RESPIRATORY Last edited: 3/9/2024

11. RESPIRATORY FAILURE

I. PATHOPHYSIOLOGY & CAUSES III. COMPLICATIONS OF IV. DIAGNOSTIC APPROACH TO RESPIRATORY FAILURE
A. TYPE I (HYPOXEMIC) RESPIRATORY FAILURE RESPIRATORY FAILURE A. ASSESS FOR TYPE OF RESPIRATORY FAILURE
B. TYPE II (HYPERCAPNIC) RESPIRATORY FAILURE A. HYPOXEMIC RESPIRATORY FAILURE B. ASSESS FOR THE CAUSE OF TYPE I (HYPOXEMIC) RESPIRATORY FAILURE
II. CLASSIC FINDINGS OF RESPIRATORY FAILURE B. HYPERCAPNIC RESPIRATORY V. TREATMENT OF RESPIRATORY FAILURE
A. HYPOXEMIC RESPIRATORY FAILURE FAILURE A. TREAT THE CAUSE OF RESPIRATORY FAILURE
B. HYPERCAPNIC RESPIRATORY FAILURE B. SUPPORTIVE CARE OF RESPIRATORY FAILURE

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I. Pathophysiology & Causes
A. Type I (Hypoxemic) Respiratory Failure
1. V/Q Mismatch
Pathophysiology: Causes:
o Alveolar filling, alveolar collapse, or pulmonary artery o Alveolar Filling:
occlusion → Impaired ventilation/perfusion to alveoli →  Pneumonia
Impaired gas exchange at alveoli → Hypoxemia • Suspected when there is fever, productive cough, and
leukocytosis
 Pulmonary Edema
• Suspected when there are crackles on auscultation and a
history of CHF
 Alveolar Hemorrhage
• Suspected in the setting of massive hemoptysis
o Alveolar Collapse:
 Atelectasis
• Suspected in a patient avoiding deep breaths secondary to
pain or poor positioning (e.g. lying in bed)
o Pulmonary Artery Occlusion:
 Pulmonary Emboli
• Suspected in a patient who has been immobile (e.g.
postoperative) and now has tachypnea and tachycardia

RR
VE
WOB

V
V V
V

O2 Alveolar Collapse
Q Atelectasis
Q
Alveolar Filling O2

PNA Pulmonary
Pulmonary Edema Embolism
Alveolar Hemorrhage

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2. Pulmonary Shunt
Pathophysiology:
o Severe alveolar filling or alveolar collapse → No ventilation to
many alveoli → Little to no gas exchange at many alveoli →
Severe hypoxemia
Causes:
o Severe Alveolar Filling:
RR
VE
 Bilateral Lobar Pneumonia WOB
• Suspected when there is fever, productive cough, and
leukocytosis
 Bilateral Pulmonary Edema
• Suspected when there are crackles on auscultation and a
history of CHF
V
 Diffuse Alveolar Hemorrhage V
• Suspected in the setting of massive hemoptysis
 Acute Respiratory Distress Syndrome (ARDS) O2
• Suspected in a patient with acute onset severe hypoxemia Q
with bilateral infiltrates that is not due to pulmonary
edema (e.g. noncardiogenic) Severe Alveolar Filling Alveolar Collapse
o Severe Alveolar Collapse:
 Severe Atelectasis secondary to a mucus plug ARDS Severe Atelectasis
• In the ICU, patients suspected of hypoxia often show a Severe PNA Mucus Plug
drastic improvement in oxygenation when suctioned Severe Pulmonary Edema
through the endotracheal tube Diffuse Alveolar Hemorrhage

