Acute Respiratory Failure

See Also

Definitions

Bellow Failure
1. Respiratory "pump" failure to expand chest and trigger inspiration
2. Due to insufficient effort or respiratory drive, neuromuscular Impairment, muscle Fatigue, inefficient bellows

Background

Respiratory Failure represents a loss of the normal, substantial Ventilatory reserve
1. In those without Bellows Failure, Minute Ventilation may increase 20 fold over a baseline of 6 l/min

Types
Hypoventilatory Respiratory Failure with Hypercapnia due to Bellows Failure

Defining features
1. High PaCO2 >50 mmHg
2. Normal A-a Gradient
  1. Contrast with decompensated COPD in which pCO2 is increased, but A-a Gradient is high
  2. Normal A-a Gradient suggests external cause, with normal lungs and normal alveolar gas exchange
Causes: Compromised lung mechanics
1. Background
  1. Work of breathing costs increase significantly with impaired lung mechanics
  2. Patients with normal lungs expend only 1 ml oxygen per 1 liter of Minute Ventilation
  3. Patients with impaired lungs may expend 10-20 ml oxygen per 1 liter of Minute Ventilation
  4. Respiratory muscles Fatigue and fail at acute, persistent workloads >40% of maximal workload
2. Upper airway obstruction
  1. Infection (Epiglottitis, Bacterial Tracheitis, croup)
  2. Adenotonsillar Hypertrophy
  3. Neck Mass
  4. Thyroid Goiter
  5. Obstructive Sleep Apnea
  6. Vocal Cord Paralysis (bilateral)
  7. Laryngeal Foreign Body
3. Pulmonary muscle Fatigue (Skeletal muscle Fatigues at >40% of maximum load)
  1. Obesity
  2. Supine position
  3. Kyphoscoliosis
  4. Ankylosing Spondylitis
  5. Hypercarbia (fever, Sepsis, burns)
4. Inefficient breathing
  1. Obstructive Lung Disease (flat diaphragm, high Residual Volume)
    1. Asthma
    2. COPD (Emphysema or Chronic Bronchitis)
  2. Restrictive Lung Disease
    1. Anatomic Dead Space accounts for a large percentage of a fixed, reduced Tidal Volume
5. Chest Trauma
  1. Pneumothorax
    1. Air in the pleural space prevents negative pressure from forming within the chest
    2. Loss of negative pressure results in lung failing to expand with diaphragmatic excursion
  2. Flail Chest or multiple Rib Fractures
  3. Diaphragmatic Rupture
  4. Hemothorax
6. Other chest conditions interfering with ventilation
Causes: Loss of Inspiratory Drive (Insufficient Effort)
1. Drug Overdose or depressant drugs
  1. Opioids
  2. Benzodiazepines
  3. Barbiturates
  4. Procedural Anesthesia (e.g. Propofol)
  5. Phencyclidine (PCP)
2. Brainstem injury
  1. See Breathing Patterns in Brain Injury
  2. Brainstem Herniation
3. Severe global CNS injury
  1. Head Trauma
  2. Intracranial Hemorrhage
  3. CNS Infection (Meningitis, Encephalitis, Brain Abscess, West Nile Encephalitis, Poliomyelitis)
  4. Central Sleep Apnea
  5. Central Alveolar Hypoventilation Syndrome (CHS)
4. CO2 Retention
  1. Blue Bloaters (Chronic Bronchitis)
    1. Obese with hypoventilation despite Hypoxia
    2. Hypercarbia resulting in increased sedation
    3. Cyanotic (polycythemic with increased desaturated Hemoglobin)
Causes: Neuromuscular
1. Toxins (or other medication adverse effects)
2. Electrolyte and endocrine abnormalities
  1. Hyponatremia
  2. Hypocalcemia
  3. Hypokalemia
  4. Hyperkalemia
  5. Hypomagnesemia
  6. Severe Hypophosphatemia
  7. Hypothyoidism
3. Nerve dysfunction
  1. Spinal cord injury
  2. Polyneuritis (e.g. Guillain-Barre Syndrome)
  3. Amyotrophic Lateral Sclerosis
  4. Multiple Sclerosis
  5. Nerve Agent Exposure (e.g. Organophosphates)
  6. Phrenic nerve injury
    1. Example: Phrenic Nerve Injury from Birth Trauma
4. Muscular dysfunction
  1. Congenital Muscular Dystrophy
  2. Myasthenia Gravis
  3. Polymyositis
  4. Tetanus

