Mechanical Ventilation in Critical Care: A Practical Guide for the Internist

Dr Neeraj Manikath , claude.ai

Abstract

Mechanical ventilation remains a cornerstone intervention in critical care medicine, with internists frequently encountering patients requiring ventilatory support. Despite its life-saving potential, mechanical ventilation carries significant risks including ventilator-induced lung injury, hemodynamic compromise, and ventilator-associated complications. This comprehensive review provides internists with practical insights into the fundamental principles of mechanical ventilation, mode selection, initial settings, troubleshooting common problems, and liberation strategies. We emphasize evidence-based approaches while highlighting clinical pearls that bridge the gap between theory and bedside practice.

Introduction

Mechanical ventilation is initiated in approximately 40% of intensive care unit (ICU) admissions, with acute hypoxemic respiratory failure and acute exacerbations of chronic obstructive pulmonary disease (COPD) being the most common indications (1). While pulmonologists and intensivists may manage complex ventilatory strategies, internists must possess foundational competence in initiating, monitoring, and recognizing complications of mechanical ventilation. The principles established by landmark trials—particularly the ARDSNet low tidal volume strategy—have fundamentally altered our approach to mechanical ventilation (2).

This review synthesizes current evidence and practical wisdom to equip internists with the essential knowledge required for competent ventilator management.

Indications for Mechanical Ventilation

Absolute Indications

Mechanical ventilation becomes necessary when spontaneous breathing fails to maintain adequate gas exchange or imposes excessive work of breathing. The primary indications include:

Hypoxemic respiratory failure (PaO₂ <60 mmHg despite supplemental oxygen)
Hypercapnic respiratory failure (PaO₂ >50 mmHg with pH <7.25)
Airway protection (Glasgow Coma Scale <8, absent gag reflex)
Respiratory arrest or agonal breathing
Hemodynamic instability requiring reduced work of breathing

Pearl: The decision to intubate should never rely solely on blood gas values. Clinical assessment—including respiratory rate >35/min, use of accessory muscles, diaphoresis, altered mentation, and inability to speak in complete sentences—often precedes laboratory confirmation of respiratory failure.

Fundamental Ventilator Mechanics

Understanding Compliance and Resistance

Two mechanical properties govern ventilation: compliance (the ease of lung inflation) and resistance (opposition to airflow).

Compliance (C) = ΔVolume/ΔPressure

Normal respiratory system compliance approximates 50-80 mL/cmH₂O. Reduced compliance characterizes restrictive pathologies (ARDS, pulmonary fibrosis, pulmonary edema), while resistance predominantly affects obstructive diseases (asthma, COPD) (3).

Hack: The plateau pressure (Pplat) reflects compliance, while the difference between peak inspiratory pressure (PIP) and Pplat indicates resistance. If PIP rises with stable Pplat, suspect increased resistance (bronchospasm, secretions, endotracheal tube obstruction). If both rise together, compliance has decreased (worsening ARDS, pneumothorax, main-stem intubation).

The Pressure-Volume Relationship

Modern ventilators deliver breaths through either volume-controlled or pressure-controlled modes. Understanding this distinction is crucial:

Volume control (VC): Delivers a set tidal volume regardless of pressure required
Pressure control (PC): Delivers breaths to a set pressure limit, with tidal volume varying based on compliance

Initial Ventilator Settings: A Systematic Approach

Mode Selection

Assist-Control Ventilation (AC) remains the preferred initial mode for most patients. In AC mode, the ventilator delivers a full tidal volume with every breath, whether initiated by the patient (assisted) or the ventilator (controlled).

Synchronized Intermittent Mandatory Ventilation (SIMV) delivers mandatory breaths at a set rate while allowing spontaneous breaths between. However, SIMV prolongs weaning time and is generally avoided except in specific circumstances (4).

Pearl: Start simple. Most patients do well with volume-controlled assist-control ventilation. Reserve advanced modes (pressure-regulated volume control, airway pressure release ventilation) for refractory cases or specific indications.

Setting Tidal Volume

The ARDSNet trial revolutionized mechanical ventilation by demonstrating that low tidal volume ventilation (6 mL/kg predicted body weight) reduced mortality in ARDS compared to traditional volumes of 12 mL/kg (2). This protective lung strategy has since been extrapolated to all mechanically ventilated patients.

