PULMONARY EDEMA

Transcription

PULMONARY EDEMA

PULMONARY EDEMA
by
Kevin T. Martin
BVE, RRT, RCP
RC Educational Consulting Services, Inc.
16781 Van Buren Blvd, Suite B, Riverside, CA 92504-5798
(800) 441-LUNG / (877) 367-NURS
www.RCECS.com
PULMONARY EDEMA
BEHAVIORAL OBJECTIVES
UPON COMPLETION OF THE READING MATERIAL, THE PRACTITIONER WILL BE
ABLE TO:
1. Define cardiogenic pulmonary edema.
2. Compare and contrast the two categories of pulmonary edema.
3. Compare and contrast the three mechanisms for the normal leak.
4. Briefly outline the factors affecting lung water.
5. Outline the common causes of cardiogenic pulmonary edema
6. Describe the normal mechanism of fluid removal from the lungs.
7. List the symptoms of pulmonary edema.
Describe the diagnostic findings of a patient with pulmonary edema.
Outline the basic treatment strategies for neurogenic pulmonary edema.
10. List therapies used to treat cardiogenic pulmonary edema
11. Identify the causes of high altitude pulmonary edema
12. Describe the problem(s) associated with an increase in capillary hydrostatic pressure
13. Describe the chest x-ray of a patient with fluid concentrating in hilar areas
14. Describe the action(s) of Morphine in the treatment of pulmonary edema
15. Explain affect of a decreased oncotic pressure with liver disease
16. List causes of noncardiogenic pulmonary edema
17. Identify the role of adult respiratory distress syndrome in pulmonary edema
18. Describe the barriers to pulmonary edema
19. Identify therapy used in the initial treatment of pulmonary edema.
20. Discuss the use of nitroglycerin in the treatment of pulmonary edema
This material is copyrighted by RC Educational Consulting Services, Inc. Unauthorized duplication is prohibited by law.
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21. Discuss the terminology used in describing the chest X-ray of a patient with pulmonary
edema.
22. Apply knowledge acquired through this learning activity and critical thinking skills during a
clinical practice exercise.
COPYRIGHT © 1991 By RC Educational Consulting Services, Inc.
COPYRIGHT © April, 2000 By RC Educational Consulting Services, Inc.
(# TX 0-480-589)
Authored by: Kevin T. Martin, BVE, RRT, RCP
Revised 1994, 1997 by Kevin T. Martin, BVE, RRT, RCP
Revised 2001 by Susan Jett Lawson, RCP, RRT-NPS
ALL RIGHTS RESERVED
This course is for reference and education only. Every effort is made to ensure that the clinical
principles, procedures and practices are based on current knowledge and state of the art
information from acknowledged authorities, texts and journals. This information is not intended
as a substitution for a diagnosis or treatment given in consultation with a qualified health care
professional.
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TABLE OF CONTENTS
INTRODUCTION ...............................................................................................................6
CAPILLARIES ....................................................................................................................6
INTERSTITIUM..................................................................................................................7
ALVEOLI ............................................................................................................................9
FACTORS AFFECTING LUNG WATER .......................................................................10
DRIVING PRESSURES...............................................................................................10
Capillary hydrostatic pressure..................................................................................10
Interstitial hydrostatic pressure ................................................................................10
Capillary oncotic pressure........................................................................................11
Interstitial oncotic pressure ......................................................................................11
BARRIERS ...................................................................................................................12
Capillary wall...........................................................................................................12
Oncotic reflection coefficient ..................................................................................12
Alveolar wall............................................................................................................12
CAUSES OF PULMONARY EDEMA.............................................................................12
Increased capillary hydrostatic pressure .......................................................................13
Decreased capillary oncotic pressure............................................................................13
Increased capillary / alveolar permeability ...................................................................13
CAUSES OF NONCARDIOGENIC PULMONARY EDEMA .......................................14
CAUSES OF CARDIOGENIC PULMONARY EDEMA ................................................15
SYMPTOMS......................................................................................................................16
DIAGNOSIS ......................................................................................................................17
CHEST RADIOGRAPHIC COMPARISON ....................................................................19
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TREATMENT ...................................................................................................................20
Immediate therapy ........................................................................................................20
Vasodilators ..................................................................................................................21
Diuretics........................................................................................................................22
Inotropic agents.............................................................................................................23
NEUROGENIC PULMONARY EDEMA ........................................................................26
PROGNOSIS AND OUTCOME.......................................................................................27
CLINICAL PRACTICE EXERCISE ................................................................................28
SUMMARY.......................................................................................................................29
PRACTICE EXERCISE DISCUSSION ...........................................................................30
SUGGESTED READING AND REFERENCES .............................................................32
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INTRODUCTION
P
ulmonary edema can loosely be divided into two categories, based upon why the blood
vessels are leaking. Leakage occurs from an increase in pressure or an increase in
permeability. Increased pressure edema is caused by an increase in driving (transmural)
pressure across the blood vessel membrane. An example of increased pressure edema is
congestive heart failure (congestive heart failure). The term “cardiogenic” pulmonary edema is
used to describe edema from increased pressure. Increased permeability edema is a result of an
alteration of the blood vessel wall. Injury or inflammation of the vessel membrane increases
permeability resulting in leakage. Increased permeability edema is associated with acute
respiratory distress syndrome (adult respiratory distress syndrome) and is termed
“noncardiogenic pulmonary edema”. The two types are not mutually exclusive. There can be an
overlap or combination of the two in a given patient at a given time. This is particularly true of
the critical care unit patient who may have multiple causes of edema.
This course devotes itself primarily to describing increased pressure edema. Increased
permeability edema is mentioned briefly when appropriate. (For a detailed discussion on
increased permeability edema refer to courses on adult respiratory distress syndrome). We begin
the discussion with a review of the normal anatomy and physiology of the lung in relation to how
fluids are removed. Specific areas of review are the pulmonary capillaries, interstitium and
alveoli. These are the structures responsible for keeping the lungs “dry.”
CAPILLARIES
M
ost fluid leakage takes place in the alveolar area, since this is where the capillaries are
located. Capillaries have very thin walls with little to no smooth muscle, media, or
adventitia. They offer little resistance to leakage and there is always a net outward flux
of both fluid and protein. However, the bulk of the leakage is fluid because most protein
molecules are too large to pass through cellular junctions. There are three proposed mechanisms
for the normal leak present: transcellular transport, vesicular transport, and leakage through
intercellular junctions.
Transcellular transport involves substances passing through the endothelial cells. Water,
electrolytes, and lipid-soluble substances may go transcellular through the endothelial cell
cytoplasm and membrane. This is a minor source of leakage. Vesicular transport is debatable as
a mechanism of leakage. It is doubtful vesicular transport plays much of a role in leakage
because the process is too slow to explain pulmonary edema. It has also been noted that
vesicular volume densities are not increased in pulmonary edema.
The primary pathway of leakage is probably through intercellular junctions or “pores” of the
capillary membrane. In addition, there appears to be more than one size of intercellular junction.
This allows molecules of varying size to leak through the capillary membrane. Narrow junctions
allow small molecules, like water, to escape. Wider junctions allow larger molecules, like
protein, to escape.
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Intercellular junctions are normally about 40-50 angstroms wide. This size prevents the escape
of most large molecules. However, they can be stretched by high pressure allowing larger
molecules to escape. At normal pressures, junction size prevents passage of molecules greater
than a molecular weight of 90,000. When pressure rises about three times normal, even these
large molecules pass through the junction.
INTERSTITIUM
T
he popular model of the alveolar-capillary (A-C) membrane describes the alveolar wall,
interstitium, and capillary wall as a relatively uniform structure. The textbook model
makes it appear that between every capillary and alveolus is a certain amount of
interstitial tissue. This is not entirely accurate.
Alveolar capillaries are arranged in the alveolar septum with a “thick” and a “thin” side. The
thick side does indeed have interstitium separating it from the alveoli. The interstitium supplies
the necessary connective tissue to support the capillary. It also allows for fluid exchange, which
is also necessary. In pulmonary edema, the interstitium widens due to excess fluid leakage. The
thin side has virtually no interstitium separating it from the alveolus. The capillary wall is fused
with the alveolar wall. This thin side is designed for gas exchange. The presence of interstitium
would obviously interfere with diffusion.
Adjacent to collagen fibers in the thick interstitial side are juxtacapillary or “j” receptors. (These
are often described as “stretch” receptors). J receptors are part of a complex reflex that results in
both stimulation of ventilation and relaxation of the extremities. J receptors are stimulated by
deformation (stretching) of collagen fibers. As collagen fibers are stretched from excess
interstitial fluid, the j receptors are stimulated. Ventilation is then increased to aid fluid removal.
Alveolar expansion increases drainage of fluid by pushing it towards the lymphatics. (The j
receptors are responsible for the rapid breathing pattern in pulmonary edema even when there are
adequate blood gases). J receptors also cause relaxation of the extremities to promote bed rest.
This helps to slow further leakage.
