where J is the net fluid movement out of the capillary, K is the capillary permeability factor, Pc and Pi are the hydrostatic pressures in the capillary and interstitial space, and πc and πi are the oncotic pressures in the capillary and interstitial space.

Although conceptually valuable, this equation has limited practical use. Of the four pressures, only the oncotic and hydrostatic pressures of blood in the pulmonary capillaries can be measured with any certainty. The oncotic and hydrostatic pressures within the interstitial compartments cannot be readily determined.

When the hydrostatic pressure within the pulmonary vascular system rises to more than 25 to 30 mm Hg, the oncotic pressure loses its holding force over the fluid within the pulmonary capillaries. Consequently fluid starts to spill into the interstitial and air spaces of the lungs (see Figure 19-1).

Clinically, the patient with left ventricular failure often has anxiety, delirium, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, fatigue, and adventitious breath sounds. Because of poor peripheral circulation, such patients often have cool skin, diaphoresis, cyanosis of the digits, and peripheral pallor. Increased pulmonary capillary hydrostatic pressure is the most common cause of pulmonary edema. Box 19-1 provides common causes of cardiogenic pulmonary edema. Box 19-2 provides common risk factors for coronary heart disease (CHD).

Although the exact mechanisms are not known, Box 19-3 provides other causes of conditions associated with noncardiogenic pulmonary edema.

OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Pulmonary Edema

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Atelectasis (see Figure 9-8), Increased Alveolar-Capillary Membrane Thickness (see Figure 9-10), and, in severe cases, Excessive Bronchial Secretions (see Figure 9-12)—the major anatomic alterations of the lungs associated with pulmonary edema (see Figure 19-1).

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

The Physical Examination

Vital Signs

Increased Respiratory Rate (Tachypnea)

Several pathophysiologic mechanisms operating simultaneously may lead to an increased ventilatory rate:

• Stimulation of peripheral chemoreceptors (hypoxemia)

• Decreased lung compliance–increased ventilatory rate relationship

• Stimulation of J receptors

• Anxiety

Increased Heart Rate (Pulse) and Blood Pressure

Cheyne-Stokes Respiration

Cheyne-Stokes respiration may be seen in patients with severe left-sided heart failure and pulmonary edema. Some authorities have suggested that the cause of Cheyne-Stokes respiration in these patients may be related to the prolonged circulation time between the lungs and the central chemoreceptors. Cheyne-Stokes respiration is a classic clinical manifestation in central sleep apnea (see Chapter 30).

Paroxysmal Nocturnal Dyspnea (PND) and Orthopnea

Patients with pulmonary edema often awaken with severe dyspnea after several hours of sleep. This condition is called paroxysmal nocturnal dyspnea. This condition is particularly prevalent in patients with cardiogenic pulmonary edema. While the patient is awake, more time is spent in the erect position and, as a result, excess fluids tend to accumulate in the dependent portions of the body. When the patient lies down, however, the excess fluids from the dependent parts of the body move into the bloodstream and cause an increase in venous return to the lungs. This action raises the pulmonary hydrostatic pressure and promotes pulmonary edema. The pulmonary edema in turn produces pulmonary shunting, venous admixture, and hypoxemia. When the hypoxemia becomes severe, the peripheral chemoreceptors are stimulated and initiate an increased ventilatory rate (see Figure 4-4). The decreased lung compliance, J receptor stimulation, and anxiety also may contribute to the paroxysmal nocturnal dyspnea commonly seen in this disorder at night. A patient is said to have orthopnea when dyspnea increases while the patient is in a recumbent position.

Cyanosis

Cough and Sputum (Frothy and Pink in Appearance)

Chest Assessment Findings

• Increased tactile and vocal fremitus

• Crackles, rhonchi, and wheezing

CLINICAL DATA OBTAINED FROM LABORATORY TESTS AND SPECIAL PROCEDURES

Pulmonary Function Test Findings (Moderate to Severe) (Restrictive Lung Pathology)

FORCED EXPIRATORY FLOW RATE FINDINGS

FVC	FEV_T	FEV₁/FVC ratio	FEF_25%-75%
↓	N or ↓	N or ↑	N or ↓
FEF_50%	FEF_200-1200	PEFR	MVV
N or ↓	N or ↓	N or ↓	N or ↓

