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52 terms

Pathophysiology- resp disease

Test 3
Subjective sensation of uncomfy breathing, feeling of not getting enough air
Dyspnea when a person is laying down
normal breathing that's rhythmic and effortless; slight pause between breaths
Kussmaul respiration (hypernea)
increased breathing rate, large Tidal volume and no pause
large airway obstruction (blockage)
increase work of breathing, slow breaths, large tidal volume, big breaths and audible wheezing
small airway obstruction (blockage)
ex. asthma and copd; rapid breathing, small tidal volume, increased effort, long exhales
Cheyne-stokes respiration
apnea followed by deep breathing = neurological origin; slows blood flow to the brain stem and slows impulses sending info to respiratory centers of brain stem
inadequate alveolar breathing related to metabolic demands (overlooked because breathing is normal); occurrs when tidal volume and respiratory rate reduce (decreased resp rate)
CO2 removal can't keep up with CO2 production and level of CO2 increases in arterial blood and makes blood more acidic
alveolar breathing exceeds metabolic demands (increased resp rate)
blue discoloration of the skin and mucous membranes caused by increased amounts of reduced hemoglobin
causes of cyanosis
causes of? -decreased arterial O2, pulmonary/cardiac right to left shunts (lungs/heart blood doesn
diverted from one pathway to another
reduced blood oxygen levels; ie. clubbing; common cause of abnormal v/q blance
enlargement of end of toe/finger equals sign of chronic hypoxemia
protective reflex that cleanses lower airways by an explosive expiration
cough up blood or bloody secretions
vomiting of blood
acute respiratory failure
bad gas exchange (can happen to anyone) ;abrupt build up of CO2 and O2
pulmonary edema
excess water in lungs that leads to heart failure
collapse of lung tissue
compression atelectasis
caused by external pressure (ie exerted by tumor, fluid, or air in lung space) causing alveoli to collapse because of pressure on lung
absorption atelectasis
results from removal of air because of destroyed alveoli or from inhaling pure O2 (ie. drugs- becomes hypoxemic b/c can't exchange gases or ie after surgery due to inhaling anesthetics)
persistent abnormal dialation of the bronchi- persistent dialation hard to maintain pressure on inside and outside b/c can't adequately empty lung; too much equal pressure in atm and inside of lung- want different pressures
presence of air or gas in the pleural space caused by a rupture in the visceral pleura (surrounds lungs) or parietal pleural and chest wall; air separates the visceral and parietal pleurae, it destroys the neg pressure of the pleural space and disrupts the equilibrium of lung causing it to collapse
spontaneous pneumothorax
unexpected in healthy people (men) happens suddenly- spontaneous rupture of blebs (blisters) on visceral pleura; unknown cause
secondary pneumothorax
cause- chest trauma, ie. stab wound or rib fracture, bullet- anything that tears the pleura
pleural effusion
presence of fluid in pleural space (effects lungs)
ARDS (acute respiratory distress syndrome)
characterized by acute lung inflammation and diffusion (much spreading) alveolarcapillary injury ; main causes: sepsis and multiple trauma
metabolic acidosis
loss of HCO3 occurs in bloodstream
resp acidosis
pH inbalances in bloodstream
lipoprotein that reduced surface tension of pulmonary fluids allowing exchange of gas in alveoli of lungs
obstructive pulmonary disease
airway obstruction that is worse with expiration; common symptoms- dyspnea, wheezing; common obstructive (blockage) disorders- asthma, emphysema, chronic bronchitis
most common pleural abnormality- disease resulting in episodic narrowing and inflammation of airways
COPD (chronic obstructive pulmonary disease)
lung changes with emphysema and chronic bronchitis; a main cause is cigarette smoke
chronic bronchitis
hypersecretion of mucus and chronic cough over 3 months of a year for 2 years. Inflammation and fibrosis of bronchial wall.
abnormal enlargement of gas exchange airways lead to destruction of alveolar walls without obvious fibrosis-loss of elastic recoil of bronchi walls
chronic bronchitis features
features: shortness of breath, abnormal blood gases leading to pulmonary hypertension and edema, hypoxemia and cyanosis
emphysema features
features: overventilation, dyspnea, resp muscle overuse,airway resp collapse, pulmonary hypertension
pulmonary embolism
respiratory manifestations = dyspnea and increase resp. rate; death of tissue b/c bad blood supply (infarction) causes pain assoc with breathing leading to gas exchange problems (hypoxemia); it is the block of part of pulmonary vascular bed by an embolus ie blood clot, fat, air bubbles
pulmonary hypertension
pulmonary artery increases blood pressure
primary pulmonary hypertension
rare family illness when small pulmonary arteries are blocked and pressure is increased
secondary pulmonary hypertension
increase pulmonary artery pressure because left ventricular failure
cor pulmonale
pro-longed pulmonary hypertension, hypertrophy, dialation of right ventrical
amount of air getting into alveoli and balance
amount of blood perfusing capillaries around alveoli
alveolar dead space
area well ventilated no perfusion
Poor perfusion
high ratio
poor ventilation
low ratio
palpable swelling because expansive increase in interstitial fluid volume (extracellular)
localized edema
limited swelling to site of trauma ex sprained finger
generalized edema
fluid in gravity-dependent areas of body ex. pitting edema (manifest in a uniform fashion)