Respiratory Failure:
Respiratory System Review Main function→ gas exchange
 Transfer of oxygen (O2) with carbon dioxide
 Alveoli = chief units of gas exchange
 Hypoxemia→ insufficient oxygen in the blood
o Measured by SpO2/SaO2
o Can lead to hypoxia
 Hypoxia→ lack of oxygen available to tissues; cannot be measured
 Oxygen saturation (O2, Sat, SaO2, SpO2) → percent of hemoglobin binding sites in the blood
that are carrying oxygen
o % of hemoglobin molecules in the arterial blood that are saturated with oxygen
o SaO2 90% = 90% of hemoglobin attachments have O2 bound
 Arterial partial pressure of oxygen (PaO2) → measure of the actual O2 content in arterial blood
o Amount of O2 dissolved in plasma
o Normal = 90-100mmHg
 Ventilation → inspiration (inhalation) or expiration
o Air moves in & out of the lungs
 Perfusion → flow of blood to the alveolar capillaries
 V/Q ratio→ expresses the effectiveness of gas exchange
o Ventilation & perfusion should match closely (4:5)
Acute Respiratory Failure Oxygenation or ventilation is inadequate
 NOT a disease; SYMPTOM that reflects lung function
 2 types→ hypoxemic respiratory failure & hypercapnic respiratory failure
Hypoxemic respiratory failure Aka oxygen failure
 PaO2 < 60mmHg when patient receiving inspired O2 concentration of 60% or more
 Inadequate O2 saturation despite supplemental O2
 Problem→ inadequate exchange of O2 between alveoli & pulmonary capillaries
 4 physiologic mechanismso Mismatch between ventilation (v) & perfusion (q) → V/Q mismatch
o Shunt
o Diffusion limitation
o Alveolar hypoventilation
 V/Q mismatcho Normal → volume of blood perfusing lungs & amount of gas reaching alveoli are almost
identical
o Normal alveolar ventilation 4-6 L/min
o Normal pulmonary blood flow 4-6 L/min
o Perfect match→ ratio or 1:1, V/Q = 1; V/Q = 0.8 (if not 1:1 = V/Q mismatch)

Pain:
What causes V/Q mismatch? → most common → dx with increased secretions in the airways or
alveoli
o May also result from pain, alveolar collapse (atelectasis), pulmonary emboli (PE)
o O2 = first step to reverse hypoxemia
o Treat hypoxemia by treating the cause



Increased muscle tension → compromises ventilation
Patient may be unwilling to take deep breaths→ short, shallow breaths→ atelectasis→ V/Q
mismatch
Activates stress response→ increasing metabolic state
o Increases O2 consumption & CO2 production = decreased O2 supply→ increase
ventilation demands
o No effect on blood flow to the lungs, result is V/Q mismatch
Pulmonary emboli:
 Embolus means “plug” or “stopper”
 Mobile clots→ lodge into narrow part of circulatory system
 embolus→ travels with blood flow until lodges & obstructs perfusion of alveoli
 Lower lobes of lungs
 Blockage of 1 or more pulmonary arteries by thrombus, air emboli, fat emboli, tumor tissue
 Affect the PERFUSION part of the V/Q mismatch
 PE limits flow distal to the occlusion
 So → there are areas of normal lung ventilation BUT decreased perfusion due to vessel occlusion
= V/Q mismatch
 If PE is large→ hemodynamic instability due to blockage of a large pulmonary artery
 Most arise from DVT in legs; other sites→ femoral/iliac veins, right side of heart
 DVT upper extremities due to central venous catheter (CVS) or arterial lines (A-line)
 Venous thromboembolism (VTE) → describes the spectrum of pathologic conditions from DVT
to PE
 Saddle emboli → large thrombus at arterial bifurcation
 PE risk factors:
o Immobility/reduced mobility
o Recent surgery (esp. Pelvis & lower extremity surgery)
o History of VTE
o Cancer
o Obesity
o Oral contraceptives, hormone therapy
o Cigarette smoking
o Prolonged air travel
o Heart failure
o Pregnancy
o Clotting disorders
 PE clinical manifestations:
o Depends on type, location, & size
o Small → may be undetectable
o Begin slowly, or appear suddenly
o Tachypnea or dyspnea
o Mild to moderate hypoxemia
o Tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, accentuation of
pulmonic heart sound, increased HR, syncope
o Massive PE→ sudden change in mental status, hypotension “I feel like i’m going to die”
 PE complications:
o 10% die within the first hour
o Pulmonary infarct (death of lung tissue)
o Most likely to happen if Occlusion in large or medium sized pulmonary vessel (>2mm in diameter)
 Insufficient collateral blood flow from the bronchial circulation