LUNG VOLUME AND CAPACITY FINDINGS

V_T	IRV	ERV	RV
N or ↓	↓	↓	↓
VC	IC	FRC	TLC	RV/TLC ratio
↓	↓	↓	↓	N

Arterial Blood Gases

MILD TO MODERATE PULMONARY EDEMA

Acute Alveolar Hyperventilation with Hypoxemia (Acute Respiratory Alkalosis)

pH	Paco₂		Pao₂
↑	↓	↓ (slightly)	↓

SEVERE STAGE PULMONARY EDEMA

Acute Ventilatory Failure with Hypoxemia (Acute Respiratory Acidosis)

pH*	Paco₂	*	Pao₂
↓	↑	↑ (slightly)	↓

^*When tissue hypoxia is severe enough to produce lactic acid, the pH and values will be lower than expected for a particular Paco₂ level.

Oxygenation Indices *

	Do₂^†		C(a-)o₂	O₂ER
↑	↓	N	N	↑	↓

^†The Do₂ may be normal in patients who have compensated to the decreased oxygenation status with (1) an increased cardiac output, (2) an increased hemoglobin level, or (3) a combination of both. When the Do₂ is normal, the O₂ER is usually normal.

^*C(a-)O₂, Arterial-venous oxygen difference; DO₂, total oxygen delivery; O₂ER, oxygen extraction ratio; , pulmonary shunt fraction; , mixed venous oxygen saturation; , oxygen consumption.

Hemodynamic Indices ‡

Cardiogenic Pulmonary Edema Moderate to Severe Stages

CVP	RAP		PCWP	CO	SV
↑	↑	↑	↑	↓	↓
SVI	CI	RVSWI	LVSWI	PVR	SVR
↓	↓	↑	↓	↑	↑

^‡CO, Cardiac output; CVP, central venous pressure; LVSWI, left ventricular stroke work index; , mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RAP, right atrial pressure; RVSWI, right ventricular stroke work index; SV, stroke volume; SVI, stroke volume index; SVR, systemic vascular resistance.

ABNORMAL LABORATORY TEST AND PROCEDURE RESULTS

• Serum chloride: low

• Serum potassium: low

• Serum sodium: low

Hypokalemia, hyponatremia and hypochloremia are often seen in patients with left-sided heart failure and may result from diuretic therapy or excessive fluid retention.

RADIOLOGIC FINDINGS

Chest Radiograph

• Bilateral fluffy opacities

• Dilated pulmonary arteries

• Left ventricular hypertrophy (cardiomegaly)

• Kerley A and B lines

• Bat’s wing or butterfly pattern

• Pleural effusion

Cardiogenic Pulmonary Edema

The radiographic findings associated with left heart failure are commonly described as follows:

• Mild left-sided heart failure: Pulmonary venous congestion with dilated pulmonary arteries is present.

• Moderate left-sided heart failure: Cardiomegaly, engorgement of the pulmonary arteries, and Kerley A and Kerley B lines are present. When cardiomegaly is present, the heart is greater than half the diameter of the thorax in a posterior-anterior chest radiograph (Figure 19-2). Because radiographic densities primarily reflect alveolar filling and not early interstitial edema, by the time abnormal findings are encountered, the pathologic changes associated with pulmonary edema are advanced. Chest x-ray films typically reveal dense, fluffy opacities that spread outward from the hilar areas to the peripheral borders of the lungs (Figure 19-2).

FIGURE 19-2 Cardiomegaly *(arrow)*, hilar prominence, and pulmonary edema in congestive heart failure. Note that the heart diameter is greater than half the diameter of the thorax.

Kerley A lines, which represent deep interstitial edema, radiate out from the hilum into the central portions of the lungs. Kerley A lines do not reach the pleura and are most prevalent in the middle and upper lung regions. Kerley B lines are short, thin, horizontal lines of interstitial edema, usually less than 1 cm in length, that extend inward from the pleural surface. They appear peripherally in contact with the pleura and are parallel to one another at right angles to the pleura. Although they may be seen in any lung region, they are most commonly seen in the lung bases (Figure 19-3).

