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110 Cards in this Set
- Front
- Back
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Volume of air that can be expired with maximal effort after maximal inspiration
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Forced vital capacity
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Volume of gas expired during 1st second
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FEV1
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OBSTRUCTIVE DISEASE:
TLC ? RV? FRC? FVC? FEV1? FEV1/FVC? What is most diagnostic change? |
TLC +
RV ++ FRC ++ FVC no change or - FEV 1 -- FEV1/FVC -- Most diagnostic - decreased FEV1/FVC with increase in TLC |
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RESTRICTIVE DISEASE:
TLC? RV? FRC? FVC? FEV1? FEV1/FVC? Most diagnostic? |
TLC --
RV - FRC - FVC -- FEV1 - FEV1/FVC no change or increased Most diagnostic decrease of FVC with decrease in TLC |
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FEV1/FVC = 80% - normal, restrictive or obstructive
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Normal
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FEV1/FVC = 50% - normal restrictive or obstructive
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Obstructive
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FEV1/FVC = 88% - normal restrictive or obstructive
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Restrictive
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Airway resistance is increased and expiration is impaired - all measures of expiration are decreased - FVC, FEV1, FEV1/FVC, air is trapped so increased FRC
What disease |
Obstructive - ASTHMA
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Increased compliance, expiration is impaired, air is trapped - increased FRC
What disease? |
COPD - obstructive
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Impaired alveolar ventilation - severe hypoxemia with cyanosis and increased PCO2 - blue and edematous from R heart failure
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Blue bloaters --> Chronic bronchitis
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Alveolar ventilation is maintained so they have normal PCO2 and only mild hypoxemia, they have reddish complexion and breathe with pursed lips at increased respiratory rate
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Pink puffers --> emphysema
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There is decreased compliance and inspiration is impaired - all lung volumes are decreased but because FEV1 decreases less than FVC, FEV1/FVC may be increased or normal
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Restrictive pattern --> fibrosis
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Daltons law of partial pressures
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Partial pressure = total pressure * fractional gas concentration
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Alveolar gas equation
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PAO2 = PIO2 - PCO2/R
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Alveolar ventillation equation
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Alveolar ventilation = (Vt-Vd) * F
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Ficks Law of diffusion
What changes in disease |
Vgas = D (P1-P2) * A/T
A and T are physical factors that change mainly in disease |
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Diffusion constant of CO2 is bigger or smaller than of O2
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CO2 bigger than O2
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RBC remians in capillary for _ seconds
Equilibrium is reached in _ seconds in normal lung at resting state _ reduces equilibration time but there is still enough reserve for full equillibration of oxygen in healthy individual |
0.75
0.25 Exercise |
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Gases that EQUILIBRATE between alveolar gas and pulmonary capillaries are _
The amount of gas transferred is dependent on properties of blood gas barrier? Examples of those gases |
PERFUSION LIMITED
NO O2 - under normal conditions N2O CO2 |
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Gases that DO NOT EQUILIBRATE between alveolar gas and pulmonary capillaries are _
The amount of gas transferred is dependent on properties of blood gas barrier? Give examples of those gases |
DIFFUSION LIMITED
YES O2 - abnormally CO |
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Why is CO a diffusion limited gas
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Binds so avidly to hemoglobin, PaCO doesnt increase too much - used to measure PULMONARY DIFFUSION CAPACITY
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Name conditions under which O2 becomes diffusion limited gas
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- Blood gas barrier is thickened in FIBROSIS
- Surface area is decreased in EMPHYSEMA - INTENSE EXERCISE decreases time for equilibration in pulmonary capillaries (can occur in normal lungs) - LOW O2 GAS MIXTURE (less partial pressure gradient, can occur in normal lungs) |
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Each Hb molecule has _ subunits
Each subunit has _ moiety with iron in ferrous state (Fe2+) and two _ and two _ polypeptide chains |
4
Heme, alpha and beta |
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Maximal amount of O2 that can bind to Hb
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O2 capacity
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Total O2 in blood (bound + dissolved)
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O2 content
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_ reflects O2 bound to Hb (the amount of O2 that is dissolved is trivial compared to bound)
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CONTENT
