pulmonary edema
TRANSCRIPT
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
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