fibers are stretched further, producing a greater force of ventricular contraction to eject the increased blood volume.
The progression of heart failure starts with impaired cardiac function. It is important to note that a myocardial infarction in itself is not heart failure, but it can contribute to heart failure. Suppose, for example, you have a patient who has suffered a significant right ventricular infarction with a resultant reduction in right ventricular contractile force. A reduction in contractile force may lead to a decrease in the amount of blood being effectively ejected by the right ventricle, which may lead to stagnation of blood and a reduced LVEDFV and preload. The decrease in preload will reduce the amount of blood ejected with each contraction (stroke volume). The decrease in preload and stroke volume will cause a reduction in cardiac output. A drop in cardiac output will result in a decrease in the pressure in the aorta and systemic arteries, which will be sensed by the baroreceptors located in the carotid bodies and aortic arch. As the arterial pressure decreases, there is a reduction in the number of impulses sent to the hypothalamus. The hypothalamus in turn triggers the sympathetic nervous system (the fight-or-flight nervous system). The resultant neural (direct nerve stimulation) and hormonal (epinephrine and norepinephrine) response will promote vasoconstriction, increased heart rate and increased myocardial contractile force, and stimulate the release of hormones to reduce urine output and increase fluid retention in an attempt to increase preload and arterial pressure for the purpose of restoring blood flow.
In heart failure, these compensatory mechanisms may actually worsen the cardiac compromise. An increase in heart rate and force of contraction will increase myocardial workload, thereby increasing oxygen demand and consumption, and may actually lead to or exacerbate myocardial ischemia. Fluid retention, coupled with the inability of the ventricles to completely fill in the presence of significant tachycardia, may lead to pulmonary congestion with a reduction in gas diffusion in the alveoli and a more severe state of hypoxia. Vasoconstriction increases vessel resistance, which in turn increases the pressure in the aortic root, requiring a greater force of contraction to overcome the pressure to eject the blood out of the ventricle. This results in an increased myocardial workload, oxygen demand and consumption in an already hypoxic heart muscle.
As the amount of cardiac tissue necroses and cellular ischemia increases, the cardiovascular reserve becomes inadequate, compromising cardiac output and tissue perfusion. As the ventricular volume continues to decrease, the amount of blood available for coronary artery perfusion is decreased, leading to further myocardial ischemia and failure. The failure of cardiac compensatory mechanisms occurs in part because the degree of vasoconstriction is not sufficient to maintain the necessary pressure to support blood flow through the core organs, including the coronary arteries. Initially, assuming the patient can compensate well enough, the pressure begins to increase systemically, leading to increased right-sided heart volume. The increase in right heart volume promotes further right ventricular failure, which leads to peripheral venous congestion and a consistently high right ventricular preload.
The systemic increase in vessel resistance will exacerbate pump failure and further reduce blood flow through the coronary vessels. Additionally, this higher resistance will require an increased force of ventricular contraction, resulting in an elevated myocardial oxygen demand and consumption, further worsening ischemia and decreasing cardiac output. Prolonged states of cellular ischemia eventually lead to lactic acid accumulation in the myocardial cells (lactic acidosis), which causes irreversible cellular membrane damage and, ultimately, complete and irreversible loss of pump function.
Heart failure is difficult to diagnose in the field, but suspicion for heart failure is not. Left heart failure should be considered in the patient who presents with unexplained hypotension, impaired mental function and pulmonary congestion. The unexplained clinical signs mentioned above should be used as differential diagnosis criteria, not definitive measures of the presence of heart failure. The single greatest differential for left heart failure versus right heart failure is the presence of dyspnea. Other signs or symptoms of left heart failure include tachycardia, cyanosis, peripheral edema, altered mental status, tachypnea and reduced urine output.
Table 1 lists assessment pearls that can be used when heart failure is suspected.
