Non-Invasive Ventilation (NIV): A Comprehensive Review for MD Anesthesia

1. Definition and Historical Background

• Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 230
• Fishman's Pulmonary Diseases and Disorders, p. 2620

2. Methods of Non-Invasive Ventilation

A. Negative-Pressure Ventilation

• Historically used (tank ventilator/"iron lung," cuirass shell, poncho wrap)
• Generates subatmospheric pressure around the chest, causing passive lung expansion
• Rarely used today except in select neuromuscular conditions
• Major limitations: immobility, poor access to patient, risk of upper-airway obstruction

B. Positive-Pressure Noninvasive Ventilation (NPPV)

i. Continuous Positive Airway Pressure (CPAP)

• Delivers a single, fixed positive pressure throughout the entire respiratory cycle (both inspiration and expiration)
• A fixed pressure, variable flow mode
• Relies entirely on the patient's intrinsic respiratory drive; does not augment tidal volume or minute ventilation
• Acts as a pneumatic splint to the pharyngeal airway and prevents alveolar collapse at end-expiration
• Increases functional residual capacity (FRC), improves V/Q matching, reduces intrapulmonary shunting
• Hemodynamic effects: reduces left ventricular preload and afterload (beneficial in cardiogenic pulmonary edema)
• Delivered via nasal mask, full face mask, or helmet (the latter used during COVID-19)
• Traditional use: OSA management; now used in acute cardiogenic pulmonary edema and postoperative atelectasis

• Fischer's Mastery of Surgery, p. 275-276

ii. Bilevel Positive Airway Pressure (BiPAP / BPAP)

• Delivers two independently adjustable pressures:
  • IPAP (Inspiratory Positive Airway Pressure): higher pressure during inspiration, augments tidal volume, reduces work of breathing, assists CO2 clearance
  • EPAP (Expiratory Positive Airway Pressure): lower pressure during expiration, equivalent to PEEP, maintains alveolar recruitment, improves oxygenation
• The difference between IPAP and EPAP (IPAP - EPAP = pressure support) determines the degree of ventilatory assist
• Supports both CO2 clearance AND oxygenation simultaneously
• Newer devices include a backup respiratory rate for patients with central apnea
• Initial settings: IPAP 12-15 cm H2O, EPAP 5 cm H2O; titrate based on clinical response
• BiPAP is the proprietary name (Philips Respironics) for bilevel PAP; the generic terms are BPAP or bilevel NPPV

• ROSEN's Emergency Medicine, p. 2613-2615
• Roberts and Hedges', p. 230-231

iii. High-Flow Nasal Cannula Oxygen (HFNC / HFNCO2)

1. Flow rates up to 60 L/min closely match patients' peak inspiratory flow demand, reducing entrainment of room air and delivering a reliable, high FiO2
2. Washes out anatomical dead space, replacing it with oxygen-enriched gas
3. FiO2 and flow rate can be titrated independently
4. Generates a small amount of PEEP (1-3 cm H2O)
5. Heated and humidified gas is better tolerated
6. Large nasal prongs occlude the nares, reducing ambient air entrainment during closed-mouth breathing

• ROSEN's Emergency Medicine, p. 1044-1045
• Fischer's Mastery of Surgery, p. 276

iv. Pressure Support Ventilation via Mask (PSV/NPPV)

• In many systems, NPPV delivered in spontaneous mode is functionally equivalent to PSV applied non-invasively
• The ventilator delivers a set inspiratory pressure every time the patient initiates a breath; inspiratory flow and inspiratory time are patient-mediated
• Many devices also offer volume-targeted modes (volume-assured pressure support, VAPS), which automatically adjust pressure to deliver a target tidal volume - useful for neuromuscular disease and OHS

v. Interfaces for NIV Delivery

3. Physiological Effects of NIV

Pulmonary Effects

• Increases alveolar recruitment and size, improving the area for gas exchange
• Improves V/Q matching
• IPAP offloads respiratory muscles and overcomes intrinsic PEEP (iPEEP) in COPD/asthma
• Changes breathing pattern: decreases respiratory rate, allows larger tidal volumes, improving alveolar ventilation

