Overview

Respiratory Failure

Quick Reference

Critical Alerts

ABG defines type: Type 1 (hypoxemic) vs Type 2 (hypercapnic) vs mixed
P/F ratio <300 = ALI; <200 = ARDS: Defines severity
Intubation is a clinical decision: Don't wait for perfect numbers
NIPPV can prevent intubation: In appropriate patients (COPD, CHF)
Treat the cause while supporting ventilation: Always look for etiology
Low tidal volume ventilation saves lives: 6 mL/kg IBW in ARDS

Key Diagnostics

Test	Finding	Significance
SpO2	<92% on room air	Hypoxemia
ABG	PaO2 <60 mmHg or PaCO2 >0 mmHg	Defines respiratory failure
P/F ratio	PaO2/FiO2	Severity of hypoxemic failure
CXR	Infiltrates, edema, effusion	Etiology
A-a gradient	Elevated	Confirms pulmonary cause
pH	Acidotic with elevated PaCO2	Acute hypercapnic failure

Emergency Treatments

Condition	Treatment	Details
Supplemental O2	Nasal cannula → HFNC → NIPPV	Titrate to SpO2 ≥92%
Hypercapnic failure (COPD)	BiPAP	IPAP 10-12, EPAP 5, titrate
Cardiogenic pulmonary edema	CPAP or BiPAP + Diuretics	May avoid intubation
Severe/refractory	Endotracheal intubation	RSI with hemodynamic support
ARDS	Low tidal volume ventilation	6 mL/kg IBW, plateau <30

Definition

Overview

Respiratory failure is the inability of the respiratory system to meet the metabolic demands of the body, resulting in hypoxemia (low oxygen) and/or hypercapnia (elevated carbon dioxide). It may be acute, chronic, or acute-on-chronic and ranges from mild supplemental oxygen need to life-threatening cardiopulmonary collapse.

Classification

By Type:

Type	PaO2	PaCO2	Mechanism	Examples
Type 1 (Hypoxemic)	<60 mmHg	Normal or low	V/Q mismatch, shunt, diffusion impairment	Pneumonia, ARDS, PE
Type 2 (Hypercapnic)	Variable	>0 mmHg	Hypoventilation	COPD, neuromuscular, overdose
Type 3 (Perioperative)	Variable	Variable	Atelectasis	Post-surgery
Type 4 (Shock)	Low	Variable	Hypoperfusion	Cardiogenic, septic shock

By Acuity:

Acuity	Definition	pH
Acute	New onset, hours to days	Acidotic if hypercapnic
Chronic	Weeks to months	Compensated pH
Acute-on-Chronic	Acute decompensation of chronic	Partially compensated

ARDS Definition (Berlin Criteria)

Component	Criteria
Timing	Within 1 week of known insult
Imaging	Bilateral opacities not fully explained by effusions, collapse, or nodules
Origin	Not fully explained by cardiac failure or fluid overload (need echo)
Oxygenation	P/F ratio with PEEP ≥5 cm H2O

ARDS Severity:

Severity	P/F Ratio	Mortality
Mild	200-300	27%
Moderate	100-200	32%
Severe	<100	45%

Epidemiology

Incidence of ARF: 10-40% of ICU admissions
ARDS incidence: 200,000 cases/year in US
Mortality: Type 1: 10-30%; Type 2: Variable; ARDS: 30-45%
Leading causes in ED: COPD exacerbation, pneumonia, CHF, PE

Etiology

Type 1 (Hypoxemic) Causes:

Mechanism	Causes
V/Q mismatch	Pneumonia, asthma, COPD, PE, atelectasis
Shunt	ARDS, pulmonary edema, pneumonia, AVM
Diffusion impairment	Pulmonary fibrosis, emphysema
Low FiO2	High altitude

Type 2 (Hypercapnic) Causes:

Category	Causes
CNS depression	Overdose, stroke, brain injury
Neuromuscular	Myasthenia gravis, GBS, ALS, muscular dystrophy
Chest wall	Kyphoscoliosis, obesity hypoventilation
Airway obstruction	COPD, severe asthma, upper airway obstruction
Increased CO2 production	Fever, sepsis (with underlying disease)

Pathophysiology

Mechanisms of Hypoxemia

Mechanism	Response to O2	A-a Gradient	Examples
V/Q mismatch	Improves	Increased	Pneumonia, PE
Shunt	Minimal improvement	Increased	ARDS, ASD
Diffusion impairment	Improves	Increased	ILD
Hypoventilation	Improves	Normal	Overdose, neuromuscular
Low FiO2	Improves	Normal	Altitude