Preexisting lung disease
Infarction → alveolar necrosis & hemorrhage
Necrotic tissue can become infected & abscess may develop
Pleural effusion
Pulmonary hypertension
PE diagnostics:
o D-dimer → measures amount of cross-linked fibrin fragments
 Result of clot degradation
 Rarely found in “healthy people”
 Rule out PE, but can’t use to rule in
 Spiral (helical) CT scan
o Aka CT angiography or CTA
o IV contrast to view pulmonary vessels; scanner rotates & gives various views
 V/Q scan
o If patient unable to have contrast
o 2 parts:
o 1. Perfusion scan → IV injection to look at pulmonary circulation
o 2. Ventilation scan → inhalation of a gas (xenon); scan will reflect distribution of
gas through lung
 MUST have patient’s cooperation
Additional PE assessments:
o ABG → PaO2 will be low (pH is usually normal)
o Abnormal chest x-ray (Atelectasis & pleural effusion)
o Abnormal EKG (ST segment & T wave changes)
o Serum troponins/B-type natriuretic peptide (BNP)
o Ultrasound lower extremities
Interprofessional care:
o Assess cardiac status → O2 required?
o Monitor ABG
o Respiratory measures→ turning, coughing, deep breathing, incentive spirometry
o Intubation; IV fluids, vasopressors
o Treat pain
o Heart failure? → diuretics given
PE treatment:
o Provide adequate tissue perfusion & respiratory function
o Prevent further growth or extension of thrombi in lower extremities
o Prevent embolization from the upper or lower extremities to the pulmonary vasculature
system
o Prevent recurrence of PE
PE drug therapy:
o Immediate anticoagulation
o Unfractionated heparin (UFH)
 If stable → heparin drip (gtt)
 Weight based dosing; bolus then continuous drip
 Goal aPTT 50-80 seconds
o Oral: warfarin (coumadin); apixaban (Eliquis), dabigatran (Pradaxa)
o Contraindicated → liver dx, clotting issues, history of hemorrhagic stroke
o Fibrinolytic agents→ tissue plasminogen activator (tPA) or alteplase (Activase)
PE surgical therapy:
o Pulmonary embolectomy → removal of emboli
o Inferior vena cava (IVC) filter→ inserted percutaneously through femoral vein



Placed at the level of the renal veins in the IVC
Filter expands & prevents migration of large clots into pulmonary system
Misplacement, migration, perforation
Pulmonary hypertension Normal → pulmonary circuit is low resistance/low pressure
 Normal → 25/10 → quarter over dime
 High pressure in pulmonary vasculature
o Increase in resistance to blood flow through pulmonary circulation
 Workload of the right ventricle increases → right ventricular hypertrophy (cor pulmonale) →
eventually heart failure
 Goals of treatment → pulmonary vasodilation, reduce right ventricular overload, diuretics
 Diuretics, anticoagulants, calcium channel blockers, phosphodiesterase, enzyme inhibitors
 Oral → sildenafil (viagra)
o Rapid → continuous IV epoprostenol (flolan)
Hypoxemic Respiratory failure- Shunt
 When blood exits the heart without taking part in gas exchange
 Extreme V/Q mismatch
 Alveoli are perfused but NOT ventilated
 Blood flow past poorly ventilated alveoli → doesn’t pick up O2 → returns unoxygenated blood to
heart & mixes with oxygenated blood
 Mixture lowers total O2 content of arterial blood → hypoxemia
 2 types:
o Anatomic → blood passes through anatomical channel in heart (ventricular septal defect)
& bypasses lungs
o Intrapulmonary → blood flows through pulmonary capillaries without taking part in gas
exchange (PNA)
What’s so bad about hypoxemia?
 Can lead to hypoxia
 PaO2 falls low enough→ s/s of inadequate oxygenation
 Severe hypoxia and/or hypoxemia = cells shift from aerobic to anaerobic metabolism
 Anerobic = uses more fuel, produces less energy & is less sufficient → produces lactic acid
 Lactic acid → hard to remove from body; needs a buffer (sodium bicarbonate NaHCO3)
 Body may not have enough NaHCO3 → metabolic acidosis
 tissue/cell damage → cell death
Hypercapnic Respiratory failure Lungs are often normal; respiratory system can’t keep up
 Increase in CO2 production or decrease in alveolar ventilation
 Acute or chronic
 Indicates problems with respiratory system
 Causes:
o Central nervous system problems → suppress drive to breathe
 Overdose
 Brain-stem infarct/TBI
 High level spinal cord injuries
o Neuromuscular conditions
 Guillain-Barre syndrome, multiple sclerosis → weakness or paralysis
 Exposure to toxins
 Critical illness → muscle wasting
o Chest wall abnormalities→ prevent normal movement/limit lung expansion
 Flail chest, kyphoscoliosis, obesity
Problems of airway/alveoli
 Asthma, COPD, cystic fibrosis
Body can tolerate increased CO2 → compensation
o Ex. COPD → slow increase in PaCO2 after respiratory tract infection
 slow/over several days→ kidneys have time to compensate
 Retaining bicarbonate
 If left untreated, will get worse
o