Clearance of water, protein and debris from the interstitium is accomplished by the lymphatic
system. There is always a very slight leakage of fluid from the capillaries to the interstitium as
mentioned above. This helps to lubricate pleural surfaces and is drained by lymph vessels. The
amount of leakage is normally insignificant. Brief surges in leakage, as what may occur during
exercise, are not unusual. In fact, the amount has to be three times normal to be clinically
detectable. Normally, the body accommodates considerable fluctuations in interstitial fluid with
no adverse effects. This is a result of both lymph system drainage and the effect of spontaneous
ventilation.
Normal interstitial pressure (commonly referred to as interstitial hydrostatic pressure) is subatmospheric (negative). This interstitial pressure is not uniformly distributed. The interstitium
directly around the alveoli has a higher (closer to atmosphere) pressure than the interstitium
around bronchi and blood vessels. Alveolar expansion raises the interstitial pressure in the
immediate area of the alveoli. This creates a pressure gradient for interstitial fluid flow away
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from the alveolar gas-exchanging areas on every breath. These interstitial pressure gradients
coupled with normal ventilatory movements help to remove interstitial fluid. Therefore, fluid in
the interstitium flows away from the alveoli and towards the lymph capillaries on inspiration.
The fluid continues to move toward the hilum on each breath. It is eventually returned to the
systemic circulation via the thoracic and lymphatic ducts.
INSPIRATION
Lymph Capillary
Increased (more negative)
pressure in this area.
The expansion of alveoli and increased negative pressure
around airways push fluid towards the lymph vessels.
The pushing of interstitial fluid by inspiration probably explains the typical “butterfly”
appearance of the chest x-ray (CXR) in acute pulmonary edema. The periphery of the lungs,
where alveoli are expanding, are cleared better than central areas. This causes fluid to
concentrate in the hilar area.
Another reason for the butterfly appearance is that airway interstitial tissue is less dense than
alveoli interstitial tissue. Therefore, it absorbs much more fluid than alveolar interstitial tissue.
In fact, airway interstitial tissue can absorb as much as a 100% increase in lung water. This
allows more fluid to collect centrally and enhances the butterfly CXR appearance.
Initial lymph capillaries are located in the spaces around respiratory bronchioles. Fluid and
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proteins in the interstitium move towards the capillaries by the interstitial pressure gradient
previously described, the contraction of ductal smooth muscle in larger lymphatics, and by
changes in intrathoracic pressure from breathing. Larger lymphatics contain one-way valves to
keep the flow heading towards the hilum.
Pulmonary Lymphatic
Loose Connective Tissue
Dense Connective Tissue
Capillary
Interstitial fluid flows away from the dense connective tissue
around alveoli and towards the pulmonary lymphatics located in
loose connective tissue around airways.
ALVEOLI
L
ast, and certainly not least, a discussion of the alveolar wall is warranted. Alveolar walls
are much less permeable than capillary walls so interstitial edema is far more common
than alveolar edema. Because of their low permeability, transcellular transport has been
suggested as the main mechanism of alveolar flooding. Some believe edema fluid is
“transported” to the alveolar space. Initially, small amounts of fluid appear only in the corners of
alveoli. Later, alveoli fill individually or in an “all or none” manner.
There are two more popular theories of how alveoli flood: direct leakage or the “overflowing
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bathtub” theory. Direct leakage is leakage through intercellular junctions. These junctions are
very tight in alveoli, so some type of injury (adult respiratory distress syndrome) must be present
to explain flooding. The overflowing bathtub theory proposes that leakage actually occurs above
the alveoli through terminal airway walls. The fluid then “overflows” into the alveolar space.
This is more plausible than direct leakage since there is more fluid around airways and airway
walls are more permeable than alveolar walls.
FACTORS AFFECTING LUNG WATER
P
ulmonary edema results from a change in driving pressure or a change in barrier
conductance (permeability). There are 4 driving pressures and 3 barriers to discuss in
regards to pulmonary edema. They are:
DRIVING PRESSURES
BARRIERS
Capillary hydrostatic pressure
Interstitial hydrostatic pressure
Capillary oncotic pressure
Interstitial oncotic pressure
Capillary wall
Oncotic reflection coefficient
Alveolar wall
The normal function of each will be briefly described. However, the main causes of pulmonary
edema are simply due to changes in capillary hydrostatic or oncotic (osmotic) pressures for
cardiogenic pulmonary edema.
DRIVING PRESSURES
CAPILLARY HYDROSTATIC PRESSURE - The mean capillary hydrostatic pressure at the
left atrium is equal to the left atrial pressure (LAP) plus 40% of the difference between the
pulmonary artery pressure (PAP) and left atrial pressure. The hydrostatic pressure varies across
the capillary bed from close to the PAP in pre-alveolar arterioles to close to the LAP in postalveolar venoules. Therefore, there is a 45% drop in pressure across the alveolar capillary bed.
This drop in pressure slows blood flow considerably past the alveoli. The resistance to flow
across the pulmonary capillary bed also is high in comparison to flow across systemic capillary
beds. This further slows blood flow past alveoli and aids diffusion. Slowing pulmonary capillary
flow keeps blood in contact with air for a maximum length of time.
In addition to a pressure gradient between arteries and veins in the pulmonary circulation, there
is also a pressure gradient from the apex to the base of the lungs. A significant vertical pressure
gradient exists due to gravity. Under normal conditions, this causes no significant change in
leakage or filtration throughout the lungs. However, if hydrostatic pressure increases, there is
more leakage from the dependent portions of the lung than the superior portions.
INTERSTITIAL HYDROSTATIC PRESSURE - The interstitial hydrostatic pressure varies
from the periphery to the hilum as described in the previous section. It is highest (closest to
atmospheric) near the alveoli and lowest (more negative) near the hilum. This provides a
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pressure gradient to provide flow from the alveolar area to the hilum. The mean interstitial
hydrostatic pressure increases in edema but the alveolar-hilar gradient remains. There is no
vertical pressure gradient for interstitial hydrostatic pressure as with capillary hydrostatic
pressure. The gradient is “longitudinal” rather than vertical. It is therefore highest in the
periphery of the lung.
CAPILLARY ONCOTIC PRESSURE - Molecules smaller than plasma proteins pass easily
across the capillary wall. The material remaining exerts a capillary oncotic pressure of about 24
mm Hg. This oncotic pressure is a result of the total protein concentration and fraction of
albumin in the plasma. Normally, there are no longitudinal or vertical changes in oncotic
pressure as with hydrostatic pressures.
INTERSTITIAL ONCOTIC PRESSURE - The interstitial oncotic pressure and protein
concentration are believed to be close to lymph protein concentrations and oncotic pressure.
Therefore, interstitial oncotic pressure is estimated to be about 14.5 mm Hg in humans. There
may be a slight difference in oncotic pressure throughout the interstitium due to differences in
capillary filtration pressure. For example, there is a lower capillary filtration pressure in the apex
than in the base of the lung. Therefore, there is less filtration of fluid in the apex so protein
concentration is less diluted. Because of this, interstitial oncotic pressure in the apex may be
slightly higher than in the bases.
PRESSURES THAT AFFECTS TRANSCAPILLARY FLUID EXCHANGE
HYDROSTATIC PRESSURES
Capillary Hydrostatic Pressure (Pc)
Drives fluid out of the capillary
Highest at arteriolar end (favors filtration)
Lowest at venular end (favors reabsorption)
Influenced more by changes in Pv than by
changes in PA
Interstitial (tissue) Hydrostatic Pressure (PT)
Determined by the volume of interstitial fluid and
tissue compliance
Normal is near 0
A rise in PT that is caused by an increase of
interstitial fluid volume, decreases the hydrostatic
gradient across the capillary thereby limiting
filtration
ONCOTIC PRESSURES
Capillary (plasma) Oncotic Pressure (IIc)
Mostly determined by plasma proteins
Albumin generates approximately 70% of the
oncotic pressure
Normal is typically 25-30 mmHg
Capillary permeability to proteins depended
upon the type of capillary
Interstitial (tissue) Oncotic Pressure
Interstitial oncotic pressures increase with
increased permeability of the capillary barrier
to proteins
Normal is approximately 5 mmHg
Oncotic pressures are decreased when
increased capillary filtration decreases
interstitial protein concentration
Capillary filtration is limited by this
mechanism
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BARRIERS
CAPILLARY WALL - The permeability of the capillary wall is determined by the structure
and function of the endothelial cells. The walls, particularly the intercellular junctions, have
already been reviewed in a previous section. Despite the presence of pores, permeability is
presumed to be low since the lungs are not usually flooded.
ONCOTIC REFLECTION COEFFICIENT - The oncotic reflection coefficient is a
measurement of how easily a solute passes through a membrane. It is related to size, shape, and
electrical charge of the solute. For example, albumin is smaller than fibrinogen so it has a lower
coefficient. Therefore, albumin passes more easily through the capillary wall than fibrinogen.
Protein has a higher coefficient so it does not pass through easily. Water has a much lower
coefficient than any of these and passes “freely” through the capillary wall.
ALVEOLAR WALL - This barrier also has been previously described. Fluid and protein flow
across the alveolar wall in normal conditions is essentially zero. Surfactant also helps keep the
lungs dry by decreasing surface tension at the air-liquid interface. This lowers alveolar
interstitial hydrostatic pressure so there is less of a driving force for fluid to enter the alveolus.
