ACUTE HEART FAILURE (PULMONARY EDEMA)
Pulmonary edema is the abnormal accumulation of fluid in the lungs. The fluid may accumulate in the interstitial spaces or in the alveoli.
Pulmonary edema is an acute event that results from HF. It can occur acutely, such as with myocardial infarction, or it can occur as an exacerbation of chronic HF. Myocardial scarring as a result of ischemia can limit the ventricular distensibility and render it vulnerable to a sudden increase in workload. With in-creased resistance to left ventricular filling, the blood backs up into the pulmonary circulation. The patient quickly develops pulmonary edema, sometimes called flash pulmonary edema, from the blood volume overload in the lungs. Pulmonary edema can also be caused by noncardiac disorders, such as renal failure, liver failure, and oncologic conditions that cause the body to retain fluid. The left ventricle cannot handle the re-sulting hypervolemia, preventing blood from easily flowing from the left atrium into the left ventricle. This causes the pres-sure to increase in the left atrium. The increase in atrial pres-sure may result in an increase in pulmonary venous pressure, which produces an increase in hydrostatic pressure that forces fluid out of the pulmonary capillaries into the interstitial spaces and alveoli.
Impaired lymphatic drainage also contributes to the accumu-lation of fluid in the lung tissues. The fluid within the alveoli mixes with air, creating “bubbles” that are expelled from the mouth and nose, producing the classic symptom of pulmonary edema, frothy pink (blood-tinged) sputum. Because of the fluid within the alveoli, air cannot enter, and gas exchange is impaired. The result is hypoxemia, which is often severe. The onset may be preceded by premonitory symptoms of pulmonary congestion, but it also may develop quickly in the patient with a ventricle that has little reserve to meet increased oxygen needs.
In pulmonary edema, as well as in HF, preload, contractility, and afterload may be altered, thereby impairing CO. Techno-logical advances (eg, impedance cardiography) have made it eas-ier to implement effective pharmacologic therapy in treating acute pulmonary edema.
As a result of decreased cerebral oxygenation, the patient be-comes increasingly restless and anxious. Along with a sudden onset of breathlessness and a sense of suffocation, the patient’s hands become cold and moist, the nail beds become cyanotic (bluish), and the skin turns ashen (gray). The pulse is weak and rapid, and the neck veins are distended. Incessant coughing may occur, producing increasing quantities of mucoid sputum. As pulmonary edema progresses, the patient’s anxiety and restless-ness increase; the patient becomes confused, then stuporous. Breathing is rapid, noisy, and moist sounding. The patient’s oxygen levels (saturation) are significantly decreased. The pa-tient, nearly suffocated by the blood-tinged, frothy fluid filling the alveoli, is literally drowning in secretions. The situation de-mands immediate action.
The diagnosis is made by evaluating the clinical manifestations resulting from pulmonary congestion. Most often, a chest x-ray is obtained to confirm that the pulmonary veins are engorged. Abrupt onset of signs and symptoms of left-sided HF(eg, crackles on auscultation of the lungs, flash pulmonary edema) without evidence of right-sided HF (eg, no JVD, no dependent edema) may indicate diastolic failure due to ischemia.
Like most complications, pulmonary edema is easier to prevent than to treat. To recognize it in its early stages, the nurse aus-cultates the lung fields and heart sounds, measures JVD, and assesses the degree of peripheral edema and the severity of breath-lessness. A dry, hacking cough; fatigue; weight gain; development or worsening of edema; and decreased activity tolerance may be early indicators of developing pulmonary edema.
In an early stage, the condition may be corrected by placing the patient in an upright position with the feet and legs depen-dent, eliminating overexertion, and minimizing emotional stress to reduce the left ventricular load. A re-examination of the pa-tient’s treatment regimen and the patient’s understanding of and adherence to it are also needed. The long-range approach to pre-venting pulmonary edema must be directed at identifying its precipitating factors.
Clinical management of a patient with acute pulmonary edema due to HF is directed toward improving ventricular function and increasing respiratory exchange. These goals are accomplished through a combination of oxygen, medication therapies, and nursing support.
Various treatments and medications are prescribed for pul-monary edema, among them oxygen, morphine, diuretics, and various intravenous medications.
