The heart constantly has to beat in order to meet the metabolic demands of the body, however, in approximately 5 million people in the United States “the heart is unable to pump blood at a rate to meet” these metabolic demands. This inability for the heart to pump blood effectively results in congestive heart failure, which leads to an impaired ventricular function and is often caused by “volume overload, pressure overload, loss of myocardial tissue, and impaired contractility” (Sanders, 2007). Although congestive heart failure is often associated with left ventricular failure, the right side of the heart can fail as well. Because right and left heart failure affects different areas of the heart, patients may present differently depending on which side is affected.
When the left side of the heart fails to work as an effective forwards pump, left ventricular failure occurs. As blood gets “delivered to the left ventricle,” it cannot be fully ejected from the ventricle, leading to a “back-pressure of blood into the pulmonary circulation.” This causes an “increase in end-diastolic blood volume [which] increases left ventricular end-diastolic pressure,” which leads to fluid being backed up into the left atria and then into the pulmonary veins and capillaries. Because the “pulmonary capillary hydrostatic pressure increases, the plasma portion of blood is forced into the alveoli,” which causes the plasma to mix with air leading to the “typical finding in pulmonary edema: foamy, blood-tinged sputum.” This “foamy, blood-tinged sputum” can build up leading to hypoxia and eventually death (Sanders, 2007).
Because “left ventricular failure results in a reduction of stroke volume,” the signs and symptoms of left ventricular failure are often compensatory in nature. Respiratory distress may be seen as patients become more hypoxic. As hypoxia begins to set in, the blood pressure becomes elevated and the pulse rate becomes rapid to “compensate for low stroke volume.” As hypoxia gets worse, the patient may have an altered level of consciousness because of poor cerebral perfusion and if hypoxia is severe enough, cyanosis maybe evident. As the frothy sputum begins to accumulate the patient may begin to cough this up. The frothy sputum also leads to adventitious lung sounds including: bilateral crackles “present at the base of the lungs and up to the level of the scapulae;” rhonchi from “fluid in [the] upper airways;” and wheezing from the “airway reflex spasm” (also known as cardiac asthma). Jugular vein distension may also be seen which indicates a “back-pressure through the right heart and into the venous system.” However, many of these compensatory mechanisms “often increase myocardial oxygen demand,” which “further [decreases] the ability of the myocardium to contract,” therefore, patients who present “with pulmonary edema (particularly those with an abrupt onset) also should be suspected of having an acute myocardial infarction” (Sanders, 2007). Furthermore, patients may have “cardiac dysrhythmias such as atrial fibrillation or premature ventricular contractions” and complain of a recent history of “exertional dyspnea, paroxysmal nocturnal dyspnea, [or] orthopnea” (Ma, Cline, Tintinallu, Kelen, & Stapczynski, 2004).
In managing left sided heart failure, the goal is multifacitied, which includes “decreasing the venous return to the heart, improving myocardial contractility, decreasing myocardial oxygen demand, improving ventilation and oxygenation, and rapidly transporting the patient to a medical facility.” When treating such patients; simple, non-invasive treatments can make a great difference in the outcome. Applying high concentration oxygen ensures that every red blood cell is fully oxygenated and allowing the patient’s legs to hang off of the gurney while assuming a sitting position increases the capacity of the lungs, which aids in the work of breathing and “decreases venous return to the heart.” If non-invasive treatments do not work, more aggressive management may be needed, such as positive pressure assistance to help decrease pulmonary edema and also reduces “the need for high levels of inspired oxygen.” If cerebral hypoxia or progressive hypercapnia exist, or if the patient is unable to maintain a SpO2 reading greater than 90% with 100% oxygen, endotracheal intubation may be required (Sanders, 2007).