Alveolar Gas Equation

PAO2 = (FiO2 × [Patm - PH2O]) - (PaCO2 / RQ)

At sea level on room air: PAO2 ≈ 100 mmHg
A-a gradient = PAO2 - PaO2
Normal A-a gradient: 5-15 mmHg (increases with age)

Compensatory Mechanisms

Increased minute ventilation (tachypnea)
Increased heart rate and cardiac output
Pulmonary vasoconstriction (hypoxic)
Diaphragmatic fatigue (unsustainable)

Consequences of Respiratory Failure

System	Effect
CNS	Confusion, seizures, coma
Cardiovascular	Arrhythmias, hypotension
Metabolic	Lactic acidosis
Pulmonary	Pulmonary hypertension

Clinical Presentation

Symptoms

Hypoxemia:

Hypercapnia:

Signs of Impending Respiratory Failure:

History

Key Questions:

Physical Examination

Vital Signs:

Finding	Significance
Tachypnea (RR >4)	Early compensation
Bradypnea	Fatigue, CNS depression
Tachycardia	Compensation, hypoxemia
Hypotension	Late, ominous
SpO2 <92%	Hypoxemia

Respiratory Examination:

Finding	Significance
Accessory muscle use	Increased work of breathing
Paradoxical breathing	Diaphragm fatigue
Prolonged expiration	Obstructive disease
Crackles	Pulmonary edema, pneumonia
Wheezes	Bronchospasm, COPD
Absent breath sounds	Pneumothorax, massive effusion
Stridor	Upper airway obstruction

Other:

Dyspnea (most common)

Common presentation.

Confusion, agitation

Common presentation.

Cyanosis

Common presentation.

Tachypnea

Common presentation.

Red Flags

Impending Respiratory Arrest

Finding	Concern	Action
Severe tachypnea then slowing	Fatigue, impending arrest	Prepare for intubation
Inability to speak	Critical dyspnea	Immediate intervention
Altered mental status	Hypoxemia or hypercapnia	ABG, prepare airway
SpO2 <85% despite high-flow O2	Severe hypoxemia	Intubation likely
Accessory muscle fatigue	Imminent failure	Urgent NIPPV or intubation
Bradycardia	Hypoxic arrest imminent	Emergent intubation

Signs of Specific Diagnoses

Finding	Consider
Asymmetric breath sounds	Pneumothorax, massive effusion
Stridor	Upper airway obstruction
Tripoding	Severe obstruction, impending failure
Diffuse bilateral crackles	ARDS, CHF
Unilateral crackles + fever	Pneumonia

Differential Diagnosis

Common Causes of Acute Respiratory Failure

Diagnosis	Key Features
COPD exacerbation	Smoking history, chronic symptoms, wheeze
Asthma exacerbation	Young, atopy, wheeze, reversible
Pneumonia	Fever, productive cough, focal crackles
Pulmonary edema (CHF)	Orthopnea, JVD, bilateral crackles
ARDS	Acute onset, bilateral infiltrates, P/F <300
Pulmonary embolism	Sudden dyspnea, pleuritic pain, risk factors
Pneumothorax	Sudden onset, unilateral absent sounds
Neuromuscular weakness	Weakness, shallow breathing, normal lung sounds
Overdose	Depressed consciousness, toxidrome

Diagnostic Approach

Arterial Blood Gas (ABG)

Interpretation:

Value	Normal	Interpretation
pH	7.35-7.45	Acidemia/Alkalemia
PaO2	>0 mmHg	<60 = Hypoxemic RF
PaCO2	35-45 mmHg	>0 = Hypercapnic RF
HCO3	22-26 mEq/L	Metabolic compensation

P/F Ratio:

PaO2 / FiO2
Normal: >400
ALI: <300
ARDS: <200

Imaging

Chest X-Ray (First-line):

Finding	Consider
Bilateral infiltrates	ARDS, CHF, bilateral PNA
Focal consolidation	Pneumonia, aspiration
Hyperinflation	COPD, asthma
Cardiomegaly + cephalization	CHF
Unilateral lucency	Pneumothorax
Pleural effusion	CHF, empyema, malignancy

CT Chest:

PE protocol if suspected
Better characterization of parenchymal disease
Not always needed in ED