Unfortunately, because of the low permeability of the alveolar wall, if the alveoli fill with
something clearance is also very slow. Fluid and electrolyte solutions can be reabsorbed well,
but protein solutions cannot be reabsorbed easily. The low permeability of the alveolar wall
allows fluid to leave but prevents larger molecules from escaping. This becomes significant in
many conditions, such as adult respiratory distress syndrome. Hyaline membranes (fibrosis)
generally form in the lungs after recovery from conditions that damage the alveolar wall. The
protein left behind is a major component of hyaline membranes. This is rarely a problem with
non-adult respiratory distress syndrome forms of pulmonary edema since protein does not escape
the capillaries.
CAUSES OF PULMONARY EDEMA
A
n imbalance of driving pressures or damage to barriers/membranes are the mechanisms
for edema formation. The net flow of liquid across a semi-permeable membrane is a
product of the driving pressure and permeability of the membrane. The three main
causes of pulmonary edema are an increase in capillary hydrostatic pressure, a decrease in
capillary oncotic pressure, or an increase in capillary/alveolar permeability. The most common
cause of cardiogenic pulmonary edema is left ventricular failure or from pulmonary venous
hypertension, usually as a result of mitral valve disease.
I describe changes in pressures causing edema in detail in the following material. Damage to the
membranes causing an increase in permeability is discussed in another course on adult
respiratory distress syndrome. Most patients diagnosed with “pulmonary edema” have an
imbalance in pressures. Increased capillary hydrostatic pressure, decreased interstitial
hydrostatic pressure, or a decrease in capillary oncotic pressure all lead to pulmonary edema.
Liver cirrhosis may lead to NONCARDIOGENIC pulmonary edema, which is due to decreased
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oncotic pressure
INCREASED CAPILLARY HYDROSTATIC PRESSURE - An increase in capillary
hydrostatic pressure is probably the most common cause of pulmonary edema. The usual
problem is congestive heart failure. Fluid overload is also a common cause of an increase.
Additional causes of an increase in capillary hydrostatic pressure are: left ventricular
dysfunction, systemic hypertension, acute myocardial infarction (MI), severe coronary
insufficiency, aortic stenosis or regurgitation, various arrhythmias, and mitral valve
regurgitation. Any condition that causes an increase in left heart pressure can cause leakage
from the pulmonary capillaries.
Increases in right heart pressures do not cause pulmonary edema if the cause of the resistance is
before the pulmonary capillaries. Hypoxic pulmonary vasoconstriction, primary pulmonary
hypertension, and obstruction of pulmonary arterial vessels do not cause edema. If the
pulmonary capillary bed becomes partly obstructed, there may be edema from non-obstructed
vessels that are over-perfused. This is unlikely due to the tremendous number of pulmonary
capillaries.
DECREASED CAPILLARY ONCOTIC PRESSURE - Should the capillary protein
concentration decrease or the interstitial protein concentration increase, there is less of a pressure
gradient to hold fluid in the capillary. This results in a decrease in transmural oncotic pressure.
The decrease is usually transient until a new steady state is established. A decrease in capillary
protein or increases in interstitial protein are usually not a significant factor in edema formation
by themselves. However, they do allow capillaries to leak at much lower than normal
hydrostatic pressures. This enhances the other causes of edema formation. A small change in
hydrostatic pressure can cause pulmonary edema under such conditions. Starvation and
malnutrition are examples of conditions that change the capillary oncotic pressure. A decrease in
oncotic pressure also is associated with overhydration and renal failure. These are unusual
causes of pulmonary edema by themselves.
INCREASED CAPILLARY / ALVEOLAR PERMEABILITY
The above mechanisms explain leakage from the capillary to the interstitium. Leakage from the
interstitium into the alveoli follows the same rules, i.e.: pressure gradient differences between the
two. Alveolar edema is a result of an increase in interstitial hydrostatic pressure, a decrease in
alveolar hydrostatic pressure or an increase in the oncotic pressure difference between the two.
Increases in alveolar surface tension and loss of surfactant also have been associated with
pulmonary edema. Most causes of pulmonary edema are cardiogenic in nature and result in an
increase in the capillary hydrostatic pressure. Some less common forms of pulmonary edema are
a result of high-altitude, narcotic/sedative overdose, or neurogenic insults.
High-altitude pulmonary edema is believed to be from over-perfusion of a restricted capillary
bed. Narcotics are more commonly associated with pulmonary edema than other sedatives. The
mechanism is believed to be direct irritation from a contaminant in the drug or the drug itself.
Additional mechanisms may be left ventricular failure from hypoxia or acidosis, or a decrease in
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lymph flow due to ventilatory depression.
Neurogenic insults result in a massive sympathetic nervous system (SNS) discharge. This causes
intense systemic vasoconstriction, hypertension, and left ventricular failure. The effect is
enhanced by displacement of blood to the lungs from systemic vasoconstriction. (This is
referred to as the “blast” theory of edema formation). An after-effect of the initial SNS blast is
damage to the pulmonary endothelium from a transient increase in capillary pressure. This then
leads to a permeability defect. (The “permeability defect” theory of neurogenic pulmonary
edema states that capillary permeability increases in neurogenic insults even without an increase
in pressure). Neurogenic causes of pulmonary edema have significant effects on how the patient
is managed. This is discussed in the “treatment” section later in the course.
WHY ARE THE BLOOD VESSELS LEAKING?
CARDIOGENIC
Increased pulmonary capillary
hydrostatic pressure
Fluid leaks into the alveolar
interstitium or the alveoli
NONCARDIOGENIC
Increased capillary
permeability.
Normal hydrostatic pressure.
Decreased oncotic pressure.
Most common cause:
Left ventricular failure
Most common cause:
Damage to the A-C
membrane.
Adult respiratory distress
syndrome.
NONCARDIOGENIC
Reflex stimulation of the
adrenergic portion of the
autonomic nervous system.
This causes a rapid shift of
blood from the systemic to the
pulmonary circulation
Cause: Neurogenic
Severe central nervous trauma
CAUSES OF NONCARDIOGENIC PULMONARY EDEMA
•
Near drowning
•
Acute glomerulonephritis
•
Aspiration
•
Inhalation injury
•
Allergic reaction
•
Adult respiratory distress syndrome
•
Epileptic seizures / convulsions
•
Neurogenic (increased intracranial pressure, CNS lesions)
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•
Renal failure / fluid overload (secondary cardiac pulmonary emboli may occur)
•
Negative-pressure / upper airway obstruction (croup, epiglottitis in children) (upper
airway tumors or laryngospasm in adults)
•
Hyponatremic encephalopathy (healthy marathon runners)
•
Type 2 decompression sickness
•
Heroin and Naloxone overdose
•
Cytotoxic chemotherapy
•
Pulmonary complications of pregnancy
•
Molecular adsorbent recirculating systems (possibly due to an immune-mediated
response)
•
Transfusion-related between mother and child
•
Lung transplantation
•
Non-accidental injury of children (prolonged seizure activity, acute airway obstruction,
ingestion / inhalation of chemicals / drugs, head injury, rarely child abuse or
maltreatment)
•
High altitude induced
CAUSES OF CARDIOGENIC PULMONARY EDEMA
•
Mitral stenosis
•
Peripartum cardiomyopathy
•
Severe diastolic dysfunction
•
Restrictive cardiomyopathy
•
Constrictive pericarditis
•
Pericardial tamponade
•
Severe myocardial contusion
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•
Acute myocardial infarction / ischemia
•
Severe anemia
•
Sepsis
•
Thyrotoxicosis
•
Myocarditis
•
Myocardial toxins (e.g. alcohol)
•
Patient noncompliance with medications and / or dietary guidelines
•
Non-ischemic acute mitral regurgitation (e.g. ruptured chordae tendinea)
•
Dysrhythmias (e.g. new-onset of rapid A-fibrillation or Ventricular tachycardia)
•
Acute valvular heart disorders (left side)
•
Renal failure with fluid overload
SYMPTOMS
S
ymptoms vary in their severity and depend upon the underlying cause. Initial symptoms
are a dry cough, anxiety, restlessness, dyspnea, and tachypnea. Acute pulmonary edema
may usually results in severe respiratory distress, tachypnea and hypoxemia. There may be
mild fatigue, pedal edema, and exertional or paroxysmal nocturnal dyspnea. Those complaining
of tightness in the chest notice an increase in the work of breathing. They may begin to wheeze.
Diffuse crackles may be auscultated. Hypoxia may be present. Fluid is probably still confined
to the interstitium with these symptoms.
As the alveoli flood, symptoms progress in severity. Cough becomes productive of thin, frothy
sputum that may be blood-tinged. Dyspnea and tachypnea become severe. As the patient begins
to fatigue, ABG’s reverse from a respiratory alkalosis (from hyperventilation) to a respiratory
acidosis. Hypoxia will be apparent and continue to worsen. Rales/crackles and rhonchi become
audible and the patient appears cyanotic. They become tachycardic, if not already.
