Mechanical Ventilation

Mechanical Ventilation Intended Outcomes

  • Background to mechanical ventilation
  • Oxygen and Ventilation Consequences
  • Intrathoracic Pressures and the Effects
  • Ventilation Pressure and Stretch
  • Cardiovascular Effects
  • Lymphatic Effects
  • Effects on other organ systems

Background to Mechanical Ventilation

  1. Historical Development
       - The initial concept of mechanical ventilation originated from negative pressure ventilators first introduced in the 1830s, with early versions as far back as the 1600s.
       - These devices utilized combinations of pistons, bellows, and sealed containers to create negative pressure environments that facilitated lung ventilation.
       - Image of Negative Pressure Ventilator
       - Reference: Soni, N., & Williams, P. (2008). Positive Pressure Ventilation: What is the real cost? British Journal of Anaesthesia, 101(4), 446-457.

  2. Significant Events
       - In 1952, during the Copenhagen Polio Epidemic, Positive Pressure Ventilation (PPV) became widely implemented.
       - Early practices lacked oximetry and capnography, highlighting the delayed recognition of PPV's negative sequelae, especially after the establishment of ARDSnet (Acute Respiratory Distress Syndrome Network) in 1994.
       - Complications arising from PPV are often not immediately visible.

  3. Primary Goals of Mechanical Ventilation
       - The main objective of mechanical ventilation (MV) and PPV is to achieve optimal oxygenation.
       - The consequences of PPV and various ventilation strategies can often be detrimental.
       - Common issues include the shearing and stretching forces that result from PPV and mechanical ventilation.

Oxygenation and Ventilation Consequences

  1. Goals and Measurement Techniques
       - The primary aim remains to secure premium oxygenation.
       - Traditionally, oxygenation has been assessed through the relationship between Fraction of Inspired Oxygen (FiO2) and arterial blood gases.
       - Modern methods involve measuring ScVO2 (central venous oxygen saturation) and lactate levels to indicate tissue hypoxia.
       - Aggressive ventilation strategies are frequently employed to achieve targeted oxygenation, leading to secondary lung injury from such interventions.
       - Reference: Soni, N., & Williams, P. (2008).

  2. Understanding Tissue Oxygenation
       - It is crucial to note that adequate tissue oxygenation can exist even with relatively low arterial saturations.
       - Poor tissue oxygenation is rarely solely attributable to lung function.
       - Patients often develop tolerance to lower saturation levels.
       - More fatalities from lung injury are linked to complications resulting from mechanical ventilation rather than hypoxemia itself.
       - Reference: Soni, N., & Williams, P. (2008).

Intrathoracic Pressures and the Effects

  1. Normal and Positive Pressure Breathing
       - In typical inspiration, minimal negative changes in intrapleural, interstitial, and alveolar pressures facilitate lung expansion.
       - During expiration, intrapleural pressure returns to normal (remaining negative), while interstitial and alveolar pressures normalize or become slightly positive to aid ventilation.
       - PPV and MV disrupt this cycle, resulting in elevated intrathoracic pressure during inspiration, leading to increased pressure in interstitial and alveolar tissues. During expiration, alveoli can tend toward atmospheric pressure.
       - Reference: Soni, N., & Williams, P. (2008).

  2. Airflow Distribution Changes
       - Negative pressure breathing yields uniform air distribution.
       - Surfactant functionality mitigates the implications of Laplace’s Law, allowing for even gas distribution even under small negative intrapleural pressures.
       - Under PPV and MV, gas distribution may become concentrated in only compliant regions of the lung due to timed delivery, risking insufficient inflation of collapsed alveoli. Sustained airflow is necessary to reinflate previously normal alveoli.
       - Reference: Soni, N., & Williams, P. (2008).

Ventilation Pressure and Stretch (Important)

  1. Ventilator-Induced Lung Injury (VILI)
       - Forces encountered during MV can result in injury, characterized by stress and shearing forces that expand alveoli. This leads to increased cytokine release and white cell recruitment, termed barotrauma and volutrauma.
       - VILI can manifest through:
         - Barotrauma: Alveolar rupture or air leaks, often due to regional lung overdistension rather than solely elevated pressure; may cause pulmonary edema.
         - Reference: Soni, N., & Williams, P. (2008).
         - Reference: Slutsky, A. S., & Ranieri, V. M. (2013). Ventilator-Induced Lung Injury. NEJM, 369(22), 2126-2136.

  2. Forms of VILI
       - Volutrauma: Can occur from utilizing tidal volumes even within normal ranges that lead to persistent lung distension.
       - Atelectrauma: Results from consistently low tidal volumes and pressures, leading to both collapse (atelectasis) and expansion of alveoli.
       - Biotrauma: Arises from the aforementioned mechanisms, causing the release of mediators that may injure lung tissue or predispose it to pulmonary fibrosis, hampering ventilation and raising infection risk.
       - Reference: Soni, N., & Williams, P. (2008).
       - Reference: Slutsky, A. S., & Ranieri, V. M. (2013).

Cardiovascular Effects

  1. Normal Breathing vs. PPV/MV
       - Negative pressure breathing (normal physiology) supports venous return, alleviating pressure on pulmonary capillaries and enhancing blood flow.
       - Conversely, PPV and MV cause increased intrathoracic pressure, reducing venous return, right ventricular output, and overall pulmonary blood flow.
       - Upon expiration, pressures typically revert to normal, restoring blood flow; however, sustained positive end-expiratory pressure (PEEP) can counteract this.
       - Elevated atrial pressures can lead to water and sodium retention strategies within the kidneys.
       - Reference: Soni, N., & Williams, P. (2008).

  2. Pulmonary Blood Flow Dynamics
       - Normal pulmonary pressures hover around 7-10 mmHg, a balance between the pulmonary artery and pulmonary vein.
       - PPV and MV significantly elevate these pressures, diminishing pulmonary blood flow and prompting pulmonary vasoconstriction.
       - These mechanisms contribute to decreased lung blood flow, ultimately reducing left atrial preload.
       - A positive intrathoracic pressure also impacts systemic venous return negatively.
       - Reference: Soni, N., & Williams, P. (2008).

Lymphatic Effects

  1. Normal Lymphatic Pressure
       - In standard inspiration, lymph pressure is approximately 4 mmHg.
       - During PPV and MV, single-celled lymphatics often undergo compression, lowering lymphatic flow.
       - While PPV and MV may promote some lymph movement towards lymphatics, drainage impairment hinders this process, potentially resulting in fluid sequestration and serving as an infection reservoir.
       - Reference: Soni, N., & Williams, P. (2008).

Effects on Other Organ Systems

  1. Immediate Systemic Effects
       - Acute reductions in cardiac output are evident upon initiation of MV.
       - Decreases in Glomerular Filtration Rate (GFR) predispose kidneys to Acute Kidney Injury (AKI).
       - Increased intrathoracic pressure can also result in hepato-splanchnic congestion, complicating lymph drainage.
       - Altered fluid dynamics and decreased venous return may lead to fluid backup at the end-organ level, creating further system-level complications.
       - Reference: Soni, N., & Williams, P. (2008).