Acute respiratory failure (ARF) Sudden or gradual
 Acute increase in CO2 or decrease in PaO2 = life threatening
 S/S depend on extent of change, speed of change, & patient’s ability to compensate
 Compensatory measures fail → respiratory failure
 Can affect all body systems at any time
 Frequent assessments
 Clinical manifestations:
o Lack of O2 → decrease LOC → brain damage?
o Tachycardia, tachypnea, diaphoresis, slight HTN
 Heart & lungs attempting to compensate
o Rapid, shallow breathing (hypoxemia)
o Slow respiratory rate (hypercapnia)
o Changes from rapid to slow
o Late sign → increased PaO2/hypercapnia
 Priorities:
o Can patient breathe? Immediate intubation?
o Hemodynamic stability?
o Blood pressure, HR, respiratory rate, SpO2
o Position of patient, work of breathing, can patient speak? Pursed lip breathing?
o Retraction → belly breathing?
 Diagnostic studies: ARF
o Chest x-ray → identify possible causes of respiratory failure
o ABG → oxygenation & ventilatory status
o Acid-base (pH, bicarbonate) balance
o Labs
o EKG
o blood/sputum cultures
o CT scan or V/Q scan
 Goals:
o Independently maintain patent airway
o Baseline breathing patterns
o Effective cough→ able to clear secretions
o ABG within normal limits or patient’s baseline
o Breath sounds within patient’s baseline
 Nursing implications:
o O2 therapy Delivery devices→ dependent on what the patient’s needs are
 Chronic hypercapnia→ COPD; may require mechanical ventilation
o Mobilize secretions Secretions can worsen ARF
 Movement of O2 and CO2 can be limited or blocked

Proper positioning, effective coughing, chest physiotherapy (chest PT),
suctioning, humidification & hydration
 “Good lung down”
o Positive pressure ventilation
 Initial O2 delivery has failed → step before mechanical intubation
 Provides O2 & decreases work of breathing
 2 kinds
 Continuous positive airway pressure (CPAP) → ONE level of pressure
 Bilevel positive airway pressure (Bipap) → TWO different levels of
pressure
 Patient must be awake & alert
Drug therapy for ARF:
 Corticosteroids → reduce airway inflammation & bronchospasm
 Short acting bronchodilators → acute bronchospasm
 Diuretics → relieve pulmonary congestion and/or fluid overload
 Antibiotics → lung infection
 Benzodiazepines → anxiety, restlessness, pain
COVID:
 Highly infectious
 Transmitted by droplet & contact
 Incubation 2-14 days
 symptoms→ originally fever, sore throat, cough, SOB
 CT chest → “ground glass” opacities
 Diagnosis → PCR identifying COVID 19 RNA
 Treatment → supportive
Acute Respiratory Distress Syndrome ARF progresses/untreated → ARDS
 Inflammatory lung disease
 Alveoli → infiltrated with leukocytes
 Widespread endothelial & alveolar damage
 Lungs get stiff → decreased compliance
 Fibrin deposits in lungs
 Non-cardiopulmonary edema → leaky capillaries
 Clinical manifestationso Mild dyspnea, tachypnea, cough & restlessness
o Refractory hypoxemia → no matter how much oxygen→ condition does not improve
o Fine crackles or normal, normal or interstitial infiltrates
o Mild hypoxemia & respiratory alkalosis (hyperventilation)
o Progresses → symptoms worsen
 ABGs → hypercapnia, refractory hypoxemia
 PaO2/FIO2 ratio (P/F ratio) → <100 = severe ARDS
 White out
 Managemento Goal → PaO2 >60 mm Hg, adequate lung ventilation to maintain normal pH or back to
baseline
o O2 administration, mechanical ventilation (high flow: FIO2 80% or higher)
o Intubation:
 Supine position
 Ambu bag at bedside (self-inflating bag-valve mask)
 Preoxygenate 3-5 minutes
 Each intubation <30 seconds each
After successful intubation → cuff inflated
Confirm placement → EtCO2
Auscultate lungs bilaterally (while manually ventilating)
Chest x-ray → 2-6cm ABOVE the carina
Connect to ventilator
o Mechanical ventilation:
 FIO2 moved in/out by a ventilator, not a cure
 Support until lungs can recover
 Positive pressure ventilation - main method used
 Inspiration → vent pushes air into the lungs under positive pressure
 Expiration occurs passively → like normal ventilation
 Volume- predetermined tidal volume (Vt) delivered w/each inspiration
 Pressure-peak inspiratory pressure = predetermined
o Vt varies based on selected pressure & compliance factors
o Increased peak pressures = decreased volume
 Increases functional capacity → volume of air left in lungs at the end of
expiration; helps open up collapsed alveoli
 Complications → increased pressure in lungs & to surrounding structures
o Compromises venous return
o Decreased blood returning to right/left sides of heart
o Decreased preload, CO, BP
o Barotrauma & volutrauma
o Low tidal volume
o Permissive hypercapnia
o Positive end expiratory pressure (PEEP)
o Prone positioning
o Extracorporeal membrane oxygenation (ECMO)
Rapid sequence Intubation RSI EMERGENT!
 Sedative & paralytic are administered at the SAME time during emergency airway management
 Decreases risk for aspiration & injury to the patient
 sedative/hypnotic like Propofol → unconsciousness
 Rapid onset opioid → blunt pain from intubation
 Paralytic → Rocuronium
Medications during intubation General anesthetics:
 Propofol (Diprivan) → lipid based emulsion
 Dexmedetomidine (Precedex) → sedation in ICU
 Benzodiazepines:
o Midazolam (Versed) → sedative/hypnotics or anxiolytics. Usually administered by
injection in adults
 Opioids:
o Fentanyl → moderate to severe pain used for sedation during mechanical ventilation
 Neuromuscular-blocking (NMBDs):
o Paralyze respiratory & skeletal muscles
o MUST administer sedation & pain relief
o Mechanical ventilation is REQUIRED
 Non-depolarizing or depolarizing blocking agents:
o Succinylcholine → quick, ideal for intubation, monitor potassium
o Nimbex (cisatracurium besylate)
o *Vecuronium