There are generally signs of the underlying cause of edema. Obviously, the practitioner must
determine the cause of the edema for effective treatment. Increased pressure edema is usually
related to cardiac failure so there may be a history of cardiac disease. Elevated jugular venous
pressures with corresponding distended jugular veins may be present. There may be cardiac
enlargement on the CXR. There may be gallop rhythms, heart murmurs, arrhythmias, and/or
peripheral edema.
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DIAGNOSIS
T
he history and physical is useful to differentiate increased pressure edema from increased
permeability edema. Increased pressure edema generally has signs and a history of cardiac
disease. Increased permeability edema usually does not have signs of cardiac disease. A
careful history and physical may reveal an acute lung injury suggesting a permeability problem.
Examples include: exposure to toxic gases or chemicals, drug ingestion, trauma, or neardrowning. In addition, a clinical setting of high-altitude, burns, seizures, sepsis, or pancreatitis
suggests increased permeability edema. Sepsis and infection are major causes of increased
permeability edema, particularly in a patient with intra-abdominal problems. Chest trauma, long
bone fractures, coma, and shock also are high-risk for increased permeability edema.
Laboratory tests are generally not helpful in diagnosing pulmonary edema. By the time results
are available, the clinical picture has made the diagnosis obvious. However, some lab tests, such
as, cultures and toxicology, can help determine an underlying cause of the edema. A relatively
easy, noninvasive method of separating increased pressure edema from increased permeability
edema is comparison of edema fluid protein concentrations to plasma protein concentrations.
Edema fluid is obtained via tracheal aspiration in the acute fulminating (frothing) stage.
In increased pressure edema, the capillary membrane is generally intact. Therefore, little protein
escapes into the interstitium. The opposite is true in increased permeability edema where
considerable protein leaks. Generally, edema fluid to plasma protein concentrations less than 0.6
indicate increased pressure edema. Ratios greater than 0.7 indicate increased permeability
edema. Those between 0.6 and 0.7 probably have a little of both types. Samples of edema fluid
grossly contaminated with mucus, pus, or debris should be discarded since they give false high
concentrations.
Hemodynamic measurements vary, depending upon the cause of the edema. Central venous
pressure (CVP) is elevated in most cases, since increased hydrostatic pressure is commonly the
cause of leakage. Pulmonary artery pressure can be normal or low in increased permeability
edema and high in increased pressure edema. Leakage can occur at normal or low PAP if
oncotic pressure is low or alveolar surface tension is high. COPD patients normally have a
higher than normal PAP without leakage. Therefore, in most instances, PAP does not provide
definitive diagnostic information. Pulmonary artery (PA) measurements are not considered
essential to diagnose or manage pulmonary edema, except for selected patients. Therefore, the
practice of routine PA catheter insertion is questionable. There is a high morbidity and mortality
associated with the use of PA catheters so they should be avoided, if possible.
ABG’s vary depending upon the severity of the problem. PaO2 may actually increase in early
stages due to hyperventilation. As more fluid leaks into the interstitium there is a mild hypoxia.
This steadily worsens as leakage continues. Hypoxia, increased work of breathing, stimulation
of J receptors, and anxiety lead to tachypnea. PaCO2 may be low initially, causing a respiratory
alkalosis. As the patient enters respiratory failure, this reverses. PaCO2 rises, pH drops, and
hypoxia continues to worsen.
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PULMONARY EDEMA
Other measurements of pulmonary function reveal an increase in closing volume (the point at
which small airways close on expiration). The patient exhibits a rapid, shallow breathing pattern
due to an increase in elastic resistance. Compliance and vital capacity decrease. Diffusion also
decreases. Other pulmonary function measurements are abnormal but are of little benefit. Most
patients are far too ill to perform pulmonary function tests (PFT’s) and the clinical picture makes
the diagnosis and treatment obvious.
The chest X-ray (CXR) is probably the most practical way to diagnose pulmonary edema. The
CXR is not sensitive to small changes in lung water and is only semiquantitative, but its
advantages far outweigh its disadvantages. Initially, the CXR reveals distended vascular
shadows and a loss of definition of the hilar structures. Septal (Kerley B) lines develop as fluid
flows into interlobular septa. Definition of both peribronchial and perivascular areas are lost due
to “cuffing” of fluid in the area. A transudative pleural effusion is not uncommon as fluid
collects in the pleural space. None of these occur with increased permeability causes of edema.
Fluid rapidly fills the alveolar space so no cuffing, septal lines or effusions are present. Air
bronchograms are often present and the heart size is usually normal in increased permeability
edema.
Most edema patients have chronic heart disease, so there is cardiac enlargement. A perihilar
“haze” indicates interstitial edema. Acinar shadows indicate alveolar edema. The CXR
appearance of edema is strongly influenced by the lung volume at the time of the film. For
maximum effectiveness, the CXR should be taken at end-inspiration. Other conditions
producing a similar CXR to pulmonary edema are: bilateral pulmonary infections, alveolar
proteinosis, Goodpasture’s syndrome, and immunological disorders, to name a few.
Goodpasture’s syndrome is an uncommon hypersensitivity disorder that causes, among other
pathology, pulmonary hemorrhage and renal failure. The cause of death from Goodpasture’s
syndrome is usually respiratory failure and pulmonary hemorrhage.
To rule out pneumonia and confirm excess lung water, a gravitational shift test can be done.
Frontal x-rays are done before and after prolonged lateral decubitus positioning. Excess lung
water is confirmed by a shift in opacity to the dependent lung. Acute parenchymal hemorrhage
and acute obliterating bronchiolitis with terminal bronchial mucus plugging can give falsepositive results with this test.
The most significant CXR features to note are: distribution of pulmonary blood flow, distribution
of edema, and the vascular pedicle width. Chronic heart failure redistributes pulmonary blood
flow to the apex of the lung. Upper lobe vessels are both recruited and distended. This gives
increased vascular markings in the upper lung fields.
Cardiogenic edema gives a central distribution of fluid (butterfly appearance) or an even
distribution from the chest wall to the heart and an increase in density at the bases. In other
words, more fluid in the hilar areas and less in the periphery. Whereas, increased permeability
edema gives a more patchy peripheral distribution or a “whiteout.”
The vascular pedicle width is the width of the mediastinum above the aortic arch. It is an
18
PULMONARY EDEMA
estimate of systemic blood volume. The normal pedicle width is around 48 mm (normal range is
38-58 in the adult). In cardiogenic edema the width is normal to increased. In permeability
edema the width is normal to decreased. It should be noted that vascular pedicle width increases
10-40% simply from a supine position. The use of PEEP can also decrease the pedicle width.
Pulmonary Edema
CHEST RADIOGRAPHIC COMPARISON
CARDIOGENIC
PULMONARY EDEMA
Cardiac enlargement due to chronic heart
disease (increased cardiothoracic ratio)
Increased vascular markings in upper lung
fields (due to chronic heart disease)
“Butterfly” appearance due to more fluid in
hilar areas and less in the lung periphery
Vascular pedicle width is normal to increased
Distended vascular shadows
Loss of defined hilar structures
Kerley B lines develop due to haziness of
interlobular septa
Loss of definition of peribronchial and
perivascular areas due to “cuffing” of fluid in
the area
Possible transudative pleural effusion
No air bronchograms
NON-CARDIOGENIC
PULMONARY EDEMA
No cardiac enlargement (unless patient has, in
addition, a history of chronic heart disease)
May or may not be present
“Whiteout” or patchy peripheral appearance
(progresses into adult respiratory distress sysdrome
stages when applicable) with lung injury pulmonary
embolus.
“Bat Wing” pattern with nephrogenic etiology
Vascular pedicle width is normal to decreased
Generally none noted
Infiltrates generally diffuse, vary with type of lung
injury
No Kerley B lines
No “cuffing”
No effusions
Air bronchograms
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PULMONARY EDEMA
Pleural effusion may be present
Pleural effusion may be present
TREATMENT
T
reatment of pulmonary edema is divided into two stages. The first is aimed at immediate
life-threatening symptoms. If the patient survives the acute stage and is stabilized, the
second stage becomes necessary. The second stage of therapy consists of determining and
treating the underlying cause of the edema. Critical Pathways have been developed at most
facilities for congestive heart failure/pulmonary edema. The protocol from the American Heart
Association Advanced Cardiac Life Support is considered the present “state of the art” in the
treatment of acute pulmonary edema.
Let us start at the beginning:
•
Assess ABC’s of cardiopulmonary resuscitation
•
Secure an airway
•
Administer oxygen
•
Start an IV
•
Attach cardiac monitor, pulse oximeter, automatic sphygmomanometer
•
Assess vital signs
•
Review history
•
Perform physical examination
•
Obtain a 12-lead electrocardiogram (ECG)
•
Obtain a chest X-ray
IMMEDIATE THERAPY - The degree of treatment and immediate therapy necessary is
determined by patient symptoms. Most patients require supplemental oxygen (O2). The amount
of O2 to provide is based upon serial ABG’s and pulse oximetry. Many feel that oxygen should
be delivered via a non-rebreathing mask to obtain an FIO2 as close to 1.0 as possible due to both
pulmonary and cardiac compromise. Severe cases of fulminating edema require intubation and
suctioning. Ventilation is necessary if the PaCO2 rises and a respiratory acidosis becomes
apparent.
