Beyond the Basics: Pulmonary Edema

     This CE activity is approved by EMS Magazine, an organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS), for 1.5 CEUs.

• Review cardiac anatomy and physiology
• Discuss etiology of pulmonary edema
• Review management of the pulmonary edema patient

     There are several causes that lead to pulmonary edema, some permanent and some temporary. Pulmonary edema is due either to failure of the heart as a forward pump or maldistribution of fluid within the pulmonary circuit. The movement of excess fluid into the alveoli as a result of an alteration in one or more of Starling's forces (forces that cause interchange of fluids between the intravascular and interstitial spaces) is a key consideration in pulmonary edema. In cardiogenic pulmonary edema, high pulmonary capillary pressure (created by high pressure inside the left atrium) is responsible for the abnormal fluid movement. In contrast, noncardiogenic pulmonary edema occurs when factors other than elevated capillary pressure are responsible for changes in the internal environment of the alveoli.

     The heart itself is comprised of specialized muscle 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 conduction as it travels between fibers.

     The cardiac muscle is divided into three distinct tissue layers: 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, the middle layer of the heart, tends to be thickest due to the bulky muscle mass. Unlike other muscles in the body, the muscle cells that comprise the myocardium 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 myocardium. The ability of the myocardium to be in constant use is largely due to the vast amount of capillary bloodflow that is networked within the myocardial muscle bed. This provides the required oxygen and nutrient delivery, and, equally important, waste removal that is mandatory in order to sustain the ongoing workload. The pericardium is the layer commonly referred to as the "pericardial sac" because it is made up of a tough fibrous sac that surrounds the heart to provide protection and lubrication for the heart as it contracts.

     The heart contains four distinct chambers: the left and right atria and left and right ventricles. The ventricles are the larger of the chambers and have the primary function of ejecting blood out of the heart into either the pulmonary circulation (to the lungs) or the systemic circulation (throughout the body). The ventricle walls are much more muscular than the atria's and, as a result, have the ability to generate a greater force and pressure during contraction.

     Bloodflow through the heart originates in the right atrium, where unoxygenated blood from the venous circulation is delivered to the heart via the superior and inferior vena cava. Once unoxygenated blood enters the right atrium, it is ejected into the right ventricle with the next contraction. Upon contraction, the blood is pumped out into the pulmonary artery and into the pulmonary capillaries in the lungs, where alveolar/capillary gas exchange occurs. This process leads to arterial oxygenation and removal of carbon dioxide. 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 and eventually causes the mitral valve to open and allow 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 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.

     The most important vessels when talking about pulmonary edema are the coronary arteries. It is important to note that although the chambers of the heart may have a full blood volume, it is the coronary arteries that are responsible for delivering oxygenated blood throughout the heart and providing cardiac oxygenation. When a patient is experiencing ischemic chest pain or a myocardial infarction, it is because blood supply through the coronary arteries has been compromised. The coronary arteries originate at the base of the aorta. The root of the coronary arteries is known as the coronary sinus. The coronary sinuses provide bloodflow 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. Another important aspect of cardiac physiology is that the coronary arteries receive their blood supply at the end of diastole. As the left ventricle contracts, the coronary arteries are occluded by the opened leaflets of the aortic valve. When the heart relaxes, 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 blood volume will lead to a reduction in coronary artery perfusion, which may lead to myocardial ischemia.

     Three important attributes play a direct role in cardiac output (amount of blood ejected in one minute): preload, myocardial contractility and afterload. Understanding these will allow EMS providers to understand the complications potentially facing a patient suffering from a cardiac pump- or volume-related problem. These three attributes determine stroke volume—the amount of blood ejected with each ventricular contraction.

