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Dysnpnea (Harrison )
- Experience derives from interaction among multiple physiological , psychological , social and
environment
Mechanisms of dyspnea
Motor efferents
- Muscles
- When increase resistance or stiffness > increase work of breathing => increase effort to breathe
- The increase neural output fromt the motor cortex is sended via coroally discharge, coroally
discharge ->send to sensory cortex , at the same time motor output is directed to the ventilator
muscle.
sensory afferents
- Chemoreceptor ( carotid body and medulla ) activated by hypoxemia , acute hypercapnia and
acidemia- > increase in ventilation-> air hunger
- Mechanoreceptors -> chest tightness -> bronchospasm
- J receptor -> stimulated -> interstitial edema ,and acute changes in pulmonary artery pressure->
air hunger.
- Metaboreceptors -> located muscle -> changes in the local biochemical milieu of tissue active
during exercise and when stimulated -> breathing discomfort
anxiety
Increase respiratory rate that accompanies acute anxiety leads to hyperinflation , increased
work and effort of breathing and a sense of an unsatifying breath
Assessing dyspnea
Descriptor Pathophysiology
Chest tightness or constriction Bronchoconstriction , interstitial edema ( asthma
, myocardial ischemia
Increases work or effort of breathing COPD , asthma , airway obstruction
Air hunger , need to breathe , urge to breathe Pulmonary edema
Unsatisfying breath Hyperinflation , asthma , pulmonary fibrosis
Differential diagnosis
PULMONARY EDEMA
Fluid accumulate in the intestitium of the lung depends on the balance of hydrostatic and
oncotic forces within the pulmonary capillaries and in the surrounding tissue
Causes : cirrhosis , nephrotic syndrome
cardiogenic pulmonary edema
- Cardiac abnormalities -> increase in pulmonary venous pressure shift the balance of forces
between the capillary and the interstitium( interstitial edema alveolar edema )
- Signs : dyspnea and orthopnea , chest x ray : peribronchial thickening , prominent vascular
markings in the upper lung zones , and kerley B lines. , sever condition => alveoli fill with fluid ->
perihilar distribution.
- Lung water increase due to damage of the pulmonary capillary lining with leakage of proteins
and other macromolecules into the tissue
- Cause : dysfunction of the surfactant lining the alveoli to callapse at low lung volumes
- Categorize the cause : injury to the lung { direct( truma) , indirect( mediators reach the lung via
blood stream ) , or pulmonary vascular causes(acute changes in pulmonary vascular pressure }
diagnostic differential
Chest x ray : cardiogenic pulmonary edema > enlarged cardiac silhouette , vascular
redistribution , interstitial thinkening, and prehilar alveolar infiltrate, pleural effusions are
common., chest x ray for non card : size of heart normal , alveolar infiltrate are distributed more
uniformly throughout the lungs, and pleural effusions are uncommon,