Predicted body weight (PBW) calculation:

Males: 50 + 2.3 × (height in inches - 60)
Females: 45.5 + 2.3 × (height in inches - 60)

Or in metric:

Males: 50 + 0.91 × (height in cm - 152.4)
Females: 45.5 + 0.91 × (height in cm - 152.4)

Oyster: Many clinicians incorrectly base tidal volume on actual body weight rather than PBW, particularly in obese patients. A 180 kg, 170 cm male has a PBW of only 66 kg, requiring a tidal volume of approximately 400 mL, not 540 mL. Using actual body weight risks volutrauma.

Respiratory Rate

Initial respiratory rate typically ranges from 12-20 breaths/minute, adjusted to maintain appropriate minute ventilation (tidal volume × respiratory rate) and pH. Patients with metabolic acidosis require increased minute ventilation for respiratory compensation.

Pearl: In COPD patients, avoid excessive respiratory rates. These patients require prolonged expiratory time to prevent air trapping and auto-PEEP. Start with rates of 10-14/minute and monitor for dynamic hyperinflation.

Positive End-Expiratory Pressure (PEEP)

PEEP maintains positive pressure throughout the respiratory cycle, preventing alveolar collapse and improving oxygenation. Initial PEEP of 5 cmH₂O is standard, with adjustments based on oxygenation requirements.

For ARDS, the ARDSNet PEEP/FiO₂ table guides PEEP titration, balancing oxygenation improvement against risks of overdistension (5). Higher PEEP strategies benefit moderate-to-severe ARDS but may compromise hemodynamics in hypovolemic patients.

Hack: Use the "best PEEP" concept—titrate PEEP to optimize compliance (measured by Pplat). Recruit collapsed alveoli without overdistending healthy ones. The ideal PEEP often corresponds to the lower inflection point on a pressure-volume curve, though bedside assessment typically relies on oxygenation response and hemodynamic tolerance.

Fraction of Inspired Oxygen (FiO₂)

Start with FiO₂ of 100% immediately post-intubation, then rapidly titrate down to maintain SpO₂ 88-95% (PaO₂ 55-80 mmHg). Prolonged exposure to high FiO₂ causes oxygen toxicity and absorption atelectasis.

Pearl: Don't chase normal oxygen saturations. The "80/60 rule" guides acceptable oxygenation: SpO₂ >88% corresponding to PaO₂ >60 mmHg provides adequate tissue oxygen delivery in most patients. Exceptions include carbon monoxide poisoning, severe anemia, and pregnancy.

Inspiratory Flow Rate and I:E Ratio

Flow rate determines how rapidly tidal volume is delivered. Typical settings range from 40-80 L/min. The inspiratory-to-expiratory (I:E) ratio is normally 1:2 or 1:3, allowing adequate expiratory time.

Oyster: Obstructive lung disease requires prolonged expiratory time (I:E of 1:3 or 1:4) to prevent air trapping. Conversely, severe hypoxemia may benefit from inverse ratio ventilation (I:E >1:1), though this typically requires deep sedation and is reserved for refractory cases.

Monitoring and Target Parameters

Plateau Pressure: The Key Safety Parameter

Plateau pressure, measured during an inspiratory hold maneuver, reflects alveolar pressure and predicts overdistension risk. Maintaining Pplat ≤30 cmH₂O is the single most important target in protective ventilation (2).

Pearl: Check Pplat at least twice daily in ARDS patients or whenever ventilator changes are made. In volume control, if Pplat exceeds 30 cmH₂O despite tidal volume of 6 mL/kg PBW, accept hypercapnia (permissive hypercapnia) unless contraindicated.

Driving Pressure: An Emerging Parameter

Driving pressure (ΔP = Pplat - PEEP) represents the pressure required to inflate the lungs and strongly predicts mortality in ARDS. Values >15 cmH₂O associate with increased mortality (6). This parameter integrates both tidal volume and compliance, making it a powerful prognostic tool.

Hack: When optimizing ventilation, focus on minimizing driving pressure. If you must choose between higher PEEP with lower tidal volume versus lower PEEP with higher tidal volume to maintain the same minute ventilation, calculate which combination yields the lowest driving pressure.

