Acute Respiratory Failure

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Definitions
Background
Types: Hypoventilatory Respiratory Failure with Hypercapnia due to Bellows Failure
Types: Hypercarbic Respiratory Failure from Diffuse Severe Lung Disease (large Respiratory Dead Space)
Types: Hypoxemic Respiratory Failure without Hypercarbia from Intrapulmonary Shunting
Types: Miscellaneous Secondary Causes of Hypoxia
Symptoms
Signs
Labs
Imaging
Differential Diagnosis
Management: General
Management: Bellows Failure or apnea
Management: Hypercarbic Respiratory Failure from Diffuse Severe Lung Disease (large Respiratory Dead Space)
Management: Intrapulmonary Shunting (Pulmonary Edema, Lung Consolidation)
Management: Approach to Non-Invasive Positive Pressure Ventilation Selection
References
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II. 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

III. 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
Images

IV. 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
3. Nerve dysfunction
  1. Cervical Spine 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. Prolonged Mechanical Ventilation (see Ventilator Weaning)
  2. Congenital Muscular Dystrophy
  3. Myasthenia Gravis
  4. Polymyositis
  5. Tetanus

V. 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

VI. Types: Hypoxemic Respiratory Failure without Hypercarbia from Intrapulmonary Shunting

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. Diffuse Alveolar Hemorrhage
  4. Acute Respiratory Distress Syndrome (ARDS)
    1. Increased permeability (low pressure edema)

VII. Types: Miscellaneous Secondary Causes of Hypoxia

VIII. Symptoms

IX. 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

X. 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

XIV. Management: Bellows Failure or apnea

Findings: Increased PaCO2, normal A-a Gradient
Aggressive management is required (e.g. consider Endotracheal Intubation and Mechanical Ventilation)
Manage immediately reversible causes (e.g. coma cocktail with Naloxone, dextrose)
Consider upper airway obstruction (e.g. Anaphylaxis, Foreign Body Aspiration)
Evaluate Trauma patients for chest wall defects interfering with bellows function (e.g. Flail Chest)
Evaluate for impending Respiratory Failure (e.g. Guillain Barre Syndrome, Myasthenia Gravis)
1. Single Breath Counting <10 to 15
2. Vital Capacity <15-20 ml/kg
3. Tidal Volume <5 ml/kg
4. Maximum expiratory force <40 cm H2O (normally >100 cm H2O)
5. Maximum inspiratory pressure less negative than -30 cm H2O (normally < -100 cm H2O)

XV. Management: Hypercarbic Respiratory Failure from Diffuse Severe Lung Disease (large Respiratory Dead Space)

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
Asthma
1. See Emergency Management of Asthma Exacerbation (or Status Asthmaticus)
2. Asthma Exacerbations are acute and reversible, and Dyspnea is always present (otherwise similar to COPD)
  1. Severe V/Q mismatch with wasted gas exchange and compensatory increased Minute Ventilation
  2. Airflow obstruction with hyperinflation results in increased work of breathing and muscle Fatigue
3. Unlike COPD, most Asthma Exacerbations are without PaCO2 rise
  1. PaO2 is typically only mildly decreased and PaCO2 is typically low (not hypercarbic)
  2. Frequent Bronchodilators, initiate Corticosteroids (delayed effect), and manage Asthma triggers
4. Very Severe Asthma Exacerbation (Status Asthmaticus) is associated with Respiratory Failure
  1. See Status Asthmaticus
  2. Emergent management with continuous Bronchodilators, Epinephrine, Magnesium, NIPPV
  3. Beta Agonists are less effective in acidosis, with worsening response to maximal therapy
  4. Increased PaCO2 >40 mmHg is a harbinger of impending respiratory arrest
  5. Endotracheal Intubation if acute aggressive management of airway obstruction fails
5. Endotracheal Intubation and Mechanical Ventilation
  1. Unlike weaning in COPD, asthma Ventilator Weaning is more simple
    1. Patients tolerate removal of Mechanical Ventilation when acute airway obstruction resolves
  2. Management is challenging due to hyperinflation
    1. High pressures are required to provide even adequate Tidal Volume
  3. As with COPD, decrease air trapping by allowing greater expiration time
    1. Shorten inspiratory time by increasing inspiratory rate
    2. Decrease Respiratory Rate (requires adequate sedation)
  4. Allow for mild hypercarbia and Respiratory Acidosis
    1. PaCO2 need not be <40 mmHg
    2. pH>7.20 is sufficient

