Acute Pulmonary EdemaAcute Pulmonary Edema

Purwoko Sugeng H.

DEFINITIONDEFINITION

Abnormal accumulation of fluid in the extravascular spaces and tissues of the lung.

ETIOLOGIETIOLOGI

Cardiogenic pulmonary edema Cardiogenic pulmonary edema (also (also termed hydrostatic or hemodynamic edema) termed hydrostatic or hemodynamic edema)

Noncardiogenic pulmonary edema Noncardiogenic pulmonary edema (also (also known as increased-permeability pulmonary known as increased-permeability pulmonary edema, acute lung injury, or acute edema, acute lung injury, or acute respiratory distress syndrome) respiratory distress syndrome)

Difficult to distinguish because of their Difficult to distinguish because of their similar clinical manifestations similar clinical manifestations

Cardiogenic Pulmonary Cardiogenic Pulmonary Edema -- Causes:Edema -- Causes:

Left ventricular failureVolume overloadMechanical obstruction of left outflow tract e.g. Mitral stenosisAortic valvular diseases & also in congestive failure and hypertensionAMIcardiomiopathy

Causes of Non-cardiac Pul. Causes of Non-cardiac Pul. EdemaEdema

Toxins: eg. Smoke, ozone, phosgene, chlorine, Nitrogen dioxide, cadmium

Trauma and burns

Aspiration of gastric contents

Acute radiation Pneumonitis

D.I.C.

Near drowning

Emboli

Multiple transfusion

Drug related: Thiazides, salicylates, interleukin-2, colchicine, chlordiazepoxide

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

Microvascular Fluid Exchange in the LungMicrovascular Fluid Exchange in the Lung

Fluid and solutes that are filtered from the circulation into the alveolar interstitial space

Do not enter the alveoli because the alveolar epithelium is composed of very tight junctions

It moves proximally into the peribronchovascular space

The lymphatics remove most of this filtered fluid from the interstitium and return it to the systemic circulation

PATHOPHYSIOLOGY PATHOPHYSIOLOGY

Microvascular Fluid Exchange in the LungMicrovascular Fluid Exchange in the Lung

Increased hydrostatic pressure in the pulmonary capillaries

elevated pulmonary venous pressure increased left ventricular end-diastolic pressure and left atrial pressure

As left atrial pressure rises further (>25 mm Hg)

edema fluid breaks through the lung epithelium flooding the alveoli with protein-poor fluid

PATHOPHYSIOLOGY PATHOPHYSIOLOGY

Microvascular Fluid Exchange in the LungMicrovascular Fluid Exchange in the Lung

Noncardiogenic pulmonary edema increase in the vascular permeability of the lung

resulting in an increased flux of fluid and protein into the lung interstitium and air spaces

HistoryHistory

Interstitial edema causes dyspnea and tachypnea

Alveolar flooding leads to arterial hypoxemia

Cough and expectoration of frothy edema fluid

HistoryHistory

Cardiogenic pulmonary edemaCardiogenic pulmonary edemaischemia with or without myocardial infarctionexacerbation of chronic systolic or diastolic heart failure, and dysfunction of the mitral or aortic valve paroxysmal nocturnal dyspnea or orthopnea

Noncardiogenic pulmonary edema Noncardiogenic pulmonary edema pneumoniasepsisaspiration of gastric contentsmajor trauma associated with the administration of multiple blood-product transfusions

Physical ExaminationPhysical Examination

Cardiogenic pulmonary edema auscultation of an S3 gallop a murmur consistent with valvular stenosis or regurgitation elevated neck veins, an enlarged and tender liver, and peripheral edemacool extremities

Noncardiogenic pulmonary edemaabdominal, pelvic, and rectal examinations are important warm extremities

Clinical ManifestationsClinical Manifestations

DyspneaSuddenOrthopneaCyanotic (central)“air hunger”Tachypnea

CoughCopious sputumFrothyBlood tinged

Pink Frothy Sputum

Clinical ManifestationsClinical Manifestations

PulseTachycardia

Bounding

Breath SoundCrackles

Fine course

Engorged neck & hand veins

Clinical ManifestationsClinical Manifestations

Diaphoretic

Clammy

Anxiety

Confusion

Stupor

InvestigationInvestigation

X-rayPulse oximetry

Electrocardiography Pulmonary-Artery Catheterization Echocardiography

Laboratory TestingLaboratory Testing

Elevated troponin levels

Measurement of electrolytes, the serum osmolarity, and a toxicology screen ABG’s

PaO2 , hypoxia, metabolic acidosis

Serum amylase and lipase

TreatmentTreatment

Goal:

Remove fluid

oxygenation

O2

Mask

Non-rebreather

CPAP

Mech. Vent

PEEP

TreatmentTreatment

DiureticsLasix

Digitalis / Digoxin lanoxin Bronchodilators

Aminophylline

Morphine peripheral resistance pressure in pulmonary capillaries anxiety

Nursing managementNursing management

OxygenationIntubation/mechanical ventilation.I&O Fluid managementDiet

SodiumLow

PotassiumHigh

FluidsDecreased / restricted

Nursing managementNursing management

Position to promote circulation

HOB Pt upright with legs down

Provide psychological supportMonitor medications

1. Penurunan curah jantung yg b/d respons fisiologi gagal jantung payah, peningkatan frekuensi, dilatasi, hipertrofi atau peningkatan isi sekuncup.

2. Penurunan curah jantung yg b/d adanya kerusakan otot miokard akibat dari infark akut, perubahan struktur akut (ruptur otot papilaris, ruptur septal) atau penyakit katup.

3. Kerusakan pertukaran gas yg b/d kongesti paru, hipertensi pulmonal, penurunan perfusi perifer yg mengakibatkan asidosis laktat & penurunan curah jantung.

4. Kelebihan volume cairan yg b/d berkurangnya curah jantung, retensi cairan & natrium oleh ginjal, hipoperfusi ke jaringan perifer & hipertensi pulmonal.

Con’tCon’t5. Kelebihan volume cairan yg b/d berkurangnya curah

jantung, retensi cairan & natrium oleh ginjal, hipoperfusi ke jaringan perifer & hipertensi pulmonal.

6. Risiko tinggi intoleransi aktivitas yg b/d curah jantung rendah, ketidakmampuan utk memenuhi metabolisme otot rangka, kongesti pulmonal yg menimbulkan hipoksemia & dispnea/nutrisi buruk selama sakit kritis.

7. Risiko tinggi kurang pengetahuan yg b/d status penyakit, tindakan, obat2tan, komplikasi & perubahan gaya hidup.

8. Ansietas yg b/d penyakit kritis, takut kematian atau kecacatan, perubahan peran dlm lingkungan sosial, atau ketidakmampuan yg permanen.

SummarySummary

Acute Pulmonary Edema is life-threatening

Progressive assessment, Treatment & nursing management can improve outcome & survive of Acute Pulmonary Edema patients

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