Hemodynamic Effects

• Increases intrathoracic pressure
• Reduces systemic venous return (decreases right ventricular preload)
• Increases pulmonary vascular resistance (increases RV afterload)
• Decreases left ventricular transmural pressure (reduces LV afterload) - particularly beneficial in cardiogenic pulmonary edema
• These effects may be detrimental in patients with right heart failure, hypovolemia, or distributive shock
• Fishman's Pulmonary Diseases and Disorders, p. 2622

4. Indications for NIV

Strongly Supported (Level A Evidence)

Well-Supported

• Hypercapnic respiratory failure with respiratory acidosis and increased work of breathing
• Immunosuppressed patients with acute hypoxemic respiratory failure - avoids ET intubation complications (especially ventilator-associated pneumonia, which is often fatal in this group)
• Obesity hypoventilation syndrome (OHS) exacerbations
• Postoperative respiratory failure - both prophylactic (obese patients after abdominal/thoracic surgery) and therapeutic
• Neuromuscular disease with chronic ventilatory failure (home NIV)
• Chest wall deformity (e.g., kyphoscoliosis) with chronic hypercapnia
• DNI/DNR patients - NIV as a ceiling of care or for palliative symptom relief

Less Well-Established / Conditional

• Acute severe asthma - short trials reasonable with close monitoring and low threshold to intubate
• Acute hypoxemic, non-hypercapnic respiratory failure (pneumonia, ARDS) - benefit uncertain; NIV failure in moderate-severe ARDS is associated with high mortality
• Chest trauma / flail chest - possible benefit in reducing intubation rates
• Post-extubation in selected patients (prevention of re-intubation)

1. Exacerbation of COPD
2. Exacerbation of congestive heart failure and cardiogenic pulmonary edema
3. Exacerbation of asthma
4. Immunocompromised patients with hypoxemic respiratory failure
5. Hypoxemic respiratory failure (general)
6. Do-not-resuscitate / do-not-intubate advance directives

5. Contraindications and Limitations of NIV

Absolute Contraindications

• Inability to protect the airway (severe encephalopathy)
• High aspiration risk (vomiting, severe GI bleeding)
• Difficulty clearing secretions
• Facial trauma/surgery
• Upper airway obstruction
• Significant hemodynamic instability

Limitations of NIV

• Patient intolerance - claustrophobia, discomfort from tight mask, air leak - the most common cause of NIV failure
• Inability to cooperate - agitation, delirium, poor GCS
• Secretion management - NIV does not assist with airway suctioning; patients must clear secretions themselves (BiPAP is especially difficult in patients with copious secretions, as expectoration is nearly impossible)
• Risk of aspiration - no protective endotracheal cuff; upper airway defenses, though partially intact, are imperfect
• Neuromuscular blockade is a contraindication, as NIV (both CPAP and BiPAP) requires an open glottis

• Delayed intubation risk - delayed decision to intubate in deteriorating patients is associated with worse outcomes than early intubation; NIV failure in ARDS patients who subsequently required intubation had markedly higher mortality
• pH < 7.25 / severe acidosis - NIV is less effective; most authorities recommend proceeding to invasive MV
• NIV failure - determinants include pH <7.30 on admission, marked mental status alteration, high comorbidity burden, and high severity scores
• Monitoring intensity required - NIV requires close nursing supervision; ABG should be checked within 1-2 hours of initiation
• Interface problems - air leaks reduce efficacy; pressure sores develop over nasal bridge with prolonged use
• Gastric distension - swallowed air can cause abdominal distension
• Murray & Nadel's Respiratory Medicine, p. 3197
• ROSEN's Emergency Medicine, p. 2606

