Running a race at 12,000
feet
Respiratory Failure
By Ame Mehadi (BSc, MSc in
EMCCN)
Out line
• Terms
• Respiratory system
• Respiratory failure
– Definition
– Category
– Causes
– Diagnosis
– Presentation
– Management
Terms
• Respiratory Acidosis
• Metabolic Acidosis
• Metabolic Alkalosis
• Respiratory Alkalosis
• Ventilation
• Oxygenation
• Hypoxemia
• Hypercapnea
Respiratory system includes:
• CNS (medulla)
• Peripheral nervous system (phrenic nerve)
• Respiratory muscles
• Chest wall
• Lung
• Upper airway
• Bronchial tree
• Alveoli
• Pulmonary vasculature
Respiratory System
• Consists of two parts:
• Gas exchange organ (lung): responsible for
OXYGENATION
• Pump (respiratory muscles and respiratory control
mechanism): responsible for VENTILATION
NB: Alteration in function of gas exchange unit
(oxygenation) OR of the pump mechanism
(ventilation) can result in respiratory failure
Normal Breathing Rates
Adults 12-20 Breaths per minute
Child 15-30 Breaths per minute
Infant 25-50 Breaths per minute
Neonates 40-70 Breaths per minute
Definitions
• PACO2—Partial pressure of CO2 in the alveoli
• PaCO2—Partial pressure of CO2 in arterial blood
• PEtCO2—Partial pressure at the end of expiration
• PvCO2—Partial pressure of CO2 in mixed venous blood
• PCO2—Partial pressure of CO2
• PaO2—Partial pressure of O2 in arterial blood (hypoxemia)
• SPO2—Saturation of arterial blood (POX) percent
• SaO2—Percentage of arterial hemoglobin saturated with
O2 (POX)
• PO2—Partial pressure of O2
Arterial Blood Gases (ABG)
Normal values at sea level
pH 7.35-7.45
PaO2 >70 mmHg
PaCO2 35-45 mmHg
HCO3 22-28 mmol/l
RESPIRATORY FAILURE
• ↓pH Acidosis
• ↑pH Alkalosis
• ↓ PaO2 Hypoxemia
• ↑PaCO2 Hypercapnia
• ↓pH+ ↑PaCO2 R. acidosis
– ↑HCO3
• ↑pH+↓PaCO2 R.Alkalosis
– ↓HCO3
Cont’d…
• Arterial hypoxemia is defined as an arterial PO2
<80 mmHg, and respiratory failure as an arterial
PO2 <60 mmHg, breathing air
• Respiratory failure is subdivided according to the
arterial carbon dioxide tension (PaCO2).
– Type 1 respiratory failure is when arterial PCO2
is normal or low (<45 mmHg), and
– Type 2 respiratory failure is when arterial PCO2
is high (>45 mmHg)
Cont’d…
• “inability of the lung to meet the
metabolic demands of the body. This can
be from failure of tissue oxygenation
and/or failure of CO2 homeostasis.”
• “Acute respiratory failure developing in
hospital is usually due to pneumonia,
aspiration of secretions or gastric
contents, pulmonary edema or sedative
drugs”
Urgent investigation in
acute respiratory failure
• Chest X-ray
• Arterial blood gases and pH
• ECG
• Full blood count
• Blood glucose
• Sodium, potassium and creatinine
• Blood culture
• Sputum culture
Common causes of acute RF
• Primary cause
– Airway obstruction in the unconscious
patient
– Acute severe asthma
– Acute exacerbation of chronic obstructive
pulmonary disease
– Pneumonia
– Pulmonary embolism
– Cardiogenic pulmonary edema
– Acute respiratory distress syndrome
– Poisoning with psychotropic drugs or alcohol
Common causes ….
• Contributory factors
– Aspiration of secretions or gastric contents
– Respiratory muscle fatigue
– Severe obesity
– Chest wall abnormality, e.g. kyphoscoliosis
– Large pleural effusion
– Pneumothorax
– Sedative drugs: benzodiazepines, opioids
Potential causes of Respiratory Failure
HYPOXEMIC RF (TYPE 1)
• PaO2 <60mmHg with normal or ↓ PaCO2
normal or high pH
• Most common form of respiratory failure
• Associated with acute diseases of the lungs.
• Lung disease is severe to interfere with
pulmonary O2 exchange, but over all ventilation
is maintained
• Pulmonary edema (Cardiogenic, noncardiogenic
(ARDS), pneumonia, pulmonary hemorrhage,
and collapse.)