Once the airway is under control, an intravenous line may be established and pharmacological agents such as Nitroglycerin, Furosemide, and Morphine administered to “decrease venous return, enhance contractile function of the myocardium, and reduce dyspnea.” Nitroglycerin helps patients in congestive heart failure by reducing peripheral vasodilation which leads to a reduction in “preload and afterload, thereby reducing the myocardial workload and improving cardiac function.” Furosemide supplements Nitroglycerin by relaxing the venous system, which has a dilating effect that occurs within five minutes. Furosemide also reduces the intravascular volume by having a diruetic effect, however, this diuretic effect of Furosemide may lead to electrolyte imbalances. Morphine is used to reduce preload on the heart by decreasing the venous return by dilating “the capacitance vessels of the peripheral venous bed” and to reduce the work of the myocardium and anxiety (Sanders, 2007). It is important to note that the use of Morphine in the patient who is undergoing a CHF exacerbation is controversial. As the patient becomes hypoxic, Morphine may enhance the hypoxia by causing respiratory depression. Furthermore, it is believed that Morphine has very little benefit to the patient when compared to oxygen, diuretics, and nitrates (Ma, Cline, Tintinallu, Kelen, & Stapczynski, 2004). Furthermore, Morphine, as well as Nitroglycerin and Furosemide, lower the blood pressure; therefore the use of these medications should be used with caution or not at all in patients who have a systolic blood pressure less than 100mmHg (Sanders, 2007).
If the right ventricle of the heart “fails as an effective forward pump,” then right sided heart failure occurs which causes a “back-pressure of blood into the systemic circulation.” If this back pressure gets too high, it can result in “the plasma portion of blood [being] forced out into the interstitial tissues of the body,” thus resulting in edema, “particularly in the dependant areas of the body” (Sanders, 2007).
As the right side of the heart begins to back up, various signs and symptoms may develop in other parts of the body. Most often tachycardia is present. Venous congestion, leading to an “engorged liver, spleen, or both” may be noted. As the fluid begins to build up, edema may be seen in the lower extremities or “sacral region in bed ridden patients.” Fluid may even build up in the abdomen leading to ascities or in the pericardium leading to pericardial effusion. Often right sided heart failure is the result of left sided heart failure, therefore signs of left sided heart failure may be present as well. Furthermore, patients may have had a previous myocardial infarction along with taking medications such as digitalis or diuretics (Sanders, 2007).
Right sided heart failure is often considered a chronic condition, therefore, it rarely presents itelf in the prehospital environment. However, there are times in which right sided heart failure may be “associated with pulmonary edema or hypotension,” thus making it a medical emergency. Treatment for right sided heart failure is mainly supportive. Allowing the the patient to maintain a position of comfort, normally in a sitting position; along with maintaining an open airway with high concentration oxygen may be all that is necessary to treat such patients. In the presence of hypotension, starting an intravenous line and administering fluid may “help normalize left ventricular filling.” If hypotension is not present, an intravenous line may be established to keep the vein open. Further treatment for the patient in right sided heart failure also includes treating left sided heart failure in the event it is present (Sanders, 2007).
When treating a patient in heart failure, one must also take into account other causes of respiratory distress including, “asthma, chronic obstructive pulmonary disease, pneumonia, pulmonary embolus, allergic reactions … [and] noncardiac pulmonary edema such as drug-related alveloar capillary damage or that seen with acute respiratory distress syndrome.” Furthermore, certain “causes of pulmonary edema need to be determined rapidly because they require emergency intervention.” Acute myocardial infarction should always be considered as a possible cause of congestive heart failure exacerbation as it is often seen in left sided heart failure. Acute mitral valve or aortic valve regurgitation should also be considered as the patient may require surgery; however, prehospital providers will have no way to determine this unless the patient has a known history of these conditions. If dysrhythmias or electrolyte imbalances exist, they should be treated, however, “those therapies that impair the inotropic state of the heart should be avoided” (Ma, Cline, Tintinallu, Kelen, & Stapczynski, 2004).
Regardless of which side of the heart is affected, all patients undergoing a CHF exacerbation should receive high concentration oxygen and be allowed to maintain a position of comfort while enroute to the hospital. Furthermore, vitals signs and an electrogradiogram, along with a complete patient examination and a focused history should be performed. Complications associted with a CHF exacerbation should be treated using local protocols.
Works Cited
Ma, J., Cline, D., Tintinallu, J., Kelen, G., & Stapczynski, S. (2004). Emergency Medicine Manual(6th Edition ed.). The McGraw-Hill Companies, Inc.
Sanders, M. (2007). Mosby’s Paramedic Textbook (3rd Edition ed.). St. Louis, Missouri: Elsevier Mosby.
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