A large-bore IV is necessary. If the patient is not hypotensive, 5-10 mg of morphine sulfate
(MS) is given slowly over several minutes. MS has several positive effects: vasodilation, CNS
sedation, and mild inotrophy. MS lowers pulmonary capillary pressure resulting in less leakage.
20
PULMONARY EDEMA
Systemic vascular resistance (SVR) also may be decreased, so cardiac output improves. Patient
anxiety is decreased adding further relief. Complications of ventilatory depression and
hypotension are possible with MS but are rarely a problem. Ventilatory depression is obviously
treated with mechanical ventilation. The appearance of hypotension when MS is given indicates
the dose was too high or intravascular volume is less than predicted. Appropriate adjustments
should be made. Any problems that arise with the use of morphine can be quickly reversed with
the administration of naloxone.
If medications are not immediately available, rotating tourniquets decrease the blood volume in
the pulmonary circulation. The goal of tourniquets is to decrease venous return to the heart.
Tourniquets (blood pressure cuffs may be used) are placed on three extremities and inflated to a
pressure greater than systolic blood pressure. The inflation is rotated between the cuffs every 15
minutes. No extremity should remain without blood flow greater than 45 minutes.
Intermittent Positive Pressure Breathing (IPPB) treatments have been used as a “pulmonary
tourniquet” in the past. Providing high intrathoracic pressure decreases venous return to the
chest without danger to the extremities. IPPB also provides ventilatory support to ease the work
of breathing. Nebulization of ethyl alcohol (50%) has been used to “pop” the bubbles of
fulminating edema as it denatures the surfactant thereby decreasing the “froth”. This provides
for more efficient gas exchange as liquid occupies less space than bubbles. This treatment is
controversial at this writing. Positive end-expiratory pressure (PEEP) is used for those being
mechanically ventilated to decrease venous return and increase oxygenation. Continuous
positive airway pressure (CPAP) is used for those not being mechanically ventilated. The newer
generation noninvasive positive pressure ventilation devices are able to provide 100% oxygen,
pressure supported breaths and PEEP. This modality has been used extensively and successfully.
Inhaled bronchodilators may be useful if the patient has an underlying pulmonary disease that
responds to these types of medications.
VASODILATORS - The most useful medications for acute increased pressure edema are
vasodilators. Vasodilation decreases the transmural pressure causing leakage. Dilation of
arteries decreases systemic vascular resistance (SVR) thereby increasing cardiac output and
improving heart efficiency. There are three useful classes of vasodilators: venodilators (nitrates),
arteriolar dilators (phentolamine, hydralazine), and mixed dilators (nitroprusside).
Sodium nitroprusside is the most potent medication used. Advantages to nitroprusside are
immediate effect, short half-life and maintenance of cardiac output. The disadvantages are that
invasive hemodynamic monitoring is necessary to avoid profound hypotension and prolonged
use results in cyanide toxicity. The earliest sign of toxicity is a metabolic acidosis. Therapy for
cyanide poisoning includes administration of thiosulfate, sodium nitrate, or hydroxycobalamin.
Toxicity usually takes 2-3 days to develop so substitute drugs should be provided before this
time.
Hypoxia also can occur if pulmonary blood flow is increased and upsets V/Q relationships. (If
there is an increase in perfusion of non-ventilated alveoli, hypoxia can occur with any
vasodilator). Nitroprusside is usually started at 10 mg/min and increased by 5-10 mg every 3-5
21
PULMONARY EDEMA
minutes until the desired effect is achieved. Diastolic arterial pressure should remain above 60
mm Hg and peak systolic pressure above 100 mm Hg. Most patients require 50-100 mg/min.
Both preload and afterload are decreased by nitroprusside. Effects are very rapid and disappear
within minutes of discontinuing the drug.
Nitroglycerin is very useful for patients with increased pressure edema associated with acute MI
or myocardial insufficiency. Nitroglycerin improves blood flow to ischemic or marginally
perfused areas. It is also useful in a patient with borderline hypotension. At higher doses
nitroglycerin results in arteriolar dilator effects like nitroprusside. Its major disadvantage is that
invasive hemodynamic monitoring is necessary. Ethanol intoxication also can be a complication
of high doses.
Nitroglycerin is usually started at 10-15 mg/min and increased by 5-10 mg increments every 3-5
minutes until the mean arterial pressure falls (usually 20 mm Hg or more), the pulmonary
capillary wedge pressure is brought to the desired level, headache becomes intolerable, or angina
is relieved. The development of tachycardia indicates wedge pressure or cardiac output has
fallen. If so, nitroprusside may be a more appropriate vasodilator.
Transdermal and oral preparations also can be used but cannot be precisely controlled.
Nitroglycerin ointment (0.5-2.0 inches) or oral isosorbide dinitrate (20-100 mg) is used. Their
advantage is a long (3-5 hours) duration of action. The calcium channel blocker nifedipine also
can be used for selective coronary artery dilation.
Arteriolar dilators are seldom used because they have little to no effect on pulmonary capillary
pressure. Phentolamine is expensive and has more serious side effects than the above drugs.
Prazosin and trimazosin reduce wedge pressure and increase cardiac output. They are useful in a
slowly developing pulmonary edema. Diazoxide is useful in a patient with advanced congestive
heart failure that is unresponsive to other vasodilators.
Hydralazine induces arteriolar dilation by an unknown mechanism. Regardless of mechanism,
hydralazine increases cardiac output and stroke volume. It can be administered orally or IV.
Effects begin within 10 minutes and last up to 4 hours. Side effects include headache, nausea,
vomiting, and cardiac and GI complaints.
Captopril works by inhibiting the renin-angiotensin system. Enalapril and lisinopril work the
same way. Renin transforms angiotensinogen to angiotensin I. Angiotensin I is then converted
to Angiotensin II, a potent vasoconstrictor, by angiotensin converting enzyme (ACE). In the
case of congestive heart failure, the angiotensin system is activated to maintain blood pressure.
The result is an increase in afterload. This worsens any pulmonary edema present. Captopril
and other ACE inhibitors lower both preload and afterload thereby minimizing edema. A
significant side effect of captopril is intractable cough. This usually requires a change to another
drug.
DIURETICS - A modest immediate effect is obtained with diuretics by reducing perfusion of
flooded alveoli. The principal effect of diuretics is to increase water excretion by the kidneys.
22
PULMONARY EDEMA
This decreases pulmonary capillary pressure by reducing cardiovascular blood volume and
pressure. The result is less leakage. Furosemide (20-40 mg IV or IM) or ethacrynic acid (50 mg
IV) is given. Diuretics may cause a loss of potassium and chloride and lead to a severe
hypokalemic or hypochloremic alkalosis. Supplemental potassium chloride is usually necessary
for a patient receiving diuretics.
If there is no response to the above doses, they can be doubled in one hour. This can be
continued until diuresis begins. If there has been no response to 160-320 mg of furosemide or
100-200 mg of ethacrynic acid, it is unlikely there will be a response to increased dosage.
Increasing dosage at this point can cause serious side effects. A patient who is hypotensive has
little response to diuretics. Poor renal perfusion limits their effectiveness. Dopamine or
dobutamine should be given to increase renal blood flow. If the patient has severely diseased
kidneys, dialysis rather than diuresis, should be considered.
INOTROPIC AGENTS - Patients with poor cardiac output and are hypotensive are candidates
for inotropic agents. Inotropics increase cardiac output through improved contractility. This
helps to lower the transmural pressure. There are three classes of drugs to choose from:
catecholamines, digitalis, and nonglycosidic, nonsympathomimetic, inotropic-vasodilating
agents.
Catecholamines are the most useful in an acute situation. Catecholamines have both alpha and
beta adrenergic effects. The former cause peripheral vasoconstriction to support blood pressure.
The latter stimulate the heart to increase cardiac output. The most common medications are
dopamine and dobutamine for short-term support in acute pulmonary edema. Isoproterenol,
epinephrine, and norepinephrine have been used, but tachyarrhythmias and other side effects are
common.
At low doses, dopamine increases cardiac contractility and cardiac output without significantly
changing heart rate or myocardial O2 consumption. It also increases SVR and directly increases
renal blood flow by stimulation of dopaminergic receptors. This increases urine output and
diuresis. Dopamine’s vasopressor effects raise systolic blood pressure while maintaining cardiac
output. Ventricular filling pressures may remain unchanged or even be raised with dopamine.
This can actually increase the transmural pressure and worsen edema. Nitroglycerin or
nitroprusside may be necessary to counteract this complication. Again, invasive hemodynamic
monitoring is necessary to gauge the effect of therapy.
Dopamine is started at 2-5 mg/kg/min and titrated for the desired effect. Dosages greater than 10
mg/kg/min are associated with significant side-effects such as arteriolar vasoconstriction. This
can be so intense that digital necrosis occurs. Tissue infusion also can cause necrosis, so a largebore catheter should be used and securely attached to the patient. It should be noted that the
pupils become fixed and dilated with dopamine infusion, regardless of neurological status.
Dopamine also may cause PaO2 to decrease, if poorly ventilated units start being perfused. This
worsens V/Q relationships like that which occurs with the vasodilators.
