RESPIRATORY FAILURE

SOFIA UNIVERSITY “ST. KLIMENT OHRIDSKI”

FACULTY OF MEDICINE
DEPARTMENT ANESTHESIOLOGY AND INTENSIVE CARE
DEFINITIONS

 Respiratory failure is a syndrome in which the respiratory

system fails in one or both of its gas exchange functions:
oxygenation and carbon dioxide elimination
 Hypoxemic respiratory failure (type I) is characterized by an
arterial oxygen tension (PaO2) lower than 60 mm Hg with a
normal or low arterial carbon dioxide tension (PaCO2).
 Hypercapnic respiratory failure (type II) is characterized by a
PaCO2 higher than 50 mm Hg.
 DEFINITIONS

 Respiratory failure may be further classified as either acute or chronic.

 Although acute respiratory failure is characterized by life-threatening derangements in arterial blood
gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may
not be as readily apparent.

 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.
 The major function of the
lung is to get oxygen into the
body and carbon dioxide out

CO2 O2
RESPIRATORY PHYSIOLOGY

 The act of respiration engages the following three processes:

 Transfer of oxygen across the alveolus
 Transport of oxygen to the tissues
 Removal of carbon dioxide from blood into the alveolus and then into the environment

 The carbon dioxide is transported in 3 main forms:

 in simple solution,
 as bicarbonate,
 combined with protein of hemoglobin as a carbamino compound.
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

 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.
 The various pathophysiological mechanisms which
cause respiratory failure.
FIO2

Ventilation
without
perfusion Hypoventilation
(deadspace
ventilation)

Diffusion
abnormality
Normal

Perfusion
without
ventilation
(shunting)
 Shunting is the most common cause for
hypoxaemic respiratory failure in ICU
FIO2 patients.
It is a form of ventilation-perfusion
mismatch in which alveoli which are not
ventilated (eg due to collapse or pus or
oedema fluid) are still perfused.
Ventilation
without
perfusion Hypoventilation
(deadspace
ventilation)

Diffusion
abnormality
Normal

Perfusion
without
ventilation
(shunting)
 Respiratory failure due to shunting is
relatively resistant to oxygen therapy.
Increasing the inspired oxygen
concentration has little effect because
it can not reach alveoli where shunting
is occurring and blood leaving normal
alveoli is already 100% saturated

75% 75%

100% 75%
87.5%
PERFUSION WITHOUT VENTILATION
(SHUNTING)
 Intra-cardiac
 Any cause of right to left shunt
 eg Fallot’s, Eisenmenger

 Intra-pulmonary
 Pneumonia
 Pulmonary oedema
 Atelectasis
 Collapse
 Pulmonary haemorrhage or contusion
Intra-pulmonary
 Small airways occluded ( e.g asthma, chronic bronchitis)
 Alveoli are filled with fluid ( e.g pulm edema, pneumonia)
 Alveolar collapse ( e.g atelectasis)
V/Q MISMATCH:

Dead space ventilation

Alveoli that are normally ventilated but poorly perfused

Anatomic dead space

Gas in the large conducting airways that does not come in contact with the capillaries e.g
pharynx

Physiologic dead space

Alveolar gas that does not equilibrate fully with capillary blood
DIFFUSION ABNORMALITY

 Less common

 Abnormality of the alveolar membrane or a reduction in the number of

capillaries resulting in a reduction in alveolar surface area

 Causes include:
 Acute Respiratory Distress Syndrome
 Fibrotic lung disease
Hypoventilation can be caused by disease at
any of the anatomical sites involved in
ventilation Brainstem

Spinal cord
Airway Nerve root

Lung Nerve

Pleura

Neuromuscular
Chest wall junction

Respiratory
muscle
ETIOLOGY

Common causes of type I (hypoxemic)  Pneumoconiosis

respiratory failure include the following:
 Granulomatous lung diseases
 COPD
 Cyanotic congenital heart disease
 Pneumonia
 Bronchiectasis
 Pulmonary edema
 Acute respiratory distress syndrome (ARDS)
 Pulmonary fibrosis
 Fat embolism syndrome
 Asthma
 Kyphoscoliosis
 Pneumothorax
 Obesity
 Pulmonary embolism
 Pulmonary arterial hypertension
ETIOLOGY