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_ reflects dissolved O2
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Partial pressure
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Normal Pa O2
Normal PvO2 Normal P50 |
100
40 27 |
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At Pa O2 (100 mm Hg) saturation is _
At PvO2, saturation is _ At P50, saturation is _ |
Almost 100%
75% 50% |
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Shift of Hb curve to the right - what causes it, what does it mean, what else shifts to the right
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FACILITATES UNLOADING IN TISSUES
Increased temperature, PCO2, 2,3- DPG and decreased pH P50 also shifts to the right *** Exercising muscle is hot, acidic and hypercarbic |
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Shift of Hb curve to the left - what causes it, what does it mean, what else shifts to the left
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FACILITATES LOADING OF OXYGEN
Decreased temperature, PCO2 and DPG and increased pH P50 decreased - shifts to left **** CO poisoning |
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Polycythemia and anemia change _
What stays the same |
Arterial O2 content
PaO2 and P50 |
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CO poisoning is dangerous for 3 reasons - name them
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CO LEFT SHIFTS the curve, decreasing P50 causing decreased oxygen unloading in tissues
CO has 240 times greater affinity for Hb as O2 so it DECREASES OXYGEN CONTENT OF BLOOD CO inhibits cytochrome oxidase |
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Forms of CO2
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HCO3 = 90%
Carbamino compounds (combination of CO2 with proteins especially Hb) = 5% Dissolved CO2 = 3% |
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Resistance of pulmonary blood flow - high or low
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Very low
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Compliance of pulmonary blood flow - high or low
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Very high
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Pressure in pulmonary circulation
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Very low compared with systemic circulation
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Effect of lower PaO2 on pulmonary blood flow
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ALVEOLAR HYPOXIA CAUSES VASOCONSTRICTION
This is a local effect and the opposite of other organs where hypoxia causes vasodilation This directs blood away from hypoxic alveoli to better ventilated areas This is also why fetal pulmonary vascular resistance is so high - pulmonary resistance decreases when the first breath oxygenates alveoli causing pulmonary blood flow to rise |
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In upright posture due to effect of gravity, flow is greatest in _ and lowest in _
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Base
Apex |
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What metabolic changes take place in lungs
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Conversion of angiotensin I to angiotensin II, inactivation of bradykinin, remove prostaglandins E2 and F2alpha and leukotrienes
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BLOOD FLOW is highest at _ and lowest at _
VENTILATION is higher at _ and lowest at _ The change in ventilation is not as great as blood flow so V/Q RATIO is higher at _ and lowest at _ |
BASE = HIGH
APEX = LOW BASE = HIGH APEX = LOW BASE = LOW APEX = HIGH |
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If ventilation is 0 (airways blocked), V/Q = _ which means patient has a _ --> no gas exchange occurs and PAO2 and PCO2 are the same as _
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V/Q = 0
Shunt Mixed venous blood (O2 = 40, CO2 = 45) |
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If perfusion is 0, patient has _ , V/Q ratio = , no gas exchange occurs and PAO2 and PACO2 are the same as _
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Pulmonary embolism
V/Q = infinity - dead space Inspired air (O2 = 150, CO2 = 0) |
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Where is higher?
Ventilation Perfusion V/Q PO2 PCO2 |
Base
Base Apex Apex Base |
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In hypoventilation what happens to
PaO2 PaCO2 CaO2 Aa gradient Response to supplemental O2 |
Decreased
Increased Decreased Not changed Responds to O2 by increase in PaO2 and CaO2 |
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Decrease in inspired PO2 (high altitude)
What happens to PaO2 PaCO2 CaO2 Aa gradient Response to supplemental O2 |
Decreased
Decreased Decreased Not changed Responds to supplemental O2 by increase in PaO2 and CaO2 |
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Diffusion limitation (PAO2 and PaO2 do not fully equilibrate)
What happens to PaO2 PaCO2 CaO2 Aa gradient Response to supplemental O2 |
Decreased
Not changed Decreased Increased Respond to supplemental O2 by increase in PaO2 and CaO2 |
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Shunt (venous blood mixes with arterial bypassing ventilated areas of the lung)
What happens to PaO2 PaCO2 CaO2 Aa gradient Response to supplemental O2 |
Decreased
Not changed Decreased Increased Poor response to O2 |
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V/Q mismatch
What happens to PaO2 PaCO2 CaO2 Aa gradient Response to supplemental O2 |
Decreased
Not changed Decreased Increased Responds to O2 by increasing PaO2 and Ca O2 |
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CO poisoning (exhaust fumes)
What happens to PaO2 PaCO2 CaO2 Aa gradient Response to supplemental O2 |
Not changed
Not changed Decreased Not changed O2 results in increase of PaO2 but no changed in CaO2 (increased affinity of CO for Hb) |