6. Applications of NIV

6.1 Acute Exacerbation of COPD (AECOPD)

• Bilevel IPAP offloads respiratory muscles and overcomes iPEEP (auto-PEEP)
• Reduces respiratory rate and allows more effective lung emptying
• Increases tidal volume and improves alveolar ventilation
• Reduces work of breathing

• Reduces mortality, intubation rates, and hospital/ICU length of stay
• ERS/ATS guidelines strongly recommend BPAP for ARF from COPD with pH ≤7.35
• NIV must be started early - late initiation after medical treatment failure eliminates the benefit
• If pH <7.20, invasive MV is generally recommended

6.2 Acute Cardiogenic Pulmonary Edema (ACPE)

• Prevents alveolar collapse at end-expiration
• Forces fluid from alveolar into interstitial space by increasing hydrostatic pressure
• Improves oxygenation and gas exchange
• Reduces LV preload and afterload - particularly valuable in the failing heart
• Decreases work of breathing rapidly

• Meta-analyses demonstrate NIV (usually CPAP) significantly reduces intubation rate and improves mortality in ACPE
• No clear outcome difference between CPAP and bilevel for CPE
• An early concern about increased AMI rates with bilevel NIV has been refuted by subsequent trials

6.3 Hypoxemic Non-hypercapnic Respiratory Failure

• Evidence is less robust than for COPD or CPE
• Most benefit in patients with pulmonary edema (cardiogenic or non-cardiogenic) or pneumonia
• For moderate-severe ARDS (PaO2/FiO2 < 200), NIV failure rate is high; invasive MV is generally preferred
• NIV failure in ARDS patients who then require intubation is associated with markedly worse mortality

6.4 Acute Severe Asthma

• Bilevel NIV increasingly used but evidence remains limited
• Data from large retrospective series show NIV used in >40% of ventilated asthma patients, with failure rate (requiring intubation) of 4.7%
• In-hospital mortality: NIV 2.3% vs invasive MV 14.5%
• A short trial of BPAP is reasonable, particularly in those not responding to standard medical therapy
• Recommendation: maintain a low threshold to intubate if no improvement

6.5 Immunosuppressed Patients

• Invasive MV carries extremely high risk of ventilator-associated pneumonia (VAP), which is often fatal
• NIV keeps upper airway defenses intact, minimizes VAP risk
• Associated with lower ET intubation rate, shorter ICU stay, lower ICU mortality

6.6 Obesity Hypoventilation Syndrome (OHS)

• Bilevel NIV (with backup rate) or CPAP
• Acute exacerbations can be managed with NIV with similar efficacy as COPD exacerbations
• Nocturnal NIV forms the cornerstone of chronic management

6.7 Neuromuscular Disease and Chest Wall Deformity

• Volume-targeted modes (VAPS) particularly useful for ensuring adequate ventilation
• Home NIV in conditions like ALS, post-polio syndrome, severe scoliosis
• Reduces hospitalizations and improves quality of life and survival

6.8 Postoperative Respiratory Applications

• Large reductions in FRC
• Transient diaphragmatic dysfunction
• Atelectasis, hypoxemia, hypercapnia

• Early CPAP for ≥6 hours after thoracic/major abdominal surgery significantly reduces pulmonary complications and reintubation
• Particularly effective in obese postoperative patients - improves oxygenation and prevents atelectasis
• Helmet CPAP is widely used in the immediate post-anesthesia care period

• In one large multicenter RCT (293 patients with ARF after abdominal surgery), NIV vs standard oxygen therapy: intubation rate reduced from 46% to 33%; health care-associated infections reduced from 49% to 31%
• Airway pressures should be kept at the lowest effective level given the risk of disrupting surgical anastomoses
• Murray & Nadel's Respiratory Medicine, p. 3198-3199

