Acute pulmonary Failure

Definition

Acute respiratory failure occurs when dysfunction of the respiratory system results in

abnormal gas exchange that is potentially life-threatening. Each element of this definition is

important to understand. The term acute implies a relatively sudden onset (from hours to days)

and a substantial change from the patient’s baseline condition. Dysfunction of the respiratory

system indicates that the abnormal gas exchange may be caused by abnormalities in any element

of the respiratory system (e.g., a central nervous system abnormality affecting the regulation of

breathing or a musculoskeletal thoracic abnormality affecting ventilation; Chapter 83), in

addition to abnormalities of the lung itself. The term respiration refers, in a broad sense, to the

delivery of oxygen (O2) to metabolically active tissues for energy usage and the removal of

carbon dioxide (CO2) from these tissues (Table 104-1). Respiratory failure is a failure of the

process of delivering O2 to the tissues and/or removing CO2 from the tissues. Abnormalities in

the periphery (e.g., cyanide poisoning, pathologic distribution of organ blood flow in sepsis) can

also lead to tissue hypoxia; although these conditions represent forms of respiratory failure in the

broadest terms, this chapter focuses on respiratory failure resulting from dysfunction of the

lungs, chest wall, and control of respiration.

Risk Factors

Strong Factor cigarette smoking young age old age pulmonary infection chronic lung disease airway obstruction alveolar abnormalities perfusion abnormalities cardiac failure peripheral nerve abnormalities muscle system abnormalities opiate and sedative medications toxic fumes and gases traumatic spinal injury traumatic thoracic injury central nervous system disorders acute vascular occlusion pneumothorax hypercoagulable states

PA Clinical Signs and Symptoms of Acute Respiratory Failure Clinical manifestations of respiratory distress reflect signs and symptoms of hypoxemia, hypercapnia, or the increased work of breathing necessary. These include Altered mental status (agitation, somnolence) Peripheral or central cyanosis or decreased oxygen saturation on pulse oximetry Manifestations of a "stress response" including tachycardia, hypertension, and diaphoresis Evidence of increased respiratory work of breathing including accessory muscle use, nasal flaring, intercostal indrawing, suprasternal or supraclavicular retractions, tachypnea Evidence of diaphragmatic fatigue (abdominal paradox) Abnormal arterial blood gas results ARF : CXR Findings Clear CXR with hypoxemia and normocapnia.- Pulmonary embolus, R to L shunt, Shock Diffusely white (opacified) CXR with hypoxemia and normocapnia - ARDS, NCPE, CHF, pulmonary fibrosis Localized infiltrate - pneumonia, atelectasis, infarct Clear CXR with hypercapnia - COPD, asthma, overdose, neuromuscular weakness

Management of Acute Respiratory Failure The management of acute respiratory failure can be divided into an urgent resuscitation phase followed by a phase of ongoing care. The goal of the urgent resuscitation phase is to stabilize the patient as much as possible and to prevent any further life-threatening deterioration. Once these goals are accomplished the focus should then shift towards diagnosis of the underlying process, and then the institution of therapy targeted at reversing the primary etiology of the ARF.

DX: 1st Tests To Order Test Result pulseoximetry SpO2 <80% arterial blood gases pH<7.38; PaO2 <60 mmHg (or <50 mmHg in chronic lung disease) on room air; PaCO2 >50 mmHg on room air Other Tests to Consider Test Result CBC elevated white blood cell count screening for hypercoagulable states variable serum bicarbonate (HCO3) may be elevated ECG

