Acute Respiratory
Distress Syndrome (ARDS)
Acute respiratory
distress syndrome (ARDS) is also known as shock lung, wet lung, white lung, or
acute respiratory distress syndrome, and occurs frequently after an acute or
traumatic injury or illness involving the respiratory system. The body responds
to the injury with life-threatening respiratory failure and hypoxemia.
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| Pathway ARDS |
ARDS is usually
noted 12-24 hours after the initial insult or 5- 10 days after sepsis
occurs. Dyspnea with hyperventilation and hypoxemia are usually the first
clinical symptoms. Adventitious breath sounds frequently are not present
initially.
Some of the most
common precipitating factors are trauma, aspiration, pneumonia, near-drowning,
toxic gas inhalation, sepsis, shock, DIC, oxygen toxicity, coronary artery
bypass, pancreatitis, fat or amniotic embolism, radiation, head injury, heroin
use, massive hemorrhage, smoke inhalation, drug overdose, or uremia. Mortality
is high (60-70%) despite treatment and often, patients who do survive, may have
chronic residual lung disease. In some cases, patients may have normal
pulmonary function after recovery. The latent phase of ARDS begins when the
pulmonary capillary and alveolar endothelium become injured. The insult causes
complement to be activated, as well as granulocytes, platelets,
and the coagulation cascade. Free oxygen radicals, arachidonic acid metabolites
and proteases are released into the system. Humoral substances, such as
serotonin, histamine and bradykinin, are released. This results in red blood
cell and high plasma protein leakage into the interstitial spaces, due to
increased capillary permeability and increased pulmonary hydrostatic pressure.
Initially, there may be little evidence of respiratory problems, and
chest x-rays may be normal or show minimal diffuse haziness. The fluid leakage
increases and lymphatic flow increases with the acute phases with widespread
damage to pulmonary capillary membranes and inflammation. Increases in
intra-alveolar edema leads to capillary congestion and collagen formation.
Surfactant production and activity decreases, which causes decreased functional
residual capacity, increased pulmonary shunting with widening A-a gradients,
decreased pulmonary compliance, and ventilation/perfusion mismatching results.
Chest x-rays will then show the ground glass appearance and finally a complete
white-out of the lung.
The chronic phases
occurs when the endothelium thickens; Type I cells, which are
the gas-exchange pneumocytes, are replaced by Type II cells, which are
responsible for producing surfactant, and along with fibrin, fluid and other
cellular material form a hyaline membrane in place of the normal alveoli.
The goals of
treatment are to improve ventilation and perfusion, to treat the underlying
disease process that caused the lung injury, and to prevent progression of
potentially fatal complications. Oxygen therapy with high levels of oxygen,
mechanical ventilatory support with PEEE and fluid and drug management are
required.
MEDICAL CARE
Laboratory:
cultures to
identify causative organ- isms when bacterial infection is present and to
identify proper antimicrobial agent; C5A levels increase with disease process;
fibrin split products increase; platelets decrease; lactic acid levels increase
Chest x-ray:
used to evaluate
lung fields; early x- rays may be normal or have diffuse infiltrates;
later x-rays will show bilateral ground glass appearance or complete whiting-out of lung fields; assists with
differentiation between ARDS and cardiogenic pulmonary edema since heart size
is normal in ARDS
Oxygen:
to correct hypoxia
and hypoxemia Arterial blood gases: to identify acid-base problems, hypocapnia,
hypercapnia, and hypoxemia, and to evaluate progress of disease process and
effectiveness of oxygen therapy
Ventilation:
to provide
adequate oxygenation and ventilation in patients who are unable to maintain
even minimal levels Pulmonary function studies: used to evaluate lung
compliance and volumes which are normally decreased; physiologic dead space is
increased and alveolar ventilation is compromised
Ineffective breathing pattern
[See Mechanical
Ventilation]
Related to: decreased lung compliance, pulmonary edema, increased
lung density, decreased surfactant
Defining characteristics: use of accessory
muscles, dyspnea, tachypnea, Bradypnea, altered ABGs
Impaired gas excbange
[See Mechanical
Ventilation]
Related to: intra-alveolar edema, atelectasis,
ventilation/perfusion mismatching, decreased arterial PO,, decreased amount and
activity of surfactant, alveolar hypoventilation, formation of hyaline
membranes, alveolar collapse, decreased diffusing capacity, shunting
Defining characteristics: tachypnea,
cyanosis, use of accessory muscles, tachycardia, restlessness, mental changes,
abnormal arterial blood gases, intrapulmonary shunting increased, A-a gradient
changes, hypoxemia, increased dead space
Inefective airway clearance
[See Mechanical
Ventilation]
Related to: interstitial edema, increased
airway resistance, decreased lung compliance, pulmonary secretions
Defining Characteristics: dyspnea,
tachypnea, cyanosis, use of accessory muscles, cough with or without
production, anxiety, restlessness, feelings of impending doom
Anxiety
[See Mechanical
Ventilation]
Related to: health crisis, effects of
hypoxemia, fear of death, change in health status, change in environment
Defining characteristics: apprehension,
restless- ness, fear, verbalized concern
Knowledge deficit
[See Mechanical Ventilation]
Related to: lack of information,
inability to process information, lack of recall
Defining characteristics:
verbalized concerns and questions
Decreased cardiac output
Related to: increased positive airway
pressures, sepsis, dysrhythmias, increased intrapulmonary edema, left
ventricular failure
Defining characteristics: tachycardia,
cardiac output less than 4 L/min, cardiac index less than 2.5 Llminlm2,
cold clammy skin, decreased blood pressure
Outcome Criteria
Patient will be hemodynamically stable.