     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), which is primarily determined by venous volume and bloodflow from the right side of the heart through the pulmonary vasculature. Any patient, but specifically cardiac patients, can suffer from either increased or decreased preload. Patients with increased preload are in danger due to an overloaded state in the ventricle. Increased bloodflow 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 need for oxygen. In other words, too much preload will result in undue myocardial stress and may lead to myocardial ischemia. Conversely, if the preload volume is grossly diminished, there will not be enough blood volume to eject from the ventricles upon contraction, causing the patient to fall into a relative state of hypovolemia. This dangerous condition may affect all of the core organs, including the heart. The reduced circulating volume will be problematic because the residual volume used to perfuse the coronary vessels will be reduced and, as such, flow through the coronary sinuses will be impaired.

     Myocardial contractility is the amount of force generated by the cardiac muscle to eject blood contained within the left ventricle at the end of diastole. Based on Frank-Starling's law, a larger volume of blood in the left ventricle generates a more forceful contraction. Myocardial stretch fibers imbedded in the ventricle sense distention of the left ventricle wall created by the preload volume. A larger volume in the left ventricle causes more distensibility and creates a greater stretch of the myocardial fibers, which in turn produces a more forceful ventricular contraction to eject blood. The opposite is also true where a decreased preload volume leads to a decrease in myocardial contractile force. It is important to recognize that the myocardial stretch fibers have a limit and, if overstretched from a dilated ventricle due to a weakened ventricular wall or chronic heart failure, Frank-Starling's law is no longer effective.

     Afterload is a measure of the pressure at which the ventricle must exert its force to eject blood. Afterload is directly related to the pressure in the aorta that must be overcome with each cardiac contraction. As blood circulates through the body, it does so by means of pressure that is created within the vessels (vascular resistance). This pressure is greatest in the arterial system. One of the most significant concerns of 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 it to eject the blood, thus creating an increase in afterload. Because increased afterload requires a greater contractile force to eject blood from the ventricle, it creates an increase in myocardial workload, which translates to an increase in myocardial oxygen demand and consumption. A drastic reduction in arterial pressure reduces afterload, since it takes less force to overcome the pressure in the aorta. If the patient's arterial pressure is decreased, his heart may have to compensate by increasing the rate and strength of myocardial contractions to generate an adequate arterial pressure and maintain adequate circulation. An increase in myocardial rate and contractile force will cause an increase in oxygen demand and consumption, potentially further exacerbating an already ischemic heart.

     The most common etiology for pulmonary edema is myocardial infarction. Some of the less common causes of pulmonary edema include infectious cardiac disease processes, such as acute myocarditis or endocarditis; induced heart failure from drugs/medications like cocaine, beta-blockers or tricyclic antidepressants; trauma-related, such as a myocardial contusion; or metabolic derangements that result in cardiac arrhythmias, such as sustained tachycardias or bradycardias.

     A massive pulmonary embolism may also produce pulmonary edema. A large pulmonary embolism will impede forward bloodflow in the pulmonary vessels, leading to volume overload of the right ventricle, a drastic reduction in left ventricular filling volume and increased hydrostatic pressure in the pulmonary vessels blocked by the embolism. In addition, the large pulmonary embolism produces a ventilation disorder by causing a perfusion/ventilation mismatch, which leads to hypoxemia. Arterial hypoxemia coupled with reduced coronary bloodflow and subsequent systemic acidosis will have a deleterious effect on the cardiac pump function, which may contribute to pump failure.

     Cardiomyopathy is defined as cardiac damage caused by something other than bloodflow problems. Cardiomyopathy weakens the left ventricle to the point that it may not effectively act as a forward pump.

     In mitral or aortic valve disease, the valves either don't open wide enough or don't close completely. When the valves are narrowed, blood can't flow freely into the myocardium, and left ventricle pressures increase. These elevated pressures cause increased ventricular workload and, subsequently, decreased ventricular function.

     Untreated or uncontrolled high blood pressure causes thickening of the left ventricular muscle, accelerates coronary artery disease and ultimately leads to decreased function of the myocardium.

     In noncardiogenic pulmonary edema, the etiology for edema is not the heart. The major issue is fluid leakage from the alveolar capillaries in the absence of pump failure.

     When pulmonary edema results from lung infections, such as pneumonia, edema occurs only in the part of the lung that's inflamed.