variable CXR diffuse or patchy infiltrates; pneumothorax; pulmonary effusion; hyperinflation; asymmetric opacification of lung fields; asymmetric lucency of lung fields pulmonary function tests PEFR <35% to 50% of predicted; FEV <35% to 50% of predicted; FVC <50% to 70% of predicted; FEV1 <50% of predicted; NIF above -25 cm H2O chest CT pulmonary embolism; chronic lung disease; infection; parenchymal disease; bronchiectasis ventilation/perfusion lung scan pulmonary embolism Emerging Tests Test Result transcutaneous CO2 monitoring reduced PaCO2 cardiothoracic ultrasound evidence of effusion, pneumothorax, consolidation, or abscess Meds: Pharmacotherapy for cardiogenic pulmonary edema and acute exacerbations of chronic obstructive pulmonary disease (COPD) is discussed here. The goals of therapy in cardiogenic pulmonary edema are to achieve a pulmonary capillary wedge pressure of 15-18 mm Hg and a cardiac index greater than 2.2 L/min/m2 while maintaining adequate blood pressure and organ perfusion. These goals may have to be modified for some patients. Diuretics, nitrates, analgesics, and inotropes are used in the treatment of acute pulmonary edema. Nursing interventions for Nursing Priorities Maintain airway patency. Assist with measures to facilitate gas exchange. Enhance nutritional intake. Prevent complications, slow progression of condition. Provide information about disease process/prognosis and treatment regimen. Ineffective Airway Clearance May be related to Bronchospasm Increased production of secretions; retained secretions; thick, viscous secretions Decreased energy/fatigue Possibly evidenced by Statement of difficulty breathing Changes in depth/rate of respirations, use of accessory muscles Abnormal breath sounds, e.g., wheezes, rhonchi, crackles Cough (persistent), with/without sputum production

Auscultate breath sounds. Note adventitious Some degree of bronchospasm is present with

breath sounds, e.g., wheezes, crackles,

rhonchi.

obstructions in airway and may/may not be manifested

in adventitious breath sounds, e.g., scattered, moist

crackles (bronchitis); faint sounds, with expiratory

wheezes (emphysema); or absent breath sounds (severe

asthma).

Assess/ monitor respiratory rate. Note

inspiratory/ expiratory ratio.

Tachypnea is usually present to some degree and may

be pronounced on admission or during stress/

concurrent acute infectious process. Respirations may

be shallow and rapid, with prolonged expiration in

comparison to inspiration.

Note presence/ degree of dyspnea, e.g.,

reports of “air hunger,” restlessness, anxiety,

respiratory distress, use of accessory

muscles. Use 0–10 scale or American

Thoracic Society’s “Grade of Breathlessness

Scale” to rate breathing difficulty. Ascertain

precipitating factors when possible.

Differentiate acute episode from

exacerbation of chronic dyspnea.

Respiratory dysfunction is variable depending on the

underlying process, e.g., infection, allergic reaction,

and the stage of chronicity in a patient with established

COPD. Note: Using a 0–10 scale to rate dyspnea aids

in quantifying and tracking changes in respiratory

distress. Rapid onset of acute dyspnea may reflect

pulmonary embolus.

Assist patient to assume position of

comfort, e.g., elevate head of bed, have

patient lean on overbed table or sit on edge

of bed.

Elevation of the head of the bed facilitates respiratory

function by use of gravity; however, patient in severe

distress will seek the position that most eases breathing.

Supporting arms/legs with table, pillows, and so on

helps reduce muscle fatigue and can aid chest

expansion.

Keep environmental pollution to a

minimum, e.g., dust, smoke, and feather

pillows, according to individual situation.

Precipitators of allergic type of respiratory reactions

that can trigger/ exacerbate onset of acute episode.

Encourage/ assist with abdominal or

pursed-lip breathing exercises.

Provides patient with some means to cope with/

control dyspnea and reduce air-trapping.

Observe characteristics of cough, e.g.,

persistent, hacking, moist. Assist with

measures to improve effectiveness of cough

effort.

Cough can be persistent but ineffective, especially if

patient is elderly, acutely ill, or debilitated. Coughing is

most effective in an upright or in a head-down position

after chest percussion.

Increase fluid intake to 3000 mL/day within

cardiac tolerance. Provide warm/ tepid

liquids. Recommend intakeof fluids

between, instead of during, meals.

Hydration helps decrease the viscosity of secretions,

facilitating expectoration. Using warm liquids may

decrease bronchospasm. Fluids during meals can

increase gastric distension and pressure on the

diaphragm.

Monitor/ graph serial ABGs, pulse

oximetry, chest x-ray.

