Pulmonary Edema

a true lifethreatening emergency

What is Edema?
Is defined as an abnormal increase in interstitial fluid within a tissue

DEFINITION
Pulmonary edema is defined as abnormal accumulation of fluid in the interstitial spaces surrounding the alveoli and/or alveolar space which leads to difficulty in breathing

Acute life threatening situation, alveoli filled with serosanguineous fluid. Most common cause is Acute LVF secondary to CAD

This results from malfunctioning of the heart.

Etiology

Etiology
Cardiogenic primary cause
Increased hydrostatic pressure

Decreased oncotic pressure:

Nephroticsyndrome, hypoproteinemia Lymphatic obstruction

 Causes usually divided into

hydrostatic and increased capillary permeability, but both

mechanisms can occur in the same patient!

Oncotic pressure, or colloid osmotic pressure

A form of osmotic pressure exerted by proteins in a blood vessel's plasma (blood/liquid) that usually tends to pull water into the circulatory system. It is the opposing force to hydrostatic pressure.

Etiology
Damage to the tissue or Inadequate functioning of the heart or circulatory system.

LVF :The backup of blood into the pulmonary vasculature resulting from inadequate left ventricular function causes an increased microvascular pressure, and fluid begins to leak into the interstitial space and the alveoli. Hypervolemia :sudden increase in the intravascular pressure
in the lung

Patient Who Has Undergone Pneumonectomy: when one lung has been removed, all the
cardiac output then goes to the remaining lung

 Re-expansion Pulmonary Edema:

This may be due to a rapid reinflation of the lung after removal of air from a pneumothorax or evacuation of fluid from a large pleural effusion.

TYPES OF PULMONARY EDEMA :

Cardiogenic pulmonary edema Noncardiogenic pulmonary edema

1. Cardiogenic PE
Pulmonary edema is either due to

Causes:
Congestive heart failure Severe heart attack with left ventricular failure Severe arrhythmias (tachycardi a/fast heartbeat or bradycardia /slow heartbeat) Hypertensive crisis Pericardial effusion with tamponade Fluid overload, e.g., from kidney failure

direct damage to the cardiac tissue or a result of inadequate functioning of the heart or circulatory system

2. Non-cardiogenic PE
Defined as the

Causes:

radiographic evidence of alveolar fluid accumulation without hemodynamic evidence to suggest a cardiogenic etiology .

a. Alveolar May occur after upper airway

obstruction (Large negative intrathoracic and transpulmonary pressure. )

Toxic gases inhalation Severe Infections

Aspiration, e.g., gastric fluid or in case of drowning Reexpansion, i.e. post pneumonectomy or large volume thoracentesis lung transplantation

2. NON-CARDIOGENIC PE CTND..

b) Other/unknown Multitrauma, e.g., severe car accident Neurogenic causes e.g., subarachnoid hemorrhage (seizures, head trauma) Arteriovenous malformation Certain types of medication intravenous fluid overload, Multiple blood transfusions

PATHOPHYSIOLOGY
Normally fluids moves into the interstitial space at the end of capillaries as a result of hydrostatic pressure in the vessels, and returns to the venous end of the capillaries due to the oncotic pressure and increase in interstitial hydrostatic pressure

Pathophysiological Mechanisms
Imbalance of Starling forces
-increased pulmonary capillary pressure / hydrostatic pressure -decreased plasma oncotic pressure -increased negative interstitial pressure

Damage to Alveolar/Capillary

barrier Lymphatic obstruction/dysfunction

Cardiogenic Pulmonary Edema

increased pulmonary venous pressure / hydrostatic pressure
secondary to left ventricular failure increased pulmonary capillary pressure secondary to increased pulmonary arterial pressure

 Left sided heart failure decrease pumping ability to the systemic circulation Inc. in venous pressure congestion and accumulation of blood in the pulmonary area fluid leaks out of the intravascular space to the interstitium

