2. Pulmonary edema
• Is a broad descriptive term and is usually defined
as an abnormal accumulation of fluid in the
extravascular compartments of the lung.
(Alveoli)
3. Pathology
• Four main categories on the basis of pathophysiology which
include:
• increased hydrostatic pressure edema
• two pathophysiological and radiological phases are recognized in
the development of pressure edema
• interstitial edema
• alveolar flooding or alveolar edema
• these phases are virtually identical for left heart failure and fluid
overload
• permeability edema with diffuse alveolar damage (DAD)
• permeability edema without diffuse alveolar damage
• mixed edema due to simultaneous increased hydrostatic
pressure and permeability changes
5. Signs and Symptoms
• Difficulty breathing (acute dyspnea) or extreme shortness of
breath that worsens with activity or when lying down
• A feeling of suffocating or drowning that worsens when lying
down
• A cough that produces frothy sputum that may have blood in
it
• A rapid, irregular heartbeat (palpitations)
• Anxiety, restlessness or a feeling that something bad is about
to happen
• Cold, clammy skin
• Wheezing or gasping for breath
• orthopnea
• paroxysmal nocturnal dyspnea (PND)
7. Echocardiography
• Echocardiography:
• Assists in the diagnosis of left ventricular systolic dysfunction
and valvular dysfunction. Through modalities, including tissue
Doppler imaging of the mitral annulus, the presence and
degree of diastolic dysfunction can be assessed
• Pulmonary Artery Catheterization:
• Often considered a gold standard in the determination of the
etiology of pulmonary edema, it is an invasive test that helps
monitor systemic vascular resistance, cardiac output, and
filling pressures. An elevated pulmonary artery occlusion
pressure over 18 mm Hg is helpful in the determination of
cardiogenic pulmonary edema
8. Radiographic features
• Plain radiograph
1. upper lobe pulmonary venous diversion (stag's antler sign)
2. increased cardiothoracic ratio/cardiac silhouette size: useful for
assessing for an underlying cardiogenic cause or association
3. features of pulmonary interstitial edema:
• peribronchial cuffing and perihilar haze
• septal (Kerley) lines
• thickening of interlobar fissures
4. features of pulmonary alveolar edema:
• air space opacification classically in a batwing distribution
• may have air bronchograms
5. pleural effusions and fluid in interlobar fissures (including
'vanishing' pulmonary pseudotumor)
ABCDE
26. Differential diagnosis
• Immersion pulmonary edema from drowning
• neurogenic pulmonary edema from stroke
• head trauma
• medication hypersensitivities or toxic ingestions
• blood transfusions leading to transfusion-related acute lung
injury (TRALI)
• liver disease
• pulmonary embolism or infarct
• Uremia
27. Treatment
• Treatment of underlying cause
• Oxygen
• IV diuretics
• Nitrates
• IV inotropes
• Ventilatory assistance
• BIPAP
• Conventional Mechanical Ventilation
28. • Propped up position (Semi-sitting position)
• Airway assessment and continuous pulse oximetry to assure
adequate oxygenation and ventilation
• Supplemental oxygen and ventilatory support (noninvasive
ventilation [NIV) or intubation) as indicated.
• Non invasive ventilation(BIPAP)
• Morphine Given in 2 to 4 mg IV boluses, morphine is a transient
venodilator that reduces preload while relieving dyspnea and
anxiety. These effects can diminish stress, catecholamine levels,
tachycardia, and ventricular afterload in patients with pulmonary
edema and systemic hypertension. However, some registry trials
showed increased mortality with use of morphine.
• Diuretics:IV Furosemide 40-80 mg IV bolus if BP is stable,
infusion in hypotension, repeat if needed
29. • Inotropes (Dopamine, Dobutamine) in hypotension
• Early vasodilator therapy like NTG (for severe hypertension,
acute mitral regurgitation, or acute aortic regurgitation);
• Sublingual Nitroglycerine and IV NTG / Nitroprusside (if BP is
high)
• Nitroglycerin - It can produce more venous than arterial
vasodilation.
• Nitroprusside — In contrast to nitroglycerin, nitroprusside can
produce balanced arterial and venous dilation. Thus, while it
can be used to decrease LV filling pressures, it will cause a
concomitant decrease in systemic vascular resistance
30.
31. Treatment of Pulmonary edema
• Re-expansion pulmonary edema can develop after removal of
longstanding pleural space air or fluid.
• These patients may develop hypotension or oliguria with pulmonary
edema resulting from rapid fluid shifts into the lung.
• Diuretics and preload reduction are contraindicated, and intravascular
volume repletion often is needed while supporting oxygenation and gas
exchange.
• High-altitude pulmonary edema often can be prevented by use
of dexamethasone, calcium channel–blocking drugs, or long-acting
inhaled β2-adrenergic agonists.
• Treatment includes descent from
altitude, bed rest, oxygen, and, if feasible, inhaled NO; nifedipine
may also be effective.
• For pulmonary edema resulting from upper airway obstruction,
recognition of the obstructing cause is key because treatment then
is to relieve or bypass the obstruction