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Pathophys - respiratory alterations

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Question
Answer
s/s of respiratory alterations   dyspnea (subjective - uncomfortable breathing)---breathlessness, air hunger, SOB etc.  
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normal breathing data   8-16 rpm---Tv=600-800mL----sighs 10-12 times/HOUR  
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kassmaul breathing vs Cheyne-Stokes   rapid, deep ---- reduced blood flow to brain stem intermittent/apnea  
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hypoventilation   inadequate alveoloar ventilation---paC02 > 44 -----normal PaC02=40  
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hyperventilaiton   alveolar ventilation exceeds metabolic demands----PaC02 < 36mmHg-----normal PaC02 = 40  
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hemoptysis   blood in sputum/pulmonary secretions bwo ----inf---pulm edema---PE (pulmonary embolism) or infarction---cancer  
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cyanosis   bluish skin/mucus membranes bwo desaturated or not enough Hb  
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s/s of hypoxia or dyspnea or cyanosis or respiratory alterations in general . . .(not sure which-gen idea here)   pain upon breathing ---clubbing---abnormal sputum  
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clubbing   increase in angle of nail bed, soft nails, nail curves like upside down spoon---associated with chronic hypoxic conditions such as ---lung ca---congenital heart disease---bronchiECTASIS  
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hypercapnia is caused by pulmonary disease   increased PaC02 measured in arterial blood  
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shunting   when blood flow (Q) is OK, but we have DECREASED ventilation-----caused by any disorder causing flooding or collapse of alveoli such as -----pulm edema---pneumonia---atelectasis  
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hypoxemia is   reduced oxygenation of arterial blood caused by 5 issues  
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hypoxemia caused by #1   decreased oxygen in inspired air----high altitude, low 02 content in gas mixture, enclosed breating space  
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hyoxemia caused by #2   hypoventilation bwo ---lack of neuro stimulation  
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hypoxemia caused by #3   alveolocapillary diffusion problem bwo ----emphysema---fibrosis---pulm edema  
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hypoxemia caused by #4   V/Q mismatch bwo ---asthma---chronic bronchitis---pneoumonia  
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hypoxemia caused by #5   pulmonary right-to-left shunt bwo -----ARDs-----respiratory distress of newborn=hyaline disease---ateclectasis  
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what is a V/Q shift?    
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what manifestion do ALL V/Q shifts cause   hypoxemia is end result  
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a low V/Q is less than 0.8 and indicates   IMPAIRED ventilation, somewhat deflated alveolus-----bwo---focal pneumonia---mucus  
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a very low V/Q indicates   BLOCKED venilation, collapsed alveolus bwo-----shunting---pneumothorax---ARDs---large area atelectasis  
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a HIGH V/Q over 0.8 indicates   impaired PERFUSION resulting in alveolar dead space bwo ---pulmonary emb---extensive emphysema  
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wikipedia's definition of pulmonary shunting   A pulmonary shunt is a physiological condition which results when the alveoli of the lung are perfused with blood as normal, but ventilation fails to supply the perfused region. VQ ratio is zero  
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What is acute respiratory failure   inadequate gas exchange----indicated by hypoxemia with Pa02 < 50----or---with PaC02 > 50 with pH < 7.25 acidotic  
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pulmonary edema   increase in interstitial fluid in lungs bwo capillary injury or failure of lymph to remove excess fluid.  