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Decreased Hb (anemia)
What happens to PaO2 PaCO2 CaO2 Aa gradient Response to supplemental O2 |
Not changed
Not changed Decreased Not changed Increase in PaO2 but not in Cao2 |
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Generates breathing rhythm
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Inspiratory center in medulla
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Not active during normal passive expiration involved in active expiration (exercise)
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EXPIRATORY CENTER in medulla
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Stimulates prolonged inspiration
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Apneustic center in pons
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Trminates inspiration
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Pneumotaxic center in ponse
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Lesions above ponse eliminate _ but _ remains intact
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Voluntary control
Basic breathing pattern |
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Central (medulla) chemoreceptors respond to _
Reaction to O2 Reaction to CO2 Reaction to H+ |
Changes in pH of CSF
No response INCREASED PCO2 --> stimulate chemoreceptors --> INCREASED VENTILATION (via H+) Increased H+ --> stimulation of increased ventilation detects H+ in CSF, 80-95% response to hypercapnia |
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Peripheral cehmoreceptors (carotid and aortic bodies)
Response to O2 Response to CO2 Response to H+ |
Decreased PaO2 --> stimulates chemoreceptors --> increased ventilation
***Stimulated by changes in pressure not O2 content so wouldnt respond to anemia Increased PCO2 --> stimulation - increased ventilation but central chemoreceptor response is most important during normal breathing Increased H+ --> stimulation --> increased ventilation *** Most of the response to metabolic acidosis is peripheral because fixed acids penetrate blood brain barrier poorly |
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Patients with severe lung disease can have chronic CO2 retention and _ can return to normal despite their hypercapnia
Having lose their CO2 stimulus to ventilate their _ becomes very important Therefore you shouldnt give those patients _ because _ |
pH of CSF
Hypoxic ventillatory drive (peripheral chemoreceptors) Enriched O2 to breathe because primary ventillatory drive will be removed which cause severe depression of ventillation |
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RESPONSE TO HIGH ALTITUDE
PAO2 PaO2 Respiratory rate Pa and PA CO2 Arterial pH Hb HB % saturation Pulmonary vascular resistance 2,3 DPG HbO2 curve What problems can occur? |
PAO2 --> decreased because of decrease in barometric pressure
PaO2 --> decreased because of hypoxemia caused by decrease in PAO2 Respiratory rate --> increased --> hypoxia stimulates peripheral receptors PaCO2 and PACO2 --> increased because of hyperventilation due to hypoxemia Arterial pH --> increased because of respiratory alkalosis, later becomes normal due to renal compensation Hb --> increased = polycythemia Hb saturation ---> decreased because of decreased PO2 PVR --> increased due to hypoxic vasoconstriction, this plus polycythemia lead to increased work and hypertrophy of R heart 2,3 DPG --> increased Hb-O2 curve --> shifts to right (because of increased 2,3 DPG) Also 2 problems: Acute mountain sickness - hypoxemia and alkalosis cause headache, fatigue, nausea, dizziness, palpitations and insomnia, treat with acetozalomide Chronic mountain sickness causes reduced exercise tolerance, fatigue, hypoxemia and polycythemia |
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Increased resistance to airflow secondary to obstruction of airways - what disease
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COPD
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COPD includes _
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Chronic bronchitis
Emphysema Asthma Bronchiectasis |
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Persistent cough and copious SPUTUM PRODUCTION FOR AT LEAST 3 MONTHS each year in 2 consecutive years, highly ASSOCIATED WITH SMOKING (90%)
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CHRONIC BRONCHITIS
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Patient presents with cough, sputum production, dyspnea, frequent infections, PE shows hypoxia, cyanosis and weight gain
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Chronic bronchitis
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Associated with destruction of alveolar speta, resulting in enlarged air spaces and loss of elastic recoil and producing overinflated enlarged lungs, thought to be due to protease/antiprotease imbalance
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Emphysema
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Autopsy shows OVERINFLATED, ENLARGED LUNGS, enlarged grossly visible air spaces and formation of apical blens and bullae (which type? )
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Emphysema
Centriacinar type |
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Patient presents with progressive dyspnea, he uses pursing of lips and ACCESSORY MUSCLE to breathe. PE shows BARREL CHEST and weight loss
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Emphysema
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Centriacinar (centrilobular) emphysema
Which part of bronchioles involved Associated with ? Worst in _ |
PROXIMAL RESPIRATORY BRONCHIOLES
SMOKING Worst in apical segments of upper lobes |
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What is the most common type of emphysema (95%)
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Centriacinar (centrilobular)