 Adjunct to general anesthesia; not for long term use; 45-60 minutes
Ventilator Settings Respiratory rate → # of breaths vent delivers per minute (12-20 breaths/min)
 Tidal volume (Vt) → volume of gas delivered to patient during each breath (6-8ml/kg, 4-8ml/kg
in ARDS)
 O2 concentration (FIO2) → fraction of inspired O2 delivered to patient (21% room air-100%)
 PEEP → pressure applied at end of expiration of ventilator breaths
o 5 cm H2O (seen as high as 15 in COVID)
o Normal: pressure falls to 0 & exhalation occurs passively
o With PEEP → pressure falls to preset level (3-20) & exhalation is passive
 Settings based on patient status, ABGs, disease process, respiratory muscle strength
 Continuously evaluated & readjusted
 ALARMS!!!
Modes of Ventilation How patient & ventilator interact to deliver effective ventilation
 Based on patient status, respiratory drive, ABGs
 Controlled:
o Vent does all the work of breathing (WOB)
o Assist control (AC), synchronized intermittent mandatory ventilation (SIMV)
 Assisted:
o Patient & vent share work of breathing
o Pressure support (PS), pressure-control (PCV)
Assist control Vent delivers preset tidal volume
 Respiratory rate, inspiratory time, tidal volume & PEEP set for the patient
 Mandatory breaths
 Patient can spontaneously breath at own rates & tidal volume
 Limit spontaneous breaths with sedation
 Risk for hyperventilation/hypoventilation
 Can allow patient some control; provides assistance
Pressure support Positive pressure applied to airway ONLY during inspiration
 Used with patient’s spontaneous respirations
 Patient MUST be able to initiate own breath
 As patient starts breath→ vent supplied rapid flow of gas
 Patient determines inspiratory length, tidal volume, & respiratory rate
Nursing implications: Vents Maintain tube placement
 Maintain cuff inflation
o 20-25 cm H2O
 Monitor oxygenation & ventilation
o SpO2, ABG, use of accessory muscles, etc.
 Maintain tube patency
o Suction when needed→ hyperoxygenate before
o Complications → bleeding, hypo/hypertensive, hypoxemia, bronchospasm,
dysrhythmias
 Oral care & skin integrity
o Mouth is open the whole time; assess skin, reposition ET tube often
 Position & comfort → medications, distractions
 Communication → talking, whiteboard
Complications of endotracheal intubation-


Unplanned extubation:
o Self extubation or accidental
o Use bilateral wrist restraints → continued reassessment
o Manually ventilate
Aspiration
o Patient unable to protect airway from aspiration
o Secretions can collect above the cuff
o Use of NG or OG tube → low intermittent suction