Chap 20 Flashcards
Pulmonary edema results from
excessive movement of fluid from the pulmonary vascular system to the extravascular system and air spaces of the lungs. The abundance of fluid in the interstitial spaces causes the lymphatic vessels to widen and the lymph flow to increase
Fluid first seeps into
the perivascular and peribronchial interstitial spaces, depending on the degree of severity, fluid may progresively move into the alveoli, bronchioles, and bronchi. As a consequence of this fluid movement, the alveolar walls and interstitial spaces swell
As the swelling intensifies,
the alveolar surface tension increases and causes alveolar shrinkage and atelectasis. Moreover, much of the fluid that accumulates in the tracheobronchial tree is churned into a frothy white (sometimes blood-tinged or pink) sputum as a result of air moving in and out of the lungs
Pulmonary edema produces a what disorder
restrictive pulmonary disorder
The major pathologic or structural changes of the lungs associated with pulmonary edema are as follows
- Interstitial edema, including fluid engorgement of the perivascular and peribronchial spaces and the alveolar wall interstitium
- Alveolar flooding
- Increased surface tension of alveolar fluids
- Alveolar shrinkage and atelectasis
- Frothy white (or pink) secretions throughout the tracheobronchial tree
Most common cause of cardiac pulmonary edema is
Left sided heart failure- commonly called congestive heart failure
Heart failure is most common in people over age of
65 years
Cardiac pulmonary edema occurs when the
left ventricle is unable to pump out a sufficient amount of blood during each ventricular contracting. The ability can be determined by means of the left ventricular ejection fraction (LVEF)- a noninvasive imaging procedure Echocardiogram (systolic activity)
Diastolic function
Poor ventricular function caused by an increased ventricular stiffness or impaired myocardial relaxation
Ordinarily hydrostatic pressure of about what tends to move fluid out of the pulmonary capillaries into the interstitial space
10-15mmHg, normally offset by colloid osmotic forces of about 25-30 mmHg and tend to keep fluid in pulmonary capillaries
Onconotic pressure
Colloid osmotic pressure and is produced by albumin and gobulin in the blood
When the hydrostatic pressure within the pulmonary capillaries rises to more than 25-30mmHg, the onconic pressure
loses its holding force over the fluid within the pulmonary capillaries. Consequently fluid starts to spill into the interstitial and air spaces of the lungs
Clinical side effects of Left ventricular failure
Activity tolerance, weight gain, anxiety, delirium, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, fatigue,cardiac arrhythmia, adventitious breath sounds.
Result of hypoperfusion
major organ failure of the brain and kidney
Pulmonary edema may develop as a result of
increased capillary permeability stemming from infectious, inflammatory, and other processes.
Causes of increased capillary permeability
Alveolar hypoxia, ARDS, Pulmonary infection-pneumonia, Therapeutic radiation of the lungs, acute head injury
Should the normal lymphatic drainage of the lungs be decreased,
Intravascular and extravascular fluid begins to pool, and pulmonary, and pulmonary edema ensues. Lymphatic drainage may be slowed bc of obliteration or distortion of lymphatic be slowed because of obliteration or distortion of lymphatic vessels. Because the lymphatic vessels empty into systemic veins, increased systemic venous pressure may slow lymphatic drainage.
Reduced intrapleural pressure may cause
pulmonary edema
Decreased oncotic pressure may be caused by
- Overtransfusion and or rapid transfusion of intravenous fluids
- Uremia
- hypoproteinemia (malnutrition)
- Acute nephritis
- Polyarteritis nodosa
The treatment for pulmonary edema is based on
- the cause-that is noncardiogenic versus cardiogenic pulmonary edema 2. severity
- Largely supportive and aimed at ensuring adequate ventilation and oxygenation
- No specific treatments, noncardiogenic pulmonary edema caused by severe infection is treted with antibiotics
- High altitude is treated with lower elevation or by positive pressure ventilation
Therapeutic interventions to address the pts circulationry system has the following three main goals
Reduction of pulmonary venous return(preload reduction)
Reduction of systemic vascular resistance (afterload reduction)
Inotropic support
Reduction of the preload
decreases pulmonary capillary hydrostatic pressure and reduces fluid transudation into the pulmonary interstitium and alveoli
Reduction of the afterload
Increases cardiac output and improves renal perfusion, which in turn allows for diuresis in the pt with fluid overload
Inotropic agents are used to treat
hypotension or signs of organ hypoperfusion