Acute Pulmonary Edema

Purwoko Sugeng H.

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

ETIOLOGI
Cardiogenic pulmonary edema (also termed hydrostatic or hemodynamic edema) Noncardiogenic pulmonary edema (also known as increased-permeability pulmonary edema, acute lung injury, or acute respiratory distress syndrome) Difficult to distinguish because of their similar clinical manifestations

Cardiogenic Pulmonary Edema -- Causes:

Left ventricular failure Volume overload Mechanical obstruction of left outflow tract e.g. Mitral stenosis Aortic valvular diseases & also in congestive failure and hypertension AMI cardiomiopathy

Causes of Non-cardiac Pul. Edema

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

PATHOPHYSIOLOGY
Microvascular 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
Microvascular 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
Microvascular 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

History

Interstitial edema causes dyspnea and tachypnea Alveolar flooding leads to arterial hypoxemia Cough and expectoration of frothy edema fluid

History
Cardiogenic pulmonary edema
ischemia with or without myocardial infarction exacerbation of chronic systolic or diastolic heart failure, and dysfunction of the mitral or aortic valve paroxysmal nocturnal dyspnea or orthopnea

Noncardiogenic pulmonary edema

pneumonia sepsis aspiration of gastric contents major trauma associated with the administration of multiple blood-product transfusions

Physical 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 edema cool extremities

Noncardiogenic pulmonary edema

abdominal, pelvic, and rectal examinations are important warm extremities

Clinical Manifestations
Dyspnea
Sudden Orthopnea Cyanotic (central) air hunger Tachypnea

Cough
Copious sputum Frothy Blood tinged

Pink Frothy Sputum

Clinical Manifestations
Pulse
Tachycardia Bounding

Breath Sound
Crackles
Fine course

Engorged neck & hand veins

Clinical Manifestations
Diaphoretic Clammy Anxiety Confusion Stupor

Investigation
X-ray Pulse oximetry i Electrocardiography Pulmonary-Artery Catheterization Echocardiography

Laboratory Testing
Elevated troponin levels Measurement of electrolytes, the serum osmolarity, and a toxicology screen ABGs
PaO2 i, hypoxia, metabolic acidosis

Serum amylase and lipase

Treatment
Goal: Remove fluid h oxygenation O2 Mask Non-rebreather CPAP Mech. Vent PEEP

Treatment
Diuretics
Lasix

Digitalis / Digoxin lanoxin Bronchodilators

Aminophylline

Morphine
i peripheral resistance i pressure in pulmonary capillaries i anxiety

Nursing management
Oxygenation Intubation/mechanical ventilation. I&O Fluid management Diet Sodium
Low

Potassium
High

Fluids
Decreased / restricted

Nursing management
Position to promote circulation
HOB h Pt upright with legs down

Provide psychological support

Monitor medications

1. 2. 3. 4.

Penurunan curah jantung yg b/d respons fisiologi gagal jantung payah, peningkatan frekuensi, dilatasi, hipertrofi atau peningkatan isi sekuncup. 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. Kerusakan pertukaran gas yg b/d kongesti paru, hipertensi pulmonal, penurunan perfusi perifer yg mengakibatkan asidosis laktat & penurunan curah jantung. Kelebihan volume cairan yg b/d berkurangnya curah jantung, retensi cairan & natrium oleh ginjal, hipoperfusi ke jaringan perifer & hipertensi pulmonal.

Cont
5. 6.
Kelebihan volume cairan yg b/d berkurangnya curah jantung, retensi cairan & natrium oleh ginjal, hipoperfusi ke jaringan perifer & hipertensi pulmonal. 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. Risiko tinggi kurang pengetahuan yg b/d status penyakit, tindakan, obat2tan, komplikasi & perubahan gaya hidup. Ansietas yg b/d penyakit kritis, takut kematian atau kecacatan, perubahan peran dlm lingkungan sosial, atau ketidakmampuan yg permanen.

7. 8.

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

Thanks You