FIGURE 19-3 Kerley lines. Septal lines caused by pulmonary edema. Kerley B lines are short horizontal lines at the lung periphery *(vertical arrows).* Kerley A lines are lines radiating from the hila *(oblique arrow).* (From Hansell DM, Armstrong P, Lynch DA, McAdams HP, eds: *Imaging of diseases of the chest,* ed 4, Philadelphia, 2005, Elsevier.)

• Severe left-sided heart failure: During this stage, the patient’s chest radiograph shows cardiomegaly; pulmonary artery engorgement; interstitial pulmonary edema; fluffy, patchy areas of alveolar edema; and often the appearance of the bat’s wing pattern (also called the butterfly pattern)—the peripheral portion of the lungs often remains clear, and this produces what is described as a “butterfly” or “bat’s wing” distribution (Figure 19-4). Pleural effusion may also be seen.

FIGURE 19-4 Bat’s wing or butterfly pattern caused by pulmonary edema. This example is typical in that it is bilateral but not symmetrical. The shadowing is maximal in the central (perihilar) portions of the lung, and the outer portions of the lungs are relatively clear. (From Hansell DM, Armstrong P, Lynch DA, McAdams HP, eds: *Imaging of diseases of the chest,* ed 4, Philadelphia, 2005, Elsevier.)

Noncardiogenic Pulmonary Edema

In noncardiogenic pulmonary edema the chest radiograph commonly shows areas of fluffy densities that are usually more dense near the hilum. The density may be unilateral or bilateral. Pleural effusion is usually not present, and (most important) the cardiac silhouette is not enlarged.

General Management of Pulmonary Edema

The treatment of pulmonary edema is based on knowledge of the underlying cause. Common therapeutic interventions are discussed in the following sections.

Medications and Procedures Commonly Prescribed by the Physician

Antidysrhythmic Agents

Because cardiac dysrhythmias can cause or exacerbate left ventricular heart failure, drugs to control bradycardia (e.g., atropine) or tachycardia (e.g., procainamide, metoprolol, or bretylium) (antidysrhythmic agents) may be administered.

Positive Inotropic Agents (Improve Cardiac Output)

When left-sided heart failure is present, positive inotropic agents (e.g., digitalis, dopamine, dobutamine, and amiodarone) are commonly administered to increase cardiac output. Digitalis is the most frequently prescribed inotropic agent for heart failure and is the drug of choice (see Appendix II, Positive Inotropic Agents).

Cardiac Workload Reduction (Afterload Reduction)

The most effective way to decrease the cardiac workload is to reduce the cardiac afterload (afterload reduction). This is primarily achieved by patient lifestyle changes and use of medications. In general, important lifestyle changes include getting exercise, lowering stress, losing weight if necessary, and consuming a low-salt diet. In some cases, bed rest and sedation may be helpful in reducing anxiety and agitation. Medications used to reduce systemic hypertension—and therefore to reduce the cardiac afterload—include direct-acting vasodilators (e.g., nitroglycerin, nitroprusside, isosorbide, hydralazine, and minoxidil).

Indirect-acting vasodilators are also be used to reduce the left ventricular afterload. Such agents include the alpha-adrenergic receptor–blocking agents (e.g., prazosin, trimazosin), which block the vasoconstrictive effects of norepinephrine. Vasodilation and afterload reduction are also achieved with the administration of angiotension-converting enzyme (ACE) inhibitors (e.g., lisinopril, captopril) or calcium channel blockers (e.g., verapamil, nifedipine). Morphine sulfate is used to reduce afterload by inducing venodilation and venous pooling. It also is used for sedation and relief of anxiety.

Sodium and Fluid Retention Therapy

Common methods used to reduce sodium and fluid retention include the following: (1) bed rest in the supine position, which enhances natural diuresis by the kidneys (sitting in the upright position reduces sodium and water excretion and therefore should be avoided), (2) restriction of sodium and water intake, and (3) high-dose diuretic therapy.

Albumin and Mannitol

Albumin or mannitol is sometimes administered to increase the patient’s oncotic pressure in an effort to offset the increased hydrostatic forces of cardiogenic pulmonary edema, if the patient’s osmotic pressure is low.

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. The hypoxemia that develops in pulmonary edema is most commonly caused by the interstitial and alveolar fluid, atelectasis, and capillary shunting associated with the disorder. Hypoxemia caused by capillary shunting is at least partially refractory to oxygen therapy (see Oxygen Therapy Protocol, Protocol 9-1).