• Physiologic causes: V/Q mismatch and shunt
HYPOXEMIC RF
CAUSES OF ARTERIAL HYPOXEMIA
1.FiO2
2. Hypoventilation ( PaCO2)
3. V/Q mismatch (e.g. COPD)
4. Diffusion limitation ?
5. Intrapulmonary
- Pneumonia
- Atelectasis
- CHF (high pressure pulmonary edema)
- ARDS (low pressure pulmonary edema)
Causes of Hypoxemic RF
• Caused by a disorder of heart, lung or
blood.
• Etiology easier to assess by CXR
abnormality:
– Normal Chest x-ray
• Cardiac shunt (right to left)
• Asthma,
• COPD
• Pulmonary embolism
Hyperinflated Lungs : COPD
Causes of Hypoxemic RF (cont’d.)
• Focal infiltrates on CXR
Atelectasis
Pneumonia
Causes of Hypoxemic RF (cont’d.)
Diffuse infiltrates on CXR
– Cardiogenic Pulmonary Edema
– Non cardiogenic pulmonary edema
(ARDS)
– Interstitial pneumonitis or fibrosis
– Infections
Diffuse pulmonary infiltrates
Hypercapnic Respiratory Failure
(Type
• PaCO2 >50 mmHg II)
• Hypoxemia is common
• pH depends on level of HCO3
• HCO3 depends on duration of hypercapnia
• Renal response occurs over days to weeks
Acute Hypercapnic RF (Type II)
• Acute
– Arterial pH is low
– Causes
- sedative drug over dose
- acute muscle weakness such as myasthenia gravis
- severe lung disease: alveolar ventilation can not be
maintained (i.e. Asthma or pneumonia)
• Acute on chronic:
– This occurs in patients with chronic CO2 retention who
worsen and have rising CO2 and low pH.
– Mechanism: respiratory muscle fatigue
Causes of Hypercapnic RF
• Respiratory centre (medulla) dysfunction
• Drug over dose, CVA, tumor, hypothyroidism, central
hypoventilation
• Neuromuscular disease: Guillain-Barre, Myasthenia
Gravis, polio, spinal injuries
• Chest wall/Pleural diseases: kyphoscoliosis,
pneumothorax, massive pleural effusion
• Upper airways obstruction: Tumor, FB, laryngeal
edema
• Peripheral airway disorder: Asthma, COPD
Respitory failure
Types
Type 1 Type 2
• Hypoxemic RF • Hypercapnic RF
• PaO2 < 60 mmHg with • PaCO2 > 50 mmHg
normal or ↓ PaCO2. • Hypoxemia is
• Associated with acute common
diseases of the lungs. • Drug overdose,
• Pulmonary edema neuromuscular
(Cardiogenic, disease, chest wall
noncardiogenic (ARDS), deformity, COPD, and
pneumonia, pulmonary Bronchial asthma.
hemorrhage, and • Obesity
collapse.) hypoventilation
syndrome
• Parenchymal disease
• Kyphoscoliosis
• Hypoxic environments
Respiratory failure
Acute RF Chronic RF
• Develops over minutes • Develops over days
to hours • ↑ in HCO3
• ↓ pH quickly to <7.2 • ↓ pH slightly
• Polycythemia,
• Example; Pneumonia Corpulmonale
• Example; COPD
Pathophysiologic causes of Acute
Respiratory Failure
●Hypoventilation
●V/P mismatch
●Shunt
●Diffusion abnormality
Pathophysiologic ….
1 - Hypoventilation
• Occurs when ventilation ↓
• Causes
– Depression of CNS from drugs
– Neuromuscular disease of respiratory
muscles
• ↑PaCO2 and ↓PaO2
• COPD
2 -V/Q mismatch
• Most common cause of hypoxemia
• Low V/Q ratio, may occur either from
– Decrease of ventilation 2ry to airway or
interstitial lung disease
– Over perfusion in the presence of
normal ventilation e.g. PE
• Admin. of 100% O2 eliminate hypoxemia
Pathophysiologic….
3 -Shunt
• The deoxygenated blood bypasses the
ventilated alveoli and mixes with oxygenated
blood → hypoxemia
• Persistent of hypoxemia despite 100% O2
inhalation
• Hypercapnia occur when shunt is excessive >
60%
• Pulmonary shunt exists when there is normal
perfusion to an alveolus, but ventilation fails
to supply the perfused region.
Pathophysiologic causes ….
3 –Shunt….