3. Extrapulmonary Shunt
Pathophysiology:
o Shunting of deoxygenated blood from the right heart to the
left heart bypassing the lungs for gas exchange → Severe
hypoxemia
Causes:
o Atrial Septal Defect (ASD) or Patent Foramen Ovale (PFO):
 In patients with pulmonary hypertension, the elevated right
heart pressures can become so significant that deoxygenated
blood may shunt from the right atrium to the left atrium via
an ASD or PFO → Resulting in Systemic Hypoxemia
O2
o Ventricular Septal Defect (VSD):
 In patients with pulmonary hypertension, elevated pressures
in the right heart can result in deoxygenated blood shunting O2
from the right ventricle to the left ventricle through a VSD → Pulmonary HTN +
Resulting in Systemic Hypoxemia Cardiac Shunt
Atrial Septal Defect
Patent Foramen Ovale
Ventricular Septal Defect

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 B. Type II (Hypercapnic) Respiratory Failure
1. Respiratory Depression
Pathophysiology:
o ↓Respiratory drive from the brainstem → ↓Rate of action
RR
potentials propagate down the intercostal and phrenic nerves VE
→ ↓Rate of contraction of intercostals and diaphragm → VT
↓Respiratory rate → Impaired ventilation of multiple alveoli →
Hypercapnia +/- Hypoxemia
 This patient will breathe at a reduced RR → CNS depression
Causes:
o Drug Overdose:
O2
 Benzodiazepine and Opioid abuse
• Assess for altered mental status
CO2
o Assess for improvement with the antidote
 Benzodiazepine abuse → Flumazenil
 Opioid abuse → Naloxone
o CVA (at or near the brainstem):
 Assess for neurological deficits
CNS Depression RR
2. Neuromuscular Dysfunction
-CVA
Pathophysiology: Opiates
-Drug Overdose
o ↓Amplitude of action potentials propagate down the
Benzodiazepines
intercostal and phrenic nerves or Weak contraction of
intercostals and diaphragm → ↓Ability to take a deep breath
and expand lungs → Impaired ventilation of multiple alveoli → Neuromuscular Dysfunction TV
Hypercapnia ± Hypoxemia -Guillain-Barré Syndrome
 This patient will breathe at an ↑RR in an attempt to improve
-Spinal Cord Injury
ventilation
-Myasthenia Gravis
Causes:
o Guillain Barré Syndrome: -Fatigue
 Suspected in a patient with ascending paralysis and areflexia
o Myasthenia Gravis: Airway Obstruction TV
 Suspected in a patient with ptosis, diplopia, dysphagia, and
dysarthria -AECOPD
3. Airway Obstruction -Asthma Exacerbation
Pathophysiology:
o Obstruction of bronchioles → Inability to exhale CO2 →
Air trapping in alveoli → Dynamic hyperinflation occurs → II. Classic Findings of Respiratory Failure
Inability to take a deep breath given hyperinflated lungs →
Impaired ventilation of multiple alveoli → A. Hypoxemic Respiratory Failure
Hypercapnia ± Hypoxemia o Dyspnea, Tachypnea, ↑Work of breathing (WOB):
 This patient will increase RR in an attempt to improve  ↓O2 → Stimulates chemoreceptors → ↑Respiratory drive to
ventilation breathe
Causes: o Hypoxia (SpO2 < 90%) on pulse oximetry
o Acute COPD Exacerbation:
B. Hypercapnic Respiratory Failure
 Suspected in a patient with a history of COPD presenting
with severe wheezing, worsening dyspnea, and increased o Dyspnea:
 ↑CO2 → Stimulates chemoreceptors →
sputum production
↑Respiratory drive to breathe
o Acute Asthma Exacerbation:
o Altered Mental Status:
 Suspected in a patient with a history of Asthma presenting
 ↑CO2 → Exhibits a sedative effect
with severe wheezing or silent chest, worsening dyspnea,
(e.g. CO2 narcosis)
and difficulty speaking in full sentences
o Asterixis:
 ↑CO2 → Exhibits a flapping tremor effect

