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
Preload reducers include
Nitroglycerin, Loop diuretics, Morphine sulfate
Nitroglycerin
Very effective, predictable, and rapid acting medication for preload
Loop diuretics
(Foresmide) Considered a cornerstone in the tx of cardiogenic pulmonary edema. Presumed to decrease preload through diuresis and direct vasodilation
Morphine sulfate
may be used in some cases to reduce preload. Adverse effects (nausea, vomiting or resp depression) may outweigh the potential benefit
Reduced systemic vascular resistance
increases cardiac output and improves renal perfusion, allowing for diuresis
Afterload reducers include
Dobutamine, Dopamine, Norephinephrine, Milrinone
Dobutamine
synthetic catecholamine that mainly has beta1 receptor activity, but also has some beta2- receptor and alpha receptor activity. Commonly used for pts with mild hypotension (systolic pressure 90-100)
Dopamine
naturally occuring catecholamine that acts as a precursor to norepinephrine.
Hemodynamic effect is dose dependent
Low dose is associated with dilation in renal and splanchnic vasculature , enhancing diuresis.
Moderate dose enhances cardiac contractility and heart rate.
A high dose increases afterload due to peripheral vasoconstriction.
GENERALLY RESERved FOR PTS WITH MODERATE HYPOTENSION (systolic 70-90)
Norepinephrine
Naturally occuring catecholamine with potent alpha receptor and mild beat receptor activity.
Stimulates beta1 adrenergic and alpha1 adrenergic receptors, increasing myocardial contractility, HR and vasoconstriction.
It increases BP and afterload. Is generally reserved for pts with SEVERE HYPOTENSION (<70 systolic)
Antidysrhythmic Agents
such as drugs to control bradycardia
Albumin or mannitol
sometimes administered to increase the pts oncotic pressure in an effort to offset the increased hydrostatic forces of cardiogenic pulmonary edema, if pts osmotic pressure is extremely low
Which of the following is an afterload reducer
Nitroprusside
What is the normal hydrostatic pressure in the pulmonary capillaries
10-15 mmHg
The normal oncotic pressure of the blood
25-30mmHg
Which of the following causes cardiogenic pulmonary edema?
Excessive fluid administration
Left ventricle failure
Mitral valve disease
Pulmonary embolus
As a result of pulmonary edema the pts
RV is decreased
FRC is Decreased
VC is decreased
TLC is decreased
LVEF norm
55-70%
Pneumonia or pneumonitis with consolidation is the result of an
inflammatory process that primarily effects the gas exchange area of the lung.
Effusion
process of fluid transfer.
Surface phagocytosis
Polymorphonuclear leukocytes move into the infected area to engulf and kill invading bacteria on the alveolar walls
When alveoli become filled with fluid, RBCs, polymorphonuclear leukocytes and macrophages the lungs are said to be
consolidated
Atelectasis is often associated with what kind of pneumonia
Aspiration pneumonia
Major pathologic or structural changes associated with pneumonia are
inflammation of the alveoli, alveoli consolidation, atelectasis
Causes of pneumonia include
bacteria, viruses, fungi, protozoa, parasites, TB, anerobic organisms, aspiration, and the inhalation of irritating chemicals such as chorine
Pneumonia is an ___ disease because its symptoms vary greatly
insidious
Bronchopneumonia
is characterized by a patchy pattern of infection that is limited to the segmental bronchi and surrounding lung parenchyma.
Usually involves both lungs and is seen more often in the lower lobe of the lung
Lobar pneumonia
is a widespread or diffuse alveolar inflammation and consolidation. Typically the end result of a severe or long term bronchopneumonia in which the infection has spread from one lung segment to another until the entire lung lobe is involved
Interstitial pneumonia
is usually diffuse and often bilateral inflammation that primarily involves the alveolar septa and interstitial space.
Mycoplasma pneumonia
cause interstitial pneumonias. Causing only minor permanent alveolar damage and usually resolve without consequences
When both lungs are involved the condition is called
double pneumonia or “walking pneumonia” often used to describe a mild case of pneumonia
CAP
pneumonia acquired from normal social contact
Streptococcal Pneumonia
accounts for 80% of all the bacterial pneumonias.
Gram positive, nonmotile coccus that is found singly, in pairs and in short chains.
Streptococci Pneumonia are generally transmitted by
aerosol from a cough or sneeze of an infected individual . Commonly cultured from the sputum of patients having an acute exacerbation of chronic bronchitis
Staphylococcal Pneumonia 2 main groups
- Staphylococcus aereus-“staph infections”
2. Stephylococcus albus and epidermidis -normal skin flora
Staphylococcus aereus is commonly transmitted by
aerosol from a cough of sneeze of an infected individual and indirectly via contact with contaminated floors, bedding, clothes, and the like
Staphylococcus are a common cause of
Hospital acquired pneumonia or nosocomial pneumonia and are becoming increasingly antibiotic resistant
MDRSA
Multiple drug resistant S. aureus
Haemophilus influenzae
is a common inhabitant of human pharyngeal flora. One of the smallest gram neg bacilli.
H. influenza type B- children age 1 month-6 years, cause of epiglottitis.