Management of Pulmonary Edema 2014
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Transcript of Management of Pulmonary Edema 2014
Management of
pulmonary edemaDR ELLAHI BAKHSH
PGR PULMONOLOGY DEPTT
UNIT_C
FJGH QUETTA
OUTLINE
DEFINITION
PATHOPHYSIOLOGY
CLASSIFICATION
CAUSES
SIGN AND SYMTOMS
DIFFERENTIAL DIAGNOSIS
WORKUP
MANAGEMENT
Definition
Pulmonary Edema :
is a condition characterized by accumulation of excess fluid in
interstitium and alveoli of the lung as a result of an alteration in
one or more of starling forces.
Pathophysiology
Pulmonary edema can be caused by the following major
pathophysiologic mechanisms:
imbalance of starling force
-increase pulmonary capillary pressure (8-12mmHg)
-decrease plasma oncotic pressure (28mmHg)
-increase negative interstitial pressure
damage to alveolar- capillary barrier
lymphatic obstruction (10-20 mL/h)
Idiopathic (unknown) mechanism
Classification
Base on underlining cause
o Cardiogenic pulmonary edema
o Non-cardiogenic pulmonary edema
Cardiogenic pulmonary edema
Cardiogenic pulmonary edema :
is defined as a high pulmonary capillary hydrostatic pressure( as
estimated clinically from the PCWP )is responsible for abnormal
fluid accumulation in alveoli of the lung .
Noncardiogenic pulmonary
edema
Noncardiogenic pulmonary edema is caused by
various disorders in which factors other than
elevated pulmonary capillary pressure are
responsible for protein and fluid accumulation in
the alveoli.
Causes
Cardiogenic pulmonary edema Non cardiogenic pulmonary edema
(ARDS ) other name of NCPE
Cardiac disorders
Atrial outflow obstruction
LV systolic dysfunction
LV diastolic dysfunction
Dysrhythmias
LV hypertrophy and
cardiomyopathies
LV volume overload
Myocardial infarction
LV outflow obstruction
Direct injury to lungchest trauma
Pneumonia
Pulmonary embolism
Indirect injury to lungSepsis
Multiple transfusions
Cardiopulmonary bypass
Lung injury plus increased hydrostatic pressure
Neurogenic pulmonary edema
High altitude pulmonary edema
Reexpansion pulmonary edema
Features may differentiate CPE
from NCPE.
In CPE, a history of an acute cardiac event is usually present. Physical
examination shows an S3 gallop, jugular venous distention, and crackles
on auscultation.
Patients with NCPE have a warm periphery, a bounding pulse, and no
S3 gallop or jugular venous distention.
Definite differentiation is based on pulmonary capillary wedge
pressure (PCWP) measurements.
The PCWP is generally >18 mm Hg in CPE and < 18 mm Hg in NCPE .
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 ( 8000 ft) and who then engage in strenuous physical
exercise at that altitude, before they have become acclimatized.
Reversible (in less than 48 hours)
Presentation CPE
Clinical features of left heart failure. extreme breathlessness,
anxiety, and feelings of drowning.
Shortness of breath.
Orthopnea , and paroxysmal nocturnal dyspnea.
Cough, Pink frothy sputum
Presentation CPE
Tachypnea and tachycardia.
Hypertension
Cool extremities may indicate low cardiac output .
Auscultation reveals fine, crepitation or wheezes .
CVS findings ; S3 ,accentuation of pulmonic component of S2, jugular
venous distention…
Patients with (RV) failure may present with hepatomegaly, hepatojugular
reflux, and peripheral edema.
Change in mental status, caused by hypoxia or hypercapnia .
Workup CPE
Complete blood count .
Serum electrolyte .
(BUN) and creatinine .
Brain natriuretic peptide .
Arterial blood gas analysis .
Electrocardiography and Echocardiography.
Radiography and Ultrasonography .
PCWP can be measured with a pulmonary
arterial catheter (Swan-Ganz catheter) .
Differential diagnosis
Pumonary Edema Cariogenic Pulmonary edema
Acute Respiratory Distress Syndrome
AsthmaCardiogenic Shock
Chronic Obstructive Pulmonary Disease
Emphysema
Goodpasture Syndrome
Myocardial Infarction
Pneumocystis (carinii) jiroveci Pneumonia
Pneumonia, Bacterial
Pneumonia, Viral
Myocardial ischemia
PneumothoraxHigh-altitude pulmonary edema
Neurogenic pulmonary edema
Pulmonary embolism
Respiratory failure
Treatment CPE
Initial management
ABCs of resuscitation, that is, airway, breathing, and circulation.
