Pulmonary Edema

Pulmonary edema occurs when movement of liquid from the blood to the interstitial space and/or into the alveoli exceeds the return of liquid to the blood and its drainage through the lymphatics.

Causes of Pulmonary Edema

Imbalance of Starling Forces

•Increased pulmonary capillary pressure

•Hypoalbuminemia increased

•Negative interstitial pressure

The two most common forms of pulmonary edema are that initiated by an imbalance of Starling forces and that initiated by disruption of one or more components of the alveolar-capillary membrane.

Altered Alveolar-Capillary Membrane Permeability (ARDS)

Primary alveolar-capillary membrane damage (Acute Respiratory Distress Syndrome)

Lymphatic Insufficiency

• Post lung transplant

• Lymphangitis carcinomatosis

• Fibrosing lymphangitis

Unknown or Incompletely Understood

• High-altitude pulmonary edema

• Neurogenic pulmonary edema

• Narcotic overdose pulmonary edema

• Pulmonary embolism

• Eclampsia

• Post cardioversion

• Post anesthesia

• Post cardiopulmonary bypass

Cardiogenic Pulmonary Edema

Acute cardiogenic pulmonary edema is the symptom of left-sided heart failure.

Causes

• Impaired left ventricular systolic and/or diastolic function

• Mitral stenosis

• Any condition that elevates left atrial and pulmonary capillary pressures significantly.

Effects of Cardiogenic Pulmonary Edema
• Interference with oxygen transfer in the lungs

• Depression arterial oxygen tension

• Sense of suffocation and oppression in the chest

• Elevates heart rate and blood pressure further restricting ventricular filling.

The increased work of breathing place an additional load on the heart, and cardiac function becomes depressed further by the hypoxia leading to a vicious. Development of acute pulmonary edema is a terrifying experience with extreme breathlessness developing suddenly, and the patient becomes extremely anxious, coughs, and expectorates pink, frothy liquid, with a feeling of drowning. The patient sits upright, or may stand, exhibits air hunger, respiratory rate is elevated, the alae nasi are dilated, and there is inspiratory retraction of the intercostal spaces and supraclavicular fossae that reflects the large negative intrapleural pressures required for inspiration. The patient often grasps the sides of the bed to allow use of the accessory muscles of respiration. Respiration is noisy, with loud inspiratory and expiratory gurgling sounds that are often easily audible across the room. Sweating is profuse, and the skin is usually cold, ashen, and cyanotic, reflecting low cardiac output and increased sympathetic drive.

Auscultation reveals crepitations and occasionally rhonchi, which appear initially over the lung bases but then extend upward with worsening of the condition. An S3 gallop and loud pulmonic component of the second heart sound are frequently present.Arterial pressure is usually elevated as a result of excitement and discomfort, which cause adrenergically mediated vasoconstriction. And this usually does not represent chronic systemic hypertension. Optic fundus examination may be useful in differentiating the two conditions.Sometimes it may be difficult to differentiate between acute pulmonary edema and acute exacerbation of bronchial asthma. Some of the points that may be of clinical use in such a situation are given in the table below.

Differentiation between Pulmonary Edema and Bronchial Asthma

Management of Pulmonary Edema

Pulmonary edema is life-threatening condition and therefore, treated as a medical emergency. As is the case with chronic stable heart failure, identification and correction of any precipitating causes should be attempted. However, because of the acute nature of the problem,the initial management includes a number of additional non-specific measures:

1) The patient should be in propped up position (provided the blood pressure is adequate) with the legs dangling along the side of the bed, if possible, which tends to reduce venous return.

2) 100 per cent O 2 should be administered to improve oxygenation. If patient is not maintaining oxygen saturation with nasal oxygen intubation and mechanical ventilation should be considered. This increases intra-alveolar pressure, reduces transudation of fluid from the alveolar capillaries, and impedes venous return to the thorax, reducing pulmonary capillary pressure.

3) Morphine is the drug of choice. It is administered intravenously, in doses from 2 to 5 mg intravenously. It reduces anxiety, reduces adrenergic vasoconstrictor stimuli to the arteriolar and venous beds, and thereby helps to break a vicious cycle. An antiemetic is usually given along with morphine to reduce chance of vomiting.

4) Intravenous loop diuretics produce rapid diuresis, reduce circulating blood volume and hasten the relief from pulmonary edema. Furosemide when administered exerts a venodilator action, reducing venous return. This helps in improving pulmonary edema even before the diuresis is initiated.

5) Afterload reducing agents e.g. IV sodium nitroprusside at 20 to 30 μg/min in patients with systolic BP above 100 mmHg.

6) Inotropic support should be provided by dopamine or dobutamine where necessary.

7) Patients with systolic heart failure who are not receiving digitalis may receive 0.75 to 1.0 mg digoxin intravenously over 15 min.

8) Sometimes, aminophylline (theophylline ethylenediamine), 240 to 480 mg intravenously, is effective in diminishing bronchoconstriction, increasing renal blood flow and sodium excretion, and augmenting myocardial contractility.

9) Rotating tourniquets may be applied in an effort to reduce venous return. Once the patient has been stabilized and underlying cause determined, treatment directed at correcting/improving the cause.