Pulmonary EdemaDR. HARSH PANDYA R1

UNDER GUIDANCE OFDR.NIPA NAYAK M.D. ASSO. PROF

Outline

Definition

Epidemiology

Pathophysiology

Classifications & causes

Pathogenesis

Staging

Clinical manifestations

Complications

Differential diagnosis

Treatment

DefinitionPulmonary Edema ; is a condition

characterized by fluid accumulation in

the lungs caused by extravasation of

fluid from pulmonary vasculature in to

the interstitium and alveoli of the lungs

The extent to which fluid accumulates in the interstitium of the lung

depends on the balance of hydrostatic and oncotic forces within

the pulmonary capillaries and in the surrounding tissue.

Hydrostatic pressure

-favors movement of fluid from the capillary into the interstitium

Oncotic pressure

-favors movement of fluid into the vessel

Maintenance

-lymphatic in the tissue carry away the small amounts of protein

that may leak out

-tight junction of endothelium are impermeable to protein

Epidemiology

Pulmonary edema occurs in about 1% to 2% of the general

population.

Between the ages of 40 and 75 years, males are affected

more than females.

After the age of 75 years, males and females are affected

equally.

The incidence of pulmonary edema increases with age and may affect about 10% of the population over the age of 75

years.

Pathophysiology

imbalance of starling force

-increase pulmonary capillary pressure

-decrease plasma oncotic pressure

-increase negative interstitial pressure

damage to alveolar- capillary barrier

lymphatic obstruction

Disruption of endothelial barrier allow protein to

escape capillary bed and enhance movement of

fluid in to the tissue of the lung

idiopathic or unknown

Classification

based on inciting mechanism

1. Imbalance of Starling force

A. Increased pulmonary capillary pressure

-left ventricular failure

-Volume overload

B. Decreased plasma oncotic pressure

- Hypoalbuminemia due to different cause

C. Increased negativity of interstitial pressure

-Rapid removal of pneumothorax with large applied negative pressures (unilateral)

Classification

Based on inciting agent…..

2. Altered alveolar-capillary membrane permeability

o Infectious pneumonia

o Inhaled toxins

o Circulating foreign substances

o Aspiration

o Endogenous vasoactive substances

o Disseminated intravascular coagulation

o Immunologic—hypersensitivity pneumonitis, drugs

o Shock lung in association with non-thoracic trauma

o Acute hemorrhagic pancreatitis

Classification

Based on inciting agent….

3. Lymphatic insufficiency-After lung transplant- Lymphangitic carcinomatosis-Fibrosing lymphangitis

4. Unknown or incompletely understood- High-altitude pulmonary edema- Neurogenic pulmonary edema- Narcotic overdose- Pulmonary embolism- Eclampsia-After anesthesia- After cardiopulmonary bypass

Classification

Base on underlining cause

o Cardiogenic pulmonary edema

o Non-cardiogenic pulmonary edema

Cardiogenic pulmonary edema

Is Pulmonary edema due to

increased pressure in the pulmonary

capillaries because of cardiac

abnormalities that lead to an

increase in pulmonary venous

pressure.

o Hydrostatic pressure is increased

and fluid exit capillary at increased

rate

Cardiogenic PE

Basic pathophysiology:

A rise in pulmonary venous and

pulmonary capillary pressures pushes

fluid into the pulmonary alveoli and

interstitium.

CXR: B/L perihilar bat’s wing

appearance,symmetric opacification

of lung fields

Pathogenesis of CPE

Left sided heart failure

Decrease pumping ability to the systemic circulation

Congestion & accumulation of blood in the pulmonary area

Fluid leaks out of the intravascular space to the interstitium

Accumulation of fluid

Pulmonary edema

`

Risk Factors

Vary by cause

-Leading risk factor is clearly

underlying cardiac disease.

Causes of Cardiogenic PE

LV failure is the most common cause.

Dysrhythmia

LV hypertrophy and cardiomyopathy

LV volume over load

Myocardia infarction

left ventricular outflow obstruction

Non cardiogenic

pulmonary edema

It is defined as the evidence of alveolar

fluid accumulation with out

hemodynamic evidence that suggest a

cardiogenic etiology.

