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2.1 Dr. J. Nugroho SP - JP - Edema Paru Akut
2.1 Dr. J. Nugroho SP - JP - Edema Paru Akut
PULMONARY EDEMA
Cardiogenic Shock
Right HF
PULMONARY EDEMA
Life-threatening
Require immediate treatment
Cardiac dysfunction
PATHOPHYSIOLOGY
Pathophysiologic mechanisms:
Imbalance of Starling forces - Ie, increased
pulmonary capillary pressure, decreased
plasma oncotic pressure, increased negative
interstitial pressure
Damage to the alveolar-capillary barrier
Lymphatic obstruction
Idiopathic (unknown) mechanism
MECHANISM OF
CARDIOGENIC PULMONARY EDEMA
The progression
Elevated LA pressure distention and opening of
small pulmonary vessels
Blood gas exchange does not deteriorate
Fluid and colloid shift into the lung interstitium
Lymphatic outflow removes the fluid
Filling interstitial space (can contain up to 500mL)
Alveolar flooding
Abnormalities in gas exchange
Vital capacity and respiratory volumes
Severe hypoxemia
DIAGNOSIS
History &
Physical
Examination
Clinical features of
left heart failure
Reflect evidence of
hypoxia and
increased
sympathetic tone
History
to determine the
exact cause
Laboratory
Studies
Complete blood
count
Electrolyte
Blood urea nitrogen
(BUN) and creatinine
Blood gas analysis
Electrocardio
graphy
LA enlargement and
LV hypertrophy
Chronic LV
dysfunction
Tachydysrhythmia or
bradydysrhythmia or
acute myocardial
ischemia or
infarction
Brain-type
natriuretic peptide
(BNP)
Radiography
Enlarged heart, Kerley lines, basilar edema,
pleural effusion (particularly bilateral and
symmetrical pleural effusions)
Echocardiography
Establish the etiology of pulmonary edema
Evaluate LV systolic and diastolic function, valvular
function, and pericardial disease.
Non-invasive hemodynamic parameters appropriate
therapy
DIFFERENTIAL DIAGNOSIS
Conditions to consider in the differential
diagnosis of CPE include the following :
Pneumothorax
Pulmonary embolism
Respiratory failure
Acute Respiratory Distress Syndrome
Asthma
Chronic Obstructive Pulmonary Disease
MANAGEMENT
Medical treatment
Reduction of
pulmonary
venous
return
(preload)
Main
Goal
Inotropic
support (in
some cases)
Reduction of
systemic
vascular
resistance
(afterload)
Vasodilators ( Nitroglycerin )
Preload reduction
Vasodilation effect lowers preload reduce
pulmonary congestion
Should be avoided : Systolic blood pressure
<110 mmHg
Diuretics
Loop diuretics : Furosemide
Opiates
Nesiritide
Reduce :
Left ventricular filling pressure
Pulmonary arterial pressure
Right atrial pressure
Systemic vascular resistance
Reduce levels of :
Renin, Aldosterone
Norepinephrine, and endothelin-1
Ventricular tachycardia
Inotropes
When :
Reduction in preload and afterload still has not
improved
Impaired systolic function
Perfusion disturbances and/or congestion
Dopamine
Cardiogenic shock
Low dose
dopaminergic
receptors
increasing diuresis
Moderate dose
-receptors
Cardiac
contractility and
Heart rate
High dose
-receptors
Vasoconstriction
(increased
afterload), Blood
pressure
Dobutamine
Hypotension due to
decreased
contractility
Positive chronotropic
& inotropic
Moderate or severe
hypotension
should be avoided
Norepine
phrine
-receptors
vasoconstriction
Use in severe
hypotension
Combination with
dobutamine
improve
hemodynamic
Ultrafiltration
Ultrafiltration should be considered in acute heart failure with volume overload who
do not respond to high doses of diuretics or in patients with impaired renal function
Ventilatory Support
Mechanical ventilation
When :
Remain hypoxic with noninvasive supplemental
oxygenation
Impending respiratory failure
Hemodynamically unstable
Summary
Common cause of acute heart failure, life-threatening
and require immediate action
Defined as pulmonary edema due to increased capillary
hydrostatic pressure secondary to pulmonary venous
pressure
High mortality rate
Acute myocardial infarction, hypotension and a history
of frequent acute attacks increase the risk of mortality
BNP and echocardiography Important diagnostic tools
Therapeutic goal :
Improve the patient's symptoms
Improves fluid status
Identification of causal factors