Laboratory Studies

Test	Purpose
ABG	Define type and severity
CBC	Infection, anemia
BMP	Electrolytes, renal function
BNP	CHF vs ARDS
Lactate	Tissue hypoxia, shock
Procalcitonin	Bacterial infection
D-dimer	PE screening
Troponin	Cardiac involvement

Additional Testing

ECG (arrhythmia, RV strain, MI)
Echocardiography (RV function, PE, CHF)
Bronchoscopy (aspiration, infection, DAH)

Treatment

Principles of Management

Oxygenation: Correct hypoxemia (SpO2 ≥92-94%)
Ventilation: Correct hypercapnia if acidotic
Treat underlying cause: Infection, CHF, bronchospasm
Minimize ventilator-induced lung injury: If intubated
Supportive care: Fluids, vasopressors, nutrition

Oxygen Therapy Escalation

Device	Flow Rate	FiO2 Achieved
Nasal cannula	1-6 L/min	24-44%
Simple mask	5-10 L/min	35-50%
Non-rebreather mask	10-15 L/min	60-80%
High-flow nasal cannula	20-60 L/min	Up to 100%
NIPPV (BiPAP/CPAP)	Adjustable	Up to 100%
Mechanical ventilation	Via ETT	21-100%

Non-Invasive Positive Pressure Ventilation (NIPPV)

Best Evidence For:

Condition	Mode	Benefit
COPD exacerbation	BiPAP	Reduces intubation and mortality
Cardiogenic pulmonary edema	CPAP or BiPAP	Reduces intubation and mortality
Immunocompromised with ARF	NIPPV trial	May avoid intubation

BiPAP Settings:

IPAP: 10-12 cm H2O (increase for ventilation)
EPAP: 5 cm H2O (increase for oxygenation)
FiO2: Titrate to SpO2 ≥92%

Contraindications to NIPPV:

Absolute	Relative
Respiratory arrest	Hemodynamic instability
Inability to protect airway	Agitation, inability to cooperate
Uncontrolled vomiting	Copious secretions
Facial trauma/surgery	Recent upper GI surgery
Upper airway obstruction	Undrained pneumothorax

Signs of NIPPV Failure (Consider intubation):

No improvement in 1-2 hours
Worsening work of breathing
Worsening ABG
Altered mental status
Hemodynamic instability

Endotracheal Intubation

Indications:

Failure of NIPPV
Unable to protect airway (GCS ≤8)
Respiratory arrest
Refractory hypoxemia (SpO2 <85% on max support)
Severe work of breathing with fatigue
Need for deep sedation or surgery

RSI Considerations in Respiratory Failure:

Issue	Approach
Hypoxemia	Pre-oxygenate, HFNC during intubation
Hypotension risk	Prepare fluids/vasopressors
Asthma/COPD	Ketamine may be preferred
Avoid apnea time	Rapid sequence, experienced operator

Mechanical Ventilation

Initial Settings:

Parameter	Initial Setting
Mode	AC (Assist Control)
Tidal volume	6-8 mL/kg IBW (6 mL/kg for ARDS)
Rate	14-16 breaths/min (adjust for PaCO2)
FiO2	100% initially, wean to SpO2 >2%
PEEP	5 cm H2O; higher for ARDS
I:E ratio	1:2

Lung Protective Ventilation (ARDS):

Tidal volume: 6 mL/kg IBW
Plateau pressure: <30 cm H2O
PEEP: Titrate per ARDS Net tables
Driving pressure: <15 cm H2O

Specific Treatments

COPD Exacerbation:

Bronchodilators (albuterol, ipratropium)
Systemic corticosteroids
Antibiotics if bacterial exacerbation
NIPPV (BiPAP)

Asthma Exacerbation:

Bronchodilators, steroids
Magnesium sulfate if severe
Epinephrine if imminent arrest
Avoid NIPPV in severe cases (risk of barotrauma)

Cardiogenic Pulmonary Edema:

NIPPV (CPAP or BiPAP)
IV diuretics
Nitrates (if hypertensive)
Treat underlying cause (MI, arrhythmia)

ARDS:

Lung protective ventilation
Conservative fluid strategy
Prone positioning if P/F <150
Consider ECMO if refractory

Pneumonia:

Antibiotics (empiric, then directed)
Supportive care

Disposition

ICU Admission Criteria

Need for mechanical ventilation
NIPPV requirement
Hemodynamic instability
Refractory hypoxemia (SpO2 <90% on high-flow)
Altered mental status from respiratory failure
ARDS

