Respiratory Failure

Definition
• Respiratory failure is defined as
respiratory dysfunction resulting in
abnormalities of oxygenation or
ventilation (CO2 elimination) severe
enough to threaten the function of vital
organs

• Arterial blood gas criteria for respiratory

failure are not absolute but may be
arbitrarily established as a PO2 under 60
mm Hg or a PCO2 over 50 mm Hg
 Causes of Respiratory failure
• Airway disorders   
Asthma,  Acute exacerbation of chronic bronchitis
or emphysema,  Obstruction of pharynx, larynx,
trachea, mainstem bronchus, or lobar bronchus by
edema, mucus, mass, or foreign body
• Pulmonary edema
   Increased hydrostatic pressure, Left ventricular
dysfunction (eg, myocardial ischemia, heart failure),
Mitral regurgitation, Left atrial outflow obstruction
(eg, mitral stenosis), Volume overload states,
Increased pulmonary capillary permeability, Acute
respiratory distress syndrome, Acute lung injury,
Unclear etiology, Neurogenic, Negative pressure
(inspiratory airway obstruction), Reexpansion,
Tocolytic-associated
• Parenchymal lung disorders   
Pneumonia  Interstitial lung diseases  Diffuse
alveolar hemorrhage syndromes  Aspiration  Lung
contusion

• Pulmonary vascular disorders   

Thromboembolism  Air embolism  Amniotic fluid
embolism

• Chest wall, diaphragm, and pleural

disorders
Rib fracture   Flail chest   Pneumothorax   Pleural
effusion   Massive ascites   Abdominal distention
and abdominal compartment syndrome
• Neuromuscular and related disorders   
Primary neuromuscular diseases     Guillain-Barré
syndrome     Myastheniagravis     Poliomyelitis
    Polymyositis   Drug- or toxin induced     Botulism
    Organophosphates     Neuromuscular blocking agents
    Aminoglycosides   Spinal cord injury   Phrenic nerve
injury or dysfunction   Electrolyte disturbances:
hypokalemia, hypophosphatemia   Myxedema

• Central nervous system disorders  

 Drugs: sedative, hypnotic, opioid, anesthetics   Brain
stem respiratory center disorders: trauma, tumor,
vascular disorders, hypothyroidism   Intracranial
hypertension   Central nervous system infections

• Increased CO2 production

Fever   Infection   Hyperalimentation with excess caloric
and carbohydrate intake   Hyperthyroidism  Seizures
  Rigors   Drugs
Extensive left-lung pneumonia caused respiratory failure; the
mechanism of hypoxia is intrapulmonary shunting
 Classification
Hypoxemic respiratory failure (type I)

• It is characterized by a PaO2 of less than 60 mm Hg

with a normal or low PaCO2

• This is the most common form of respiratory failure,

and it can be associated with virtually all acute
diseases of the lung, which generally involve fluid
filling or collapse of alveolar units

• Some examples of type I respiratory failure are

cardiogenic or noncardiogenic pulmonary edema,
pneumonia, and pulmonary hemorrhage
 Hypercapnic respiratory failure (type II)

• It is characterized by a PaCO2 of more than 50 mm

Hg

• Hypoxemia is common in patients with hypercapnic

respiratory failure who are breathing room air

• The pH depends on the level of bicarbonate, which, in

turn, is dependent on the duration of hypercapnia

• Common etiologies include drug overdose,

neuromuscular disease, chest wall abnormalities, and
severe airway disorders (eg, asthma, chronic
obstructive pulmonary disease [COPD])
 Pathophysiology
Hypoxemic respiratory failure
• Ventilation-perfusion (V/Q) mismatch and shunt are
mechanisms responsible for Type I failure

• With V/Q mismatch, the areas of low ventilation relative to

perfusion (low V/Q units) contribute to hypoxemia

• An intrapulmonary or intracardiac shunt causes mixed venous

(deoxygenated) blood to bypass ventilated alveoli and results
in venous admixture

• These 2 mechanisms lead to widening of the alveolar-arterial

oxygen difference, which normally is less than 15 mm Hg

• The distinction between V/Q mismatch and shunt can be made

by assessing the response to oxygen supplementation or
calculating the shunt fraction following inhalation of 100%
oxygen.

• In most patients these 2 mechanisms coexist

 Common causes of type I
(hypoxemic) respiratory failure
– Chronic bronchitis and emphysema (COPD)
– Pneumonia
– Pulmonary edema
– Pulmonary fibrosis
– Asthma
– Pneumothorax
– Pulmonary embolism
– Pulmonary arterial hypertension
– Pneumoconiosis
– Granulomatous lung diseases
– Cyanotic congenital heart disease
– Bronchiectasis
– Adult respiratory distress syndrome
– Fat embolism syndrome
– Kyphoscoliosis
– Obesity
 Pathophysiology
Hypercapnic respiratory
failure
• At a constant rate of carbon dioxide
production, PaCO2 is determined by the level
of alveolar ventilation

• A reduction in minute ventilation is observed

primarily in the setting of neuromuscular
disorders and CNS depression

• In pure hypercapnic respiratory failure, the

hypoxemia is easily corrected with oxygen
therapy
• 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 PaCO2

• 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.
 Common causes of type II
(hypercapnic) respiratory failure
– Chronic bronchitis and emphysema (COPD)
– Severe asthma
– Drug overdose
– Poisonings
– Myasthenia gravis
– Polyneuropathy
– Poliomyelitis
– Primary muscle disorders
– Porphyria
– Cervical cordotomy
– Head and cervical cord injury
– Primary alveolar hypoventilation
– Obesity hypoventilation syndrome
– Pulmonary edema
– Adult respiratory distress syndrome
– Myxedema
– Tetanus
Distinctions between acute
and chronic respiratory
failure
• Acute hypercapnic respiratory failure develops
over minutes to hours; therefore, pH is less than 7.3

• Chronic respiratory failure develops over several

days or longer, allowing time for renal compensation
and an increase in bicarbonate concentration.
Therefore, the pH usually is only slightly decreased.

