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ASTHMA 
Pediatric Critical Care Medicine 
Emory University 
Children’s Healthcare of Atlanta
Asthma 
 Episodes of increased breathlessness, cough, 
wheezing, chest tightness. 
 Exacerbations may be abrupt or progressive 
 Always related to decreases in expiratory (also 
in inspiratory in severe cases) airflows 
 Hallmarks: airway inflammation, smooth 
muscle constriction and mucous plugs
Epidemiology 
Most common chronic disease in the world: varies 
between regions 
More prevalent in westernized countries but more severe 
in developing countries 
Yr of cost 2005 >$11.5 billion per year 
35/100.000 fatality, mostly pre-hospital & older pop 
Seasonal exacerbation pattern but ICU admission remains 
constant 
<10% life threatening exacerbation: 2-20% with ICU 
admission; 4% intubation 
Reduction in mortality (63%) in the 1980’s due to inhaled 
steroids
Asthma Prevalence 
4
Pathophysiology 
 Airway inflammation, smooth muscle constriction, and 
airway obstruction 
 VQ mismatch (<0.1)- decrease vent with normal perfusion 
 Intrapulmonary shunt is prevented due to collateral 
ventilation, hypoxic pulmonary vasoconstriction, rarely 
functionally complete obstruction  mild hypoxemia 
 Worsening of hypercapnea is indicative of impending 
respiratory failure in combination of lactic acidosis 
 Worsening of hypoxemia after beta-agonist is common due 
to removal of hypoxic induced pulmonary vasoconstriction
Asthma
Histamine 
Tryptase 
PGD2 
LTC4 
IL-4 
IL-5 
IL-6 
TNF-α 
Eosinophilic cationic proteins 
Major basic proteins 
Platelet activating factor 
LTC4, LTD4, LTE4 
IL-3 
IL-4 
IL-5 
GM-CSF
Pathophysiology 
 Lactic acidosis: 
 Changes in glycolysis due to high dose beta 
agosist; 
 Increased wob, anaerobic metabolism 
 Coexisting profound tissue hypoxia 
 Over production of lactic acid by the lungs 
 Decrease lactate clearance due to hypoperfusion
Pathophysiology 
 Significantly reduced: FEV1; FEV1/FVC, Peak 
expiratory flow; maximal expiratory flow at 75%, 
50% and 25%, and maximal exiratory flow 
between 25% and 75% of the FVC 
 Abnormally high airway resistance: 5-15x normal 
due to shortening of airway smooth muscle, 
airway edema and inflammation, excessive 
luminal secretions.

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Difference Between Search & Browse Methods in Odoo 17
 

Olumide pidan

  • 1. ASTHMA Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta
  • 2. Asthma  Episodes of increased breathlessness, cough, wheezing, chest tightness.  Exacerbations may be abrupt or progressive  Always related to decreases in expiratory (also in inspiratory in severe cases) airflows  Hallmarks: airway inflammation, smooth muscle constriction and mucous plugs
  • 3. Epidemiology Most common chronic disease in the world: varies between regions More prevalent in westernized countries but more severe in developing countries Yr of cost 2005 >$11.5 billion per year 35/100.000 fatality, mostly pre-hospital & older pop Seasonal exacerbation pattern but ICU admission remains constant <10% life threatening exacerbation: 2-20% with ICU admission; 4% intubation Reduction in mortality (63%) in the 1980’s due to inhaled steroids
  • 5. Pathophysiology  Airway inflammation, smooth muscle constriction, and airway obstruction  VQ mismatch (<0.1)- decrease vent with normal perfusion  Intrapulmonary shunt is prevented due to collateral ventilation, hypoxic pulmonary vasoconstriction, rarely functionally complete obstruction  mild hypoxemia  Worsening of hypercapnea is indicative of impending respiratory failure in combination of lactic acidosis  Worsening of hypoxemia after beta-agonist is common due to removal of hypoxic induced pulmonary vasoconstriction
  • 7. Histamine Tryptase PGD2 LTC4 IL-4 IL-5 IL-6 TNF-α Eosinophilic cationic proteins Major basic proteins Platelet activating factor LTC4, LTD4, LTE4 IL-3 IL-4 IL-5 GM-CSF
  • 8. Pathophysiology  Lactic acidosis:  Changes in glycolysis due to high dose beta agosist;  Increased wob, anaerobic metabolism  Coexisting profound tissue hypoxia  Over production of lactic acid by the lungs  Decrease lactate clearance due to hypoperfusion
  • 9. Pathophysiology  Significantly reduced: FEV1; FEV1/FVC, Peak expiratory flow; maximal expiratory flow at 75%, 50% and 25%, and maximal exiratory flow between 25% and 75% of the FVC  Abnormally high airway resistance: 5-15x normal due to shortening of airway smooth muscle, airway edema and inflammation, excessive luminal secretions.