6.9 Weaning and Extubation

• Extubation to NIV in selected patients can accelerate the weaning process
• A meta-analysis of 16 trials (n=994, predominantly COPD) found extubation to NIV vs continued invasive weaning significantly decreased mortality
• Particularly useful in patients with advanced age, underlying cardiac/respiratory disease, prolonged MV duration, or hypercapnia during weaning trials
• Does not benefit unselected post-extubation patients; should be used preventively in selected populations rather than as rescue for established post-extubation failure

6.10 DNI/DNR Patients

• NIV can provide respiratory support as a ceiling of care while underlying cause is treated
• In palliative setting, NIV may reduce dyspnea (use is controversial; no clear evidence)
• A time-limited trial may allow patient to survive until family arrival ("time bridge")

7. Advantages of NIV Over Conventional Mechanical Ventilation (CMV)

• Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 231

8. Predictors of NIV Success and Failure

Predictors of SUCCESS

• pH 7.25-7.35 (moderate acidosis that is responsive)
• PaCO2 < 92 mmHg
• Younger age
• Better neurological status / Ability to cooperate
• Lower APACHE score
• COPD or cardiogenic pulmonary edema as the underlying diagnosis
• Improvement in pH, RR, and PaCO2 within 1-2 hours of initiation

Predictors of FAILURE (criteria for immediate intubation)

• pH < 7.25 or worsening pH despite NIV
• Persistent tachypnea and acidemia at 30-60 minutes
• GCS impairment not attributable to CO2 narcosis
• Inability to tolerate mask
• Hemodynamic instability
• Respiratory or cardiac arrest
• Persistent inability to clear secretions

9. Practical Settings and Initiation Protocol

• Low-High approach: IPAP 10, EPAP 5, FiO2 100% - then titrate IPAP upward
• High-Low approach: IPAP 20-25, EPAP 5, FiO2 100% - then titrate downward
• Use EPAP 8 if morbid obesity or iPEEP
• Titrate FiO2 to maintain SpO2 88-92% (86-92% in COPD)
• Increase pressure support (IPAP-EPAP) if hypercapnic; increase EPAP if hypoxic

• Clinical reassessment at 30 minutes
• ABG at 1-2 hours after initiation
• Failure to improve: escalate to invasive MV

10. Summary Table

• Roberts and Hedges' Clinical Procedures in Emergency Medicine, Chapter 8
• ROSEN's Emergency Medicine, Chapter 60
• Fishman's Pulmonary Diseases and Disorders, Chapter 148
• Murray & Nadel's Textbook of Respiratory Medicine, Chapter on NIV
• Fischer's Mastery of Surgery, 8th ed.
• Harrison's Principles of Internal Medicine, 22nd ed., Chapter 313

PEEP (Positive End-Expiratory Pressure): A Comprehensive Review for MD Anesthesia

1. Definition and Basic Concept

• Morgan and Mikhail's Clinical Anesthesiology, 7th ed., p. 2542-2543

2. Physiological Basis and Mechanism of Action

2.1 Why PEEP Is Needed

• Supine position and general anesthesia reduce FRC by ~20% due to cephalad diaphragm shift
• Muscle paralysis eliminates the resting diaphragm tone that maintains FRC
• High FiO2 causes absorption atelectasis
• Surgical factors: abdominal insufflation (pneumoperitoneum), lateral positioning, open thorax, mediastinal weight

2.2 Primary Pulmonary Mechanism

1. Preventing alveolar collapse - shifts the end-expiratory lung volume above closing capacity
2. Increasing FRC - the major effect; maintains a larger oxygen reservoir
3. Recruiting atelectatic alveoli - opens collapsed alveoli above the lower inflection point (LIP) of the pressure-volume curve
4. Alveolar interdependence - when PEEP opens one alveolar unit, adjacent alveolar units tend to open as well (pores of Kohn, alveolar codependency)
5. Redistributing extravascular lung water - does not reduce total lung water, but shifts fluid from the alveolar/interstitial space toward peribronchial and perihilar areas, improving oxygenation
6. Improving lung compliance - recruitment of collapsed alveoli moves tidal ventilation onto the more compliant portion of the P-V curve
7. Reducing intrapulmonary shunting - more alveoli participate in gas exchange; reduces venous admixture

