Respiratory arrest should be distinguished from respiratory failure.

The former refers to

the complete cessation of breathing, while respiratory failure is the inability to provide adequate
ventilation for the body's requirements. Respiratory failure could lead to arrest.

Respiratory Failure Workup
Approach Considerations
Respiratory failure may be associated with a variety of clinical manifestations.
However, these are nonspecific, and very significant respiratory failure may be
present without dramatic signs or symptoms. This emphasizes the importance
of measuring arterial blood gases in all patients who are seriously ill or in
whom respiratory failure is suspected.
Chest radiography is essential. Echocardiography is not routinely done but is
sometimes useful. Pulmonary functions tests (PFTs), if feasible, may be
helpful, although more useful in terms of defining recovery potential.
Electrocardiography (ECG) should be performed to evaluate the possibility of
a cardiovascular cause of respiratory failure; it also may detect dysrhythmias
resulting from severe hypoxemia or acidosis. Right-sided heart catheterization
is controversial.

Laboratory Studies
Once respiratory failure is suspected on clinical grounds, arterial blood gas
analysis should be performed to confirm the diagnosis and to assist in the
distinction between acute and chronic forms. This helps assess the severity of
respiratory failure and helps guide management.
A complete blood cell (CBC) count may indicate anemia, which can contribute
to tissue hypoxia, whereas polycythemia may indicate chronic hypoxemic
respiratory failure.
A chemistry panel may be helpful in the evaluation and management of a
patient in respiratory failure. Abnormalities in renal and hepatic function may
either provide clues to the etiology of respiratory failure or alert the clinician to
complications associated with respiratory failure. Abnormalities in electrolytes
such as potassium, magnesium, and phosphate may aggravate respiratory
failure and other organ function.
Measuring serum creatine kinase with fractionation and troponin I helps
exclude recent myocardial infarction in a patient with respiratory failure. An
elevated creatine kinase level with a normal troponin I level may indicate
myositis, which occasionally can cause respiratory failure.
In chronic hypercapnic respiratory failure, serum levels of thyroid-stimulating
hormone (TSH) should be measured to evaluate the possibility of
hypothyroidism, a potentially reversible cause of respiratory failure.
Radiography
Chest radiography is essential in the evaluation of respiratory failure because
it frequently reveals the cause (see the images below). However,
distinguishing between cardiogenic and noncardiogenic pulmonary edema is
often difficult. Increased heart size, vascular redistribution, peribronchial
cuffing, pleural effusions, septal lines, and perihilar bat-wing distribution of
infiltrates suggest hydrostatic edema; the lack of these findings suggests
acute respiratory distress syndrome (ARDS).

Bilateral airspace infiltrates on

chest radiograph film secondary to acute respiratory distress syndrome that
resulted in respiratory failure.
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 Extensive left-lung pneumonia
caused respiratory failure; the mechanism of hypoxia is intrapulmonary
shunting.
Echocardiography
Echocardiography need not be performed routinely in all patients with
respiratory failure. However, it is a useful test when a cardiac cause of acute
respiratory failure is suspected.
The findings of left ventricular dilatation, regional or global wall motion
abnormalities, or severe mitral regurgitation support the diagnosis of
cardiogenic pulmonary edema. A normal heart size and normal systolic and
diastolic function in a patient with pulmonary edema would suggest ARDS.
Echocardiography provides an estimate of right ventricular function and
pulmonary artery pressure in patients with chronic hypercapnic respiratory
failure.
Pulmonary Function Tests
Patients with acute respiratory failure generally are unable to perform PFTs;
however, these tests are useful in the evaluation of chronic respiratory failure.
Normal values for forced expiratory volume in 1 second (FEV1) and forced
vital capacity (FVC) suggest a disturbance in respiratory control. A decrease
in the FEV1 -to-FVC ratio (FEV1/FVC) indicates airflow obstruction, whereas a
reduction in both FEV1 and FVC and maintenance of FEV1/FVC suggest
restrictive lung disease.
Respiratory failure is uncommon in obstructive diseases when FEV1 is greater
than 1 L and in restrictive diseases when FVC is greater than 1 L.