Step-Down Unit

Stable on low-flow O2
Resolving NIPPV
Improving trajectory

Discharge Criteria

Returned to baseline oxygenation
Stable on room air or usual home O2
Underlying cause treated
Able to manage medications
Follow-up arranged

Follow-Up

Situation	Follow-Up
COPD exacerbation	Pulmonary within 1-2 weeks
First respiratory failure	Pulmonary for workup
ARDS survivor	Pulmonary, rehab, cognitive assessment
Home O2 initiation	PCP/Pulmonary within 1 week

Patient Education

Condition Explanation

"Your lungs are not able to get enough oxygen into your blood (and/or remove enough carbon dioxide)."
"We need to help you breathe with extra oxygen (or a mask that pushes air in, or a breathing tube)."
"We are also treating the underlying cause of this problem."

Home Oxygen Use (If Applicable)

Proper use of equipment
Safety (no smoking, avoid flames)
When to call for help
Follow-up for reassessment

Warning Signs

Worsening shortness of breath
Increased cough or sputum
Fever
Confusion
Blue lips or fingertips

Special Populations

COPD Patients

May have chronic hypercarbia (baseline CO2 elevated)
Target SpO2 88-92% (avoid oxygen-induced hypercapnia)
NIPPV is highly effective
Avoid excessive oxygen

Neuromuscular Disease

Weak cough, aspiration risk
NIPPV may be long-term therapy
Watch for hypoventilation without dyspnea

Obesity Hypoventilation Syndrome

BMI >30 + daytime hypercapnia
NIPPV (BiPAP) is often effective
Higher PEEP requirements

Pregnancy

Lower physiologic PaCO2 (30-32 mmHg)
Interpret ABG in context
Maternal oxygenation priority for fetal well-being

Elderly

Frailty impacts goals of care
Higher mortality
Consider advance directives

Quality Metrics

Performance Indicators

Metric	Target	Rationale
ABG obtained in ARF	100%	Define type and severity
NIPPV for COPD/CHF	>0% (when indicated)	Reduces intubation
Lung protective ventilation	100% for ARDS	Reduces mortality
Time to antibiotics for pneumonia	<1 hour	Improves outcomes
Plateau pressure <30	100% on vent	Prevents VILI

Documentation Requirements

Vital signs and SpO2
ABG results
Type of respiratory failure (1 vs 2)
Interventions and response
Intubation indication and technique
Ventilator settings
Underlying cause and treatment

Key Clinical Pearls

Diagnostic Pearls

ABG defines the type: Type 1 hypoxemic, Type 2 hypercapnic
P/F ratio estimates severity: <200 is ARDS
Normal A-a gradient = extrapulmonary cause: Hypoventilation
Metabolic compensation takes days: Acute failure has acidotic pH
Tachypnea is compensatory: Slowing respiratory rate may indicate fatigue
BNP helps differentiate CHF from ARDS: Elevated in cardiac cause

Treatment Pearls

NIPPV prevents intubation in COPD and CHF: Strong evidence
Low tidal volume in ARDS saves lives: 6 mL/kg IBW
Plateau pressure target <30: Prevents lung injury
Target SpO2 88-92% in COPD: Avoid oxygen-induced hypercapnia
Intubation is a clinical decision: Don't wait for perfect numbers
Pre-oxygenate before intubation: Maximize safe apnea time

Disposition Pearls

All mechanical ventilation = ICU: No exceptions
NIPPV may be appropriate for step-down: If stable
ARDS survivors need follow-up: Cognitive and physical rehab
Home oxygen needs reassessment: May be temporary

References

ARDS Definition Task Force. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012;307(23):2526-2533.
Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes for acute lung injury and ARDS. N Engl J Med. 2000;342(18):1301-1308.
Rochwerg B, et al. Official ERS/ATS clinical practice guidelines: noninvasive ventilation for acute respiratory failure. Eur Respir J. 2017;50(2):1602426.
Guérin C, et al. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med. 2013;368(23):2159-2168.
Stefan MS, et al. Comparative effectiveness of noninvasive and invasive ventilation in critically ill patients with acute exacerbation of chronic obstructive pulmonary disease. Crit Care Med. 2015;43(7):1386-1394.
Weng CL, et al. Meta-analysis: Noninvasive ventilation in acute cardiogenic pulmonary edema. Ann Intern Med. 2010;152(9):590-600.
Fan E, et al. An Official American Thoracic Society/European Society of Intensive Care Medicine/Society of Critical Care Medicine Clinical Practice Guideline: Mechanical Ventilation in Adult Patients with ARDS. Am J Respir Crit Care Med. 2017;195(9):1253-1263.
UpToDate. Overview of initiating invasive mechanical ventilation in adults in the ICU. 2024.