2.3 Hemodynamic Effects (The Opposing Force)

1. Reduces systemic venous return - increased intrathoracic pressure compresses the great veins, reducing preload to the right ventricle; this is the principal mechanism of PEEP-induced hemodynamic compromise
2. Increases pulmonary vascular resistance - overdistended alveoli compress alveolar capillaries; increases RV afterload
3. Leftward shift of interventricular septum - when RV overdistends due to increased afterload, the septum shifts left, impairing LV filling (ventricular interdependence)
4. Reduces LV preload and cardiac output - net effect when PEEP exceeds 15 cm H2O commonly
5. Reduces LV afterload - positive intrathoracic pressure decreases LV transmural pressure, which can be beneficial in LV failure

• Morgan and Mikhail's Clinical Anesthesiology, 7th ed., p. 2546-2547

3. Types of PEEP

3.1 Extrinsic (Applied) PEEP (PEEPe)

• Applied to treat or prevent hypoxemia
• Levels typically 5-15 cm H2O

• Mimics the ~2-3 cm H2O of glottic resistance normally present during spontaneous breathing
• Applied to intubated patients to compensate for loss of glottic braking; typically 3-5 cm H2O

• The level at which oxygenation benefit is maximized while minimizing hemodynamic and barotrauma risk

3.2 Intrinsic (Auto) PEEP - iPEEP

• In COPD, asthma, or during high respiratory rates with short expiratory times, expiratory flow is limited by small airway obstruction, dynamic airway collapse, or diminished elastic recoil
• Gas that should have been exhaled remains trapped in the alveoli, progressively building up pressure above set PEEP

• Hemodynamic instability - same mechanism as high extrinsic PEEP; can cause circulatory collapse
• High peak inspiratory pressures (PIP)
• Difficulty triggering the ventilator - patient must generate inspiratory effort sufficient to overcome both auto-PEEP and the set trigger threshold; this markedly increases work of breathing
• Breath stacking/dynamic hyperinflation - progressively worsening situation in unrecognized cases
• Tension pneumothorax in severe cases

1. Flow-time waveform - exhalation flow does not return to zero before the next breath begins (the most reliable bedside sign)
2. Expiratory hold maneuver - occlude the expiratory port at end-expiration; the resulting airway pressure equilibrates with alveolar pressure and displays the total PEEP; auto-PEEP = total PEEP - set PEEP
3. Disconnecting patient from ventilator - additional expired gas flows out after disconnect

• Reduce respiratory rate - allow more expiratory time
• Reduce tidal volume - less gas to exhale
• Decrease inspiratory time / increase inspiratory flow - creates a longer expiratory phase
• Increase I:E ratio (1:3 or 1:4 in obstructive disease)
• Bronchodilators - reduce expiratory airway resistance
• Apply extrinsic PEEP to match auto-PEEP - paradoxically reduces triggering work in spontaneously breathing patients (does NOT increase total PEEP if set below auto-PEEP level)
• Temporary ventilator disconnect in life-threatening situations
• ROSEN's Emergency Medicine, p. 1255-1262
• Roberts and Hedges', p. 603-605
• Miller's Anesthesia, 10th ed., p. 7106

4. Indications for PEEP

4.1 Acute Respiratory Failure / ARDS

• Primary indication for higher PEEP (8-20 cm H2O)
• Reduces shunt, improves oxygenation, prevents alveolar derecruitment
• ARDSNet protocol mandates minimum 5 cm H2O; titrated upward based on FiO2/PEEP table
• In severe ARDS (PaO2/FiO2 <200), higher PEEP strategies have a mortality benefit

4.2 Acute Cardiogenic Pulmonary Edema

• CPAP/PEEP reduces LV afterload (decreases LV transmural pressure)
• Reduces preload (reduces pulmonary venous congestion)
• Reduces work of breathing
• Redistributes interstitial fluid away from alveoli