Types
Hypercarbic Respiratory Failure from Diffuse Severe Lung Disease (large Respiratory Dead Space)

Background
1. Severe, diffuse lung disease with poor gas exchange
  1. pCO2 is easily excreted even through mild-moderately disease alveoli
  2. Hypercarbia requires apnea (Bellows Failure) or diffuse, severely impaired gas exchange
2. Ventilated lung with poor gas exchange is dead space, wasted ventilation
3. Perfusion to lung units that receive less ventilation results in blood retaining more CO2 and less O2
4. Increased respiratory effort cannot fully compensate for increased dead space and CO2 production
Defining features
1. High PaCO2
  1. May be normal or low in mild to moderate disease compensated with Hyperventilation
  2. However, with decompensation, pCO2 rises
2. Low PaO2
3. Increased A-a Gradient
4. Often improves with Supplemental Oxygen
Causes:
1. Decompensated Obstructive Lung Disease
  1. Asthma or Bronchospasm
  2. Chronic Obstructive Pulmonary Disease (COPD)
2. Decompensated Interstitial Lung Disease (e.g. Idiopathic Pulmonary Fibrosis, Sarcoidosis)
3. Decompensated Cystic Fibrosis

Types
Hypoxemic Respiratory Failure without Hypercarbia

Background
1. Alveoli fill with fluid (esp. in dependent lung) and are unable to oxygenate
2. Interstitial fluid results in stiff lungs that ventilate poorly
3. Small airways collapse
4. Right to Left intrapulmonary shunt past poorly ventilated lung
5. Carbon dioxide may still be expired as dead space is not increased (contrast with hypercapnic failure)
  1. CO2 is highly soluble in fluid (contrast with O2) and diffuses well despite fluid filled alveoli
6. Patient cannot oxygenate despite increased Respiratory Rate and ventilation
  1. Blood in non-edematous lung is fully saturated with oxygen
  2. Blood in edematous lung is not able to oxygenate
Defining features
1. Low PaCO2
  1. Contrast with Bellows Failure and Decompensated Severe, Diffusely impaired alveolar gas exchange
2. Low PaO2 <50-60 mmHg on room air
3. A-a Gradient may be increased
4. May not improve with Supplemental Oxygen
Causes: Improved with Supplemental Oxygen
1. Non-specific
2. May be due to any Hypoxia cause (e.g. mild-moderate COPD, Asthma, CHF, PE)
Causes: Not improved with Supplemental Oxygen (pO2 <50 mmHg despite oxygen)
1. Suggests Physiologic right to left intrapulmonary shunting (esp. lung edema)
  1. Oxygen and Hyperventilation are unable to compensate for shunted (non-oxygenated) blood
  2. Blood has a fixed ceiling for Oxygen Saturation, above which no further oxygen is absorbed
    1. pO2 increases with FIO2 and alveolar recruitment from diseased, shunted regions
    2. Alveolar recruitment increases with NIPPV (PEEP, CPAP, BiPAP) and Mechanical Ventilation
2. Cardiac Pulmonary Edema (increased transcapillary pressure)
  1. Left Ventricular Failure
  2. Acute Myocardial Ischemia (left ventricle)
  3. Malignant Hypertension
  4. Mitral Regurgitation or stenosis
3. Lung Conditions (often with increased capillary permeability)
  1. Severe Lobar Pneumonia
    1. Autoregulatory Vasoconstriction normally decreases perfusion to non-ventilated alveoli
    2. Significant right to left shunt occurs when Vasoconstriction fails to prevent perfusion to infected lung
  2. Pulmonary Contusion
  3. Alveolar Hemorrhage
  4. Acute Respiratory Distress Syndrome (ARDS)
    1. Increased permeability (low pressure edema)
4. Miscellaneous other causes
  1. Pulmonary Embolism

Types
Miscellaneous Secondary Causes of Hypoxia

Symptoms

Signs

General appearance
1. Altered Mental Status
2. Diaphoresis
Increased work of breathing
1. Accessory muscle use
2. Intercostal retractions
3. Tachypnea
4. Paradoxical breathing patterns
  1. Abdominal wall moves inward with inspiration as respiratory Fatigue occurs
Cardiovascular changes
1. Mucous membrane and nail bed Cyanosis
2. Tachycardia
3. Hypertension

