ACUTE

PULMONARY

FAILURE

Prepared By:

BSN, Level IV

Sarah Jane A. Cristobal

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.

DEFINITION

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), in addition to

abnormalities of the lung itself.

DEFINITION

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. Respiratory failure is a failure of

the process of delivering O2 to the tissues

and/or removing CO2 from the tissues.

DEFINITION

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.

PHYSICAL

ASSESSMENT

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

PHYSICAL

ASSESSMENT

• 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

PHYSICAL

ASSESSMENT

• 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

DIAGNOSTIC

EXAMINATIONS

First Tests To Order:

• 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

DIAGNOSTIC

EXAMINATIONS

• CBC

elevated white blood cell count

screening for hypercoagulable states

Variable

serum bicarbonate (HCO3)

may be elevated

DIAGNOSTIC

EXAMINATIONS

• 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

DIAGNOSTIC

EXAMINATIONS

• chest CT

pulmonary embolism; chronic lung disease;

infection; parenchymal disease;

bronchiectasis

ventilation/perfusion lung scan

pulmonary embolism

DIAGNOSTIC

EXAMINATIONS

• ECG

Variable

• transcutaneous CO2 monitoring

reduced PaCO2

• cardiothoracic ultrasound

evidence of effusion, pneumothorax, consolidation, or abscess

RISK FACTORS

• cigarette smoking

• young age

• old age

• pulmonary infection

• chronic lung disease

• airway obstruction

• alveolar abnormalities

RISK FACTORS

• perfusion abnormalities

• cardiac failure

• peripheral nerve abnormalities

• muscle system abnormalities

• opiate and sedative medications

• toxic fumes and gases

RISK FACTORS

• traumatic spinal injury

• traumatic thoracic injury

• central nervous system disorders

• acute vascular occlusion

• pneumothorax

• hypercoagulable states

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

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.

MEDICATIONS

Pharmacotherapy for cardiogenic

pulmonary edema and acute exacerbations of

chronic obstructive pulmonary disease (COPD)

is discussed here.

MEDICATIONS

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.

MEDICATIONS

These goals may have to be modified

for some patients. Diuretics, nitrates, analgesics,

and inotropes are used in the treatment of acute

pulmonary edema.

MEDICATIONS

• First-line therapy generally includes a loop diuretic such

as furosemide, which inhibits sodium chloride

reabsorption in the ascending loop of Henle.

• Furosemide (Lasix)

This allows both superior potency and a

higher peak concentration despite an increased

incidence of adverse effects, particularly ototoxicity

MEDICATIONS

• Metolazone (Zaroxolyn)

Has been used as adjunctive therapy in

patients initially refractory to furosemide. It has been

demonstrated to be synergistic with loop diuretics in

treating refractory patients and causes a greater loss

of potassium. Metolazone is a potent thiazide-related

diuretic that sometimes is used in combination with

furosemide for more aggressive diuresis. It is also

used for initiating diuresis in patients with a degree of

renal dysfunction.

•

MEDICATIONS

Nitrates reduce myocardial oxygen

demand by lowering preload and after load. In

severely hypertensive patients, nitroprusside

causes more arterial dilatation than

nitroglycerin. Nevertheless, in view of the

possibility of thiocyanate toxicity and the

coronary steal phenomenon associated with

nitroprusside, IV nitroglycerin may be the initial

therapy of choice for afterload reduction.

•

MEDICATIONS

• Nitroglycerin sublingual (Nitro-Bid, NitroMist, Nitrostat, Nitrolingual)

Sublingual nitroglycerin tablets and spray are particularly useful in the patient who presents with acute pulmonary edema with a systolic blood pressure of at least 100 mm Hg. As with sublingual nitroglycerin tablets, the onset of action of nitroglycerin spray is 1-3 minutes, with a half-life of 5 minutes. Administration of the spray may be easier, and it can be stored for as long as 4 years.

MEDICATIONS

• Nitroprusside sodium (Nitropress)

Nitroprusside produces vasodilation of

venous and arterial circulation. At higher

dosages, it may exacerbate myocardial

ischemia by increasing heart rate. It is easily

titratable.

MEDICATIONS

Morphine IV is an excellent adjunct in

the management of acute pulmonary edema. In

addition to anxiolysis and analgesia, its most

important effect is venodilation, which reduces

preload. It also causes arterial dilatation, which

reduces systemic vascular resistance and may

increase cardiac output.

MEDICATIONS

• Morphine sulfate (Duramorph, Astramorph)

Morphine sulfate is the drug of choice

for narcotic analgesia because of its reliable and

predictable effects, safety profile, and ease of

reversibility with naloxone. Morphine sulfate

administered IV may be dosed in a number of

ways and commonly is titrated until the desired

effect is obtained.