Common causes of type II (hypercapnic)  Porphyria

respiratory failure include the following:
 Cervical cordotomy
 COPD
 Head and cervical cord injury
 Severe asthma
 Primary alveolar hypoventilation
 Drug overdose
 Obesity-hypoventilation syndrome
 Poisonings
 Pulmonary edema
 Myasthenia gravis
 ARDS
 Polyneuropathy
 Myxedema
 Poliomyelitis
 Tetanus
 Primary muscle disorders
RESPIRATORY FAILURE
SYMPTOMS
 CNS:  Dyspnea
 Headache
 Visual Disturbances Cardiac:
 Anxiety Orthopnea
 Confusion
 Memory Loss
Peripheral edema
 Weakness Chest pain
 Decreased Functional Performance

 Pulmonary: Other:
 Cough
 Chest pains Fever, Abdominal pain, Anemia, Bleeding
 Sputum production
 Stridor
CLINICAL

 Respiratory compensation  Tissue hypoxia

 Tachypnea RR > 35 Breath /min  Altered mental state
 Accessory muscles  HR and BP (late)
 Recesssion
 Nasal flaring
 Haemoglobin desaturation
 cyanosis
 Sympathetic stimulation
 HR
 BP
 sweating
MENTAL STATE

⇓PaO2 +⇑PaCO2 ⇨ acidosis ⇨ dilatation of cerebral

resistance vesseles ⇨ ⇑ICP
Disorientation Headache
Coma personality changes
DEAD
RESPIRATORY FAILURE
LABORATORY TESTING

 Arterial blood gas

PaO2
PaCO2
 Respiratory mechanics
PH  Spirometry (FVC, FEV1, Peak flow)

 Chest imaging
 Ultrasound  Respiratory muscle pressures
 Chest x-ray  MIP ( maximum inspiratory pressure)
 CT  MEP ( maximum expiratory pressure
 Ventilation–perfusion scan

Other tests • EKG, echocardiogram

• Hemoglobin • Electromyography (EMG)
• Electrolytes, blood urea nitrogen, creatinine • Nerve conduction study
• Creatinine phosphokinase, aldolase
CRITERIA FOR THE DIAGNOSIS OF ARDS

 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 [PaO 2/FiO2]
< 200)
 Normal pulmonary vascular properties - Pulmonary capillary wedge pressure
lower than 18 mm Hg
DIFFERENTIAL DIAGNOSES

 Acute Respiratory Distress  Cyanosis  Noninvasive Ventilation

Syndrome
 Diaphragmatic Paralysis  Obstructive Sleep Apnea
 Angina Pectoris
 Dilated Cardiomyopathy  Pneumothorax Imaging
 Aspiration Pneumonitis and
Pneumonia  Distributive Shock  Idiopathic Pulmonary Arterial
Hypertension
 Asthma  Emphysema
 Pulmonary Embolism
 Atelectasis  Hypertrophic Cardiomyopathy
 Respiratory Acidosis
 Bacterial Pneumonia  Idiopathic Pulmonary Fibrosis
 Restrictive Lung Disease
 Cardiogenic Pulmonary Edema  Interstitial (Nonidiopathic)
Pulmonary Fibrosis  Nonidiopathic Pulmonary
 Cardiogenic Shock Hypertension
 Mechanical Ventilation
 Community-Acquired Pneumonia  Viral Pneumonia
(CAP)  Myocardial Infarction
 Cor Pulmonale  Neurogenic Pulmonary Edema
COMPLICATIONS

 Complications of acute respiratory failure may be:

 Pulmonary
 embolism, barotrauma, pulmonary fibrosis, and complications secondary to the use of
mechanical devices
 Cardiovascular
 hypotension, reduced cardiac output, arrhythmia, endocarditis, and acute myocardial
infarction
 gastrointestinal (GI)
 hemorrhage, gastric distention, ileus, diarrhea, and pneumoperitoneum
 infectious, renal, or nutritional.
TREATMENT &
MANAGEMENT
APPROACH CONSIDERATIONS