Labs

Complete Blood Count
Comprehensive Metabolic Panel
Serum Troponin
Serum Brain Natriuretic Peptide (BNP, NT-proBNP)
D-Dimer
Arterial Blood Gas
1. See ABG Interpretation
2. Venous Blood Gas (VBG) is often used instead, but cannot use pO2 based calculations (e.g. A-a Gradient)
3. A-a Gradient
  1. Distinguishes intrinsic lung causes (e.g. V/Q mismatch) from external causes (e.g. Bellows Failure)
  2. Increased A-a Gradient suggests intrinsic lung cause, whereas A-a Gradient is normal in external causes
4. Increased pCO2 Causes
  1. Bellows Failure with inadequate ventilation (normal lungs and gas exchange)
    1. Normal A-a Gradient
  2. Severely abnormal lungs with V/Q mismatch and unable to compensate with Minute Ventilation (e.g. COPD)
    1. Increased A-a Gradient

Imaging

Chest XRay
Consider Bedside Lung Ultrasound in Emergency
Consider CT Pulmonary Angiography
1. See Pulmonary Embolism Diagnosis

Differential Diagnosis

See Causes above
See Dyspnea Causes
See Tachypnea Causes
See Hypoxia

Management
General

See Emergency Breathing Management
See Advanced Airway
See Non-Invasive Positive Pressure Ventilation
See Mechanical Ventilation
Specific Approaches
Bellows Failure or apnea (increased PaCO2, normal A-a Gradient)
1. Aggressive management is required (e.g. consider Endotracheal Intubation and Mechanical Ventilation)
2. Manage immediately reversible causes (e.g. coma cocktail with Naloxone, dextrose)
3. Consider upper airway obstruction (e.g. Anaphylaxis, Foreign Body Aspiration)
4. Evaluate Trauma patients for chest wall defects interfering with bellows function (e.g. Flail Chest)
5. In progressive neuromuscular disorders (e.g. Guillain Barre Syndrome) evaluate for impending Respiratory Failure
  1. Vital Capacity <15-20 ml/kg
  2. Tidal Volume <5 ml/kg
  3. Maximum expiratory force <40 cm H2O (normally >100 cm H2O)
  4. Maximum inspiratory force <30 cm H2O (normally >100 cm H2O)
Hypercarbic Respiratory Failure from Diffuse Severe Lung Disease (large Respiratory Dead Space)
1. COPD
  1. See Emergency Management of COPD Exacerbation
  2. Conservative management with controlled Oxygen Delivery (avoiding CO2 narcosis)
  3. Bronchodilators and Corticosteroids
  4. Non-Invasive Positive Pressure Ventilation (NIPPV) as needed
  5. Antibiotics for productive or purulent cough and increased Dyspnea or requiring NIPPV or Intubation
  6. Comorbid Right Heart Failure may Compound Presentation
  7. Avoid Endotracheal Intubation and Mechanical Ventilation if possible
    1. Ventilator Weaning may be more difficult
    2. See Mechanical Ventilation for settings
    3. Requires larger Tidal Volumes (e.g. 10 ml/kg) due to large Physiologic Dead Space
    4. Avoid excessive correction of PaCO2
      1. Correct pH, but avoid Respiratory Alkalosis
      2. Allows for pre-existing metabolically compensated hypercarbia
    5. Decrease air trapping by allowing greater time for expiration
      1. Shorten inspiratory time by increasing inspiratory rate
      2. Decrease Respiratory Rate
2. Asthma
  1. See Emergency Management of Asthma Exacerbation (or Status Asthmaticus)
Pulmonary Edema
1. See Congestive Heart Failure Exacerbation Management

Management
Approach to Non-Invasive Positive Pressure Ventilation Selection

Hypoxemic Respiratory Failure (Inadequate oxygenation)
1. Reflected by Arterial Blood Gas PaO2 and Oxygen Saturation
2. Concepts
  1. Increase oxygen delivered to the lung (esp. FIO2) or
  2. Increase mean airway pressure (or Positive End-Expiratory Pressure)
3. Interventions
  1. Continuous Positive Airways Pressure (CPAP)
Hypercarbic Respiratory Failure (Inadequate ventilation)
1. Reflected by Arterial Blood Gas PaCO2 and pH
2. Concepts (increase Minute Ventilation)
  1. Increase Tidal Volume (TV) or
  2. Increase Respiratory Rate (RR)
3. Interventions
  1. Bilevel Positive Airway Pressure (BiPap)
References
1. Mallemat and Runde in Herbert (2015) EM:Rap 15(2): 7-8

References

(2016) Fundamental Critical Care Support, p. 46-60
Davies (1986) Acute Respiratory Failure, Cyberlog
Presberg in Noble (2001) Primary Care, p. 705-16