MEDICATIONS

• Dopamine

Dopamine is a positive inotropic agent that

stimulates both adrenergic and dopaminergic

receptors. Its hemodynamic effects depend on the

dose. Lower doses stimulate mainly dopaminergic

receptors that produce renal and mesenteric

vasodilation; higher doses produce cardiac stimulation

and renal vasodilation. Doses of 2-10 µg/kg/min can

lead to tachycardia, ischemia, and dysrhythmias.

Doses higher than 10 µg/kg/min cause

vasoconstriction, which increases afterload.

MEDICATIONS

• Norepinephrine (Levophed)

Used in protracted hypotension after

adequate fluid replacement. It stimulates beta1- and

alpha-adrenergic receptors, which leads to

increased cardiac muscle contractility and heart

rate, as well as vasoconstriction. As a result,

norepinephrine increases systemic blood pressure

and cardiac output. Adjust and maintain infusion to

stabilize blood pressure (eg, 80-100 mm Hg

systolic) sufficiently to perf

MEDICATIONS

• Dobutamine

Dobutamine produces vasodilation and

increases the inotropic state. At higher dosages, it

may cause increased heart rates, thus exacerbating

myocardial ischemia. It is a strong inotropic agent

with minimal chronotropic effect and no

vasoconstriction.

MEDICATIONS

Bronchodilators are an important

component of treatment in respiratory failure

caused by obstructive lung disease. These

agents act to decrease muscle tone in both

small and large airways in the lungs. This

category includes beta-adrenergics,

methylxanthines, and anticholinergics.

MEDICATIONS

• Terbutaline (Brethaire, Bricanyl)

Terbutaline acts directly on beta2

receptors to relax bronchial smooth muscle,

relieving bronchospasm and reducing airway

resistance.

MEDICATIONS

• Albuterol (Proventil)

Albuterol is a beta-agonist useful in the

treatment of bronchospasm. It selectively

stimulates beta2-adrenergic receptors of the

lungs. Bronchodilation results from relaxation of

bronchial smooth muscle, which relieves

bronchospasm and reduces airway resistance.

NURSING

DIAGNOSIS

1. Ineffective Airway Clearance May be related to Bronchospasm, Increased production of secretions; retained secretions; thick, viscous secretion

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

NURSING

DIAGNOSIS

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

NURSING

DIAGNOSIS

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

NURSING

DIAGNOSIS

4. 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

NURSING

DIAGNOSIS

5. Self-Care deficit, specify—intolerance to activity,

decreased strength/endurance, depression,

severe anxiety.

6. Home Maintenance, ineffective—intolerance to

activity, inadequate support system, insufficient

finances, unfamiliarity with neighborhood

resources.

NURSING

DIAGNOSIS

7. Infection, risk for—decreased ciliary action,

stasis of secretions, tissue destruction,

increased environmental exposure, chronic

disease process, malnutrition.

NURSING

INTERVENTIONS

• Auscultate breath sounds. Note adventitious breath sounds, e.g., wheezes, crackles, rhonchi.

• Assess/ monitor respiratory rate. Note inspiratory/ expiratory ratio.

• 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.

NURSING

INTERVENTIONS

• 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.

• Keep environmental pollution to a minimum, e.g.,

dust, smoke, and feather pillows, according to

individual situation.

• Encourage/ assist with abdominal or pursed-lip

breathing exercises.

NURSING

INTERVENTIONS

• Observe characteristics of cough, e.g., persistent,

hacking, moist. Assist with measures to improve

effectiveness of cough effort.

• Increase fluid intake to 3000 mL/day within cardiac

tolerance. Provide warm/ tepid liquids. Recommend

intakeof fluids between, instead of during, meals.

• Monitor/ graph serial ABGs, pulse oximetry, chest x-ray.

NURSING

INTERVENTIONS

• Assess respiratory rate, depth. Note use of accessory muscles, pursed-lip breathing, inability to speak/ converse.

• Elevate head of bed, assist patient to assume position to ease work of breathing. Include periods of time in prone position as tolerated. Encourage deep-slow or pursed-lip breathing as individually needed/ tolerated.

• Assess/ routinely monitor skin and mucous membrane color.

NURSING

INTERVENTIONS

• Expectoration of sputum; suction when

indicated.

• Auscultate breath sounds, noting areas of

decreased airflow and/or adventitious sounds.

• Palpate for fremitus.

• Monitor level of consciousness/ mental status.

Investigate changes.

NURSING

INTERVENTIONS

• Assess dietary habits, recent food intake.

Note degree of difficulty with eating.

Evaluate weight and body size (mass).

• Auscultate bowel sounds.

• Give frequent oral care, remove

expectorated secretions promptly, provide

specific container for disposal of

secretions and tissues.

NURSING

INTERVENTIONS

• Encourage a rest period of 1 hr before and after

meals. Provide frequent small feedings.

• Avoid gas-producing foods and carbonated

beverages.

• Avoid very hot or very cold foods.

• Weigh as indicated.

• Administer supplemental oxygen during meals

as indicated.

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