Ch. 16 Extrapulmonary Effects of Mechanical Ventilation

Extrapulmonary Effects of Mechanical Ventilation

Cardiovascular Function

  • Spontaneous Inspiration:
    • Negative intrapleural pressures increase venous return.
    • Pressure gradient to the heart increases due to drop in vena cava pressure.
  • Right Ventricular Preload:
    • Increased during inspiration.
  • Left Ventricular Preload:
    • Decreased during passive expiration.
    • Venous return decreases as intrapleural pressure becomes less negative.
    • Right ventricular stroke volume decreases.
  • Pulmonary Capillaries:
    • Overdistension narrows capillaries, increasing pulmonary vascular resistance and right ventricular afterload.
  • High Positive Pressure:
    • Levels >15 cm H2O and volume depletion reduce cardiac output and coronary artery perfusion, potentially causing myocardial ischemia.
  • Compensatory Mechanisms:
    • Include increased sympathetic tone, systemic vascular resistance, peripheral venous pressure, and peripheral shunting of blood.
  • Measuring Blood Pressure:
    • Essential soon after initiating PPV.
  • Venous Return:
    • PPV reduces venous return, improving stroke volume by optimizing length-tension relationships.

Mean Airway Pressure

  • Formula: Mean\ Airway\ Pressure = \frac{1}{2}[PIP × (\frac{TI}{TCT})] where TCT = \frac{60}{Respiratory\ Rate}
  • Inspiratory Hold: Increases mean airway pressure.
  • Formula with PEEP: Mean\ Airway\ Pressure = \frac{1}{2}[(PIP - PEEP) × (\frac{TI}{TCT})] + PEEP

Ventilation Parameters

  • High Inspiratory Flow Rates: Can cause uneven ventilation.
  • I:E Ratio: Ratios of 1:1, 2:1, or higher can lead to air trapping and hemodynamic complications.
  • Factors Influencing Cardiovascular Effects: Inspiratory flow and pattern, I:E ratio, inflation hold, PEEP, and ventilator mode.
  • Rapid Flow Rates: Deliver desired VT quickly, shortening inspiratory time and lowering mean airway pressure.
  • PEEP: Decreases cardiac output if pressure transmits to intrathoracic space; less impact with "stiff" lungs.

Neurological Function

  • CPP (Cerebral Perfusion Pressure): CPP = MABP - ICP
  • PPV Impact: Increases central venous pressure, potentially raising ICP.
  • Increased ICP Sign: Jugular vein distention.
  • Hyperventilation: Temporarily constricts cerebral vessels by lowering PaCO2.

Renal Function

  • PPV Effects: Alters kidney function due to hemodynamic changes, humoral responses (ADH, ANF, renin-angiotensin-aldosterone), and pH/PaCO2/PaO2 abnormalities.
  • Reduced Urinary Output: Occurs when glomerular capillary pressure drops below 75 mm Hg.
  • Hormonal Influence:
    • ADH: Released due to blood pressure changes from PPV, causing oliguria.
    • Atrial Natriuretic Factor: Reduced by PPV and PEEP, leading to water and sodium retention.
    • Renin-Angiotensin-Aldosterone: Activated during PPV, causing sodium and water retention.
  • Blood Gas Impact: Decreased PaO2 and increased PaCO2 impair renal function.
  • Drug Effects: Altered renal function from PPV can prolong drug effects.

Gastrointestinal Function

  • Liver Effects: PPV and PEEP can elevate serum bilirubin, potentially from reduced cardiac output, increased diaphragmatic force, decreased portal venous flow, or increased splanchnic resistance.
  • Gastric Distention: Can result from air swallowing; managed with a gastric tube.
  • Malnutrition Risk: Seriously ill patients are at risk due to inadequate food intake and increased metabolic rate.

Additional Considerations

  • Complications of Malnutrition: Reduced response to hypoxia/hypercapnia, muscle atrophy, respiratory infections, decreased surfactant, slowed tissue healing, and lower serum albumin.
  • Overfeeding Risks: Increases oxygen consumption, carbon dioxide production, and work of breathing.
  • Nutritional Assessment: Includes body composition, weight, anthropometric measurements, protein deficiencies, and immune function.
  • Mitigation: Early recognition and intervention are crucial for reducing complications associated with PPV.