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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)

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