     Several chemicals are irritants to the lungs. Irritants like chlorine, ammonia and nitrogen dioxide can produce pulmonary edema by directly damaging the alveoli and capillaries and allowing for fluid seepage and leakage. If inhaled at high concentrations, these chemicals can be fatal. Effects of the chemicals depend on the level and duration of exposure.

     Smoke inhalation may severely injure the tracheobronchial tree. If this occurs, the epithelial lining of the airway may begin to slough around day three or four. The increase in secretions puts the patient at high risk for obstruction of distal airways, atelectasis and rapid development of pneumonia.

     The etiology for pulmonary edema in renal disease is related to sodium retention. When the kidneys fail to excrete sodium, water is retained and patients experience fluid overload and cannot effectively balance their fluid volume. The increase in water increases cardiac work and is not effectively pumped throughout the body, but remains in the pulmonary circuit. This also leads to higher hydrostatic pressure in the pulmonary capillaries that forces fluid out into the alveolar-capillary interface.

     ARDS occurs in a number of disorders, including sepsis, acute pulmonary infection, non-thoracic trauma, inhaled toxins, disseminated intravascular coagulation and cocaine smoking. Regardless of etiology, the clinical scenario is similar in most patients once membrane damage has occurred. In ARDS, the alveolar-capillary membrane becomes damaged and leaky, allowing increased movement of water and proteins from the intravascular to the interstitial space.

     High-altitude pulmonary edema generally occurs in individuals who rapidly ascend to altitudes above 12,000 to 13,000 feet and accounts for a majority of deaths due to high altitude disease. An abnormally pronounced degree of hypoxic pulmonary vasoconstriction at a given altitude is believed to be the causative factor. High pulmonary pressures create a higher hydrostatic pressure and force fluid out of the pulmonary capillaries into the alveolar-capillary interface.

     Patients with pulmonary edema often present with shortness of breath and orthopnea (dyspnea while lying flat). Chest pain also may be a prominent symptom when pulmonary edema is due to a cardiac event.

     Assessment of pulmonary edema can be easy in the patient with extremes, but in the early phase, patients may present with generalized respiratory distress. The initial exam usually reveals a tachypneic, diaphoretic patient with rales on auscultation of the chest and possibly heart murmurs. In the absence of fulminating pulmonary edema, a true diagnosis should be reserved for the hospital setting, where the presence of fluid can be confirmed by chest x-ray.

     The foremost complication of pulmonary edema is high pulmonary artery pressure. When pulmonary pressures are high, diuretics and fluid restriction can improve pulmonary function. Oxygen must be provided. A non-rebreather mask may be adequate for the patient in the early stages of failure. Once a patient develops pulmonary edema, the non-rebreather will not be effective and he will require an oxygenation device, such as CPAP or endotracheal intubation, and ventilation with positive end-expiratory pressure (PEEP). Fluid is trapped between the alveoli and capillaries, and simple oxygenation without supplemental pressure will not be successful. Pressure will be needed to increase arterial oxygen tension and force the oxygen through the fluid, and subsequently across the alveolar and capillary membranes.

     In addition to ensuring the patient can be adequately oxygenated, there are several pharmacologic agents currently used in prehospital care that may be considered when managing a pulmonary edema patient with a cardiac etiology. It should be understood that the primary goals in pharmacologic management of the pulmonary edema patient is restoration of oxygenated bloodflow in conjunction with reduction of cardiac workload and cardiac oxygen consumption. The most commonly used pulmonary edema drugs are detailed below. Standard delivery in the field is difficult because most ambulances do not carry infusion pumps and therefore cannot guarantee exact dosing of the infusion drug.

     Dopamine is an ideal inotrope (increases contractile force) for the patient in which rate is not an important factor. Dopamine, when used at higher doses (10–20mcg/kg/min) has been shown to have significant effect on increasing heart rate, which increases the amount of oxygen utilization and need. The ideal dose of dopamine, which delivers predominantly beta properties that increase inotrope, should be around 5mcg/kg/min.