Overview

Respiratory Failure

Quick Reference

Critical Alerts

ABG defines type: Type 1 (hypoxemic) vs Type 2 (hypercapnic) vs mixed
P/F ratio <300 = ALI; <200 = ARDS: Defines severity
Intubation is a clinical decision: Don't wait for perfect numbers
NIPPV can prevent intubation: In appropriate patients (COPD, CHF)
Treat the cause while supporting ventilation: Always look for etiology
Low tidal volume ventilation saves lives: 6 mL/kg IBW in ARDS

Key Diagnostics

Test	Finding	Significance
SpO2	<92% on room air	Hypoxemia
ABG	PaO2 <60 mmHg or PaCO2 >0 mmHg	Defines respiratory failure
P/F ratio	PaO2/FiO2	Severity of hypoxemic failure
CXR	Infiltrates, edema, effusion	Etiology
A-a gradient	Elevated	Confirms pulmonary cause
pH	Acidotic with elevated PaCO2	Acute hypercapnic failure

Emergency Treatments

Condition	Treatment	Details
Supplemental O2	Nasal cannula → HFNC → NIPPV	Titrate to SpO2 ≥92%
Hypercapnic failure (COPD)	BiPAP	IPAP 10-12, EPAP 5, titrate
Cardiogenic pulmonary edema	CPAP or BiPAP + Diuretics	May avoid intubation
Severe/refractory	Endotracheal intubation	RSI with hemodynamic support
ARDS	Low tidal volume ventilation	6 mL/kg IBW, plateau <30

Definition

Overview

Classification

By Type:

Type	PaO2	PaCO2	Mechanism	Examples
Type 1 (Hypoxemic)	<60 mmHg	Normal or low	V/Q mismatch, shunt, diffusion impairment	Pneumonia, ARDS, PE
Type 2 (Hypercapnic)	Variable	>0 mmHg	Hypoventilation	COPD, neuromuscular, overdose
Type 3 (Perioperative)	Variable	Variable	Atelectasis	Post-surgery
Type 4 (Shock)	Low	Variable	Hypoperfusion	Cardiogenic, septic shock

By Acuity:

Acuity	Definition	pH
Acute	New onset, hours to days	Acidotic if hypercapnic
Chronic	Weeks to months	Compensated pH
Acute-on-Chronic	Acute decompensation of chronic	Partially compensated

ARDS Definition (Berlin Criteria)

Component	Criteria
Timing	Within 1 week of known insult
Imaging	Bilateral opacities not fully explained by effusions, collapse, or nodules
Origin	Not fully explained by cardiac failure or fluid overload (need echo)
Oxygenation	P/F ratio with PEEP ≥5 cm H2O

ARDS Severity:

Severity	P/F Ratio	Mortality
Mild	200-300	27%
Moderate	100-200	32%
Severe	<100	45%

Epidemiology

Incidence of ARF: 10-40% of ICU admissions
ARDS incidence: 200,000 cases/year in US
Mortality: Type 1: 10-30%; Type 2: Variable; ARDS: 30-45%
Leading causes in ED: COPD exacerbation, pneumonia, CHF, PE

Etiology

Type 1 (Hypoxemic) Causes:

Mechanism	Causes
V/Q mismatch	Pneumonia, asthma, COPD, PE, atelectasis
Shunt	ARDS, pulmonary edema, pneumonia, AVM
Diffusion impairment	Pulmonary fibrosis, emphysema
Low FiO2	High altitude

Type 2 (Hypercapnic) Causes:

Category	Causes
CNS depression	Overdose, stroke, brain injury
Neuromuscular	Myasthenia gravis, GBS, ALS, muscular dystrophy
Chest wall	Kyphoscoliosis, obesity hypoventilation
Airway obstruction	COPD, severe asthma, upper airway obstruction
Increased CO2 production	Fever, sepsis (with underlying disease)

Pathophysiology

Mechanisms of Hypoxemia

Mechanism	Response to O2	A-a Gradient	Examples
V/Q mismatch	Improves	Increased	Pneumonia, PE
Shunt	Minimal improvement	Increased	ARDS, ASD
Diffusion impairment	Improves	Increased	ILD
Hypoventilation	Improves	Normal	Overdose, neuromuscular
Low FiO2	Improves	Normal	Altitude

