Management of

pulmonary edemaDR ELLAHI BAKHSH

PGR PULMONOLOGY DEPTT

UNIT_C

FJGH QUETTA

OUTLINE

DEFINITION

PATHOPHYSIOLOGY

CLASSIFICATION

CAUSES

SIGN AND SYMTOMS

DIFFERENTIAL DIAGNOSIS

WORKUP

MANAGEMENT

Definition

Pulmonary Edema :

is a condition characterized by accumulation of excess fluid in

interstitium and alveoli of the lung as a result of an alteration in

one or more of starling forces.

Pathophysiology

Pulmonary edema can be caused by the following major

pathophysiologic mechanisms:

imbalance of starling force

-increase pulmonary capillary pressure (8-12mmHg)

-decrease plasma oncotic pressure (28mmHg)

-increase negative interstitial pressure

damage to alveolar- capillary barrier

lymphatic obstruction (10-20 mL/h)

Idiopathic (unknown) mechanism

Classification

Base on underlining cause

o Cardiogenic pulmonary edema

o Non-cardiogenic pulmonary edema

Cardiogenic pulmonary edema

Cardiogenic pulmonary edema :

is defined as a high pulmonary capillary hydrostatic pressure( as

estimated clinically from the PCWP )is responsible for abnormal

fluid accumulation in alveoli of the lung .

Noncardiogenic pulmonary

edema

Noncardiogenic pulmonary edema is caused by

various disorders in which factors other than

elevated pulmonary capillary pressure are

responsible for protein and fluid accumulation in

the alveoli.

Causes

Cardiogenic pulmonary edema Non cardiogenic pulmonary edema

(ARDS ) other name of NCPE

Cardiac disorders

Atrial outflow obstruction

LV systolic dysfunction

LV diastolic dysfunction

Dysrhythmias

LV hypertrophy and

cardiomyopathies

LV volume overload

Myocardial infarction

LV outflow obstruction

Direct injury to lungchest trauma

Pneumonia

Pulmonary embolism

Indirect injury to lungSepsis

Multiple transfusions

Cardiopulmonary bypass

Lung injury plus increased hydrostatic pressure

Neurogenic pulmonary edema

High altitude pulmonary edema

Reexpansion pulmonary edema

Features may differentiate CPE

from NCPE.

In CPE, a history of an acute cardiac event is usually present. Physical

examination shows an S3 gallop, jugular venous distention, and crackles

on auscultation.

Patients with NCPE have a warm periphery, a bounding pulse, and no

S3 gallop or jugular venous distention.

Definite differentiation is based on pulmonary capillary wedge

pressure (PCWP) measurements.

The PCWP is generally >18 mm Hg in CPE and < 18 mm Hg in NCPE .

Unusual type pulmonary edema

Neurogenic pulmonary edema

Patients with central nervous system disorders and without apparent preexisting LV

dysfunction

Re-expansion pulmonary edema

Develops after removal of air or fluid that has been in pleural space for

some time, post- thoracentesis

Patients may develop hypotension or oliguria resulting from rapid fluid

shifts into lung.

Unusual type pulmonary edema

High altitude pulmonary edema

occurs in young people who have quickly ascended to altitudes

above2700m ( 8000 ft) and who then engage in strenuous physical

exercise at that altitude, before they have become acclimatized.

Reversible (in less than 48 hours)

Presentation CPE

Clinical features of left heart failure. extreme breathlessness,

anxiety, and feelings of drowning.

Shortness of breath.

Orthopnea , and paroxysmal nocturnal dyspnea.

Cough, Pink frothy sputum

Presentation CPE

Tachypnea and tachycardia.

Hypertension

Cool extremities may indicate low cardiac output .

Auscultation reveals fine, crepitation or wheezes .

CVS findings ; S3 ,accentuation of pulmonic component of S2, jugular

venous distention…

Patients with (RV) failure may present with hepatomegaly, hepatojugular

reflux, and peripheral edema.

Change in mental status, caused by hypoxia or hypercapnia .

Workup CPE

Complete blood count .

Serum electrolyte .

(BUN) and creatinine .

Brain natriuretic peptide .

Arterial blood gas analysis .

Electrocardiography and Echocardiography.

Radiography and Ultrasonography .

PCWP can be measured with a pulmonary

arterial catheter (Swan-Ganz catheter) .