 Fluid accumulates in the interstitium

Continual filtration overwhelms lymphatics Disrupts alveolar membrane

Transudation- Alveolar lumen is filled with

transudate (pale-eosinophilic, finely granular), a liquid which replaces the air.
Effects: Leads to hypoxemia
Decreases vital capacity Causes abnormalities in gas exchange

Elevated left atrial pressure

distention and opening of small pulmonary vessels

The interstitial space can contain up to 500 mL of fluid. With further accumulations, the fluid crosses the alveolar epithelium in to the alveoli,

HYPOXEMIA BECOMES MORE SEVERE

Non-cardiogenic Pulmonary Edema

Decreased plasma oncotic pressure Increased negativity of interstitial pressure Altered alveolar-capillary membrance permeability(ARDS) lymphatic insufficiency others: high-altitude, neurogenic, narcotic overdose

SIGNS AND SYMPTOMS

A sudden onset of extreme breathlessness,

anxiety, and feelings of drowning.

Patients may be sitting upright, they may demonstrate air hunger, and they may become agitated and confused. Cough: Pink, frothy sputum (blood ) Excessive sweating Pale skin If left untreated, it can lead to coma and even death Patients with symptoms of gradual onset (eg, over 24 h) often report dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea Nocturia Ankle edema

Diagnostic Findings
Physical examination auscultation-crackles, wheezes S3 heart sounds Blood tests Blood count : severe anemia and may suggest sepsis or infection if a markedly elevated WBC count BUN and creatinine determinations

The chest x-ray- shows

whiteouts: distinguishing CPE from other pulmonary causes

 ABG Hemodynamic monitoring: PAWP Pulse oxymeter A bedside echocardiogram :

MEDICAL MANAGEMENT
Correction of hypoxemia Reduction in preload Reduction of afterload Enhance contractility Support of perfusion

Correct hypoxemia
Oxygen therapy
- at high FiO2 level: O2 to keep SpO2 > 90%

Noninvasive Positive Pressure Ventilation(NPPV) In case of persistent hypoxemia, acidosis or altered mental status, intubation and mechanical ventilation may become necessary

NPSV= noninvasive pressure support ventilation In NPSV, the patient breathes

filled alveoli and prevents them from collapsing during exhalation.

through a face mask against a continuous flow of positive airway pressure. NPSV maintains the patency of the fluid-

As a result, the patient saves the energy spent trying to reopen collapsed alveoli. NPSV improves pulmonary air exchange, and it increases

intrathoracic pressure with reduction in preload and afterload.

Noninvasive Pressure Support Ventilation

NPPV (contd)
Two methods:
BiPAP (Bilevel Positive Airway Pressure)
CPAP (Continuous Positive Airway Pressure)

 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.

CPAP
Delivered by nasal or face mask Pt. breathes through mask against a
continuous positive a/w pressure CPAP flow generators develop a constant, controllable pressure to keep your upper airway open so that you can breath normall Can be delivered by either volume or pressure controlled ventilator Delivers set pressure with each breath, maintained throughout the respiratory cycle

CPAP (contd)
Mechanism:
expiration)

Incresaes FRC( Vol of air remaining in lungs at end of

Prevents alveolar collapse during exhalation by
maintaining a positive intra-alveolar pressure Increases gas exchange 2 to increased alveolar ventilation

Increases intrathoracic pressure, reducing

preload/afterload and improving cardiac output

CPAP (contd)
Benefits/Advantages of CPAP
CPAP reduces work of breathing by keeping the wet alveoli open If the alveoli are open at the end of expiration, energy is not consumed on the next inhalation Work of breathing is reduced relieving respiratory muscle fatigue

Benefits/Advantages of CPAP
A higher alveoli pressure will result in a stoppage of fluid movement into the alveoli Increase in airway pressure results in improved gas exchange

2; REDUCTION IN PRELOAD
reduction of pulmonary venous return

Preload reduction decreases pulmonary

capillary hydrostatic pressure and reduces fluid transudation into the pulmonary interstitium and alveoli.