Causes
•Intracardiac
– Right to left shunt
• Fallot’s tetralogy
• Eisenmenger’s syndrome
•Pulmonary
– A/V malformation
– Pneumonia
– Pulmonary edema
– Atelectasis/collapse
– Pulmonary Hemorrhage
– Pulmonary contusion
Pathophysiologic causes….
4 - Diffusion abnormality
• Less common
• Due to
– abnormality of the alveolar
membrane
– ↓ the number of the alveoli
• Causes
– ARDS
– Fibrotic lung disease
COMMON PRESENTATIONS
Respiratory failure
• Clinical features of acute respiratory failure
– Respiratory distress (dyspnea, tachypnea, ability
to speak only in short sentences or single words,
agitation, sweating)
– Respiratory rate <8 or >30/min
– Accessory muscles of breathing active
– Feeble respiratory efforts, silent chest
– Tremor, asterisk
– Cyanosis
– Agitation, confusion
– Reduced LOC, coma
– Bradycardia or hypotension
Clinical and Laboratory Manifestation
(non-specific and unreliable)
• Cyanosis
- bluish color of mucous membranes/skin
indicate hypoxemia
- unoxygenated hemoglobin 50 mg/L
- not a sensitive indicator
• Dyspnea
– secondary to hypercapnia and hypoxemia
• Paradoxical breathing
• Confusion, somnolence and coma
• Convulsions
Clinical & Laboratory Manifestations
• Circulatory changes
– tachycardia, hypertension, hypotension
• Polycythemia
– Chronic hypoxemia - erythropoietin synthesis
• Pulmonary hypertension
• Cor-pulmonale or right ventricular failure
Assessment of hypoxaemia
• Detection of cyanosis -fraught with error ie hypoxaemia often
missed specially if anaemic – oximetry much better
• Tachypnoea, tachycardia often present but not always
• Confusion, restlessness maybe more prominent especially in
the elderly
• respiratory rate is the single best predictor of severe illness- but
beware the calm patient hypoventilating from opiates!
• Hx and examination
• Previously healthy or features of COPD
• Other illnesses predisposing to CO2 retention
• Clinical picture will usually point towards correct diagnosis
• In dire emergencies resuscitate first then go through above
steps
Management: general principles
• Maintain patent airway
• Increase inspired oxygen concentration if needed to
achieve target SaO2 >90% (>88% in acute
exacerbation of COPD)
• Treat underlying cause and contributory factors
• If feasible, sit the patient up to improve diaphragmatic
descent and increase tidal volume
• Clear secretions: encourage cough, physiotherapy,
aspiration, hydration
• Drain large pleural effusion if present
• Drain pneumothorax if present
• Optimize CO: treat hypotension and heart failure
• Consider ventilatory support
Management of RF 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
Oxygen Therapy
• Supplemental O2 therapy essential
• Titration based on SaO2, PaO2 levels and PaCO2
• Goal is to prevent tissue hypoxia
• Tissue hypoxia occurs (normal Hb & C.O.)
– venous PaO2 < 20 mmHg or SaO2 < 40%
– arterial PaO2 < 38 mmHg or SaO2 < 70%
• Increase arterial PaO2 > 60 mmHg(SaO2 > 90%) or
venous SaO2 > 60%
• O2 dose either flow rate (L/min) or FiO2 (%)
Physiology of CO2
• Concentration of CO2 in alveoli is
determined by:
Perfusion (Q)
Ventilation (V)
• Concentration of CO2 in alveoli is:
• Varies indirectly with ventilation
Oxygenation
• Measured by pulse oximetry (SpO2)
– Noninvasive measurement
– Percentage of oxygen in red blood cells
– Changes in ventilation take several minutes to
be detected
– Affected by motion artifact, poor perfusion,
temperature
Ventilation
• Measured by the end-tidal CO2
– Partial pressure (mm Hg) or volume (%) of CO2
in the airway at end of exhalation
– Breath-to-breath measurement provides
information within seconds
– Not affected by motion artifact, distal
circulation, temperature
Normal Ventilation/Perfusion
Ratio
• The volume of blood returning to the
lungs matches the capacity of the
lungs to exchange gases
• Ventilation
• Cardiac Output
Ventilation-Perfusion (V/Q)
Mismatch
• Phenomenon where either perfusion or
ventilation to an area of lung decreases;
results in diminished gas exchange,
hypoxemia, and hypercapnia
• •If ventilation is held constant, then changes in
EtCO2 are due to changes in cardiac output.
Summary
• Exacerbation of COPD is a classical
example of type 1 respiratory failure