The New York Heart Association (NYHA) developed a classification of patients with heart disease based on the relation between symptoms and the amount of effort required to provoke them. Although assigning numerical values to subjective findings has clear limitations, this classification is nonetheless useful in comparing groups of patients, as well as in trending the same patient at different times. Using this classification, the degree of heart failure can be symptomatically classified according to the amount of effort required to produce symptoms of failure. These signs are as follows:
- Class I: no limitation. Ordinary physical activity does not cause undue fatigue, dyspnea or palpitations. Patients have symptoms only at exertion levels similar to those of relatively healthy individuals.
- Class II: slight limitation of physical activity. Patients with class II disease are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea or angina. Patients exhibit symptoms with ordinary exertion.
- Class III: marked limitation of physical activity. Although patients are comfortable at rest, less-than-ordinary activity leads to symptoms. Patients exhibit symptoms with minimal exertion.
- Class IV: inability to carry on any physical activity without discomfort. Symptoms of congestive failure are present even at rest. Increased discomfort is experienced with any physical activity.
First and foremost, because the primary problem with the heart failure patient is related to ischemia, oxygen must be provided. A non-rebreather mask may be adequate for managing the patient in the early stages of heart failure. Once the patient develops pulmonary edema, the non-rebreather may no longer be effective in maintaining adequate arterial oxygen levels. The patient may require oxygenation via continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP) or endotracheal intubation and ventilation using positive end-expiratory pressure (PEEP). Similar to pulmonary edema in the CHF patient, fluid is trapped between the alveoli and pulmonary capillaries in the alveolar/capillary interface. The fluid accumulation increases the distance between alveoli and pulmonary capillaries and leads to poor diffusion of oxygen and carbon dioxide. Simple oxygenation without positive airway pressure will not likely be successful in increasing arterial oxygenation. Positive airway pressure will be needed to force oxygen through the fluid, across the alveolar and capillary membranes, and into the pulmonary capillaries.
In addition to ensuring adequate oxygenation, there are several pharmacological agents currently used in the prehospital setting that may be considered. It should be understood that the primary goals in pharmacologic management of the heart failure patient are to: 1) restore circulation of oxygenated blood; 2) reduce myocardial workload; and 3) reduce myocardial oxygen consumption. The most commonly used drugs are detailed below. Standard delivery of infusions in the field is difficult, because many ambulances do not carry infusion pumps and therefore cannot guarantee exact dosing of the infusion drug.
Dopamine is an ideal positive inotrope (increases contractile force) when rate is not a factor. Dopamine, when delivered at higher doses (10-20mcg/kg/min), exerts a greater alpha effect and has been shown to have significant effects on increasing the heart rate, which increases the myocardial oxygen demand. The ideal dose of dopamine that delivers predominantly beta properties, which exert primarily a positive inotrope effect, is 5 to 10 mcg/kg/min.
Dobutamine, a synthetic amine, has strong positive inotropic properties. It is not uncommon to infuse dobutamine in conjunction with low doses of dopamine. Dobutamine is a more potent inotrope than dopamine and has less influence on heart rate. However, dobutamine, when administered at high doses, may promote production of norepinephrine, which will increase myocardial ischemia and death, thus worsening the degree of shock. This is a reason why ambulances without IV pumps rarely carry dobutamine.
Nitroglycerin is a potent coronary and peripheral vasodilator that has proved to be highly beneficial when used in patients with heart failure. Nitroglycerin is beneficial because it dilates the coronary vessels, allowing for greater myocardial oxygenation. In addition, the peripheral vasodilatory effects lead to a reduction in preload and arterial pressure, and subsequently to afterload, thereby reducing the myocardial workload and myocardial oxygen demand. A reduction in myocardial oxygen demand requires less coronary artery perfusion.
In the patient with a confirmed right ventricular infarction, nitroglycerin should be withheld in the prehospital setting. The patient may already present as hypotensive due to an inadequate preload. Nitroglycerin will have little benefit in this patient and may lead to a further decrease in cardiac output and blood pressure by further reduction in the preload. Consider a fluid bolus instead of nitroglycerin.