Dobutamine does not cause systemic vasoconstriction like dopamine. It is primarily a positive
23
PULMONARY EDEMA
inotropic agent with mild vasodilating properties. Ventricular filling pressures tend to fall, rather
than rise, as with dopamine. Cardiac output increases, resulting in improved renal blood flow.
Dobutamine is particularly useful for treatment of pulmonary edema due to a loss of ventricular
contractility. It is more effective and predictable than parenteral digitalis in acute MI.
Dobutamine is usually started at 2-3 mg/kg/min and increased every 10-30 minutes until the
desired effect is achieved. Maximum effect is delayed for 10 minutes or more. Usually 7-15
mg/kg/min is sufficient. Above this range is when problems (like tachycardia) begin to appear.
Administer dobutamine cautiously in patients with atrial fibrillation because it facilitates AV
nodal conduction. This causes ventricular rate to increase. Digitalis is more appropriate in such
patients.
Digitalis is the drug of choice for long-term inotropic therapy. It is much less useful than
dopamine or dobutamine for acute pulmonary edema. It is less predictable and its effects are not
as great as either dopamine or dobutamine. Digitalis also has a narrow therapeutic to toxic dose
ratio. Patients with chronic heart failure are often treated with digitalis as an outpatient.
Digitalis should not be used in an acute situation for these patients. They can be put in a toxic
situation rapidly. The major use for digitalis is in atrial fibrillation with a rapid ventricular
response.
Newer nonglycosidic, nonsympathomimetic, inotropic vasodilators have been studied. The
bypyridine derivative amrinone and its analog milrinone are two such drugs. They increase
intracellular cyclic AMP levels by inhibition of phosphodiesterase. An increase in intracellular
calcium also occurs and may be the cause of a positive inotropic effect. These drugs also
decrease SVR through peripheral vasodilation. This decreases hydrostatic pressure in the lungs
and decreases edema formation. An advantage to nonsympathomimetic inotropic vasopressors is
that they have little chance of inducing arrhythmias.
A few patients with severe pulmonary edema that do not respond to the above therapies may
require mechanical circulatory support. Intraaortic balloon pumps or ventricular assist devices
may be used. Extracorporeal membrane oxygenation (ECMO), heart transplant, and heart-lung
transplant also may be used for a very few patients.
All of the above are used for the immediate salvage of the patient. If this is successful, the goal
of therapy becomes decreasing the hydrostatic pressure causing the pulmonary edema.
Hydrostatic pressure must be decreased to near normal to prevent further leakage. In increased
pressure edema this should be sufficient, since the capillary membrane is undamaged. Wedge
pressures less than 20 mm Hg should be adequate to prevent further leakage. Some patients may
need a higher pressure to maintain cardiac output. (COPD patients often have a higher than
normal pressure due to chronic hypoxic vasoconstriction. They may not tolerate wedge
pressures less than 20 mm Hg). Therapy should be aimed at decreasing the work of the heart and
increasing its efficiency. Bed rest, adequate oxygenation and salt restriction are basic principles
24
PULMONARY EDEMA
of care.
All correctable causes of failure should be treated. Arrhythmias, hypertension, acute MI,
digitalis toxicity, infection, and severe anemia are common causes that can be reversed. One
also should restrict physical activity and prevent pain and anxiety. These will decrease the work
of the heart. Sitting them upright, providing O2, a potent diuretic, and relieving anxiety usually
stabilize patients. Do not overtreat the patient because that causes more harm than good.
INITIAL MEDICATION GUIDELINES BASED ON BLOOD PRESSURE WITH A
CARDIAC “PUMP” PROBLEM:
BLOOD PRESSURE (in mmHg)
SUGGESTED PHARMACEUTICAL INTERVENTION
Systolic < 70
Norepinephrine
Dopamine
Dopamine
Norepinephrine
Dobutamine
Systolic 70-100
Systolic > 100 and normal
diastolic
Diastolic > 110
Nitroglycerin
Nitroprusside
FURTHER INTERVENTIONS SPECIFIC TO ACUTE CARDIOGENIC PULMONARY
EDEMA:
First line action
Second line action
Third line action
Furosemide
Morphine
Nitroglycerin
Oxygen/intubate as indicated
Nitroglycerin if BP > 100
Nitroprusside if BP > 100
Dopamine if BP < 100
Dobutamine if BP > 100
PEEP
CPAP
NIPPV with IPAP/EPAP
Amrinone (if other drugs fail)
Aminophylline (if wheezing)
Thrombolytic (if not in shock)
Digoxin (if in atrial fibrillation or
supraventricular tachycardias)
Angioplasty (if drugs fail)
25
PULMONARY EDEMA
Intra-aortic balloon pump-IAPB (bridge to
surgery)
Surgical intervention (valves, coronary artery
bypass-CABG, heart transplant)
COMMON TREATMENTS FOR PULMONARY EDEMA
•
Oxygen
•
CPAP/BIPAP
•
Intubation (severe)
•
Mechanical ventilation with PEEP (severe)
•
Morphine
•
Nitroprusside (vasopressor)
•
Furosemide (diuretics)
•
Digitalis
•
Bed rest
•
Salt restriction
NEUROGENIC PULMONARY EDEMA
I
t should be noted that general supportive care of the patient with neurogenic pulmonary
edema (NPE) differs markedly from the patient with cardiogenic pulmonary edema. For
NPE, the goal of care is centered on maintaining the patient while preventing increases in
intracranial pressure (ICP). This is not a consideration in the patient with cardiogenic pulmonary
edema. Many of the procedures and medications that are commonplace for patients with
cardiogenic pulmonary edema are detrimental to the patient with NPE. Positioning, turning,
suctioning, sedation, and the diuretic used are different for the NPE patient. The following
describes the differences.
Cardiogenic pulmonary edema requires the patient to be in an upright position with the feet and
legs dependent. NPE requires the head of the bed to be elevated (up to 30 degrees) while
avoiding hip flexion. Frequent turning of the cardiac patient is recommended while slow,
26
PULMONARY EDEMA
cautious turning is used for the neurological patient. (A slowly rotating bed is probably the best
option for the neurological patient). Suctioning for the NPE patient should be done only when
necessary, not routinely or frequently. Suctioning results in a valsalva maneuver and coughing.
These raise the ICP considerably. One must avoid all procedures that increase ICP in the
neurological patient, if possible. These include suctioning, coughing, positive pressure
ventilation, and placing the patient in a head down position. For sedation, use codeine sulfate
instead of morphine sulfate. And finally, oncotic diuretics (mannitol) should be used instead of
loop diuretics (furosemide).
PROGNOSIS AND OUTCOME
W
ater, protein, and cellular debris must be removed from the alveolar and interstitial
spaces following resolution of the cause of the edema. Edema fluid is removed via the
lymphatics, airways, blood vessels, pleural space, or the mediastinum. However, the
exact pathway for resolution of water and protein is not known. Cellular debris is removed by
macrophage ingestion.
There are two possible pathways to clear water and protein from the alveoli. They can be
removed directly through the alveolar or terminal airway epithelium. The alveolar route is slow
because the alveolar wall is relatively impermeable to large molecules (unless it is severely
damaged). If the edema fluid clots, removal is even slower. Surfactant in the alveoli activates
the clotting system so clotting of edema fluid is common.
Fluid (water) is readily absorbed into the interstitium, leaving protein and other large molecules
in the alveoli. This contributes to hyaline membrane formation. Fluid in the interstitium is
removed via the lymph system or by migrating to loose airway and vascular connective tissue
spaces. Large amounts of fluid are cleared into these spaces through hypothesized leaky
terminal airway walls (“leaking bathtub” theory in reverse). Coughing clears an insignificant
amount of fluid.
Most interstitial water in pulmonary edema is in the connective tissue rather than the alveolar
area. The lymph capillaries are arranged to drain only the alveolar walls so most interstitial
water is not removed via the lymphatics. Some of the fluid may drain directly into the
bloodstream through vessel walls in the lung. A significant portion of the fluid probably follows
prevailing pressure gradients to drain into the mediastinum. Mediastinal lymphatics then drain
the fluid.
The outcome of increased pressure edema is determined by the underlying cause and the skill
and promptness in treatment. Most cases are a result of heart disease, so the outcome depends on
the severity of cardiac dysfunction. Patients who do not have significant peripheral
hypoperfusion generally do well with a mortality rate of about 10%. Those with significant
peripheral hypoperfusion have a mortality of approximately 50%. Those who recover from an
acute episode caused by heart disease require long-term outpatient management. Iatrogenic
causes of edema, such as, volume overload or inappropriate cardiac medications, usually do well
once the cause is removed. Obviously, any precipitating factors should be sought and
27
PULMONARY EDEMA
eliminated.
Mortality for patients requiring mechanical ventilation is related to systolic blood pressure at the
time of intubation and the need for vasopressor medications 24 hours later. A systolic blood
pressure less than 130 mm Hg when intubated and the need for vasopressors at 24 hours have a
higher mortality. The prognosis depends heavily upon the severity of the acute left ventricular
injury and not the degree of respiratory failure.