     Dobutamine, a synthetic amine, has strong inotropic properties and is ideal for managing pulmonary edema. 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, when administered at high doses, dobutamine may promote production of norepinephrine, which increases myocardial ischemia and death, thus worsening the degree of shock. This is why few ambulances without IV pumps carry dobutamine.

     Nitroglycerin is a potent coronary vasodilator and a peripheral vasodilator that has proven to be highly beneficial when used in patients with pulmonary edema, as it dilates the coronary vessels, allowing for greater myocardial oxygenation. In addition, the peripheral vasodilatory effects lead to reduced preload and arterial pressure and subsequently to afterload, thus reducing the myocardial workload. The reduction in arteriolar pressure will also decrease hydrostatic pressure in the capillary bed, thereby reducing the fluid being forced out of the capillary. A reduction in workload requires less myocardial oxygen and less coronary artery perfusion. The exception to using NTG in the pulmonary edema patient is the presence of hypotension. When a patient is hypotensive, the most likely etiology is right ventricular infarction. Hypotension is most likely due to inadequate preload. Nitroglycerin will have little benefit in this patient and may lead to a further decrease in blood pressure by an additional reduction in preload. Instead of nitroglycerin, consider a fluid bolus in the right ventricular infarct patient. Nitroglycerin infusion in a hypotensive patient may be accomplished through simultaneous administration of an inotrope. At lower doses, inotropes like dopamine and dobutamine will help maintain adequate pressure through increasing the strength of cardiac contractile force, while the concurrent vasodilation will help reduce the force at which the ventricle must eject blood and thereby reduce the myocardial workload.

     Lasix is a diuretic that could be used in the patient with clinical signs of heart failure, including peripheral and/or pulmonary edema. Lasix may reduce edema by increasing fluid excretion through the kidneys by reducing sodium reabsorption in the loop of Henle and the distal tubules. It is also thought that Lasix exerts a venodilator effect, which reduces vascular volume and hydrostatic pressure. Again, like nitroglycerin, diuretics should be used with caution, as they will promote water loss and, in the patient with a right ventricular infarct, further decrease preload, causing the patient to become more hypotensive. It is important to note that the use of diuretics in noncardiogenic pulmonary edema will have minimal benefit, since the etiology for this form of pulmonary edema is not volume-related but rather mediated by increases in capillary permeability.

     Morphine has long been believed effective in pulmonary edema management because of its anxiolytic (anxiety reducing) and vasodilatory properties. A study published in March 2008 demonstrated that morphine was associated with increased adverse events in acute decompensated heart failure. Complications included a greater frequency of mechanical ventilation, prolonged hospitalization, more ICU admissions and higher mortality. As a result, the use of morphine in prehospital management should be evaluated closely and reconsidered.

     Pulmonary edema may have numerous etiologies, but the result is still the same: compromised perfusion. What has long been traditional in management of pulmonary edema should be evaluated in the field as it has been in the hospital. EMS providers across the country continue to use the Lasix, nitroglycerin, morphine mantra because they always have. Is this the best way to treat the pulmonary edema patient? The simple answer is no. In the field, EMS should adhere to evidence-based practices, and the evidence is conclusive: Global treatment of pulmonary edema with Lasix, morphine and nitroglycerin is not appropriate. Nitroglycerin remains the universal therapy and, in some cases, Lasix is appropriate, but consider modifying routine practice. As a prehospital care provider, you must ensure the pulmonary edema patient has adequate oxygenation and can be effectively treated before it is too late.

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     William S. Krost, MBA, NREMT-P, is director of Emergency Services & Health System Access for Blanchard Valley Health System in Findlay, OH.

     Joseph J. Mistovich, Med, NREMT-P, is a professor and chair of the Department of Health Professions at Youngstown (OH) State University.

     Daniel D. Limmer, AS, EMT-P, is a paramedic with Kennebunk Fire-Rescue in Kennebunk, ME.