Hydrostatic pressure is normal

Leakage of protein and other molecule

in to the tissue

Non cardiogenic PE

o Associated with dysfunction of

surfactant lining the alveoli,

increased surface force and a

propensity for the alveoli to

collapse at low volume.

o Characterized by intra pulmonary

shunt with hypoxemia and

decrease lung compliance

Non cardiogenic

pulmonary edema

Mechanism include:

Increased alveolar–capillary membrane permeability

Decreased plasma oncotic pressure

Increased negativity of pulmonary interstitial pressure

Lymphatic insufficiency or obstruction

Non- cardiogenic PE

cause

I. Direct injury to the lung

II. Hematogenous injury to the

lung

III. possible lung injury plus

elevated hydrostatic pressure

Staging of PE

Three stages of PE can be distinguished based on

the degree of fluid accumulation:

Stage-1 : all excess fluid can still be cleared by lymphatic drainage.

Stage-2 : characterized by the presence of interstitial

edema.

Stage-3 : characterized by alveolar edema due to

altered alveolor- capillary permeability

Mild: Only engorgement of pulmonary vasculature is seen.

Moderate: There is extravasation of fluid into the interstitial space due to changes in oncotic pressure.

Severe: Alveolar filling occurs.

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 and who then engage in strenuous physical exercise at that

altitude, before they have become acclimatized.

Reversible (in less than

48 hours)

Pathophysiology

on ascending to high altitude, falling level of Po2 trigger hypoxic

pulmonary vasoconstriction

This directs blood flow away from hypoxic areas of lung towards area

that are well oxygenated

This results in a rise in mean pulmonary artery pressure & a

heterogeneous blood flow to different parts of the lung

Cont…

In areas that receive high blood flow the capillary trans-mural pressure rises & walls of the capillary &alveolus are exposed to stress failure

Extensive damage to alveolar capillary membrane

Edema which is rich in high molecular weight proteins & RBCs to pass freely in to the alveoli & impair oxygenation.

patient present with

Headache, Insomnia, Fluid retention, Cough,Shortness of breath

Symptom of pulmonary

edema

ACUTE

Shortness of breath

A Feeling of suffocating

Anxiety ,restlessness

Cough-frothy sputum that may be tinged with

blood

excessive sweating

pale skin

chest pain if PE is cause by cardiac abnormality

palpitation

Symptom……

Long term(chronic)

Paraxosomal nocturnal dyspnea

orthopnea

Rapid weight gain

Loss of appetite

fatigue

ankle and leg swelling

Signs

Tachycardia

Tachypnea

Confusion

Agitation

Anxious

Diaphoric

Hypertension

Cool extremities

Rales

Wheezing

CVS findings ; S3 ,accentuation of pulmonic component of S2, jugular venous distention…..

Special considerations

Unilateral pulmonary edema after rapid

evacuation of large pneumothorax

Findings may be apparent only by radiography.

Occasionally, dyspnea with physical findings

localized to edematous lung

Special consideration

Lymphatic blockade secondary to fibrotic and

inflammatory diseases or lymphangitic

carcinomatosis

Both clinical and radiographic manifestations are

dominated by the underlying disease process.

Neurogenic pulmonary edema

Symptoms usually occur within minutes to hours of

the injury

Complications

leg swelling(edema),

abdominal swelling(ascites),

Pleural effusion,

Congestion & swelling of liver,

acute heart attack (myocardial infarction [MI]),

cardiogenic shock,

arrhythmias,

electrolyte disturbances,

mesenteric insufficiency,

protein enteropathy,

respiratory arrest, and death.

Differential diagnosis

Pneumothorax

Bronchitis

Cardiac tamponed

COPD

Pericarditis

Pneumonia (bacterial ,viral , PCP)

Pulmonary embolism

Shocks (cardiogenic ,septic ,anaphylactic)

Venous air embolism

Distinguishing Cardiogenic from

Non-cardiogenic Pulmonary Edema

Finding suggesting cardiogenic edema

-S3 gallop

-elevated JVP

-Peripheral edema

Findings suggesting non-cardiogenic edema

-Pulmonary findings may be relatively normal in the early stages

-.

Distinguishing ….. Chest radiography

A cardiogenic cause is favored with

Cardiomegaly

Kerley B lines and loss of distinct vascular margins

Cephalization: engorgement of vasculature to the apices

Perihilar alveolar infiltrate

Pleural effusion

Non cardiogenic cause

-Heart size is normal

-Uniform alveolar infiltrate

-pleural effusion is uncommon

-lack of cephalization

Distinguishing…..