4.3 Intraoperative Use (Routine)

• Low PEEP 5-8 cm H2O is standard in modern lung-protective ventilation
• Prevents anesthesia-induced atelectasis
• Reduces postoperative pulmonary complications (PPCs)
• Particularly important in obese patients, where atelectasis is more pronounced
• During pneumoperitoneum for laparoscopy - PEEP improves oxygenation and lung compliance

4.4 Post-extubation / Postoperative

• Continued PEEP (via CPAP/NIV) after major abdominal/thoracic surgery
• Prevents atelectasis during the vulnerable postoperative period

4.5 Obese Patients

• Obesity significantly impairs FRC and causes basal atelectasis
• Higher PEEP (10-15 cm H2O) combined with recruitment maneuvers may be needed
• PEEP + recruitment maneuvers improve oxygenation without significant hemodynamic compromise in hemodynamically stable obese patients

4.6 One-Lung Ventilation (OLV)

• PEEP applied to the ventilated lung to maintain FRC near normal
• Reduces auto-PEEP that commonly develops in COPD patients during OLV
• Typical starting point: 5 cm H2O PEEP, then titrate based on driving pressure

4.7 COPD Exacerbations

• External PEEP may be applied to match (but not exceed) auto-PEEP levels
• Reduces triggering effort in spontaneously breathing patients on assist modes

5. Determination of "Optimal" / "Best" PEEP

5.1 Stepwise Incremental PEEP Titration

• Start at PEEP 5 cm H2O
• Increase in steps of 2-5 cm H2O
• At each step, assess: SpO2, compliance, driving pressure, cardiac output, blood pressure
• The "best PEEP" maximizes compliance (or oxygenation) without causing hemodynamic deterioration
• End point: SpO2 ≥88-90% at FiO2 ≤0.5

5.2 ARDSNet FiO2/PEEP Tables

5.3 Pressure-Volume Curve Method

• Plot the static P-V curve by sequential inflation with small volumes
• Lower inflection point (LIP): pressure below which alveoli begin to collapse - set PEEP above LIP to prevent atelectrauma
• Upper inflection point (UIP): pressure above which overdistension begins - keep plateau pressure below UIP
• Limitation: time-consuming, requires sedation/paralysis; less practical at bedside

5.4 Driving Pressure (ΔP) Minimization

• Driving pressure normalizes tidal volume to the functional lung size (the "baby lung" in ARDS)
• Studies show driving pressure is a stronger predictor of ARDS mortality than either VT or plateau pressure alone
• PEEP is titrated to minimize ΔP (ideally <15 cm H2O; some recommend <13 cm H2O)
• During controlled ventilation: ΔP = Pplat - PEEP

5.5 Esophageal Manometry / Transpulmonary Pressure

• Esophageal balloon catheter estimates pleural pressure
• Transpulmonary pressure (PL) = Airway pressure - Pleural pressure (Pesoph)
• PEEP is titrated to maintain positive end-expiratory transpulmonary pressure (preventing end-expiratory lung collapse)
• Particularly valuable in patients with abnormal chest wall compliance: obesity, anasarca, abdominal compartment syndrome
• A clinical trial showed improved oxygenation but no difference in overall mortality versus standard titration

5.6 Decremental PEEP Trial (after Recruitment Maneuver)

• Apply recruitment maneuver (e.g., sustained 30-40 cm H2O for 30-40 seconds)
• Start at high PEEP (20-25 cm H2O)
• Decrease PEEP in stepwise decrements every 3-5 minutes
• Set PEEP at the level that maximized compliance (lowest driving pressure / tidal volume ratio)
• Caution: largest prospective RCT of open lung protocol showed increased 6-month mortality, pneumothorax risk, and hemodynamic instability - use with caution

5.7 Monitoring Hemodynamic Response

• SpO2 and PaO2
• Blood pressure and cardiac output (via thermodilution, pulse contour analysis)
• Mixed venous O2 saturation (SvO2 > 50-60%)
• Urine output
• If cardiac output decreases significantly, volume loading or inotropic support may be needed
• Roberts and Hedges', p. 567-597
• Miller's Anesthesia, 10th ed., p. 11889-11891
• Current Surgical Therapy, 14th ed.