Oxygen is administered in concentrations ad-equate to relieve hypoxemia and dyspnea. Usually, a face mask or non-rebreathing mask is initially used. If respiratory failure is severe or persists despite optimal management, endotracheal intubation and mechanical ventilation are required. The use of positive end-expiratory pressure (PEEP) is effective in reducing venous return, decreasing fluid movement from the pulmonary capillaries to the alveoli, and improving oxygenation. Oxy-genation is monitored with pulse oximetry and by measurement of arterial blood gases.
Morphine is administered intravenously in small doses(2 to 5 mg) to reduce peripheral resistance and venous return so that blood can be redistributed from the pulmonary circulation to other parts of the body. This action decreases pressure in the pul-monary capillaries and decreases seepage of fluid into the lung tis-sue. The effect of morphine in decreasing anxiety is also beneficial.
Diuretics promote the excretion of sodium and waterby the kidneys. Furosemide (Lasix), for example, is administered intravenously to produce a rapid diuretic effect. Furosemide also causes vasodilation and pooling of blood in peripheral blood vessels, which reduces the amount of blood returned to the heart, even before the diuretic effect. Some physicians may prescribe bumetanide (Bumex) and metolazone (Mykrox, Zaroxolyn) in place of furosemide.
Dobutamine (Dobutrex) is an intravenous medica-tion given to patients with significant left ventricular dysfunction. A catecholamine, dobutamine stimulates the beta1-adrenergic receptors. Its major action is to increase cardiac contractility. However, at higher amounts, it also increases the heart rate and the incidence of ectopic beats and tachydysrhythmias. Because it also increases AV conduction, care must be taken in patients who have underlying atrial fibrillation. A medication that pro-tects the AV node, such as digitalis, a beta-blocker, or a calcium channel blocker, may be indicated before dobutamine therapy is initiated to prevent increased ventricular response rate.
Milrinone (Primacor) is a phosphodiesterase in-hibitor that delays the release of calcium from intracellular reser-voirs and prevents the uptake of extracellular calcium by the cells. This promotes vasodilation, decreasing preload and afterload, re-ducing the workload of the heart. Milrinone is administered in-travenously, usually to patients who have not responded to other therapies. It is not usually used to treat patients with renal failure. The major side effects are hypotension (usually asymptomatic), gastrointestinal dysfunction, increased ventricular dysrhythmias, and decreased platelet counts. The patient’s blood pressure is monitored closely.
Nesiritide (Natrecor) is an intravenous medicationthat is indicated for acutely decompensated HF. Natriuretic pep-tides are produced by the myocardium as a compensatory re-sponse to increased ventricular end-diastolic pressure and myocardial wall stress and to the increased release of neuro-hormones (eg, norepinephrine, renin, aldosterone) that occur with HF. Nesiritide is a human B-type natriuretic peptide (BNP) made from Escherichia coli using recombinant technology. Human BNP binds to vascular smooth muscle and endothelial cells, causing dilation of arteries and veins and suppression of the neu-rohormones. The result is improved stroke volume and reduced preload and afterload (Colucci et al., 2000). This medication causes rapid improvement in the symptoms of HF and may be used with other HF medications (eg, beta-blockers, digoxin). The most common side effect is dose-related hypotension.
Proper positioning can help reduce venous return to the heart. The patient is positioned upright, preferably with the legs dan-gling over the side of the bed. This has the immediate effect of decreasing venous return, lowering the output of the right ven-tricle, and decreasing lung congestion. If the patient is unable to sit with the lower extremities dependent, the patient may be placed in an upright position in bed.
As the ability to breathe decreases, the patient’s sense of fear and anxiety rises proportionately, making the condition more severe. Reassuring the patient and providing skillful anticipatory nursing care are integral parts of the therapy. Because this patient feels a sense of impending doom and has an unstable condition, the nurse must remain with the patient. The nurse should give the patient simple, concise information in a reassuring voice about what is being done to treat the condition and the expected results. The nurse should also identify any anxiety-inducing factors (eg, a pet left alone at home, presence of an unwelcome family member at the bedside, a wallet full of money) and initiate strategies to elim-inate the concern or reduce its effect.
The patient receiving morphine is observed for respiratory de-pression, hypotension, and vomiting; a morphine antagonist, such as naloxone hydrochloride (Narcan), is kept available and given to the patient who exhibits these side effects.
The patient receiving diuretic therapy may excrete a large vol-ume of urine within minutes after a potent diuretic is adminis-tered. A bedside commode may be used to decrease the energy required by the patient and to reduce the resultant increase in car-diac workload induced by getting on and off a bedpan. If neces-sary, an indwelling urinary catheter may be inserted.
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