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lets say there are 3 things leading to pulmonary edema   increased left atrial pressure --- increased capillary perm/disruption of surfactant production---lymph obstruction/alteration  
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manifestations of pulmonary edema   dyspnea---hypoxemia---increased work of breathing---frothy sputum  
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aspiration commonly happens bwo   stroke pts aspirate food---kids inhale toys---ICU pts aspirate oropharyngeal contents  
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atelectasis   collapse of (alveoli) lung tissue caused by -----obesity---post op complication---endobronchial tumors---foreign body  
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bronchiectasis   is persistent dilation of bronchi--> easily collapse/obstruction most common and secondary to-----cystic fybrosis-----MOSTLY CAUSED BY mycobacterium avium  
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pneumothorax   gas or air trapped in pleural space bwo tear in visceral or parietal pleura  
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what can cause pneumothorz   chest wall trauma---inc airway pressure causing alveloi to rupture---spontaneous like ruptpure of COPD bleb, trauma  
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pleural effusion   shift of blood/fluid into pleura ---MOST OFTEN CAUSED BY CHF-----also nephrotic syndrome---cirrhosis---infections/pneumonia---cancer---PE  
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pleurisy   inflammation of pleural lining  
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what causes pleurisy   infection---inhaled chemical---collagen vascular disease---PE---trauma---pancreatitis/abd problems  
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ARDS = acute respiratory failure syndrome   sever form of failure with acute lung clincial lung injury----inflamm and diffuse alveolocapillary injury and NONCARDICAC PE  
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what is a very common cause of ARDs   severe aspiration of stomach contents, usually postop resp failure  
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obstructive pulmonary diseases   characterized by airway obstruction that makes it difficult to EXPIRE  
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examples of obstructive pulmonary diseases   asthma---chronic bronchitis---emphysema---  
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COPD   chronic obstructive pulmonary disease used to describe chronic BRONCHITIS AND EMPHYSEMA  
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asthma - chronic inflamm disorder of airways characterized by   bronchial hyperresponsiveness----episodic episodes of wheezing/breathlessness/chest tightness/coughing  
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pathophys of asthma   allergens---mast cells---release mediators---vasoactive cytokines increase cap perm---inflamm causes bronchial sm musc contr---vascular congestion/edema/mucus---mucociliary fxn impaired---epi cells damaged---airway walls thicken---obstruction  
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left untreated, asthma causes   causes irreversible airway damage  
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chronic bronchitis - can have seasonal cycles - defined as   hypersecretion of mucus and chronic/productive cough for at least 3 months for 2 consecutive years---higher incidence in smokers/high pollutants---repeaded infections a problem  
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pathophys bronchitis   irritant---inflamm cells---inc goblet cells---inc mucous can't be cleared---bronchospasm/dyspnea/cough---starts in lg airways, then smaller---airways close during expiration and trap air---V/Q mismatch---hypoxemia  
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take home on bronchitis   air can move in during INSPIRATION but during EXPIRATION, bronchial muscles relax, bronchial walls collapse around mucus----air cant escape---impaired ventilation leads to air trapping and increase in C02  
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emphysema   abn permanent enlargement of gas exchange airways accomp by DESTRUCTION of alveolar walls  
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in emphysema, what is obstruction caused by   caused by changes in lung tissue NOT BY mucus/inflamm  
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causes of emphysema   cig smoking---pollution ---childhood infection  
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what is the genetic component to emphysema   Alpha-1 antitrysin deficiency ---which inhibits many proteolytic enzymes. people lacking this enzyme, proteolysis of lung occurse --> homozygotes 75% chance of emphysema------smokers also deficient in alpha-1 antitrypsin  
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pathophys of emphysema   destruction of alveolar septa---destroys capillaries---increase volume of air in acinus---irritants may inhibit antiproteases---loss of elastic recoil/expiration.  
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what does hyperinflation in emphysema lead to   leads to air spaces (bullae) and blebs---then V/Q mismatch & hypoxia---air trapping---hypovent and hypercapnia late in dx  
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pulmonary hypertension = PAH   when pulmonary arterial pressure (PAP) exceeds 25 mmHg at rest, 30 exercising  
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pathophys of PAH   endothelial dysfunction --- xs vasoCONstrictors thromboxane/endothelin-----decreased vasoDILATORS NO/prostaglandin---fibrosis/thickening of vessel wall---lumen narrowing  
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PAH is associated with a ton of dxs   idiopathic--familial--CT dx--portal HTN---drugs/toxins---HF---thrombic/embolic dx---lung/hypoxia dxs  
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PAH clinical manifestations   often masked by u/l CV or pulm dx---dyspnea on exertion---fatigue---palpitations---chest pain  
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PE = pulmonary vascular disease-pulmonary embolus   occlusion by embolus---blood, fat, tissue, air  
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risk factos PE   conditions promoting clotting/venous stasis---hypercoagulability---endothelial injury  
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PE is 3rd leading cause of death in US   often bwo DVT - small emboli lodge in small bv---large occlude blood flow to lung = death  
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