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 III. Complications of Respiratory Failure
A. Hypoxemic Respiratory Failure B. Hypercapnic Respiratory Failure
1. Multi-Organ Dysfunction 1. ↑Intracranial Pressure
Pathophysiology: Pathophysiology:
o Severe hypoxia → ↑Oxygen delivery to tissues → o Severe and sustained hypercapnia → Cerebral vasodilation →
Organ ischemia → Organ dysfunction Cerebral blood flow → ↑ICP
Presentation: Presentation:
o Encephalopathy: o Encephalopathy:
 Confusion → Stupor → Coma  Confusion → Stupor → Coma
o Arrhythmias: o Pupillary Changes:
 Atrial fibrillation  Pupil dilation not reactive to light → Suggests 3rd nerve
 Ventricular tachycardia compression and impending herniation (uncal herniation)
o Myocardial Ischemia:
 Angina, ST changes, and ↑Troponin
o Lactic Acidosis:
Intracranial Pressure
 ↑Lactate level
 ABG with ↓pH and ↓HCO3-

Multi-Organ Dysfunction

PH
CO2
Lactate
+
Asterixis +
ICP
O2 +
Encephalopathy + Cerebral
Vasodilation
+ + Arrhythmias

Encephalopathy Myocardial Cerebral

+ Ischemia Blood Flow

2. Pulmonary Hypertension
Pathophysiology:
o Chronic hypoxia or extremely severe acute hypoxemia →
↑Hypoxic pulmonary vasoconstriction → ↑PVR →
↑Pulmonary BP
Presentation:
o Dyspnea on exertion
o ↑Risk of Right Heart Failure (e.g. Cor Pulmonale)

Pulmonary
Vasoconstriction
PVR

FIGURE 1. EXTERNAL VENTRICULAR DRAIN FOR MEASURING ICP

PAP

O2 (Hypoxemia)
Pulm HTN

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IV. Diagnostic Approach to Respiratory Failure

A. Assess for type of Respiratory Failure

1. Obtain an ABG 2. Administer 100% FiO2 Challenge
Purpose: Purpose:
o Differentiate between Type I and Type II respiratory failure o Differentiate between V/Q mismatch and Shunt in Type I
Abnormal Findings: respiratory failure
o Type I (Hypoxemic) Respiratory Failure: Abnormal Findings:
 PaO2 < 60 mmHg o V/Q Mismatch:
 Normal or Low PaCO2  Hypoxemia improves with oxygen supplementation
o Type II (Hypercapnic) Respiratory Failure: o Shunt:
 PaO2 < 60 mmHg  Hypoxemia DOES NOT improve with oxygen
 ↑PaCO2 (> 45 mmHg) supplementation

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 B. Assess for the cause of type I (hypoxemic) Respiratory Failure
1. Obtain a CXR or Chest CT (e.g. CTPA) 2. Obtain an Echocardiogram
Purpose: Purpose:
o To assess for the presence of Pneumonia, Pulmonary Edema, o Assess for Intracardiac Shunt (e.g. ASD, PFO, VSD)
Atelectasis, Alveolar Hemorrhage, ARDS o Assess for evidence of Cardiogenic Pulmonary Edema
o To assess for the presence of PE (use CTPA study) Abnormal Findings:
Abnormal Findings: o Right to left shunting of blood on echocardiogram in the
o Consolidation on imaging → Pneumonia, Atelectasis presence of elevated pulmonary artery pressure
o Diffuse infiltrates → ARDS, Pulmonary Edema, Alveolar o ↓LVEF or Diastolic dysfunction → Diffuse infiltrates may be
Hemorrhage from pulmonary edema that is cardiogenic in origin
o Pulmonary occlusion on CTPA → PE

FIGURE 2. FIGURE 1. CXR SHOWING BILATERAL PULMONARY INFILTRATES FIGURE 4. APICAL 4 CHAMBER VIEW SHOWING NORMAL LVEF & DIASTOLIC FUNCTION