Physical Examination
The signs and symptoms of acute respiratory failure reflect the underlying
disease process and the associated hypoxemia or hypercapnia. Localized
pulmonary findings reflecting the acute cause of hypoxemia (eg, pneumonia,
pulmonary edema, asthma, or chronic obstructive pulmonary disease
[COPD]), may be readily apparent. In patients with ARDS, the manifestations
may be remote from the thorax, such as abdominal pain or long-bone fracture.
Neurologic manifestations include restlessness, anxiety, confusion, seizures,
or coma.
Asterixis may be observed with severe hypercapnia. Tachycardia and a
variety of arrhythmias may result from hypoxemia and acidosis.
Cyanosis, a bluish color of skin and mucous membranes, indicates
hypoxemia. Visible cyanosis typically is present when the concentration of
deoxygenated hemoglobin in the capillaries or tissues is at least 5 g/dL.
Dyspnea, an uncomfortable sensation of breathing, often accompanies
respiratory failure. Excessive respiratory effort, vagal receptors, and chemical
stimuli (hypoxemia and/or hypercapnia) all may contribute to the sensation of
dyspnea.
Both confusion and somnolence may occur in respiratory failure. Myoclonus
and seizures may occur with severe hypoxemia. Polycythemia is a
complication of long-standing hypoxemia.
Pulmonary hypertension frequently is present in chronic respiratory failure.
Alveolar hypoxemia potentiated by hypercapnia causes pulmonary arteriolar
constriction. If chronic, this is accompanied by hypertrophy and hyperplasia of
the affected smooth muscles and narrowing of the pulmonary arterial bed. The
increased pulmonary vascular resistance increases afterload of the right
ventricle, which may induce right ventricular failure. This, in turn, causes
enlargement of the liver and peripheral edema. The entire sequence is known
as cor pulmonale.
Criteria for the diagnosis of ARDS include the following:
 Clinical presentation - Tachypnea and dyspnea; crackles upon
auscultation
 Clinical setting - Direct insult (aspiration) or systemic process
causing lung injury (sepsis)
 Radiologic appearance - 3-quadrant or 4-quadrant alveolar flooding
 Lung mechanics - Diminished compliance (< 40 mL/cm water)
 Gas exchange - Severe hypoxia refractory to oxygen therapy (ratio
of arterial oxygen tension to fractional concentration of oxygen in
inspired gas [PaO2/FiO2] < 200)
 Normal pulmonary vascular properties - Pulmonary capillary wedge
pressure lower than 18 mm Hg

AMBOSS

Respiratory failure
Summary
Respiratory failure is the acute or chronic inability of the respiratory system to
maintain gas exchange (PaO  of < 60 mmHg, PaCO > 50 mmHg). Causes can be
2 2 

extrapulmonary (e.g., CNS depression due to narcotic overdose) as well as

pulmonary (e.g., acute exacerbation of COPD). Respiratory failure can be
classified as hypoxemic (type 1) or hypercapnic (type 2). Clinical features of
hypoxemia include respiratory distress, cyanosis, tachycardia, and altered mental
status. Clinical features of hypercapnia include hypoventilation, headache, warm
extremities, and asterixis. Diagnostics include arterial blood gas analysis and
possibly chest imaging to detect the underlying disease. Treatment includes
supportive measures (oxygen delivery and/or ventilator support) and treatment of
the underlying condition. Complications may arise due to
prolonged hypoxemia and can affect various organs (e.g., renal/heart failure, brain
damage).

Clinical features of hypoxemia

o Tachypnea, dyspnea
o Cyanosis
 o Pleuritic chest pain
o Tachycardia, arrhythmia
o Confusion, somnolence
Clinical features of hypercapnia
o Hypoventilation
o Headache, daytime sleepiness
o Anxiety
o Warm extremities
o Papilledema
o Asterixis
o Coma
o Paralytic ileus
Diagnostics
 Arterial blood gas analysis (ABG): to confirm diagnosis
o Alveolar-arterial gradient: ([P  - 47] × FiO  - [PaCO /0.8]) - PaO
atm 2 2 2

o Normal Aa gradient: hypoventilation or ↓ oxygen uptake

o ↑ Aa gradient: V/Q mismatch or shunting
 Chest imaging (x-ray, CT): to assess for chest wall, pleural,
and/or lung lesions (e.g.,
trauma, ARDS, pneumonia, pneumothorax, atelectasis, pleural effusion)

Management

Supportive measures  [1]

 Nonmechanical ventilation/oxygen support

o Goal
 Correction of hypoxemia
 Mechanical ventilation
o Goal
 Correct hypercapnia and possible hypoxemia
o Oxygenation and ventilation are affected via change of the
following mechanical ventilator parameters:
 ↑ Respiratory rate and/or ↑ tidal volume → ↑
ventilation
 ↑ FiO  and/or ↑ PEEP → ↑ oxygenation
2
Etiology
 Pulmonary causes
o Airway obstruction (hypoventilation) and/or
increased physiologic dead space (e.g., due to exacerbation
of COPD, acute severe bronchial asthma, bronchiolitis)
o Impaired alveolar diffusion (e.g., due to pulmonary edema,
severe pneumonia, pulmonary hemorrhage , idiopathic
pulmonary fibrosis)
o Right-to-left shunt
 Pulmonary right-to-left shunt (e.g., due to ARDS,
pulmonary contusions/hemorrhage, lung collapse)
o V/Q mismatch (e.g., due to severe pneumonia, pulmonary
edema, pulmonary embolism, atelectasis)
o Decreased FiO  (e.g., due to asphyxiant gas exposure, high
2

altitude)
 Extrapulmonary causes
o CNS depression (e.g., due to narcotic or sedative overdose, brain
trauma/herniation, stroke)
o Respiratory muscle weakness (e.g., due to myasthenia
gravis, Guillain-Barre syndrome, myopathies, ALS, high
cervical spinal cord injury, poliomyelitis)
o Decreased chest wall compliance (e.g., due to rib
fractures, tension pneumothorax, tetanus, seizures, fibrothorax)
o Increased O  consumption and/or CO  production (e.g., due to
2 2

severe sepsis, toxic shock syndrome, cardiogenic

shock, multiorgan dysfunction)
o Electrolyte disturbances (e.g., anorexia nervosa)