Differential diagnosis

Pumonary Edema Cariogenic Pulmonary edema

Acute Respiratory Distress Syndrome

AsthmaCardiogenic Shock

Chronic Obstructive Pulmonary Disease

Emphysema

Goodpasture Syndrome

Myocardial Infarction

Pneumocystis (carinii) jiroveci Pneumonia

Pneumonia, Bacterial

Pneumonia, Viral

Myocardial ischemia

PneumothoraxHigh-altitude pulmonary edema

Neurogenic pulmonary edema

Pulmonary embolism

Respiratory failure

Treatment CPE

Initial management

ABCs of resuscitation, that is, airway, breathing, and circulation.

Oxygen should be administered to all patients to keep oxygen saturation at greater than

90%.

Methods of oxygen delivery include the use of a face mask, (NPSV (which includes [BiPAP] and [CPAP]), and intubation and mechanical ventilation.

Medical treatment of CPE focuses on 3 main goals:

(1) reduction of pulmonary venous return (preload reduction),

(2) reduction of systemic vascular resistance (afterload reduction)

(3) inotropic support.

Ventilatory support (CPE)

Noninvasive pressure-support ventilation

NPSV maintains the patency of the fluid-filled alveoli and prevents them from collapsing

during exhalation.

NPSV improves pulmonary air exchange, and it increases intrathoracic pressure with

reduction in preload and afterload.

Two types of NPSV are CPAP and BiPAP.

In CPAP, a single airway pressure is maintained throughout all phases of the respiratory

cycle.

In BiPAP, high pressures can be applied during inspiration and low pressures during

expiration, increasing the patient's comfort.

Mechanical ventilation

In general, use endotracheal intubation and mechanical ventilation

when patients with CPE remain hypoxic despite maximal noninvasive

supplemental oxygenation, when patients have evidence of

impending respiratory failure or when patients are hemodynamically

unstable

Mechanical ventilation maximizes myocardial oxygen delivery and

ventilation

Preload Reduction (CPE )

Preload reduction decreases pulmonary capillary hydrostatic

pressure and reduces fluid transudation into the pulmonary

interstitium and alveoli.

Nitroglycerin : oral or I/v 10 -100 mcg/min

Diuretics :

Morphine sulfate

Afterload Reduction (CPE )

Afterload reduction increases cardiac output and improves renal

perfusion, which allows for diuresis in the patient with fluid overload.

ACE inhibitors : Enalapril 1.25mg I/v or captopril 25mg subligually

Angiotensin II receptor blockers

Nitroprusside for 3-4mcg/kg/min IV infusion:

Inotropic agents

Dobutamine

Dopamine

Intra-aortic balloon pumping (CPE )

The IABP is inserted percutaneously through the femoral artery to

descending aorta using a modified technique. Fluoroscopy may be used

for correct positioning of the balloon, and Helium, gas is used to inflate the

balloon.

The IABP decreases afterload as the pump deflates; during diastole the

pump inflates to improve coronary blood flow.

Ultrafiltration (CPE )

Ultrafiltration is a fluid removal procedure that is

particularly useful in patients with renal

dysfunction and expected diuretic resistance.

Noncardiogenic Pulmonary Edema

High-Altitude Pulmonary Edema Treatment

includes rest, administration of oxygen, and descent to a lower altitude.

If diagnosed early, recovery is rapid with a descent of only 500-1000 m.

A portable hyperbaric chamber or supplemental oxygen administration

immediately increases oxygen saturation and reduces pulmonary artery

pressure, heart rate, respiratory rate,

Nifedipine, by reducing pulmonary arterial pressure, may be effective in

treating HAPE .

Acetazolamide and dexamethasone have been shown to be effective

agents for prophylaxis against high-altitude illness.

Treatment of Noncardiogenic

Pulmonary Edema

Neurogenic Pulmonary Edema Treatment

Supplemental oxygen

Mechanical ventilation may be necessary, either noninvasive with a

face mask or via an endotracheal tube.

Pharmacological agents are not used routinely in the treatment of

neurogenic pulmonary edema.

But sometimes include alpha-adrenergic antagonists (eg,

phentolamine) and Beta-adrenergic agonists (eg, dobutamine,

dopamine, norepinephrine).

Reexpanison pulmonary edema

Reexpanison pulmonary edema is a rare but serious complication

of thoracentesis.

This case was unusual in that RPE developed on the side

contralateral to the lung that was drained.

If RPE occurs, the treatment is mostly supportive, including

supplemental oxygen, positive pressure ventilation, and diuresis.

However, if there is radiographic evidence of RPE but the patient is

asymptomatic, no treatment is necessary.

Complication

Respiratory failure

Cardiac arrest

Sudden Death secondary to cardiac arrhythmia

Prognosis

In a high-acuity setting, in-hospital death rates are as

high as 15-20%.

Myocardial infarction, associated hypotension, and a

history of frequent hospitalizations for CPE generally

increase the mortality risk.