Alveolar Gas Equation

PAO2 = (FiO2 × [Patm - PH2O]) - (PaCO2 / RQ)

At sea level on room air: PAO2 ≈ 100 mmHg
A-a gradient = PAO2 - PaO2
Normal A-a gradient: 5-15 mmHg (increases with age)

Compensatory Mechanisms

Increased minute ventilation (tachypnea)
Increased heart rate and cardiac output
Pulmonary vasoconstriction (hypoxic)
Diaphragmatic fatigue (unsustainable)

Consequences of Respiratory Failure

System	Effect
CNS	Confusion, seizures, coma
Cardiovascular	Arrhythmias, hypotension
Metabolic	Lactic acidosis
Pulmonary	Pulmonary hypertension

Clinical Presentation

Symptoms

Hypoxemia:

Hypercapnia:

Signs of Impending Respiratory Failure:

History

Key Questions:

Physical Examination

Vital Signs:

Finding	Significance
Tachypnea (RR >4)	Early compensation
Bradypnea	Fatigue, CNS depression
Tachycardia	Compensation, hypoxemia
Hypotension	Late, ominous
SpO2 <92%	Hypoxemia

Respiratory Examination:

Finding	Significance
Accessory muscle use	Increased work of breathing
Paradoxical breathing	Diaphragm fatigue
Prolonged expiration	Obstructive disease
Crackles	Pulmonary edema, pneumonia
Wheezes	Bronchospasm, COPD
Absent breath sounds	Pneumothorax, massive effusion
Stridor	Upper airway obstruction

Other:

Dyspnea (most common)

Common presentation.

Confusion, agitation

Common presentation.

Cyanosis

Common presentation.

Tachypnea

Common presentation.

Red Flags

Impending Respiratory Arrest

Finding	Concern	Action
Severe tachypnea then slowing	Fatigue, impending arrest	Prepare for intubation
Inability to speak	Critical dyspnea	Immediate intervention
Altered mental status	Hypoxemia or hypercapnia	ABG, prepare airway
SpO2 <85% despite high-flow O2	Severe hypoxemia	Intubation likely
Accessory muscle fatigue	Imminent failure	Urgent NIPPV or intubation
Bradycardia	Hypoxic arrest imminent	Emergent intubation

Signs of Specific Diagnoses

Finding	Consider
Asymmetric breath sounds	Pneumothorax, massive effusion
Stridor	Upper airway obstruction
Tripoding	Severe obstruction, impending failure
Diffuse bilateral crackles	ARDS, CHF
Unilateral crackles + fever	Pneumonia

Differential Diagnosis

Common Causes of Acute Respiratory Failure

Diagnosis	Key Features
COPD exacerbation	Smoking history, chronic symptoms, wheeze
Asthma exacerbation	Young, atopy, wheeze, reversible
Pneumonia	Fever, productive cough, focal crackles
Pulmonary edema (CHF)	Orthopnea, JVD, bilateral crackles
ARDS	Acute onset, bilateral infiltrates, P/F <300
Pulmonary embolism	Sudden dyspnea, pleuritic pain, risk factors
Pneumothorax	Sudden onset, unilateral absent sounds
Neuromuscular weakness	Weakness, shallow breathing, normal lung sounds
Overdose	Depressed consciousness, toxidrome

Diagnostic Approach

Arterial Blood Gas (ABG)

Interpretation:

Value	Normal	Interpretation
pH	7.35-7.45	Acidemia/Alkalemia
PaO2	>0 mmHg	<60 = Hypoxemic RF
PaCO2	35-45 mmHg	>0 = Hypercapnic RF
HCO3	22-26 mEq/L	Metabolic compensation

P/F Ratio:

PaO2 / FiO2
Normal: >400
ALI: <300
ARDS: <200

Imaging

Chest X-Ray (First-line):

Finding	Consider
Bilateral infiltrates	ARDS, CHF, bilateral PNA
Focal consolidation	Pneumonia, aspiration
Hyperinflation	COPD, asthma
Cardiomegaly + cephalization	CHF
Unilateral lucency	Pneumothorax
Pleural effusion	CHF, empyema, malignancy

CT Chest:

PE protocol if suspected
Better characterization of parenchymal disease
Not always needed in ED

Laboratory Studies

Test	Purpose
ABG	Define type and severity
CBC	Infection, anemia
BMP	Electrolytes, renal function
BNP	CHF vs ARDS
Lactate	Tissue hypoxia, shock
Procalcitonin	Bacterial infection
D-dimer	PE screening
Troponin	Cardiac involvement