Troubleshooting Common Ventilator Problems

High-Pressure Alarms

When peak pressures rise, systematically evaluate:

Patient factors: Bronchospasm, secretions, pneumothorax, patient-ventilator dyssynchrony
Ventilator factors: ETT obstruction (kinking, biting, mucus plug)
Position: Main-stem intubation (check ETT depth, auscultate bilaterally)

Pearl: The quickest diagnostic maneuver—disconnect the patient from the ventilator and manually bag. If resistance normalizes, the problem lies with the ventilator or circuit. If resistance persists, the problem involves the patient or endotracheal tube.

Low Tidal Volume Alarms

Common causes include circuit leaks, ETT cuff leaks, and (in pressure control modes) decreased compliance. Check cuff pressure (should be 25-30 cmH₂O) and assess for air audible around the ETT.

Auto-PEEP and Air Trapping

Auto-PEEP (intrinsic PEEP) occurs when insufficient expiratory time prevents complete exhalation before the next breath. This is particularly problematic in COPD and asthma.

Detection: Perform an expiratory hold maneuver and observe if flow reaches zero before the next breath. Alternatively, measure auto-PEEP directly (displayed on most modern ventilators).

Management strategies:

Decrease respiratory rate
Decrease tidal volume
Increase inspiratory flow (shortens inspiratory time)
Decrease minute ventilation (accept higher PaCO₂ if tolerated)
Optimize bronchodilation

Oyster: Paradoxically, adding external PEEP (up to 80% of measured auto-PEEP) can sometimes improve patient comfort and reduce work of breathing by helping trigger the ventilator, though this remains controversial (7).

Patient-Ventilator Dyssynchrony

Dyssynchrony manifests as patient distress, tachypnea, accessory muscle use, or "fighting the ventilator." Common causes include:

Flow starvation: Inspiratory flow rate too low for patient demand
Trigger sensitivity: Patient efforts fail to trigger assisted breaths
Double-triggering: Ventilator delivers two breaths for one patient effort
Premature cycling: Breath terminates before patient finishes inspiration

Hack: Watch the flow-time waveform. In flow starvation, the flow curve shows a "scooped out" appearance as the patient actively inhales against inadequate flow. Increase flow rate to 60-80 L/min to match patient demand.

Special Populations and Disease-Specific Strategies

ARDS Management

Beyond low tidal volume ventilation, additional strategies for moderate-to-severe ARDS include:

Higher PEEP: Use ARDSNet PEEP/FiO₂ tables to guide titration
Prone positioning: In severe ARDS (PaO₂/FiO₂ <150), prone positioning for 16+ hours daily reduces mortality (8)
Neuromuscular blockade: Early use (48 hours) of cisatracurium improved outcomes in severe ARDS in the ACURASYS trial, though the more recent ROSE trial showed no benefit with lighter sedation strategies (9,10)
Recruitment maneuvers: Controversial; may transiently improve oxygenation but lack mortality benefit
ECMO: Consider for refractory hypoxemia (PaO₂/FiO₂ <80) despite optimal ventilation

Pearl: The PaO₂/FiO₂ ratio quickly categorizes ARDS severity: mild (200-300), moderate (100-200), severe (<100). This prognostic tool guides treatment escalation.

COPD and Asthma

Obstructive diseases require strategies preventing dynamic hyperinflation:

Lower respiratory rates (10-14/min)
Shorter inspiratory times (increase flow rate)
Lower tidal volumes acceptable
Monitor auto-PEEP closely
Aggressive bronchodilator therapy

Pearl: In status asthmaticus, ketamine provides both sedation and bronchodilation. Consider 1-2 mg/kg bolus followed by infusion of 0.5-2 mg/kg/hour.

Cardiogenic Pulmonary Edema

Positive pressure ventilation improves cardiac function in pulmonary edema by:

Reducing preload (increased intrathoracic pressure decreases venous return)
Reducing afterload (decreased transmural pressure)
Improving oxygenation
Decreasing work of breathing

Hack: When intubating for acute decompensated heart failure, anticipate hypotension post-intubation. Preload reduction from positive pressure ventilation may unmask hypovolemia. Have vasopressors prepared, but avoid aggressive fluid resuscitation.