Oxygen should be administered to all patients to keep oxygen saturation at greater than
90%.
Methods of oxygen delivery include the use of a face mask, (NPSV (which includes [BiPAP] and [CPAP]), and intubation and mechanical ventilation.
Medical treatment of CPE focuses on 3 main goals:
(1) reduction of pulmonary venous return (preload reduction),
(2) reduction of systemic vascular resistance (afterload reduction)
(3) inotropic support.
Ventilatory support (CPE)
Noninvasive pressure-support ventilation
NPSV maintains the patency of the fluid-filled alveoli and prevents them from collapsing
during exhalation.
NPSV improves pulmonary air exchange, and it increases intrathoracic pressure with
reduction in preload and afterload.
Two types of NPSV are CPAP and BiPAP.
In CPAP, a single airway pressure is maintained throughout all phases of the respiratory
cycle.
In BiPAP, high pressures can be applied during inspiration and low pressures during
expiration, increasing the patient's comfort.
Mechanical ventilation
In general, use endotracheal intubation and mechanical ventilation
when patients with CPE remain hypoxic despite maximal noninvasive
supplemental oxygenation, when patients have evidence of
impending respiratory failure or when patients are hemodynamically
unstable
Mechanical ventilation maximizes myocardial oxygen delivery and
ventilation
Preload Reduction (CPE )
Preload reduction decreases pulmonary capillary hydrostatic
pressure and reduces fluid transudation into the pulmonary
interstitium and alveoli.
Nitroglycerin : oral or I/v 10 -100 mcg/min
Diuretics :
Morphine sulfate
Afterload Reduction (CPE )
Afterload reduction increases cardiac output and improves renal
perfusion, which allows for diuresis in the patient with fluid overload.
ACE inhibitors : Enalapril 1.25mg I/v or captopril 25mg subligually
Angiotensin II receptor blockers
Nitroprusside for 3-4mcg/kg/min IV infusion:
Inotropic agents
Dobutamine
Dopamine
Intra-aortic balloon pumping (CPE )
The IABP is inserted percutaneously through the femoral artery to
descending aorta using a modified technique. Fluoroscopy may be used
for correct positioning of the balloon, and Helium, gas is used to inflate the
balloon.
The IABP decreases afterload as the pump deflates; during diastole the
pump inflates to improve coronary blood flow.
Ultrafiltration (CPE )
Ultrafiltration is a fluid removal procedure that is
particularly useful in patients with renal
dysfunction and expected diuretic resistance.
Noncardiogenic Pulmonary Edema
High-Altitude Pulmonary Edema Treatment
includes rest, administration of oxygen, and descent to a lower altitude.
If diagnosed early, recovery is rapid with a descent of only 500-1000 m.
A portable hyperbaric chamber or supplemental oxygen administration
immediately increases oxygen saturation and reduces pulmonary artery
pressure, heart rate, respiratory rate,
Nifedipine, by reducing pulmonary arterial pressure, may be effective in
treating HAPE .
Acetazolamide and dexamethasone have been shown to be effective
agents for prophylaxis against high-altitude illness.
Treatment of Noncardiogenic
Pulmonary Edema
Neurogenic Pulmonary Edema Treatment
Supplemental oxygen
Mechanical ventilation may be necessary, either noninvasive with a
face mask or via an endotracheal tube.
Pharmacological agents are not used routinely in the treatment of
neurogenic pulmonary edema.
But sometimes include alpha-adrenergic antagonists (eg,
phentolamine) and Beta-adrenergic agonists (eg, dobutamine,
dopamine, norepinephrine).
Reexpanison pulmonary edema
Reexpanison pulmonary edema is a rare but serious complication
of thoracentesis.
This case was unusual in that RPE developed on the side
contralateral to the lung that was drained.
If RPE occurs, the treatment is mostly supportive, including
supplemental oxygen, positive pressure ventilation, and diuresis.
However, if there is radiographic evidence of RPE but the patient is
asymptomatic, no treatment is necessary.
Complication
Respiratory failure
Cardiac arrest
Sudden Death secondary to cardiac arrhythmia
Prognosis
In a high-acuity setting, in-hospital death rates are as
high as 15-20%.
Myocardial infarction, associated hypotension, and a
history of frequent hospitalizations for CPE generally
increase the mortality risk.