Additional Testing

ECG (arrhythmia, RV strain, MI)
Echocardiography (RV function, PE, CHF)
Bronchoscopy (aspiration, infection, DAH)

Treatment

Principles of Management

Oxygenation: Correct hypoxemia (SpO2 ≥92-94%)
Ventilation: Correct hypercapnia if acidotic
Treat underlying cause: Infection, CHF, bronchospasm
Minimize ventilator-induced lung injury: If intubated
Supportive care: Fluids, vasopressors, nutrition

Oxygen Therapy Escalation

Device	Flow Rate	FiO2 Achieved
Nasal cannula	1-6 L/min	24-44%
Simple mask	5-10 L/min	35-50%
Non-rebreather mask	10-15 L/min	60-80%
High-flow nasal cannula	20-60 L/min	Up to 100%
NIPPV (BiPAP/CPAP)	Adjustable	Up to 100%
Mechanical ventilation	Via ETT	21-100%

Non-Invasive Positive Pressure Ventilation (NIPPV)

Best Evidence For:

Condition	Mode	Benefit
COPD exacerbation	BiPAP	Reduces intubation and mortality
Cardiogenic pulmonary edema	CPAP or BiPAP	Reduces intubation and mortality
Immunocompromised with ARF	NIPPV trial	May avoid intubation

BiPAP Settings:

IPAP: 10-12 cm H2O (increase for ventilation)
EPAP: 5 cm H2O (increase for oxygenation)
FiO2: Titrate to SpO2 ≥92%

Contraindications to NIPPV:

Absolute	Relative
Respiratory arrest	Hemodynamic instability
Inability to protect airway	Agitation, inability to cooperate
Uncontrolled vomiting	Copious secretions
Facial trauma/surgery	Recent upper GI surgery
Upper airway obstruction	Undrained pneumothorax

Signs of NIPPV Failure (Consider intubation):

No improvement in 1-2 hours
Worsening work of breathing
Worsening ABG
Altered mental status
Hemodynamic instability

Endotracheal Intubation

Indications:

Failure of NIPPV
Unable to protect airway (GCS ≤8)
Respiratory arrest
Refractory hypoxemia (SpO2 <85% on max support)
Severe work of breathing with fatigue
Need for deep sedation or surgery

RSI Considerations in Respiratory Failure:

Issue	Approach
Hypoxemia	Pre-oxygenate, HFNC during intubation
Hypotension risk	Prepare fluids/vasopressors
Asthma/COPD	Ketamine may be preferred
Avoid apnea time	Rapid sequence, experienced operator

Mechanical Ventilation

Initial Settings:

Parameter	Initial Setting
Mode	AC (Assist Control)
Tidal volume	6-8 mL/kg IBW (6 mL/kg for ARDS)
Rate	14-16 breaths/min (adjust for PaCO2)
FiO2	100% initially, wean to SpO2 >2%
PEEP	5 cm H2O; higher for ARDS
I:E ratio	1:2

Lung Protective Ventilation (ARDS):

Tidal volume: 6 mL/kg IBW
Plateau pressure: <30 cm H2O
PEEP: Titrate per ARDS Net tables
Driving pressure: <15 cm H2O

Specific Treatments

COPD Exacerbation:

Bronchodilators (albuterol, ipratropium)
Systemic corticosteroids
Antibiotics if bacterial exacerbation
NIPPV (BiPAP)

Asthma Exacerbation:

Bronchodilators, steroids
Magnesium sulfate if severe
Epinephrine if imminent arrest
Avoid NIPPV in severe cases (risk of barotrauma)

Cardiogenic Pulmonary Edema:

NIPPV (CPAP or BiPAP)
IV diuretics
Nitrates (if hypertensive)
Treat underlying cause (MI, arrhythmia)

ARDS:

Lung protective ventilation
Conservative fluid strategy
Prone positioning if P/F <150
Consider ECMO if refractory

Pneumonia:

Antibiotics (empiric, then directed)
Supportive care

Disposition

ICU Admission Criteria

Need for mechanical ventilation
NIPPV requirement
Hemodynamic instability
Refractory hypoxemia (SpO2 <90% on high-flow)
Altered mental status from respiratory failure
ARDS

Step-Down Unit

Stable on low-flow O2
Resolving NIPPV
Improving trajectory

Discharge Criteria

Returned to baseline oxygenation
Stable on room air or usual home O2
Underlying cause treated
Able to manage medications
Follow-up arranged

Follow-Up

Situation	Follow-Up
COPD exacerbation	Pulmonary within 1-2 weeks
First respiratory failure	Pulmonary for workup
ARDS survivor	Pulmonary, rehab, cognitive assessment
Home O2 initiation	PCP/Pulmonary within 1 week

Patient Education

Condition Explanation

"Your lungs are not able to get enough oxygen into your blood (and/or remove enough carbon dioxide)."
"We need to help you breathe with extra oxygen (or a mask that pushes air in, or a breathing tube)."
"We are also treating the underlying cause of this problem."

