HEART FAILURE (PULMONARY EDEMA)
edema is the abnormal accumulation of fluid in the lungs. The fluid may
accumulate in the interstitial spaces or in the alveoli.
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.
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
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.
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
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.
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.
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
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
treatments and medications are prescribed for pul-monary edema, among them
oxygen, morphine, diuretics, and various intravenous medications.
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
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
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
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.
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.
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
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.