6. Adverse Effects of PEEP

6.1 Cardiovascular

• Reduced cardiac output - the most clinically important adverse effect; from reduced venous return (most common mechanism). Circulatory depression is most often associated with PEEP >15 cm H2O
• Hypotension - especially in hypovolemic patients; preload depletion compounds the problem
• Right ventricular failure - increased pulmonary vascular resistance from alveolar overdistension compresses alveolar capillaries, increasing RV afterload
• Leftward interventricular septal shift - impairs LV filling
• Note: patients with decreased lung compliance (ARDS) transmit less airway pressure to the pleural space; thus, they are less hemodynamically affected by PEEP than patients with normal compliance

6.2 Pulmonary / Barotrauma

• Pneumothorax - alveolar rupture from overdistension; most dangerous complication
• Pneumomediastinum
• Pneumopericardium
• Subcutaneous emphysema
• Ventilator-Induced Lung Injury (VILI) - both overdistension injury (volutrauma/barotrauma) and atelectrauma (cyclic opening/closing) contribute

6.3 Renal Effects

• PEEP-induced reduction in cardiac output decreases renal blood flow
• Decreases urinary output, GFR, and free water clearance
• May activate renin-angiotensin-aldosterone system and increase ADH release (contributing to fluid retention)

6.4 Hepatic Effects

• Reduced hepatic blood flow from decreased cardiac output and increased hepatic venous pressure
• May impair hepatic drug metabolism

6.5 Neurological Effects

• Increases intracranial pressure (ICP) - PEEP increases intrathoracic pressure, which impedes cerebral venous drainage
• Significant concern in TBI, stroke, intracranial hypertension
• Must carefully balance oxygenation requirements against ICP effects

6.6 Worsening V/Q Mismatch in Focal Disease

• PEEP is most effective in diffuse parenchymal disease (e.g., ARDS)
• In focal disease (e.g., lobar pneumonia, unilateral contusion), PEEP may simply overdistend already-aerated lung units, shunting blood toward diseased areas and paradoxically worsening hypoxemia

6.7 Increased Dead Space

• Overdistension of alveoli compresses alveolar capillaries, increasing alveolar dead space
• Can worsen hypercapnia despite adequate tidal volumes
• Morgan and Mikhail's Clinical Anesthesiology, 7th ed., p. 2547
• ROSEN's Emergency Medicine

7. PEEP in ARDS and Lung-Protective Ventilation

1. Atelectrauma - cyclic collapse and re-expansion of unstable alveoli; PEEP prevents this by maintaining end-expiratory lung volume
2. Volutrauma - excessive distension from large tidal volumes; PEEP distributes tidal volume more uniformly across recruited alveoli
3. Barotrauma - excessive pressures; PEEP reduces the pressure swings needed if compliance improves

• Overdistension / volutrauma of already-open alveoli when PEEP is set too high

8. PEEP in the Intraoperative / Anesthetic Context

8.1 General Anesthesia and Atelectasis

• All patients under GA develop some degree of atelectasis (typically 5-10% of total lung area)
• Caused by: supine position, diaphragm cephalad displacement, absorption atelectasis with 100% FiO2, muscle paralysis
• PEEP 5-8 cm H2O is recommended during routine mechanical ventilation under GA

8.2 Lung-Protective Ventilation During Surgery

• VT: 6-8 mL/kg IBW
• PEEP: 5-10 cm H2O (higher in obese patients)
• Recruitment maneuvers if significant atelectasis occurs
• FiO2: lowest effective level
• Goal: reduce postoperative pulmonary complications (PPCs)