Liberation from Mechanical Ventilation

Weaning represents the most time-consuming phase of mechanical ventilation. Approximately 40% of total ventilator time involves weaning (11).

Assessing Readiness

Daily spontaneous breathing trials (SBTs) identify patients ready for extubation. Prerequisites include:

Resolution/improvement of indication for intubation
Adequate oxygenation (PaO₂/FiO₂ >150, PEEP ≤8, FiO₂ ≤0.5)
Hemodynamic stability (no/minimal vasopressors)
Ability to initiate breaths
No planned procedures requiring sedation

Conducting the Spontaneous Breathing Trial

Place the patient on minimal support for 30-120 minutes:

T-piece (disconnected from ventilator, receiving supplemental oxygen)
Pressure support 5-7 cmH₂O with PEEP 5 cmH₂O
CPAP 5 cmH₂O

Success criteria:

Respiratory rate <35/min
SpO₂ >90%
Heart rate change <20%
Systolic BP change <180 or >90 mmHg
No distress (diaphoresis, agitation, altered mentation)

Pearl: The rapid shallow breathing index (RSBI = respiratory rate/tidal volume in liters) predicts extubation success. RSBI <105 suggests successful extubation, while >105 indicates likely failure (12). For example, RR 30/min with tidal volume 250 mL yields RSBI of 120 (30/0.25), predicting failure.

Managing Extubation Failure

Approximately 10-15% of patients require reintubation within 48-72 hours. Risk factors include:

Age >65 years
Cardiac disease
High illness severity
Copious secretions
Upper airway obstruction

Oyster: The cuff-leak test helps predict post-extubation stridor. Deflate the ETT cuff and measure exhaled tidal volume. A leak <110 mL (or <12% of delivered volume) suggests significant laryngeal edema. Consider corticosteroids (methylprednisolone 20 mg IV q4h × 4 doses) before planned extubation in high-risk patients (13).

Complications of Mechanical Ventilation

Ventilator-Associated Pneumonia (VAP)

VAP develops in 10-25% of intubated patients and significantly increases mortality. Prevention strategies (the "ventilator bundle") include:

Elevation of head of bed 30-45°
Daily sedation interruption and SBT assessment
Peptic ulcer prophylaxis
DVT prophylaxis
Oral care with chlorhexidine

Pearl: Suspect VAP when a ventilated patient develops new infiltrates plus two of: fever >38°C, leukocytosis, or purulent secretions. However, diagnosis remains challenging as these findings are nonspecific in ICU patients.

Ventilator-Induced Lung Injury (VILI)

VILI encompasses multiple injury mechanisms:

Volutrauma: Overdistension from excessive tidal volumes
Barotrauma: High pressures causing pneumothorax
Atelectrauma: Repetitive opening/closing of alveoli
Biotrauma: Inflammatory cascade triggered by mechanical injury

The protective ventilation strategy prevents VILI:

Tidal volume 6 mL/kg PBW
Plateau pressure ≤30 cmH₂O
Driving pressure <15 cmH₂O
Adequate PEEP

Hemodynamic Compromise

Positive pressure ventilation decreases venous return, potentially causing hypotension, especially in hypovolemic patients. The "squeeze test" helps diagnose—temporary disconnection from the ventilator with return of blood pressure suggests positive pressure as the culprit.

Conclusion

Mechanical ventilation remains simultaneously one of the most powerful and potentially harmful interventions in internal medicine. The modern approach emphasizes protective ventilation strategies, derived from landmark trials demonstrating that gentler ventilation improves outcomes. Internists must master fundamental principles—appropriate mode selection, lung-protective tidal volumes, plateau pressure monitoring, recognition of patient-ventilator dyssynchrony, and evidence-based liberation strategies.

The clinical pearls highlighted in this review bridge theoretical knowledge and bedside practice. Remember that successful mechanical ventilation requires more than protocol adherence—it demands vigilant monitoring, systematic troubleshooting, and individualized adjustments based on patient physiology and disease state. As ventilator technology continues evolving, these fundamental principles remain constant, providing the foundation for competent critical care practice.

References

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