Reduce preload ctd.

Diuretics
Loop diuretics are presumed to decrease preload through 2 mechanisms: diuresis and direct vasoactivity (venodilation).

Nitrates
Nitroglycerin (NTG) is the most effective, predictable, and rapid-acting medication available for preload reduction. Venous dilation result in peripheral pooling of blood, dec. venous return and thus preload. IV NTG can be started with 10 mcg/min and then rapidly uptitrated to >100 mcg/min. The other alternative is NTG given as 3-mg IV boluses every 5 minutes.

3. REDUCE AFTER LOAD

Reduced systemic vascular resistance increases cardiac output and improves renal perfusion, allowing for diuresis. Antihypertensive agents ACE inhibitors
Potent vasodilator that lowers aldosterone secretion. Enalapril 1.25 mg IV or captopril 25 mg given sublingually

Catecholamines
These agents produce vasodilation and increase inotropic state, increased cardiac output Dobutamine, Dopamine

Morphines to reduce anxiety from the dyspnea

Nitroprusside (Nitropress) Potent direct smooth-musclerelaxing agent that primarily reduces afterload but can mildly reduce preload. Improves cardiac output but can precipitously decrease BP.

4. ENHANCE CONTRACTILITY
DIGOXIN

INOTROPES

5. SUPPORT PERFUSION
IABP decreases afterload as the pump deflates, and it inflates during diastole to improve coronary blood flow. The intra-aortic balloon pump is inserted percutaneously through the femoral artery. The distal end of the pump is placed just distal to the origin of the left subclavian artery. Helium, a lowdensity gas with minimal water solubility, is used to inflate the balloon. Proper timing of counterpulsation is necessary for maximum hemodynamic support. Inflation of the balloon should occur in early diastole, just after the aortic valve closes. Balloon deflation should occur in early systole, just before the aortic valve opens.

NURSING DIAGNOSIS Impaired Gas Exchange related to excess fluid in the lungs Anxiety related to sensation of suffocation and fear.

 Monitor oxymetry and report the findings of <92% Monitor ABG results for presence of hypoxemia(decrease PaO2) and hypercapnia(Increase PcO2) Assess for signs of hypoxia: restlessness, confusion, headache. Monitor ECG for dysrrhythmia development that may be related to hypoxemia, acid-base imbalance, or ventricular irritability. Closely monitor I/O chart Record weight daily and report if steady gaining. Monitor vital signs every 15 to 30 minutes or more often as indicated.

ASSESSMENT

ASSESSMENT CTD.
Assess the patients condition frequently Auscultate the lung fields for breath sounds and be alert for crackles(Rales) Watch for complications of treatment such as electrolyte depletion. Be alert for signs of increasing respiratory distress Assess for edema especially in dependent areas such as the ankles and sacrum.

Initial Nursing Management

Supplementary oxygen with face mask Elevate the head side or keep in sitting posture Monitor Vital Signs Cardiac monitoring ECG Pulse oxymetry I/v line Catheterization

 Help the patient relax to promote oxygenation. Place the patient in high Fowlers position to enhance lung expansion. Administer oxygen as ordered. Carefully record the time morphine is given and the amount administered. Kept ready the emergency equipments (Airway, Ambu bag, Intubation tray) Provide frequent mouth care to reduce dryness of mucous membrane. Keep environment calm and quiet

NURSING INTERVENTION

Nursing Management
Assisting with administration of oxygen and intubation Mechanical ventilation if respiratory failure occurs. Administers medications (ie, morphine, vasodilators, inotropic medications, preload and afterload agents) as prescribed Monitors the patients response.

Outcome Criteria
RR 12 to 20 breaths/min :Eupnea Lungs clear to auscultation pH 7.35 to 7.45: Pao2 80 to 100 mm Hg: Paco2 35 to 45 mm Hg: O2 sat > 95% Appears calm; rests comfortably