PEEP in Mechanical Ventilation: Definition, Settings, Nursing Care

Mechanical ventilation requires four foundational settings: PEEP (Positive End Expiratory Pressure, 5-20 mmHg) maintains constant pressure to improve oxygenation; FiO2 (Fraction of Inspired Oxygen, 21-100%) controls oxygen concentration; Respiratory Rate (8-32 breaths/minute) determines ventilation frequency; and Tidal Volume (6-8 cc/kg ideal body weight) or Inspiratory Pressure (above PEEP) controls volume delivery. These settings operate in either Volume Control (setting tidal volume) or Pressure Control (setting pressure above PEEP) modes, with Respiratory Rate × Tidal Volume calculating Minute Ventilation for carbon dioxide elimination.

Volume control ventilation maintains constant tidal volume while pressure varies, with key settings including tidal volume (VT), respiratory rate (RR), FIO2, PEEP (minimum 5 cm H2O), and pressure support (5-20 cm H2O); monitoring parameters include minute ventilation (target 5-10 L/min), peak inspiratory pressure (<35 cm H2O), and plateau pressure (<30 cm H2O for lung compliance). The basic volume control modes progress from most to least supportive: Assist Control delivers full tidal volume regardless of patient effort, SIMV allows spontaneous breaths with pressure support assistance, and Pressure Support provides minimal mandatory breaths with patient-driven breathing, forming a hierarchy of ventilatory support that enables gradual weaning from mechanical ventilation.

Mechanical ventilation supports patients with apnea, acute respiratory failure, airway protection needs, severe hypoxia, or respiratory muscle fatigue. Two fundamental approaches exist: negative pressure ventilation (iron lung) which expands around the chest for neuromuscular disorders, and positive pressure ventilation which delivers air through artificial airways. Positive pressure has two modes: volume-controlled (preset tidal volume, passive exhalation) and pressure-controlled (preset pressure, tidal volume adjusts with compliance/resistance). Essential ventilator settings include tidal volume (6-10 mL/kg ideal body weight), FIO2 (21-100%), respiratory rate, peak pressure, pressure support (6-18 cm H2O), and I:E ratio. The high pressure limit (10-20 cm H2O above peak) prevents alveolar rupture. Two primary modes exist: assist control (delivers preset tidal volume with any spontaneous breath above set rate) and SIMV (synchronizes mandatory breaths with patient efforts, allowing self-regulated tidal volume during spontaneous breaths).

Mechanical ventilation requires multidisciplinary coordination among house officers, nursing staff, respiratory therapists, and intensivists to ensure consistent patient care. Two fundamental types of mechanical ventilation exist: fully supported modes and weaning modes. Assist control is the classic fully supported mode where clinicians set respiratory rate (12-16 bpm), tidal volume (300-400 mL or 6 mL/kg for ARDS), FiO2, and PEEP (starting at 5 cm H2O). PRVC (Pressure Regulated Volume Control) is a dual-mode system where clinicians set tidal volume and the ventilator automatically adjusts pressure targets, providing benefits like demand flow and automatic compensation for changing pulmonary compliance.

Three basic ventilation modes: Volume Control (VC), Pressure Control (PC), and Pressure Support Ventilation (PSV). No mode is inherently better; choice depends on team experience. Basic concepts: pressure is force on surface, volume is space occupied by air, flow is gas displacement over time. In Volume Control, the ventilator delivers set tidal volume (6-8 ml/kg predicted body weight), with pressure as consequence. Key parameters: tidal volume, respiratory frequency, PEEP, FiO2. The ventilator displays pressure, flow, and volume curves. Patients can trigger breaths if not fully sedated. Volume Control is preferred for neurocritical patients and passively ventilated patients.

Surface tension at the air-fluid interface in alveoli creates an elastic force that tends to cause alveolar collapse, with smaller alveoli being more prone to collapse due to Laplace's law (P = 2T/r); surfactant, produced by type II alveolar epithelial cells, reduces this surface tension by acting as a surface-active agent composed primarily of phospholipids like dipalmitoylphosphatidylcholine, thereby increasing lung compliance and preventing neonatal respiratory distress syndrome.

Atelectasis is the collapse of alveoli, primarily caused by obstruction (mucus plugs, tumors), external compression, hypoventilation, or surfactant deficiency. When obstruction occurs, alveoli distal to the blockage become trapped and cannot exchange gases. Trapped air and fluids are absorbed into the pleural space, creating negative pressure that collapses pliant lung tissue. Rigid tissues resist collapse but still develop fluid accumulation. This cascade of events begins the physiological deterioration of lung function.

Pulmonary atelectasis is the collapse of previously inflated lung tissue, classified into three main types: obstructive/reabsorption atelectasis (caused by bronchial blockages from foreign bodies, mucus plugs, tumors, or inflammation, characterized by mediastinal shift toward the affected lung), compressive atelectasis (resulting from pleural effusion, pneumothorax, tumors, or lymphadenopathy, with mediastinal shift away from the affected lung), and contraction/scarring atelectasis (due to pulmonary fibrosis, which is typically irreversible). The pathophysiology involves alveolar reabsorption of gases when ventilation is blocked, leading to alveolar collapse, local pulmonary vasoconstriction to maintain ventilation-perfusion balance, and compensatory collateral ventilation through pores of Kohn and Lambert canals. Clinical manifestations include dyspnea, cyanosis, chest pain, and fever, though many patients remain asymptomatic.

