Nursing Care Plan for Acute Respiratory Distress Syndrome (ARDS)

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.

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.

INTERVENTIONS	RATIONALES
Monitor vital signs every 1-2 hours, and prn.	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.
Obtain PA pressures every hour, cardiac output/index every 4 hours, and calculate other hemodynamic values.	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.
Monitor for mental changes, decreased peripheral pulses, cold or clammy skin.	May indicate decreased cardiac output and decreased perfusion.

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.

INTERVENTIONS	RATIONALES
Monitor for peripheral or dependent edema, or distended neck veins.	May indicate fluid excess that results in venous congestion and leads to respiratory failure.
Auscultate lung fields for adventitious breath sounds.	Broncho vesicular sounds heard over entire lung fields result when lung density increases. Crackles and rhonchi may be auscultated in pulmonary edema.
Monitor intake and output every hour. Notify MD if urine less than 30 cc/hr.	Identifies fluid imbalances and possible sources.
Weigh every day.	Weight gains of > 2 Ibs./day or 5 Ibs./week indicate fluid retention.
Monitor for vocal fremitus.	May be present due to increased lung density resulting from pulmonary edema.
Monitor vital signs.	Tachycardia and elevated blood pressure may result from fluid excess and heart failure.
Restrict fluids as warranted.	May be required to help with fluid balance regulation.

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.

INTERVENTIONS	RATIONALES
Monitor vital signs every 1-2 hours, and prn.	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.
Monitor intake and output every hour, and notify MD of significant fluid imbalances.	Continuing negative balances may result in volume depletion.
Weigh daily.	Changes in weight from day to day may correlate to fluid shifts that may occur.
Observe skin turgor and hydration status.	Decreases in skin turgor, tenting of skin, and dry mucous membranes may indicate fluid volume deficits.
Administer IV fluids as ordered.	Replaces fluids and maintains circulating volume.
Monitor labwork for sodium and potassium levels.	Diuretic therapy may result in hypokalemia and hyponatremia.

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.

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