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OBJECTIVES:
- Definition of Pulmonary Edema
- Causes of Pulmonary Edema
DEFENITION
Pulmonary edema is fluid accumulation in the lungs leads to impaired gas exchange and may cause respiratory failure. It is due to either failure of the heart to remove fluid from the lung circulation ("cardiogenic pulmonary edema") or a direct injury to the lung parenchyma ("noncardiogenic pulmonary edema").
CAUSES
A.
Cardiogenic
Severe Severe CHF Hypertension
B. o
Non-cardiogenic May occur after upper airway obstruction, intravenous fluid overload, neurogenic causes (seizures, head trauma, strangulation, electrocution).
Alveolar
Inhalation of toxic gases Pulmonary contusion, i.e., high-energy trauma Aspiration, e.g., gastric fluid or in case of drowning Multiple blood transfusions Infection
Other/unknown
Multitrauma, e.g., severe car accident Neurogenic, e.g., subarachnoid hemorrhage Certain types of medication
Upper airway obstruction, i.e. negative pressure pulmonary edema Arteriovenous malformation
Anxiety
Pale skin
Wheezing
Cyanosis
(bluish discoloration of the skin due to poor blood circulation , lack of O2)
CONT.
A classic sign of pulmonary edema is the production of pink frothy sputum. If left untreated, it can lead to coma and even death, in general, due to its main complication of hypoxia. Other symptoms:
Paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night). Orthopnea (inability breathlessness). to lie down flat due to
PATHOPHYSIOLOGY
left-sided congestive heart failure left ventricle can't eject blood increase pulmonary vein pressure Fluid accumulates initially in the basal regions of the lower lobes because hydrostatic pressure is greater in these sites . Histologically, the alveolar capillaries are engorged, and an intra-alveolar granular pink precipitate is seen. Alveolar microhemorrhages may be present.
CONT.
MICROVASCULAR
INJURY (INCREASE IN CAPILLARY PERMEABILITY)
6 PHASES
1- Injury reduce normal blood flow to the lungs platelets aggregate and release histamine (H), serotonin (S), and bradykinin (B).
2those substance - especially histamine - inflame and damage the alveolocapillary membrane, increase capillary permeability fluids shift into interstitial space.
CONT.
3capillary permeability increase proteins and fluids leak out increase interstitial osmotic pressure and causing pulmonary edema
4- decrease blood flow and fluids in the alveoli damage surfactant alveoli collapse, impeding gas exchange and decrease lung compliance.
CONT.
5- O2 cant cross the alveolocapillary membrane, but CO2 can and is lost with every exhalation O2 & CO2 level decrease in blood.
6- pulmonary edema worsens, inflamation leads to fibrosis, and gas exchange is further impeded.
MANAGMENT
It
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CONT.
1) Cardiogenic pulmonary edema : Due to left ventricular failure 2) Non cardiogenic pulmonary edema : Due to increased permeiability secondary to
sepsis
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CONT.
Treatment of pulmonary edema depends upon the specific etiology BUT Given the fact that this condition is very serious then : Number of measures must be applied immediately to support : 1) The circulation 2) Gas exchange 3) Lung mechanics
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with
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of oxygenation is essential to ensure a dequate oxygen delivery to the peripheral tissues including the heart . Oxygen is given by mask and start with high concentration to keep the Oxygen saturation above 90 %
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2]
Reduction of Preload :
For
most cases of pulmonary edema, the quantity of extravascular lung water is related to the intravascular volume status
N.B The ascending loop of Henle has active reabsorbtion of more than 35% of the filtered Na
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FRUSEMIDE
PHARMACOLOGIC CATEGORY: Diuretic, Loop DOSING: ADULTS I.M., I.V.: 20-40 mg/dose, may be repeated in 1-2 hours as needed
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FRUSEMIDE CONT.
Hemodynamic effects By reducing intravascular volume, diuresis will eventually lower central venous and pulmonary capillary wedge pressures.
the absence of symptomatic hypotension, intravenous, Nitroprusside may be considered as an addition to diuretic therapy for rapid improvement of congestive symptoms in patients admitted with Acute cardiogenic pulmonary edema 23
CONT.
B) Nitrates : are the most commonly used vasodilators.They reduce LV filling pressure primarily via venodilation . Options for nitrate therapy include the following: 1) Nitrglycerin ( short acting ) An initial dose of 5-10 g/min of intravenous nitroglycerin is commonly used Or Sublingual nitroglycerin .4 mg every 5 minutes 2) Isosorbide dinitrate ( long acting ) It has longer half-life compared to intravenous nitroglycerin
Both drugs act predominantly as venodilator and coronary vasodilator as well They are rapid in onset and effective We need to monitor the blood pressure .
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The digitalis glycosides show only a small Difference betwwen a therapeutics effective Dose and dose that are toxic or even fatal So .. These drugs have a low therapeutics index
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6]
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If atrial fbrilation is the cause for the pulmonary edema or if the ventricular rate is fast, then a drug to control the rate is recommonded :
1)short-acting IV formulations of such drugs (eg, Esmolol or Diltiazem) are often used. 2) Digoxin is also potentially useful in this setting.
The
AHA guidelines on ADHF recommend a low sodium diet (2 g daily) The AHA guidelines recommend fluid restriction (<2 L/day)
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RESOURCES
Harrison's Principles of Internal Medicine 17th ed. Katzungs Basic and Clinical Pharmacology, 10th ed. Lippincott pharmacology 3rd ed.
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ANY QUESTIONS ?
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