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INTERVENTIONS
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RATIONALES
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Monitor vital signs every 1-2
hours, and prn.
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Mechanical ventilation and the
use of PEEP increase the intrathoracic pressures which results in compression
of the large vessels in the chest and this causes decreased venous return to
the heart and decreased blood pressure.
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Obtain PA pressures every hour,
cardiac output/index every 4 hours, and calculate other hemodynamic values.
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PA pressures will be elevated but
wedge pressure will be normal. This is the classic marker to differentiate
between cardiogenic and non-cardiogenic pulmonary edema. Most ARDS patients
have adequate cardiac function at least initially, unless decreases in CO/CI are due to
PEEP.
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Monitor for mental changes,
decreased peripheral pulses, cold or clammy skin.
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May indicate decreased cardiac
output and decreased perfusion.
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Discharge or
Maintenance Evaluation
· Patient will have adequate perfusion and cardiac output/index
within normal limits for physio- logic condition.
· Patient will have no mental status changes or peripheral perfusion
impairment.
Risk for fluid volume
excess
Related to: interstitial edema, increased
pulmonary fluid with normal intravascular volume, transfusions, resuscitative
fluids
Defining characteristics: edema, dyspnea,
orthopnea, rales, wheezing
Outcome Criteria
Patient will be hemodynamically stable, with no signs of pulmonary
edema.
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INTERVENTIONS
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RATIONALES
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Monitor for peripheral or dependent edema, or distended neck
veins.
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May indicate fluid excess that results in venous congestion and
leads to respiratory failure.
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Auscultate lung fields for adventitious breath sounds.
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Broncho vesicular sounds heard over entire lung fields result
when lung density increases. Crackles and rhonchi may be auscultated in
pulmonary edema.
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Monitor intake and output every hour. Notify MD if urine less
than 30 cc/hr.
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Identifies fluid imbalances and possible sources.
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Weigh every day.
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Weight gains of > 2 Ibs./day or 5 Ibs./week indicate
fluid retention.
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Monitor for vocal fremitus.
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May be present due to increased lung density resulting from
pulmonary edema.
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Monitor vital signs.
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Tachycardia and elevated blood pressure may result from fluid
excess and heart failure.
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Restrict fluids as warranted.
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May be required to help with fluid balance regulation.
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Discharge or
Maintenance Evaluation
Patient will have
no edema or weight gain. Patient will be eupneic with no adventitious breath
sounds to auscultation.
Risk for fluid volume deficit
Related to: fluid shifts, diuretics,
hemorrhage
Defining characteristics: decreased blood
pressure, oliguria, anuria, low pulmonary artery wedge pressures
Outcome Criteria
Patient will achieve and maintain a normal and balanced fluid
volume status and be hemodynamically stable.
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INTERVENTIONS
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RATIONALES
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Monitor vital signs every 1-2 hours, and prn.
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Tachycardia, hypotension and decreases in pulse quality may
indicate fluid shifting has resulted in volume depletion. Temperature
elevations with diaphoresis may result in increased insensible fluid loss.
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Monitor intake and output every hour, and notify MD of
significant fluid imbalances.
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Continuing negative balances may result in volume depletion.
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Weigh daily.
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Changes in weight from day to day may correlate to fluid shifts
that may occur.
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Observe skin turgor and hydration status.
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Decreases in skin turgor, tenting of skin, and dry mucous
membranes may indicate fluid volume deficits.
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Administer IV fluids as ordered.
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Replaces fluids and maintains circulating volume.
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Monitor labwork for sodium and potassium levels.
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Diuretic therapy may result in hypokalemia and hyponatremia.
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Discharge or Maintenance
Evaluation
· Patient will achieve normal fluid balance.
· Patient will have urine output within normal limits.
· Patient will be hemodynamically stable, with no weight change.