Bronchopulmonary Hygiene Therapy Protocol

Because of the excessive frothy white secretions associated with pulmonary edema, bronchial hygiene treatment modalities may be used to enhance the mobilization of bronchial secretions (see Bronchopulmonary Hygiene Therapy Protocol, Protocol 9-2).

Lung Expansion Therapy Protocol

Lung expansion therapy is commonly prescribed to offset the fluid accumulation and alveolar shrinkage associated with pulmonary edema. For example, high-flow mask continuous positive airway pressure (CPAP) has been shown to produce a significant and rapid improvement in oxygenation and ventilatory status in patients with pulmonary edema. Mask CPAP improves decreased lung compliance, decreases the work of breathing, enhances gas exchange, and decreases vascular congestion in patients with pulmonary edema. In fact, mask CPAP is prescribed (at least for a trial period) for patients with pulmonary edema who have arterial blood gas values that reveal impending or acute ventilatory failure—the hallmark clinical manifestation for mechanical ventilation. Often, mask CPAP dramatically improves oxygenation and ventilatory status in these patients and eliminates the need for mechanical ventilation (see Lung Expansion Therapy Protocol, Protocol 9-3).

Aerosolized Medication Protocol

Both sympathomimetic and parasympatholytic agents are commonly used to induce bronchial smooth muscle relaxation (see Aerosolized Medication Protocol, Protocol 9-4 and Appendix II). They often are not effective in this disorder, however.

Alcohol (Ethanol, Ethyl Alcohol)

Because alcohol is a specific surface-active agent, it may be aerosolized into the patient’s lungs to lower the surface tension of the frothy secretions. This action enhances the mobilization of secretions. Generally, 5 to 15 mL of 30% to 50% alcohol solution is administered. Such therapy is rarely used today.

Decreasing Hydrostatic Pressure

In an effort to lower hydrostatic pressure, the physician may order the following:

• Positioning the patient in Fowler’s position (sitting up)

• Rotating tourniquets (rarely used)

• Phlebotomy (rarely used)

CASE STUDY

Pulmonary Edema

Admitting History and Physical Examination

This 76-year-old man was admitted to the emergency room in obvious respiratory distress. His wife reported that her husband had gone to bed feeling well. He woke up with chest pain at about 2:30 am, very short of breath. She became concerned and called an ambulance. Neither the patient nor the wife were good historians, but they did report that the patient had been under a physician’s care for some time for “heart trouble” and that he was taking “little white pills” on a daily basis. For the previous 3 days, he had not taken any medication.

On admission to the emergency room, the patient was mildly disoriented and slightly cyanotic. He repeatedly tried to take the oxygen mask from his face. He complained of a feeling of suffocation. His neck veins were distended, and the skin of his extremities was mottled. On auscultation, there were coarse rhonchi and crackles in both lower lung fields and some crackles in the middle and upper lung fields.

His cough was productive of pinkish, frothy sputum. His vital signs were as follows: blood pressure 105/50, heart rate 124/min, and respiratory rate 28/min. He was afebrile. ECG showed evidence of an old infarct, sinus tachycardia, and an occasional premature ventricular contraction. X-ray films taken in the emergency room with the patient in a sitting position revealed bilateral fluffy infiltrates, more marked in the lower lung fields. The heart was enlarged. All other laboratory findings were within normal limits. Blood gases on an Fio₂ of 0.30 were pH 7.11, Paco₂ 72, 27, and Pao₂ 56. His oxygen saturation by oximetry (Spo₂) was 87%. The respiratory therapist working in the emergency room during the night shift recorded the following SOAP note.

Respiratory Assessment and Plan

S Patient states “a feeling of suffocation.”

O Cyanosis, disorientation. Distended neck veins and mottled extremities. BP 105/50, HR 124, RR 28. ECG: sinus tach and occasional PVCs. Distended neck veins, mottled extremities, coarse rhonchi and crackles bilaterally. Frothy pink sputum. CXR: Bilateral fluffy infiltrates and an enlarged heart. ABG: pH 7.11, Paco₂ 72, 25, and Pao₂ 56 (Fio₂ 0.30). Spo₂ 87%.