8.3 One-Lung Ventilation (OLV)

• Loss of the non-ventilated lung creates obligate shunt
• PEEP applied to the ventilated lung: maintains FRC near normal, prevents auto-PEEP accumulation
• CPAP applied to the non-ventilated lung: reduces shunt (blood now encounters some oxygen in upper-airway filled alveoli)
• Auto-PEEP is common during OLV in COPD patients (auto-PEEP averages 4-6 cm H2O in lung cancer/COPD series)
• External PEEP benefit during OLV depends on whether it moves the end-expiratory equilibration point toward or away from the LIP

8.4 Laparoscopic Surgery / Pneumoperitoneum

• Pneumoperitoneum raises intra-abdominal pressure, displaces the diaphragm cranially, and reduces FRC
• PEEP 5-10 cm H2O + recruitment maneuvers improve oxygenation and compliance
• In obese patients, this combination does not appear to harm cardiac output significantly

8.5 Special Patient Groups

• Significant reduction in FRC; atelectasis exacerbated in supine/Trendelenburg position
• Higher PEEP (10-15 cm H2O) combined with ARMs generally required
• Esophageal manometry can guide PEEP to overcome elevated pleural pressure from abdominal weight

• Post-CPB lung dysfunction common; PEEP helps prevent/treat atelectasis and improve oxygenation after weaning from bypass
• Must be balanced against hemodynamic effects in a potentially compromised heart

9. Summary Table: PEEP vs Auto-PEEP vs CPAP

10. Clinical Monitoring Points

1. SpO2 / PaO2 - is oxygenation improving?
2. Blood pressure and HR - hemodynamic compromise?
3. Airway pressures (PIP and plateau) - overdistension? Plateau >30 cm H2O signals danger
4. Driving pressure (Pplat - PEEP) - <15 cm H2O target in ARDS
5. Compliance = VT / (Pplat - PEEP) - improvement indicates successful recruitment
6. Urine output - declining urine output suggests reduced cardiac output and renal hypoperfusion
7. ICP (if monitored) - relevant in TBI patients

11. Key Exam Points (Summary)

1. PEEP primarily improves oxygenation (not CO2 clearance) by increasing FRC and recruiting atelectatic alveoli
2. The major adverse effect is reduced cardiac output from decreased venous return; most clinically significant at PEEP >15 cm H2O
3. Patients with low lung compliance (ARDS) tolerate PEEP hemodynamically better than patients with normal lungs
4. Auto-PEEP is detected by the flow-time waveform (no return to zero flow) and measured by the expiratory hold maneuver
5. Driving pressure (Pplat - PEEP) is a powerful predictor of ARDS mortality; minimizing it is a key ventilatory goal
6. Optimal PEEP methods: FiO2/PEEP table (ARDSNet), P-V curve (LIP method), driving pressure minimization, esophageal manometry, decremental PEEP trial
7. PEEP is harmful in focal lung disease (worsens V/Q by overdistending normal alveoli) but beneficial in diffuse disease (ARDS)
8. Intraoperatively, PEEP 5-10 cm H2O is part of lung-protective ventilation in all patients under GA
9. PEEP and ICP: PEEP increases intrathoracic pressure, which impedes cerebral venous drainage and can worsen intracranial hypertension - use cautiously in head-injured patients
10. The maximal safe plateau pressure is 30-32 cm H2O; if this is exceeded, PEEP or VT must be reduced

• Morgan and Mikhail's Clinical Anesthesiology, 7th ed., Chapter 58
• Miller's Anesthesia, 10th ed., Chapters 33 and 49
• ROSEN's Emergency Medicine, Chapter 2
• Roberts and Hedges' Clinical Procedures in Emergency Medicine, Chapter 8
• Murray & Nadel's Textbook of Respiratory Medicine, Chapter 135
• Current Surgical Therapy, 14th ed.
• Barash, Cullen, and Stoelting's Clinical Anesthesia, 9th ed.