Establishes baseline for monitoring progression/

regression of disease process and

complications. Note: Pulse oximetry readings detect

changes in saturation as they are happening, helping to

identify trends before patient is symptomatic. However,

studies have shown that the accuracy of pulse oximetry

may be questioned if patient has severe peripheral

vasoconstriction.

2. Impaired Gas Exchange May be related to Altered oxygen supply (obstruction of airways by secretions, bronchospasm; air-trapping) Alveoli destruction Possibly evidenced by Dyspnea Confusion, restlessness Inability to move secretions Abnormal ABG values (hypoxia and hypercapnia) Changes in vital signs Reduced tolerance for activity

Assess respiratory rate, depth. Note use

of accessory muscles, pursed-lip

breathing, inability to speak/ converse.

Useful in evaluating the degree of respiratory distress

and/or chronicity of the disease process.

Elevate head of bed, assist patient to

assume position to ease work of

Oxygen delivery may be improved by upright position and

breathing exercises to decrease airway collapse, dyspnea,

breathing. Include periods of time in

prone position as tolerated. Encourage

deep-slow or pursed-lip breathing as

individually needed/ tolerated.

and work of breathing. Note: Recent research supports use

of prone position to increase Pao2.

Assess/ routinely monitor skin and

mucous membrane color.

Cyanosis may be peripheral (noted in nailbeds) or central

(noted around lips/or earlobes). Duskiness and central

cyanosis indicate advanced hypoxemia.

Encourage expectoration of sputum;

suction when indicated.

Thick, tenacious, copious secretions are a major source of

impaired gas exchange in small airways. Deep suctioning

may be required when cough is ineffective for

expectoration of secretions.

Auscultate breath sounds, noting areas of

decreased airflow and/or adventitious

sounds.

Breath sounds may be faint because of decreased airflow

or areas of consolidation. Presence of wheezes may

indicate bronchospasm/ retained secretions. Scattered

moist crackles may indicate interstitial fluid/ cardiac

decompensation.

Palpate for fremitus. Decrease of vibratory tremors suggests fluid collection or

air-trapping.

Monitor level of consciousness/ mental

status. Investigate changes.

Restlessness and anxiety are common manifestations of

hypoxia. Worsening ABGs accompanied by confusion/

somnolence are indicative of cerebral dysfunction due to

hypoxemia.

Evaluate level of activity tolerance.

Provide calm, quiet environment. Limit

patient’s activity or encourage bed/chair

rest during acute phase. Have patient

resume activity gradually and increase as

individually tolerated.

During severe/ acute/ refractory respiratory distress,

patient may be totally unable to perform basic self-care

activities because of hypoxemia and dyspnea. Rest

interspersed with care activities remains an important part

of treatment regimen. An exercise program is aimed at

increasing endurance and strength without causing severe

dyspnea and can enhance sense of well-being.

Evaluate sleep patterns, note reports of

difficulties and whether patient feels

well rested. Provide quiet environment,

group care/ monitoring activities to

allow periods of uninterrupted sleep;

limit stimulants, e.g., caffeine;

encourage position of comfort.

Multiple external stimuli and presence of dyspnea may

prevent relaxation and inhibit sleep.

Monitor vital signs and cardiac rhythm. Tachycardia, dysrhythmias, and changes in BP can reflect

effect of systemic hypoxemia on cardiac function.

3. Nutrition: imbalanced, less than body requirements May be related to Dyspnea; sputum production Medication side effects; anorexia, nausea/vomiting Fatigue Possibly evidenced by Weight loss; loss of muscle mass, poor muscle tone Reported altered taste sensation; aversion to eating, lack of interest in food

Assess dietary habits, recent

food intake. Note degree of

difficulty with eating. Evaluate

weight and body size (mass).

Patient in acute respiratory distress is often anorectic because of

dyspnea, sputum production, and medications. In addition, many

COPD patients habitually eat poorly, even though respiratory

insufficiency creates a hypermetabolic state with increased caloric

needs. As a result, patient often is admitted with some degree of

malnutrition. People who have emphysema are often thin with

wasted musculature.

Auscultate bowel sounds.

