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NURS 350 Patho resp

Pathophys - respiratory alterations

s/s of respiratory alterations dyspnea (subjective - uncomfortable breathing)---breathlessness, air hunger, SOB etc.
normal breathing data 8-16 rpm---Tv=600-800mL----sighs 10-12 times/HOUR
kassmaul breathing vs Cheyne-Stokes rapid, deep ---- reduced blood flow to brain stem intermittent/apnea
hypoventilation inadequate alveoloar ventilation---paC02 > 44 -----normal PaC02=40
hyperventilaiton alveolar ventilation exceeds metabolic demands----PaC02 < 36mmHg-----normal PaC02 = 40
hemoptysis blood in sputum/pulmonary secretions bwo ----inf---pulm edema---PE (pulmonary embolism) or infarction---cancer
cyanosis bluish skin/mucus membranes bwo desaturated or not enough Hb
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
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
hypercapnia is caused by pulmonary disease increased PaC02 measured in arterial blood
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
hypoxemia is reduced oxygenation of arterial blood caused by 5 issues
hypoxemia caused by #1 decreased oxygen in inspired air----high altitude, low 02 content in gas mixture, enclosed breating space
hyoxemia caused by #2 hypoventilation bwo ---lack of neuro stimulation
hypoxemia caused by #3 alveolocapillary diffusion problem bwo ----emphysema---fibrosis---pulm edema
hypoxemia caused by #4 V/Q mismatch bwo ---asthma---chronic bronchitis---pneoumonia
hypoxemia caused by #5 pulmonary right-to-left shunt bwo -----ARDs-----respiratory distress of newborn=hyaline disease---ateclectasis
what is a V/Q shift?
what manifestion do ALL V/Q shifts cause hypoxemia is end result
a low V/Q is less than 0.8 and indicates IMPAIRED ventilation, somewhat deflated alveolus-----bwo---focal pneumonia---mucus
a very low V/Q indicates BLOCKED venilation, collapsed alveolus bwo-----shunting---pneumothorax---ARDs---large area atelectasis
a HIGH V/Q over 0.8 indicates impaired PERFUSION resulting in alveolar dead space bwo ---pulmonary emb---extensive emphysema
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
What is acute respiratory failure inadequate gas exchange----indicated by hypoxemia with Pa02 < 50----or---with PaC02 > 50 with pH < 7.25 acidotic
pulmonary edema increase in interstitial fluid in lungs bwo capillary injury or failure of lymph to remove excess fluid.
lets say there are 3 things leading to pulmonary edema increased left atrial pressure --- increased capillary perm/disruption of surfactant production---lymph obstruction/alteration
manifestations of pulmonary edema dyspnea---hypoxemia---increased work of breathing---frothy sputum
aspiration commonly happens bwo stroke pts aspirate food---kids inhale toys---ICU pts aspirate oropharyngeal contents
atelectasis collapse of (alveoli) lung tissue caused by -----obesity---post op complication---endobronchial tumors---foreign body
bronchiectasis is persistent dilation of bronchi--> easily collapse/obstruction most common and secondary to-----cystic fybrosis-----MOSTLY CAUSED BY mycobacterium avium
pneumothorax gas or air trapped in pleural space bwo tear in visceral or parietal pleura
what can cause pneumothorz chest wall trauma---inc airway pressure causing alveloi to rupture---spontaneous like ruptpure of COPD bleb, trauma
pleural effusion shift of blood/fluid into pleura ---MOST OFTEN CAUSED BY CHF-----also nephrotic syndrome---cirrhosis---infections/pneumonia---cancer---PE
pleurisy inflammation of pleural lining
what causes pleurisy infection---inhaled chemical---collagen vascular disease---PE---trauma---pancreatitis/abd problems
ARDS = acute respiratory failure syndrome sever form of failure with acute lung clincial lung injury----inflamm and diffuse alveolocapillary injury and NONCARDICAC PE
what is a very common cause of ARDs severe aspiration of stomach contents, usually postop resp failure
obstructive pulmonary diseases characterized by airway obstruction that makes it difficult to EXPIRE
examples of obstructive pulmonary diseases asthma---chronic bronchitis---emphysema---
COPD chronic obstructive pulmonary disease used to describe chronic BRONCHITIS AND EMPHYSEMA
asthma - chronic inflamm disorder of airways characterized by bronchial hyperresponsiveness----episodic episodes of wheezing/breathlessness/chest tightness/coughing
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
left untreated, asthma causes causes irreversible airway damage
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
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
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
emphysema abn permanent enlargement of gas exchange airways accomp by DESTRUCTION of alveolar walls
in emphysema, what is obstruction caused by caused by changes in lung tissue NOT BY mucus/inflamm
causes of emphysema cig smoking---pollution ---childhood infection
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
pathophys of emphysema destruction of alveolar septa---destroys capillaries---increase volume of air in acinus---irritants may inhibit antiproteases---loss of elastic recoil/expiration.
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
pulmonary hypertension = PAH when pulmonary arterial pressure (PAP) exceeds 25 mmHg at rest, 30 exercising
pathophys of PAH endothelial dysfunction --- xs vasoCONstrictors thromboxane/endothelin-----decreased vasoDILATORS NO/prostaglandin---fibrosis/thickening of vessel wall---lumen narrowing
PAH is associated with a ton of dxs idiopathic--familial--CT dx--portal HTN---drugs/toxins---HF---thrombic/embolic dx---lung/hypoxia dxs
PAH clinical manifestations often masked by u/l CV or pulm dx---dyspnea on exertion---fatigue---palpitations---chest pain
PE = pulmonary vascular disease-pulmonary embolus occlusion by embolus---blood, fat, tissue, air
risk factos PE conditions promoting clotting/venous stasis---hypercoagulability---endothelial injury
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
Created by: lorrelaws