PRE FINAL OSCE

 

1) Criteria for weaning patient off of ventilator? 


 -> Subjective assessment:

     Adequate cough
     No neuromuscular blocking agents 
     Absence of excessive trachea bronchial secretions 
     Reversal of underlying cause of respiratory failure 
     

 -> Objective assessment:

     Stable cardiovascular status
     Heart rate <140 beats/min
     No active myocardial ischemia 
     Adequate heamoglobin level >8g/dL
     Systolic blood pressure 90-160mmHg
    

 -> Adequate oxygenation:

      Tidal volume >5mL/kg
      Vital capacity >10mL/kg
      Proper Inspiratory effort 
      Respiratory rate <35/min
      PaO2 >60mmHg, PCO2 <60mmHg
      No significant respiratory acidosis 


• Reference-




2) CPAP for pneumonia treatment 

• The Cpap does not treat pneumonia directly but can reduce the work of breathing often seen with pneumonia. In most cases rpneumonia is unilateral and can interfere with gas exchange on the effected side. 

• There may be additional areas of the lung that could be ventilated by using Cpap to recruit unventilated alveoli. The goal is to offset what the pneumonia is blocking with recruited alveoli (or) open small airways previously obstructed.


• Reference- 




3) Alveolar changes in respiratory distress? 


• An uninjured healthy lung contains an intact respiratory epithelial layer and alveolar space patrolled by resident alveolar macrophages. Type I and type II pneumocytes contribute to regulation of alveolar contents, including surfactant, and maintain the integrity of the alveolar-capillary barrier. 
Following infection or injury, an influx of innate immune cells such as neutrophils and monocytes migrate from the circulation into the interstitial and alveolar spaces, 

• During respiratory distress, damage to the epithelial and endothelial layers results in breakdown of the alveolar-capillary barrier and accumulation of edematous fluid and debris in the alveolar spaces. Pro-inflammatory and destructive functions of alveolar macrophages, monocytes, and neutrophils contribute to disease pathology. 

• The consequence is the loss of alveolar-capillary barrier function. This disruption permits the accumulation of proteinaceous fluid in the alveolar space coupled with decreased compliance due to loss of surfactant. 

• In many cases, the severe hypoxemia necessitates life-supportive mechanical ventilation and the delivery of high concentrations of supplemental oxygen.

• Reference:
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