PULMONARY EDEMA

Objectives:

- Definition of Pulmonary Edema

- Causes of Pulmonary Edema

- Sign & symptoms of Pulmonary Edema

- Pathophysiology of Pulmonary Edema

- Management 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 heart attack with left ventricular failure

Severe arrhythmias (tachycardia/ bradycardia)

CHF

Hypertension

B. Non-cardiogenic
o 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
 Sign & Symptoms
Difficulty, Shortness of breathing
Coughing up blood
Excessive sweating
Anxiety
Pale skin
Wheezing
Cyanosis
(bluish discoloration of the skin due to poor blood circulation , lack of O2)
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 to lie down flat due to
breathlessness).
 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.
 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).

2- those substance - especially histamine

- inflame and damage the alveolocapillary
membrane, increase capillary
permeability fluids shift into interstitial
space.
 3- capillary 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.
 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
 Treatment of Pulmonary Edema, Introduction

ItIs an Acute Life-Threatening

Condition therefore Therapeutic
Should be Applied Immediately

14
 Treatment of Pulmonary Edema, Introduction

Pulmonary edema is of different types :

1) Cardiogenic pulmonary edema : Due to left

ventricular failure

2) Non cardiogenic pulmonary edema : Due to

increased permeiability secondary to sepsis

15
 Treatment of Pulmonary Edema, Introduction

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

16
 Treatment of Acute Pulmonary Edema
1] Support of Oxygenation and Ventilation for
a
patient with acute cardiogenic pulmonary
edema generally have an identifiable
cause of acute left venticular failure Such
as
A) Arrhythmia
B) Ischemia/ infarction
C) Myocardial decompensation
These can be treated rapidly with
improvement in Gas exchange

17
 Treatment of Acute Pulmonary Edema

1] Oxygen therapy :
Support 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 %

18
 TREATMENT OF ACUTE PULMONARY EDEMA

2] Reduction of Preload :
Formost cases of pulmonary edema, the quantity of
extravascular lung water is related to the intravascular
volume status

How To Reduce The Preload

On The Heart?

19
 Treatment of Acute Pulmonary Edema
A) Diuretics :
The loop diuretics is preferred (Why?)
Examples of loop diuretics:

1) Frusemide
2) Bumetanide
3) Torsemide

N.B
The ascending loop of Henle has active reabsorbtion of
more than 35% of the filtered Na

20
 Frusemide
PHARMACOLOGIC CATEGORY:
Diuretic, Loop

DOSING: ADULTS
I.M., I.V.: 20-40 mg/dose, may be repeated in 1-2 hours as
needed

USE Management of pulmonary edema associated with

congestive heart failure

21
 Frusemide
Hemodynamic effects By reducing
intravascular volume, diuresis will eventually
lower central venous and pulmonary capillary
wedge pressures.

Adverse effects :
a. Hyperuricemia
b. Acute hypovolemia
c. potassium depletion
e. hypomagnesemia

22
 Treatment of Acute Pulmonary Edema

B) Vasodilator therapy :
Patients with acute cardiogenic pulmonary
edema are often treated with vasodilators in
an attempt to reduce preload and pulmonary
capillary wedge pressure

Inthe 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
 Treatment of Acute Pulmonary Edema
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 .

24
 Treatment of Acute Pulmonary Edema

4] Angiotensin-Converting Enzyme
Inhibitors:
These drugs reduce both the
afterload as well as the preload.
They work by inhibiting angiotensin
II production which is a potent
vasoconstrictor and this leads to
vasodilatation
example :
Captopril
25
 Treatment of Acute Pulmonary Edema

5] Digitalis Glycosides :
It has positive inotropic action ..(rarely used
nowadays)
It is useful for control of ventricular rate in
patient with rapid atrial fibrillation .

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

26
 Treatment of Acute Pulmonary Edema

6] Arrhythmia management Both supraventricular and

ventricular arrhythmias can occur in association with
pulmonary edema.
Atrial fibrillation Atrial fibrillation (AF) is a common
arrhythmia, particularly in patients with underlying
heart disease. Among patients with both HF and AF,
there are several possible relationships :
Acute HF can precipitate AF due to increases in left atrial
pressure and wall stress .
AF can cause acute HF, particularly if the ventricular
response is rapid

27
 Treatment of Acute Pulmonary Edema
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.

3) Amiodarone can be considered.

28
 Treatment of Acute Pulmonary Edema

8] Sodium and Water Restriction :

Dietary sodium restriction is an

important component of therapy to
restore euvolemia

The AHA guidelines on ADHF

recommend a low sodium diet (2 g
daily)
The AHA guidelines recommend fluid
restriction (<2 L/day)
29
 Resources

Harrison's Principles of Internal Medicine 17th ed.

Katzungs Basic and Clinical Pharmacology, 10th ed.
Lippincott pharmacology 3rd ed.

30
THANK YOU !!