 The risks of oxygen therapy are oxygen toxicity and carbon dioxide narcosis. Pulmonary oxygen toxicity
rarely occurs when a fractional concentration of oxygen in inspired gas (FiO2) lower than 0.6 is used;
therefore, an attempt to lower the inspired oxygen concentration to this level should be made in
critically ill patients.
 Carbon dioxide narcosis occasionally occurs when some patients with hypercapnia are given oxygen to
breathe. Arterial carbon dioxide tension (PaCO2) increases sharply and progressively with severe
respiratory acidosis, somnolence, and coma. The mechanism is primarily the reversal of pulmonary
vasoconstriction and the increase in dead space ventilation.
 Hypoxemia is the major immediate threat to organ function. After the patient’s hypoxemia is corrected
and the ventilatory and hemodynamic status have stabilized, every attempt should be made to identify
and correct the underlying pathophysiologic process that led to respiratory failure in the first place. The
specific treatment depends on the etiology of respiratory failure.
 Patients generally are prescribed bed rest during early phases of respiratory failure management.
However, ambulation as soon as possible helps ventilate atelectatic areas of the lung.
 Consultation with a pulmonary specialist and an intensivist are often required. Patients with acute
respiratory failure or exacerbations of chronic respiratory failure need to be admitted to the intensive
care unit for ventilatory support.
 Etiology management
 Keep airway open
 Oxygen therapy and correction of
Hypoxemia
 Respiratory stimulant
 Non - invasive ventilation
 Invasive ventilation
 General supportive care
 Transfer to ICU
 Infection control
 Management of electrolyte and acid-
base disturbance
 Management of cor pulmonale,
pulmonary encephalopathy, multi-organ
disfunction syndrome
 Nutrition support
NONINVASIVE VENTILATORY SUPPORT

 Ventilatory support via a nasal or full-face mask rather than via an endotracheal
tube (see the images below) is increasingly being employed for patients with
acute or chronic respiratory failure.
 Noninvasive ventilation should be considered in patients with mild-to-moderate
acute respiratory failure.
 The patient should have an intact airway, airway-protective reflexes, and be alert
enough to follow commands.
MEDICATION

 Diuretics
 Furosemide (Lasix)
 Nitrates
 Nitroglycerin sublingual
 Nitroprusside sodium
 Analgesics
 Opioid Analgesics
 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.

 Inotropes
 Dopamine
 Norepinephrine
 Dobutamin
MEDICATION

 Bronchodilators
 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.
 Anticholinergics /ipratropium bromide/
 Anticholinergics antagonize the action of acetylcholine with muscarinic receptor on
bronchial smooth muscle.
 Corticosteroids
 Corticosteroids have been shown to be effective in accelerating recovery from acute
COPD exacerbations and are an important anti-inflammatory therapy in asthma.
Although they may not make a clinical difference in the emergency department (ED),
they have some effect 6-8 hours into therapy; therefore, early dosing is critical.
PROGNOSIS

 The mortality associated with respiratory failure varies according to the etiology.
For ARDS, mortality is approximately 40-45%;
 Younger patients (< 60 y) have better survival rates than older patients.
 Significant mortality also occurs in patients admitted with hypercapnic respiratory
failure.
 This is because these patients have a chronic respiratory disorder and other
comorbidities such as cardiopulmonary, renal, hepatic, or neurologic disease.
 For patients with COPD and acute respiratory failure, the overall mortality has
declined from approximately 26% to 10%.
 Acute exacerbation of COPD carries a mortality of approximately 30%. The mortality
rates for other causative disease processes have not been well described.
REFERENCES
 Intensive and Critical Care Medicine, WFSICCM World Federation of Societies of Intensive and Critical Care Medicine, Besso, José, Lumb, Philip
D., Williams, Ged (Eds.), ISBN 978-88-470-1436-7

 Clinical Anesthesia, seventh edition, Paul G. Barash, ISBN-13: 978-1451144192;

 Miller's Anesthesia, seventh edition, Ronald D. Miller MD MS, ISBN-13: 978-0702052835;

 Morgan and Mikhail's Clinical Anesthesiology, 5th edition, John Butterworth, ISBN-13: 978-0071627030.