Compliance (distensibility) is the lung's capacity to expand per pressure change: Compliance = ΔVolume / ΔPressure. High compliance (emphysema) means easy expansion; low compliance (fibrosis) means rigidity. Elastance is inversely proportional to compliance. Pulmonary surfactant (phospholipids and proteins from type II pneumocytes) reduces surface tension, preventing alveolar collapse, increasing compliance, and stabilizing alveoli of different sizes. Alveolar stability also depends on elastic recoil and residual volume containing poorly diffusible gases like nitrogen.

Surface tension at alveolar air-water interfaces tends to collapse alveoli. Type II alveolar cells produce surfactant (protein-lipid complex) that decreases surface tension. Without surfactant (infant respiratory distress syndrome), compliance decreases dramatically. Chest wall disorders like ankylosing spondylitis, kyphosis, scoliosis, and cartilage calcification reduce chest wall compliance, impairing lung expansion. Neuromuscular problems including diaphragm injury, intercostal paralysis, and ALS decrease compliance by impairing inspiratory muscles. Pneumothorax causes atmospheric pressure to enter the pleural cavity, pushing against lungs and causing collapse. As intrapleural pressure rises toward atmospheric levels, lung volume decreases, decreasing compliance. Mucus buildup from chronic bronchitis or cystic fibrosis also decreases compliance by preventing proper air distribution to alveoli.

Arterial Blood Gases (ABGs) measure pH, PaCO2, HCO3-, PaO2, and base excess to assess a patient's oxygenation, ventilation, and acid-base status. Normal values are pH 7.35-7.45, PaCO2 35-45 mmHg, HCO3- 22-26 mEq/L, and PaO2 80-100 mmHg on room air. Interpretation follows a systematic approach: pH determines the primary disorder (acidosis if <7.35, alkalosis if >7.45), then identify the compensatory mechanism by comparing PaCO2 and HCO3- values. Respiratory acid-base disturbances affect PaCO2, while metabolic disturbances affect HCO3-. Compensation status is determined by whether pH returns to normal range. For example, pH 7.46 with PaCO2 34 and HCO3- 23.5 indicates uncompensated respiratory alkalosis, while pH 7.36 with PaCO2 75 and HCO3- 40.6 indicates compensated respiratory acidosis.

Arterial blood gas (ABG) analysis determines oxygenation and ventilation and indicates acidosis or alkalosis. Normal values: pH 7.35-7.45, PaCO2 (carbon dioxide) 35-45 mmHg, PaO2 (oxygen) 80-100 mmHg, HCO3 (bicarbonate) 22-26 mEq/L. Acidosis is pH below 7.35; alkalosis is pH above 7.45. PaCO2 above 45 indicates acidosis (hypoventilation); PaCO2 below 35 indicates alkalosis (hyperventilation). HCO3 below 22 indicates acidosis; HCO3 above 26 indicates alkalosis.

Arterial Blood Gas (ABG) analysis measures partial pressure of oxygen (PaO2), partial pressure of carbon dioxide (PaCO2), pH, and calculated bicarbonate (HCO3-) to assess a patient's oxygenation, ventilation, and acid-base status. Normal values are: pH 7.35-7.45, PaCO2 35-45 mmHg, PaO2 75-100 mmHg, and HCO3- 22-26 mEq/L. PaCO2 reflects ventilation status, while PaO2 indicates oxygenation status and must be correlated with clinical context such as oxygen therapy.

This comprehensive lecture covers the complete fundamentals of Arterial Blood Gas (ABG) interpretation. ABG stands for Arterial Blood Gas, involving blood samples drawn from arteries (typically radial artery) to measure gas levels. The three main parameters are: (1) pH (7.35-7.45 normal) indicating acid-base status; (2) PaO2 (80-100 mmHg) reflecting oxygenation; (3) PaCO2 (35-45 mmHg) representing respiratory ventilation. HCO3- (22-26 mEq/L) is the metabolic component controlled by kidneys. Respiratory acidosis occurs when PaCO2 increases above 45 mmHg, while respiratory alkalosis occurs when PaCO2 decreases below 35 mmHg. Metabolic acidosis occurs when HCO3- decreases below 22 mEq/L, and metabolic alkalosis occurs when HCO3- increases above 26 mEq/L. The respiratory system controls PaCO2, while the kidneys control HCO3-. Compensation occurs when one body system attempts to correct an acid-base disturbance caused by another system. The systematic approach to ABG interpretation: (1) Check pH to determine acidosis or alkalosis; (2) Check if PaCO2 matches the pH change; (3) Check if HCO3- matches the pH change; (4) Assess compensation. Disorders are classified as uncompensated, partially compensated, or fully compensated based on whether pH has returned to normal range. The 7.40 threshold determines whether a normal pH represents acidosis (below 7.40) or alkalosis (above 7.40).

Arterial blood gas analysis provides critical information about acid-base status and oxygenation. Key parameters: pH (7.35-7.45 normal), PaO2 (oxygenation), PaCO2 (ventilation), HCO3- (metabolic component). Normal values depend on pH - when pH is outside normal range, values are considered abnormal. The interpretation involves determining primary disturbance (respiratory vs metabolic) and compensation. This systematic approach guides treatment decisions.