Diminished/ hypoactive bowel sounds may reflect decreased gastric

motility and constipation (common complication) related to limited

fluid intake, poor food choices, decreased activity, and hypoxemia.

Give frequent oral care,

remove expectorated secretions

promptly, provide specific

container for disposal of

secretions and tissues.

Noxious tastes, smells, and sights are prime deterrents to appetite

and can produce nausea and vomiting with increased respiratory

difficulty.

Encourage a rest period of 1

hr before and after meals.

Provide frequent small

feedings.

Helps reduce fatigue during mealtime, and provides opportunity to

increase total caloric intake.

Avoid gas-producing foods

and carbonated beverages.

Can produce abdominal distension, which hampers abdominal

breathing and diaphragmatic movement and can increase dyspnea.

Avoid very hot or very cold

foods.

Extremes in temperature can precipitate/ aggravate coughing

spasms.

Weigh as indicated.

Useful in determining caloric needs, setting weight goal, and

evaluating adequacy of nutritional plan. Note: Weight loss may

continue initially, despite adequate intake, as edema is resolving.

Administer supplemental

oxygen during meals as

indicated.

Decreases dyspnea and increases energy for eating, enhancing

intake.

4. Risk for Infection Risk factors may include Inadequate primary defenses (decreased ciliary action, stasis of secretions) Inadequate acquired immunity (tissue destruction, increased environmental exposure) Chronic disease process Malnutrition

Monitor temperature. Fever may be present because of infection

and/or dehydration.

Review importance of breathing exercises, effective

cough, frequent position changes, and adequate fluid

intake.

These activities promote mobilization and

expectoration of secretions to reduce risk of

developing pulmonary infection.

Observe color, character, odor of sputum. Odorous, yellow, or greenish secretions

suggest the presence of pulmonary infection.

Demonstrate and assist patient in disposal of tissues

and sputum. Stress proper handwashing (nurse and

patient), and use gloves when handling/ disposing of

Prevents spread of fluid-borne pathogens.

tissues, sputum containers.

Monitor visitors; provide masks as indicated.

Reduces potential for exposure to infectious

illnesses, e.g., upper respiratory infection

(URI).

Encourage balance between activity and rest.

Reduces oxygen consumption/ demand

imbalance, and improves patient’s resistance

to infection, promoting healing.

Discuss need for adequate nutritional intake. Malnutrition can affect general well-being

and lower resistance to infection.

Recommend rinsing mouth with water and spitting, not

swallowing, or use of spacer on mouthpiece of inhaled

corticosteroids.

Reduces localized immunosuppressive

effect of drug and risk of oral candidiasis.

Obtain sputum specimen by deep coughing or

suctioning for Gram’s stain, culture/ sensitivity.

Done to identify causative organism and

susceptibility to various antimicrobials.

Administer antimicrobials as indicated.

May be given for specific organisms

identified by culture and sensitivity, or be

given prophylactically because of high risk.

6. Knowledge Deficit May be related to Lack of information/unfamiliarity with information resources Information misinterpretation Lack of recall/cognitive limitation Possibly evidenced by Request for information Statement of concerns/misconception Inaccurate follow-through of instructions Development of preventable complications

Other Possible Nursing Diagnoses

1. Self-Care deficit, specify—intolerance to activity, decreased strength/endurance, depression,

severe anxiety.

2. Home Maintenance, ineffective—intolerance to activity, inadequate support system, insufficient

finances, unfamiliarity with neighborhood resources.

3. Infection, risk for—decreased ciliary action, stasis of secretions, tissue destruction, increased

environmental exposure,chronic disease process, malnutrition.

Pathophysiology

Respiratory failure can arise from an abnormality in any of the components of the respiratory system, including the airways, alveoli, central nervous system (CNS), peripheral nervous system, respiratory muscles, and chest wall. Patients who have hypoperfusion secondary to cardiogenic, hypovolemic, or septic shock often present with respiratory failure.

Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue. Ventilatory demand is the spontaneous minute ventilation that results in a stable Pa CO2.

Normally, ventilatory capacity greatly exceeds ventilatory demand. Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both). Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller. Ventilatory demand is augmented by an increase in minute ventilation and/or an increase in the work of breathing