FIGURE 3. CT SHOWING BILATERAL PULMONARY INFILTRATES FIGURE 5. PARASTERNAL SHORT AXIS SHOWING NORMAL LVEF & DIASTOLIC FUNCTION

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V. Treatment of Respiratory Failure
A. Treat the cause of Respiratory Failure
1. Pneumonia 3. COPD/Asthma Exacerbation 5. Pulmonary Embolism
Treatment: Treatment: Treatment:
o Antibiotics o Bronchodilators and Steroids o Heparin vs IVC filter if not massive PE
o tPA vs embolectomy if massive PE
2. Pulmonary Edema 4. Atelectasis
Treatment: Treatment:
o Diuretics o Incentive spirometry and deep
breathing

B. Supportive care of Respiratory Failure

1. Non-Invasive Oxygen Supplementation

Types of Supplementation: Purpose:
o Nasal cannula o NC, NRB, HFNC
o Non-rebreather  Improve oxygenation
o High-flow nasal cannula o BIPAP
o Bilevel positive airway pressure (BIPAP)  Improves work of breathing
Indications:  Improves cardiogenic pulmonary edema
o Nasal cannula (NC)  Improves CO2 clearance
 Best for Mild hypoxia Monitoring:
 Can administer up to 60% FiO2 o Monitor for improvement in SpO2 via pulse oximetry or PaO2
 Can administer up to 1-10L via ABG
o Non-rebreather (NRB) (NC) (NRB) o Monitor for improvement in Dyspnea, RR, and WOB
 Best for Mild hypoxia not o Monitor for improvement in hypercapnia on serial ABGs
responding to NC
 Can administer 100% FiO2
 Can administer up to 15L
o High-flow nasal cannula (HFNC)
 Best for moderate to severe hypoxia
not responding to NRB
 Can administer 100% FiO2
 Can administer up to 50L (HFNC)
o Bilevel positive airway pressure (BIPAP)
 Best for cardiogenic pulmonary edema or
hypercapnic respiratory failure
 Can administer 100% FiO2
 Can administer IPAP (Inspiratory pressure
support) and EPAP (Expiratory pressure
support)

(BiPAP)

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2. Invasive Oxygen Supplementation 24:36

Types of Supplementation: Monitoring:

o Intubation and Mechanical ventilation o Monitor Peak Inspiratory Pressures (PIP)
Indications:  ↑PIP → Monitor for bronchospasm, mucus plugging, kinked
o Hypoxemia refractory to non-invasive ventilation ETT
o Hypercapnia refractory to non-invasive ventilation • Indicates there is significant resistance in ETT or airway
o Inability to maintain a patent airway (e.g. prevent aspiration in o Monitor Plateau Pressures (Pplat)
altered mental status)  ↑Pplat → Assess for increased risk of barotrauma in ARDS
Modes of Ventilation: • This is an indication of poor lung compliance
o Controlled Mechanical Ventilation (CMV) o Monitor for Extubation via Spontaneous Breathing Trials (SBT)
 Used in patients who require diaphragmatic rest allowing the  Requires little support for oxygenation
ventilator to do all of the work • FiO2 < 40% and PEEP < 5
o Pressure Support Ventilation (PSV)  Require little support for breathing at a normal rate and tidal
 Allows the patient to breathe on their own with supportive volume
pressure support to prepare the patient for extubation • RSBI < 105
Purpose:  Require resolution of an underlying cause that required
o Improve Oxygenation intubation
 Use of FiO2 • Improvement in mental status reducing risk of aspiration
• ↑FiO2 in hypoxia
• ↓FiO2 in hyperoxia
o Prevent free radical reactions
 Use of PEEP
• ↑PEEP in hypoxia
• ↓PEEP in hyperoxia and elevated Plateau pressures
o Prevent barotrauma
o Improve CO2 Clearance
 Use of Tidal volume and RR
• ↑TV and RR in hypercapnia
• ↓TV and RR in hypocapnia

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