CLINICAL PRACTICE EXERCISE
The following practice exercise is discussed at the end of the course. Discussion answers are
based upon the text. Individual experience may provide alternative correct responses.
1. The patient is a 68 year old male admitted to the critical care unit for acute respiratory failure.
He has underlying COPD and appears emaciated. He was recently extubated after 5 days of
mechanical ventilation. After extubation, respiratory rate has increased gradually from 16 to 30.
Heart rate is now 140 and BP is 120/80. CXR shows increasing perihilar infiltrates. Pulmonary
wedge pressure is stable at 15 mm Hg. ABG’s are pH 7.47, PaCO2 40, PaO2 70, % sat. 93%,
HCO3 28 on 2 lpm nasal cannula. Lab data reveals hypoalbuminemia and an elevated BUN.
Evaluate this information.
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
2. The patient is placed on a 40% venti-mask and given an IPPB treatment with a
bronchodilator. His symptoms remain unchanged, except for a slight increase in SpO2 to 95%.
STAT CXR reveals distended vascular shadows and Kerley B lines. The patient is given
furosemide and morphine. BP decreases to 90/60 and there is no response to the diuretic. There
has been minimal urine output over the last 24 hours. Evaluate this information and make
recommendations.
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
28
PULMONARY EDEMA
3. Prior to your suggestions being implemented, the patient becomes cyanotic, lethargic, and
begins producing copious amounts of thin, frothy sputum. The patient is intubated and placed
back on the mechanical ventilator. Evaluate this information.
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
SUMMARY
here are two types of pulmonary edema, increased pressure edema and increased
permeability edema. Increased pressure edema is a result of an imbalance in driving
pressures within the capillary. This results in fluid leakage. Causes of increased pressure
edema are often cardiogenic. Increased permeability edema is due to damage to the alveolarcapillary membrane. This results in the syndrome known as “adult respiratory distress
syndrome”. This course primarily describes increased pressure edema.
There is normally a small amount of fluid leakage from the pulmonary capillaries to the
interstitium. Most leakage is removed by the interstitial lymph system. Fluid movement in the
interstitium is due to interstitial pressure gradients, ventilatory movements, lymph vessel smooth
muscle and one-way valves.
Alveoli are significantly less permeable to fluid than capillaries so alveolar edema is less
common than interstitial edema. Alveolar edema may be a result of direct leakage through the
wall or from excess fluid overflowing from terminal airways.
Factors affecting lung water consist of: capillary hydrostatic pressure, interstitial hydrostatic
pressure, capillary oncotic pressure, interstitial oncotic pressure, the capillary wall, the oncotic
reflection coefficient, and the alveolar wall. Causes of pulmonary edema include increased
capillary hydrostatic pressure, decreased interstitial hydrostatic pressure, decreased transmural
oncotic pressure differences, high-altitude, narcotics, and neurogenic insults. Increased capillary
hydrostatic pressure due to left ventricular failure or pulmonary venous hypertension (usually
due to mitral valve disease) is the most common cause.
•
Left ventricular failure may lead to CARDIOGENIC pulmonary edema caused by
increased hydrostatic pressure.
•
Liver cirrhosis may lead to NONCARDIOGENIC pulmonary edema, which is due to
decreased oncotic pressure.
•
Adult respiratory distress syndrome is NONCARDOGENIC pulmonary edema brought
on my increased permeability.
Symptoms of pulmonary edema depend largely upon the cause of the leakage. Initial symptoms
29
PULMONARY EDEMA
include a dry cough, anxiety, restlessness, dyspnea, and tachypnea. As the edema progresses,
breathing becomes more labored and cough becomes productive of thin, frothy sputum. ABG’s
reverse from a respiratory alkalosis and mild to no hypoxia to respiratory acidosis and severe
hypoxia.
The history and physical help differentiate increased pressure from increased permeability
edema. The former is usually related to cardiac disease, so there is a history of heart symptoms
and signs of chronic heart disease. A useful laboratory test is the edema fluid (tracheal aspirate)
protein to plasma protein concentration ratio. Ratios less than 0.6 indicate increased pressure
edema. Ratios greater than 0.7 indicate increased permeability edema. Hemodynamic
measurements are nonspecific, but increases are generally associated with increased pressure
edema.
The CXR is probably the most practical tool for diagnosing pulmonary edema. The initial CXR
reveals distended vascular shadows and ill-defined hilar structures. Kerley lines and a perihilar
haze then develop. It can progress to a complete “white-out”. Generally, the CXR has a
“butterfly” appearance, being dense in the middle and clearing towards the periphery. This is a
result of fluid migrating to the hilum due to interstitial pressure gradients.
Initial treatment is aimed at immediate life-threatening symptoms. If the patient survives,
treatment is aimed at determining and treating the underlying cause. Immediate therapy consists
of maintaining a patent airway and providing oxygen and ventilation as necessary. An IV should
be started for administration of MS, vasodilators, diuretics, and inotropic agents. In the absence
of medications or their ineffectiveness, rotating tourniquets and IPPB can be used. Most cases of
increased pressure edema do well if the underlying cause is promptly treated. Cases caused by
cardiac disease require long-term outpatient management.
PRACTICE EXERCISE DISCUSSION
1. Increasing respiratory rate and heart rate indicate respiratory distress. Blood pressure and
PA pressures are normal. The CXR is compatible with interstitial edema. The ABG shows a
normal PaCO2 which is probably low for this patient with COPD. This indicates
hyperventilation, possibly in response to “j” receptor stimulation. Interstitial edema also
may trigger hyperventilation by increasing the work of breathing. The PaO2 is low
considering the degree of hyperventilation. Edema may be impeding diffusion. Normal BP
and wedge pressures are not compatible with increased hydrostatic pressure as the
mechanism of leakage. Emaciated appearance, five days of intubation and hypoalbuminemia
are compatible with malnutrition. Capillary oncotic pressure is probably low, allowing for
leakage at normal hydrostatic pressures. Elevated BUN raises possibility of renal
insufficiency.
2. Lack of response to hyperinflation and bronchodilation help rule out a pulmonary cause of
the distress. CXR helps to confirm this by indicating imminent alveolar flooding. The BP
decrease is probably in response to morphine. A lack of urine output helps confirm renal
insufficiency. Hypotension compounds this problem by decreasing kidney perfusion.
30
PULMONARY EDEMA
Diuretic response will be minimal until kidney function improves. Suggest dopamine or
dobutamine to increase blood pressure and renal flow, increase furosemide dose to attempt
diuresis. CPAP or BIPAP may help decrease venous return and further leakage. It may also
relieve some of the work of breathing and increase oxygenation.
3. Patient is in acute pulmonary edema with alveolar flooding evident by secretions. Low
albumin levels, renal insufficiency, and positive water balance have combined to produce
acute excessive leakage. Nutritional and kidney status must be improved to resolve edema.
31
PULMONARY EDEMA
SUGGESTED READING AND REFERENCES
1. Burton, G.G., et al. (1997) Respiratory Care: A Guide to Clinical Practice. (4th ed)
Philadelphia: Lippincott-Raven.
2. Dettbarn C, Davidson L., “Pulmonary Complications in the Patient with Acute Head
Injury: Neurogenic Pulmonary Edema”, Nov. 1989, HEART AND LUNG, Vol. 18,
#6, pp 583-588
3.
Emergency Cardiac Care Committee and Subcommitties, American Heart Association:
Guidelines for cardiopulmonary resuscitation and emergency cardiac care, III; Adult
advanced cardiac life support; JAMA 1992.
4.
Fedullo A, Swinburne A, Wahl G, Bixby K., “Acute Cardiogenic Pulmonary Edema Treated
with Mechanical Ventilation”, May, 1991, CHEST, Vol. 99, #5, pp 1220-1226
5. Fishman A. (editor), PULMONARY DISEASES AND DISORDERS, Vol.I, 3rd Edition,
1998, McGraw-Hill Co. pp. 733-752 B. Saunders Co.
6.
Khan, A.N. & Kasthuri, R.S. Pulmonary Edema, Noncardiogenic, June 17, 2005,
www.emedicine.com
7.
Klabunde, R. E., Cardiovascular Physiology Concepts, www.cvphysiology.com
8.
Mattu, A. et al. Pulmonary Edema, Cardiogenic, February 7, 2003,
www.emedicine.com
9.
Merck Manual, Sec. 6, Ch 77, Goodpasture’s Syndrome, www.merck.com
10. Murray J, Nadel J. (editors), TEXTBOOK OF RESPIRATORY MEDICINE, 1988, W.B.
Saunders Co. pp. 1359-1409
11. Putnam C., REVISITING THE CHEST FILM IN PULMONARY EDEMA, Journal of
Respiratory Diseases, Sept. 1994, Vol. 15, #9, pp 819-831
12. Reimer, S.E. & Morrison, S.C. Case Sixty Six-Lung Injury Pulmonary Edema, Pediatric
Teaching Files, uhrad.com
13. Seaton A, Seaton D, Leitch A., CROFTON AND DOUGLAS’S RESPIRATORY
DISEASES, 5th edition, 2000, Blackwell Scientific Publications, pp. 584-597
14. Scanlon C, Spearman C, Sheldon R., EGAN’S FUNDAMENTALS OF
RESPIRATORY CARE, 7th edition. 1999, Mosby Yearbook, Inc.