Hypoxemia

Cardiogenic

- due to ventilation perfusion miss match

-respond to administration of oxygen

Non cardiogenic

-due to intrapulmonary shunting

-persist despite oxygen supplimentation

Exertional Dyspnea

Orthopnea

Aspiration of food or foreign body

Direct Chest injuries

Walking High altitude

Chest Pain(right or left)

Leg pain or swelling(Pulmonary Embolism)

A cough that produces frothy sputum that may be tinged with blood(cardiogenic)

History Taking

Approach a Patient with

Pulm.Edema

Cont…

Palpitations

Excessive sweating

Skin color change-Pale skin

Chest pain(if it is Cardiogenic)

Rapid weight gain(cardiogenic)

Fatigue

Loss of appetite

Smoking History

Past Medical History

COPD,

heart failure,

HIV risk factors

(pulmonary Kaposi’s sarcoma).

Prior chest X-rays,

CT scans,

tuberculin testing (PPD).

Medications

Anticoagulants

Aspirin

NSAIDs

Narcotic

Heroin

Morphine

Methadone and

Dextropropoxyphene

INVESTIGATIONS

CXR-PA view:

unilateral or bilateral involvement,cardiogenicpattern or non cardiognic pattern(air bronchogramsigns, fluffy opacities, asymmetrical inhomogenousinvolvement),lobar involvement in post infectious PE.

ABG analysis:

hypoxia and hypocapnia initially with respi. alkalois

hypercapnea in later stage with respi and metabolic acidosis

Hemodynamic measurement with Swan-Ganzcatheter

Blood work up and septic screen

Management stretagy

Treat underlying cause : Sepsis,heart failure,highaltitude hypoxia,obstruction,fluidoverload,hypoproteinemia etc.

Respi support: NIV vs Intubation f/b venti support

Indication for intubation f/b venti support

Refractive hypoxia

Excessive work of breathing : rate > 35/min , MV>12L/min

Hemodynamic instability

Inability to protect airway

Anticipated rapid clinical deterioration

Management stretagy…..

NIV support:CPAP

Reasonable initial venti settings are EPAP 7 cmH2O

and IPAP of around 15 cm H2O with adjustment according to patient tolerance and maintaining

SaO2>90%

Decreases work of breathing,FRC is

increased,collapse of alveoli due to edema fluid is

prevented and helps in opening up of already

collapsed alveoli

Good response is generally observed in 30 minutes,ifnot so or worsening is seen, consider elective intubation f/b venti support

Management stretagy…

Principles of mechanical ventilation

Two fundamental principles

1. Prevention of overdistension of alveoli-limiting

tidal volume or inspiratory pressure

2. Choose the level of PEEP sufficiently high to

prevent derecruitment of alveoli at end of

expiration

1. Limiting tidal volume

High TV 12-15 ml per kg are

dangerous in patient with PE

Can lead to VOLUTRAUMA

Tidal volume kept at 6-8 ml per kg

to start with in patient of PE

Then adjusted to keep the plateau

pressure below 30 cm of H2O

2. Use of PEEP

Recruits collapsed alveoli,prevents collapse,improvesV/Q mismatch,decreases shunt and venous admixture,increases FRC,reduces pathological dead space

Can allow adequate oxygenation at lower FiO2,protects from oxygen toxicity

Most patients with ARDS will need PEEP of more than 10 cm H2O at FiO2<0.6

If high level of PEEP causes hemodynamic instability, use of pressure controlled – inverse ratio ventilation , prone posture can be beneficial

Inverse ratio venti:changes inspiration-expiration ratio,lower peak pressure can be achieved,auto-PEEP develops,higher mean alveolar pressure with low peak pressure

Treatment in special

conditions

High altitude pulmonary edema

Slow ascent ,prophylactically tab.nifedipine 20mg sustained release 8hrly, or tab dexamethasone 8 mg 12hrly,or inhaled salmeterol

Descent and supplemental O2 are definitive Rx

If descent not possible and O2 not available,startpharmacotherapy to reduce pulmonary artery pressure

Tab nifedipine 10mg sublingual f/b 20 mg SR tab 6hrly

Also hydralazine,inhaled nitrous oxide acetazolamide are helpful

Post Aspiration PE

Preop gastric emptying by physical means(ryle’stube aspiration) or pharmacological means(perinorm,atropine,glocopyrolate)

Anti ematics ondensatron,granisatron injectable

Induction in lateral position

Head low position

Bronchoscopic removal of particulate aspirate material

NO BRONCHO-ALVEOLAR LAVAGE-removes surfactant and promotes collapse

Supportive sterids

PEEP and mechanical venti till edema clears

THANK YOU