A nitroglycerin infusion in a hypotensive heart failure patient may be accomplished through concurrent administration of a positive inotrope. Inotropic agents such as dopamine and dobutamine at lower doses help maintain adequate systemic pressure by increasing the strength of cardiac contractile force, while the concurrent vasodilation reduces the systemic resistance and assists in reducing the ventricular force that must be generated to eject the blood, thereby reducing the myocardial workload.
Lasix is a loop diuretic that may be used in patients with clinical signs of heart failure, including peripheral and pulmonary edema. Lasix reduces edema by increasing fluid excretion through the kidneys and by reducing sodium reabsorption in the Loop of Henle and the distal tubules. Like nitroglycerin, diuretics should be used with caution, since the water and electrolyte loss may further decrease preload and lead to hypotension, which increases the risk of cardiac dysrhythmias.
Heart failure is a pathophysiologic cascade that, if improperly identified and managed, may lead to death. If heart failure is identified early enough, development of irreversible end-stage heart failure may be avoided. The goal of the prehospital care provider in managing heart failure is directed at maintenance of adequate cellular oxygenation, reduction of preload and afterload to improve forward blood flow, and, ultimately, improve cardiac output.
Bledsoe BE, Porter RS, Cherry R. Paramedic Care: Principles and Practice, Volume 3. Medical Emergencies. Upper Saddle River: Prentice-Hall, 2001.
Berne RM, Levy MN. Cardiovascular Physiology, 6th Edition, St. Louis, MO: Mosby, 1992.
Civetta JM, Taylor RW, Kirby RR. Critical Care, 2nd Edition. Philadelphia: JB Lippincott Company, 1992.
Chizner MA. Clinical Cardiology Made Ridiculously Simple. Miami: MedMaster, 2006.
Dalton AL, Limmer DA, Mistovich JA, Werman HA. Advanced Medical Life Support, 2nd Edition. Upper Saddle River: Prentice-Hall, 2003.
Guyton AC, Hall JE. Textbook of Medical Physiology, 11th Edition. Philadelphia: Elsevier, 2006.
Hollenberg SM, Kavinsky CJ, Parrillo JE. Heart failure. Ann Intern Med 131(1):47-59, 6 Jul 1999.
Huether SE, McCance KL. Understanding Pathophysiology, 3rd Edition. St. Louis, MO: Mosby, 2004.
Klabunde RR. Cardiovascular Physiology Concepts. Philadelphia: Lippincott, Williams, & Wilkins, 2005.
Martini FH, Bartholomew EF, Bledsoe BE. Anatomy and Physiology for Emergency Care. Upper Saddle River: Pearson Education, 2002.
McPhee SJ, Vishwanath RL, et al. Pathophysiology of Disease: An Introduction to Clinical Medicine, 3rd Edition. Lange-McGraw-Hill, 2000.
Rosen P, Barkin RM, et al. Emergency Medicine Concepts and Clinical Practice, 5th Edition. St. Louis, MO: Mosby, 2002.
Semonin-Holleran RA. Air and Surface Patient Transport Principles and Practice, 3rd Edition. St. Louis, MO: Mosby, 2003.
Tintinalli JE. Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill, 2000.
William S. Krost, BS, EMT-P, is an operations manager and flight paramedic with the St. Vincent/Medical University of Ohio/St. Rita's Critical Care Transport Network (Life Flight) in Toledo, Ohio, and a nationally recognized lecturer. Joseph J. Mistovich, MEd, NREMT-P, is a professor and the chair for the Department of Health Professions at Youngstown (OH) State University, author of several EMS textbooks and a nationally recognized lecturer. Daniel Limmer, AS, EMT-P, is a paramedic with Kennebunk Fire-Rescue in Kennebunk, Maine, and a faculty member at Southern Maine Community College. He is the author of several EMS textbooks and a nationally recognized lecturer.