Home Oxygen Use (If Applicable)

Proper use of equipment
Safety (no smoking, avoid flames)
When to call for help
Follow-up for reassessment

Warning Signs

Worsening shortness of breath
Increased cough or sputum
Fever
Confusion
Blue lips or fingertips

Special Populations

COPD Patients

May have chronic hypercarbia (baseline CO2 elevated)
Target SpO2 88-92% (avoid oxygen-induced hypercapnia)
NIPPV is highly effective
Avoid excessive oxygen

Neuromuscular Disease

Weak cough, aspiration risk
NIPPV may be long-term therapy
Watch for hypoventilation without dyspnea

Obesity Hypoventilation Syndrome

BMI >30 + daytime hypercapnia
NIPPV (BiPAP) is often effective
Higher PEEP requirements

Pregnancy

Lower physiologic PaCO2 (30-32 mmHg)
Interpret ABG in context
Maternal oxygenation priority for fetal well-being

Elderly

Frailty impacts goals of care
Higher mortality
Consider advance directives

Quality Metrics

Performance Indicators

Metric	Target	Rationale
ABG obtained in ARF	100%	Define type and severity
NIPPV for COPD/CHF	>0% (when indicated)	Reduces intubation
Lung protective ventilation	100% for ARDS	Reduces mortality
Time to antibiotics for pneumonia	<1 hour	Improves outcomes
Plateau pressure <30	100% on vent	Prevents VILI

Documentation Requirements

Vital signs and SpO2
ABG results
Type of respiratory failure (1 vs 2)
Interventions and response
Intubation indication and technique
Ventilator settings
Underlying cause and treatment

Key Clinical Pearls

Diagnostic Pearls

ABG defines the type: Type 1 hypoxemic, Type 2 hypercapnic
P/F ratio estimates severity: <200 is ARDS
Normal A-a gradient = extrapulmonary cause: Hypoventilation
Metabolic compensation takes days: Acute failure has acidotic pH
Tachypnea is compensatory: Slowing respiratory rate may indicate fatigue
BNP helps differentiate CHF from ARDS: Elevated in cardiac cause

Treatment Pearls

NIPPV prevents intubation in COPD and CHF: Strong evidence
Low tidal volume in ARDS saves lives: 6 mL/kg IBW
Plateau pressure target <30: Prevents lung injury
Target SpO2 88-92% in COPD: Avoid oxygen-induced hypercapnia
Intubation is a clinical decision: Don't wait for perfect numbers
Pre-oxygenate before intubation: Maximize safe apnea time

Disposition Pearls

All mechanical ventilation = ICU: No exceptions
NIPPV may be appropriate for step-down: If stable
ARDS survivors need follow-up: Cognitive and physical rehab
Home oxygen needs reassessment: May be temporary

References

ARDS Definition Task Force. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012;307(23):2526-2533.
Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes for acute lung injury and ARDS. N Engl J Med. 2000;342(18):1301-1308.
Rochwerg B, et al. Official ERS/ATS clinical practice guidelines: noninvasive ventilation for acute respiratory failure. Eur Respir J. 2017;50(2):1602426.
Guérin C, et al. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med. 2013;368(23):2159-2168.
Stefan MS, et al. Comparative effectiveness of noninvasive and invasive ventilation in critically ill patients with acute exacerbation of chronic obstructive pulmonary disease. Crit Care Med. 2015;43(7):1386-1394.
Weng CL, et al. Meta-analysis: Noninvasive ventilation in acute cardiogenic pulmonary edema. Ann Intern Med. 2010;152(9):590-600.
Fan E, et al. An Official American Thoracic Society/European Society of Intensive Care Medicine/Society of Critical Care Medicine Clinical Practice Guideline: Mechanical Ventilation in Adult Patients with ARDS. Am J Respir Crit Care Med. 2017;195(9):1253-1263.
UpToDate. Overview of initiating invasive mechanical ventilation in adults in the ICU. 2024.