15. Staton, G. W. Pulmonary Edema, ACP Medicine, Sept. 2004, WebMD.
16. Witek, T., Schachter E., PHARMACOLOGY AND THERAPEUTICS IN
RESPIRATORY CARE, 1994, W. B. Saunders Co., pp 432-436
17. Zucker, M. Noninvasive PSV May Obviate ICU Admission for Cardiogenic
Pulmonary Edema, Oct. 2003, www.pulmonaryreviews.com
32
PULMONARY EDEMA
POST TEST
DIRECTIONS: IF COURSE WAS MAILED TO YOU, CIRCLE THE MOST CORRECT
ANSWERS ON THE ANSWER SHEET PROVIDED AND RETURN TO: RCECS, 16781
VAN BUREN BLVD, SUITE B, RIVERSIDE, CA 92504-5798 OR FAX TO: (951) 789-8861.
IF YOU ELECTED ONLINE DELIVERY, COMPLETE THE TEST ONLINE – PLEASE
DO NOT MAIL OR FAX BACK.
1. Treatment of cardiogenic pulmonary edema includes:
1.
2.
3.
4.
a.
b.
c.
d.
chest physical therapy
vasodilators
aerosol therapy
diuretics
1, 2
2, 3
3, 4
2, 4
2. A useful diagnostic test to help differentiate increased pressure from increased
permeability edema is:
a.
b.
c.
d.
ABG’s.
PFT’s.
Sputum culture.
Edema fluid to plasma protein concentration ratio.
3. Clearance of water, protein, and debris from the interstitium is accomplished by the:
a.
b.
c.
d.
e.
Systemic capillaries.
Pulmonary capillaries.
Lymphatic system.
a & b.
None of the above.
4. Which of the following aids removal of interstitial fluid?
a.
b.
c.
d.
e.
Venous vessel smooth muscle
Ventilatory movements
Interstitial pressure gradients
Pulmonary venoules
b&c
5. High altitude pulmonary edema is believed to be from:
a.
b.
c.
d.
Increased capillary oncotic pressure
Overperfusion of a restricted capillary bed
Decreased interstitial hydrostatic pressure
None of the above
33
PULMONARY EDEMA
6. Cardiogenic pulmonary edema is best defined as:
a.
b.
c.
d.
Edema caused by increased capillary hydrostatic pressure
Edema caused by increased capillary permeability
Adult respiratory distress syndrome
None of the above
7. Which of the following are early, initial symptoms of pulmonary edema?
1.
2.
3.
4.
a.
b.
c.
d.
e.
dry cough
dyspnea
thick, copious sputum
tachypnea
2, 3
1, 3, 4
1, 2, 3, 4
1, 2, 4
1 only
8. A patient in acute pulmonary edema will demonstrate the following on ABG results:
a.
b.
c.
d.
Extreme hypoxemia
Acute respiratory acidosis
Acute respiratory alkalosis
Variable results dependent upon the stage and severity of the problem
9. Sputum in pulmonary edema is characteristically:
a.
b.
c.
d.
e.
Foul-smelling.
Thin, frothy and possible blood tinged.
Thick and yellow.
Cream-colored.
Purulent
10. What is the usual problem that results in increased capillary hydrostatic pressure?
a.
b.
c.
d.
Congestive heart failure
Sepsis
Asthma
Dehydration
11. The goal in the treatment of the patient with neurogenic pulmonary edema is to:
a.
b.
c.
d.
Use loop diuretics to decrease intracellular fluid
Turn the patient frequently to keep fluid from pooling
Prevent increases in intracranial pressure (ICP)
Suction frequently to maintain a patent airway
34
PULMONARY EDEMA
12. The most practical way to diagnose pulmonary edema is via:
a.
b.
c.
d.
Chest X-ray.
ABG’s.
Vital Capacity.
ECG’s.
13. Pulmonary edema caused by liver cirrhosis is an example of:
a.
b.
c.
d.
Increased hydrostatic pressure
Decreased oncotic pressure
Increased permeability of the a-c membrane
None of the above
14. The typical “butterfly” appearance of the chest X-ray in acute cardiogenic pulmonary edema
is probably due to:
a.
b.
c.
d.
Engorgement of the pulmonary periphery
Fluid concentrating in the hilar areas
Uniform distribution of interstitial pressure
None of the above
15. The two most common causes of cardiogenic pulmonary edema are:
1.
2.
3.
4.
5.
a.
b.
c.
d.
Goodpasture’s syndrome
Aspiration of gastric contents
Pulmonary alveolar proteinosis
Left ventricular failure
Pulmonary venous hypertension
1&2
2&3
4&5
1&3
16. Morphine sulfate is useful in pulmonary edema because:
a.
b.
c.
d.
e.
It provides vasodilation.
It results in CNS sedation.
It causes mild inotrophy.
All the above.
It provides ventilatory depression.
35
PULMONARY EDEMA
17. The following are causes of noncardiogenic (increased permeability) pulmonary edema:
a.
b.
c.
d.
Cytotoxic chemotherapy
Inhalation of toxic chemicals
Drug ingestion
All of the above
18. Adult respiratory distress syndrome is an example of:
a.
b.
c.
d.
e.
Noncardiogenic pulmonary edema
Increased capillary permeability
Damage to the a-c membrane
a and b
a, b and c
19. The proposed mechanisms for the normal capillary leak are:
a.
b.
c.
d.
Transcellular and vesicular transport and leakage through intercellular junctions
Thick collagen fibers, interstitial fibrosis and pneumonia
Low hydrostatic pressures and decreased capillary permeability
High oncotic and hydrostatic pressures
20. The barriers to pulmonary edema include:
a.
b.
c.
d.
21.
Capillary and interstitial hydrostatic pressures
Capillary and oncotic pressure
Capillary and alveolar walls and oncotic reflection coefficient
None of the above
Mr. Jones, a 67 year old male with a history of cardiac disease presents to the Emergency
Department complaining of severe respiratory distress. He is obviously tachypneic. Your
most appropriate initial step in the treatment of this patient would be to:
a.
b.
c.
d.
22.
Administer oxygen via a non-rebreathing mask
Review the patient’s history with him
Listen to his breath sounds
Attach a cardiac monitor
Which of the following statements regarding the use of nitroglycerin is true?
a.
b.
c.
d.
Decreases blood flow to poorly perfused areas
Is useful in patients with borderline hypotension
Decreases cardiac output
None of the above
36
PULMONARY EDEMA
23.
Jane Doe is in the Critical Care Unit. She arrived in the Emergency Department last night.
Her diagnosis is heroin overdose. She remains unconscious. The paramedics intubated her
successfully in the field with an 8.0 ETT and she has been on the ventilator overnight. Her
FIO2 requirements to maintain an acceptable SpO2 have increased. Breath sounds are
equal, but crackles (rales) are significant bilaterally. What would you expect the chest Xray to reveal this morning?
a.
b.
c.
d.
24.
A second line intervention specific to acute cardiogenic pulmonary edema is:
a.
b.
c.
d.
25.
Right mainstem intubation
Increased fluid confined to the hilar areas
Diffuse, patchy, peripheral distribution of fluid
Enlarged cardiac shadow
Aminophylline
Oxygen
Angioplasty
PEEP
Ms. Smith, a 28 year old otherwise healthy female arrives in the Emergency Department.
She was severely injured in a motor vehicle accident, is intubated and being successfully
oxygenated and ventilated. The trauma physician and team assess her injuries. Among the
injuries is head trauma, fractured right femur and chest contusions. Which type(s) of
pulmonary edema would most likely occur in this patient?
a.
b.
c.
d.
Cardiac and neurogenic
Noncardiac and cardiac
Noncardiac only
None of the above
KM: Test Version E
37
PULMONARY EDEMA
ANSWER SHEET
NAME____________________________________ STATE LIC #______________________
ADDRESS_________________________________ AARC# (if applic.)__________________
DIRECTIONS: (REFER TO THE TEXT IF NECESSARY – PASSING SCORE FOR CE
CREDIT IS 70%). IF COURSE WAS MAILED TO YOU, CIRCLE THE MOST CORRECT
ANSWERS AND RETURN TO:
RCECS, 16781 VAN BUREN BLVD, SUITE B,
RIVERSIDE, CA 92504-5798 OR FAX TO: (951) 789-8861. IF YOU ELECTED ONLINE
DELIVERY, COMPLETE THE TEST ONLINE – PLEASE DO NOT MAIL OR FAX BACK.
1.
a b c d
17. a b c d
2.
a b c d
18. a b c d e
3.
a b c d e
19. a b c d
4.
a b c d e
20. a b c d
5.
a b c d
21. a b c d
6.
a b c d
22. a b c d
7.
a b c d e
23. a b c d
8.
a b c d
24. a b c d
9.
a b c d e
25. a b c d
10. a b c d
11. a b c d
12. a b c d
13. a b c d
14. a b c d
15. a b c d
16. a b c d e
KM: Test Version E
38
PULMONARY EDEMA
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39

PULMONARY EDEMA

Transcription

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