XVI. Management: Intrapulmonary Shunting (Pulmonary Edema, Lung Consolidation)

Acute Respiratory Distress Syndrome (ARDS or noncardiac Pulmonary Edema)
1. See Acute Respiratory Distress Syndrome
2. Typically a previously healthy patient with serious triggering event (e.g. Trauma, Sepsis)
  1. Trigger causes diffuse alveolar-capillary membrane injury with increased permeability
  2. Protein rich fluid extravasates from capillaries and floods the alveoli
  3. Alveoli are without ventilation, but still perfused
3. Presents with Dyspnea, Tachypnea, Tachycardia with diffuse interstitial lung edema (and no Peripheral Edema)
  1. Shunting blood through unventilated alveolar capillaries results in severe Hypoxemia
  2. PaCO2 remains low, as CO2 may still be cleared through remaining lung (esp. upper fields)
4. Oxygenation
  1. Provide adequate Supplemental Oxygen
  2. Avoid excessive oxygen which is toxic to damaged lung alveoli
5. Supportive Care
  1. See Acute Respiratory Distress Syndrome for full supportive measures
  2. Conservative IV hydration to prevent Fluid Overload
    1. Excess intravascular fluid increases hydrostatic pressures at alveolar capillary, increased Pulmonary Edema
    2. Maintain adequate Cardiac Output but keep Central Venous Pressures and Wedge Pressure lower
  3. Treat the underlying condition that triggered ARDS
  4. Beta Agonists and consider Corticosteroids
  5. Antibiotics for primary and secondary infections
  6. Body position changes (prone)
  7. Consider ECMO
6. Mechanical Ventilation: Lung Protective strategy (limit Barotrauma)
  1. Start with low Tidal Volumes (e.g. 6 ml/kg based on Ideal Body Weight)
  2. Lower FIO2 to avoid alveolar toxicity
    1. Titrate FIO2 down to 0.60 to keep O2 Sat at 88-95% (PaO2 goal 55 to 85 mmHg)
  3. Adjust Positive End Expiratory Pressure (PEEP) in step with FIO2 (See PEEP Table)
    1. Start with PEEP 5 cm H20 and ideally titrate PEEP >12 cm H2O
    2. PEEP expands collapsed airways and recruits more alveoli
    3. PEEP decreases right to left intrapulmonary shunt and improves Hypoxia
    4. PEEP decreases lung stiffness and decreases work of breathing
  4. Allow some hypercapnia to reduce Barotrauma risk (permissive hypercapnia)
    1. Lower minute volumes (lower Tidal Volume and rate)
    2. Titrate to pH of 7.20 to 7.30, PaCO2 up to 50 mmHg (permissive hypercapnia)
Cardiogenic Pulmonary Edema
1. See Congestive Heart Failure Exacerbation Management
2. Similar pathophysiology to ARDS, despite the different underlying cause
  1. Fluid filled alveoli and airway collapse result in right to left intrapulmonary shunt
  2. Hypoxemia predominates and PaCO2 is typically low to start, but increases with progression
  3. Alveolar dead space increases with V/Q mismatch and inefficient respirations (high rate, low TV)
3. Unlike ARDS, Hypoxemia may respond rapidly to emergent management (BiPaP, high dose IV Nitroglycerin, diuresis)
  1. However, if Hypoxemia is refractory, Mechanical Ventilation is effective at improving oxygenation
  2. Cardiogenic Shock tolerates poorly the increased work of breathing, and Ventilator may unload workload
Lobar Bacterial Pneumonia
1. See Pneumonia Management
2. Intrapulmonary shunting due to lung consolidation
3. Presenting with fever, Pleuritic Chest Pain, Purulent Sputum, Tachycardia, Tachypnea and dense Alveolar Infiltrate
4. As with other intrapulmonary shunting, Hypoxemia (low PaO2) with low PaCO2 is typical
  1. Response to Supplemental Oxygen is poor, except in regions of poor ventilation (low V/Q)
    1. Supplemental Oxygen does not compensate for intrapulmonary shunt
  2. Hypoxemia is worsened by concurrent Septic Shock with lower mixed venous PO2
    1. Correction of shock state may improve oxygenation by raising venous PO2
5. Positioning
  1. Positioning of good lung down, favors perfusion to the lung better able to ventilate
6. Mechanical Ventilation
  1. Consider in Unstable Patients, unable to sustain high work of breathing
  2. Oxygenation may remain poor despite Mechanical Ventilation
  3. Exercise caution with PEEP
    1. PEEP may increase capillary resistance, decreasing perfusion to normally ventilated lung
    2. PEEP may therefore force more blood through consolidated, shunted lung

XVII. 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

XVIII. References

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

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