• The distinction between acute and chronic

hypoxemic respiratory failure cannot readily be
made on the basis of arterial blood gases. The
clinical markers of chronic hypoxemia, such as
polycythemia or cor pulmonale, suggest a long-
standing disorder
Pathophysiologic causes of
acute respiratory failure
• Hypoventilation
• V/Q mismatch
• Shunt

These are the most common

pathophysiologic causes of acute
respiratory failure
 Clinical Findings
• The symptoms and signs of acute respiratory
failure are both insensitive and nonspecific;
therefore, the physician must maintain a high
index of suspicion and obtain arterial blood
gas analysis if respiratory failure is suspected

• Symptoms and signs of acute respiratory

failure are those of the underlying disease
combined with those of hypoxemia or
hypercapnia
• The chief symptom of hypoxemia is dyspnea

• Signs of hypoxemia include cyanosis,

restlessness, confusion, anxiety, delirium,
tachypnea, bradycardia or tachycardia,
hypertension, cardiac dysrhythmias, and tremor

• Dyspnea and headache are the cardinal

symptoms of hypercapnia

• Signs of hypercapnia include peripheral and

conjunctival hyperemia, hypertension,
tachycardia, tachypnea, impaired consciousness,
papilledema, and asterixis
 Treatment
• Treatment of the patient with acute
respiratory failure consists of

• (1) specific therapy directed toward

the underlying disease

• (2) respiratory supportive care

directed toward the maintenance of
adequate gas exchange

• (3) general supportive care

Management of Respiratory
Failure Principles
• Hypoxemia may cause death in RF
• Primary objective is to reverse and
prevent hypoxemia
• Secondary objective is to control
PaCO2 and respiratory acidosis
• Treatment of underlying disease
• Patient’s CNS and CVS must be
monitored and treated
 Respiratory Support
• Respiratory support has both nonventilatory and
ventilatory aspects
Nonventilatory aspects
• The main therapeutic goal in acute hypoxemic
respiratory failure is to ensure adequate
oxygenation of vital organs
• Inspired oxygen concentration should be the lowest
value that results in an arterial hemoglobin saturation
of 90% (PO2 60 mm Hg)
• Higher arterial oxygen tensions are of no proven
benefit
• Hypoxemia in patients with obstructive airway disease
is usually easily corrected by administering low-flow
oxygen by nasal cannula (1–3 L/min) or Venturi mask
(24–28%)
• Higher concentrations of oxygen are necessary to
correct hypoxemia in patients with ARDS, pneumonia,
and other parenchymal lung diseases
 Ventilatory aspects
• Ventilatory support consists of maintaining
patency of the airway and ensuring adequate
alveolar ventilation

• Noninvasive positive-pressure ventilation

• NPPV delivered via a full face mask or nasal mask

has become first-line therapy in COPD patients
with hypercapnic respiratory failure who can
protect and maintain the patency of their airway,
handle their own secretions, and tolerate the
mask apparatus

• Patients with acute lung injury or ARDS or those

who suffer from severely impaired oxygenation
do not benefit and should be intubated if they
require mechanical ventilation.
Headgear and full face mask commonly are used as the
interface for noninvasive ventilatory support
 A Bilevel positive airway pressure support machine is shown
here. This could be used in spontaneous mode or timed mode
• Tracheal intubation
• Indications for tracheal intubation include

• (1) hypoxemia despite supplemental oxygen

• (2) upper airway obstruction
• (3) impaired airway protection
• (4) inability to clear secretions
• (5) respiratory acidosis
• (6) progressive general fatigue, tachypnea,
use of accessory respiratory muscles, or
mental status deterioration
• (7) apnea
• Mechanical ventilation

• Indications for mechanical ventilation include

• (1) apnea
• (2) acute hypercapnia that is not quickly reversed by
appropriate specific therapy
• (3) severe hypoxemia
• (4) progressive patient fatigue despite appropriate
treatment.

• Several modes of positive-pressure ventilation

are available

• PEEP is useful in improving oxygenation in patients with

diffuse parenchymal lung disease such as ARDS. It
should be used cautiously in patients with localized
parenchymal disease, hyperinflation, or very high airway
pressure requirements during mechanical ventilation
 General Supportive Care
• Maintenance of adequate nutrition is vital;.
Overfeeding, especially with carbohydrate-rich
formulas, should be avoided, because it can increase
CO2 production and may potentially worsen or induce
hypercapnia

• Hypokalemia and hypophosphatemia may worsen

hypoventilation due to respiratory muscle weakness

• Sedative-hypnotics and opioid analgesics should be

titrated carefully to avoid oversedation, leading to
prolongation of intubation

• Temporary paralysis with a neuromuscular blocking

agent is occasionally used to facilitate mechanical
ventilation and to lower oxygen consumption.
Prolonged muscle weakness due to an acute myopathy
is a potential complication of these agents
• Psychological and emotional support of the patient and family

• Skin care to avoid decubitus ulcers

• Meticulous avoidance of nosocomial infection and

complications of tracheal tubes are vital aspects of
comprehensive care for patients with acute respiratory failure

• Stress gastritis and ulcers may be avoided by administering

sucralfate, histamine H2-receptor antagonists, or proton pump
inhibitors but many clinicians therefore prefer sucralfate

• The risk of DVT and pulmonary embolism may be reduced by

subcutaneous administration of heparin (5000 units every 12
hours), the use of LMW heparin or placement of a sequential
compression device on an extremity