• Acute pulmonary edema (CXR)

• Acute ventilatory failure with moderate hypoxemia (ABG)

• Large and small airway secretions (rhonchi and crackles)

P Oxygen Therapy Protocol: Increase Fio₂ to 0.60 via continuous CPAP mask at 25 cm H₂O per Lung Expansion Therapy Protocol. Remain on standby for emergency endotracheal intubation and ventilator support. Continue ECG and oximetry monitoring, and repeat ABG in 30 minutes.

The patient was admitted on the cardiology service with a diagnosis of pulmonary edema–CHF. ECG monitoring and continuous oximetry were followed. Treatment consisted of intravenous furosemide, dopamine, and nitroprusside, as well as mask CPAP at 25 cm H₂O pressure with an Fio₂ of 0.6. A Foley catheter was placed.

Two hours later, the patient’s condition was very much improved, and he was no longer cyanotic. Vital signs were as follows: blood pressure 126/70, heart rate 96/min, and respiratory rate 18/min. ECG revealed mild sinus tachycardia and no ectopic beats. Auscultation showed considerable improvement. There were still some basilar crackles, but the upper lung fields were clear. Cough was much reduced and no longer productive. Repeat chest x-ray examination at the bedside showed considerable improvement. Urine output was in excess of 600 mL/hr. The patient was calm and rational, stating that he was less short of breath and had no pain. Repeat arterial blood gases revealed pH 7.35, Paco₂ 46, 24, and Pao₂ 120 on an Fio₂ of 0.50. The following respiratory therapy SOAP note was made at the time.

Respiratory Assessment and Plan

S Patient states, “I’m less short of breath. No pain.”

O Not cyanotic. BP 126/70, HR 96, RR 18. ECG: Mild sinus tachycardia without ectopic beats. Fewer crackles; no sputum production; CXR: Improved. ABG: pH 7.35, Paco₂ 46, 24, Pao₂ 120 (Fio₂ 0.50).

• Decreased pulmonary edema (overall impression from the data)

• No longer in ventilatory failure (ABG)

• Acceptable acid-base status with excessively corrected hypoxemia (ABG)

• Secretions controlled (no sputum and fewer crackles)

P Reduce O₂ per Oxygen Therapy Protocol to 2 L/min by nasal cannula. Discontinue CPAP per Lung Expansion Therapy Protocol. Continue ECG and oximetric monitoring. Repeat ABG in 60 minutes.

Discussion

Acute pulmonary edema is a classic finding in CHF. Several clinical manifestations associated with Increased Alveolar-Capillary Membrane Thickness (see Figure 9-10) were present in this case. For example, the patient’s decreased lung compliance was manifested in his tachycardia and tachypnea, whereas his hypoxemia reflected diffusion blockade associated with classic pulmonary edema. His lung compliance was so reduced that he had progressed to acute ventilatory failure—the severe stage of pulmonary edema. Some Atelectasis (see Figure 9-8) was doubtless also present and was the rationale for CPAP therapy. In addition, the clinical scenario associated with Excessive Bronchial Secretions (see Figure 9-12) also was evident initially with frothy blood-tinged sputum and coarse rhonchi and crackles in both lower lung fields. The patient was too ill to allow valid pulmonary function testing, but the suspicion is that a combined obstructive and restrictive pattern may have been present at the time of the first assessment.

The Aerosolized Medication Protocol and Bronchopulmonary Hygiene Therapy Protocol were not used in this case. Often, the first-line management of pulmonary edema consists only of improving myocardial efficiency, decreasing the cardiovascular afterload, decreasing the hypervolemia, providing CPAP, and improving oxygenation. Furosemide (Lasix) is a potent loop diuretic, dopamine has direct inotropic effects, and nitroprusside is a potent peripheral vasodilator. The combination of these drugs, along with CPAP and oxygen therapy, resulted in marked improvement of the patient’s myocardial activity and a rapid change in the clinical picture.

In short, this patient had an acute respiratory problem, but the basic cause was cardiac. After the cardiac condition was treated, the respiratory symptoms rapidly disappeared. CPAP and an increased Fio₂ were adequate, and this patient was spared the trauma and risk associated with intubation and mechanical ventilation. No evidence of acute myocardial infarction was found. He was discharged after 48 hours, his condition much improved. He was instructed to take his cardiac medication and diuretics without fail and to return to his family physician in 3 days.