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Panacinar (panlobular) emphysema
- Which part involved? _ Associated with? - Distribution? |
ENTIRE ACINUS INVOLVED, distal alveoli spared
ALPHA 1 ANTITRYPSIN DEFFICIENCY Distribution - whole lung, worse in bases of lower lobes |
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- Due to hyperreactive airways resulting in episodic BRONCHOSPASM, producing WHEEZING, severe DYSPNEA and coughing
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Asthma
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Biopsy of the lung shows inflammation, edema, hypertrophy of mucous glands with GOBLET CELL HYPERPLASIA AND MUCUS PLUGS, also hypertrophy of bronchial wall smooth muscle and thickened basement membranes
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ASTHMA
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Exrinsic asthma
Mechanism What type is most common Who usually gets it What triggers it |
TYPE I HYPERSENSITIVITY reaction
ALLERGIC (ATOPIC) - most common type Childhood and young adults, especially with POSITIVE FAMILY HISTORY Allergens - pollen, dust, food, molds, animals, occupational exposure |
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Intrinsic asthma
Possibel triggers |
RESPIRATORY INFECTIONS (usually viral)
STRESS EXERCISE COLD temperatures Drug induced - ASPIRIN |
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Bronchiectasis - an abnormal permanent airway dilation due to _
Who usually gets it? |
CHRONIC NECROTIZING INFECTION
Most patients have underlying lung disease such as bronchial obstruction, necrotizing pneumonias, CYSTIC FIBROSIS or KARTAGENER SYNDROME |
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Give examples of restrictive lung disease
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CHEST WALL DISORDERS- obesity, kyphoskoliosis, polio
INTRINSIC LUNG DISEASE - ARDS, NRDS, pneumoconioses, sarcoidosis, fibrosis, Goodpastures and WG syndrome, eosinophillic granulomas, collagen vascular disorders, hypersenstivity pneumonias, drug exposure |
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Diffuse damage to alveolar epithelium and capillaries resulting in progressive respiratory failure unresponsive to oxygen therapy
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ARDS
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What are the possible causes of ARDS
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Shock, sepsis, trauma, gastric aspiration, radiation, oxygen toxicity, drugs, pulmonary infections, etc
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Patient presents with dyspnea, tachypnea, hypoxemia and cyanosis and is using accessory respiratory muscles, x ray shows BILATERAL LUNG OPACITY ("white out"). Patient dies and autopsy shows heavy STIFF NON COMPLIANT LUNGS, interstitial and intra alveolar edema, interstitial inflammation, loss of type I pneumocytes and HYALINE MEMBRANE FORMATION
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ARDS
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Causes respiratory distress wihin hours after birth and seen in infants with _ secondary to prematurity, maternal diabetes, multuple births or C section - diagnossi
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Defficiency of surfactant
NRDS |
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Baby girl was born at 26 weeks, was normal at birth but within few hours developed increasing respiratory effort, tachypnea, nasal flaring, use of accessory muscles of respiration, expiratory grunt and cyanosis, x ray shows GROUND GLASS reticulogranular densities, labs show lecithin:sphingomyelin ratio of 1.5. Lung biopsy shows atelectasis and HYALINE MEMBRANE FORMATION
Diagnosis Treatment Prevention |
Diagnosis- NRDS
Treatment -surfactant replacement and oxygen Complications of oxygen treatment - BRONCHOPULMONARY DYSPLASIA AND RETROLENTAL FIBROPLASIA (retinopathy in newborns) Prevention- delay labor and corticosteroids to mature the lung |
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Pulmonary edema common causes
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L sided heart failure
MV stenosis fluid overload nephrotic syndrome liver disease infections drugs shock radiation |
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Pulmonary emboli mostly rise from _ and may be asymptomatic, cause pulmonary infarction or cause sudden death - severity related to size of embolus and other comorbid conditions
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DEEP VEIN THROMBOSIS in the leg (also arise from pelvic veins)
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_ forms in the ventral wall of foregut
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Respiratory (laryngotracheal) diverticulum
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Divides foregut into esophagus and trachea
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Tracheoesophageal septum
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Abnormal communication between trachea and esophagus caused by malformation of tracheoesophageal septum
90% occur between esophagus and _ Generally associated with what conditions? Symptoms? |
Tracheoesophageal fistula
Distal 1/3 of trachea Esophageal atresia and polyhydramnios Gagging and cyanosis after feeding and reflux of gastric contents into lungs causing pneumonitis |
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Terminal bronchioles divide into _ which contain alveoli and branch to form alveolar ducts, ducts terminate in _ and are lined by _
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RESPIRATORY BRONCHIOLES
alveolar sacs Squamous alveolar epithelium |
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Thin walled sacs responsible for gas exchange
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Alveoli
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Provide thin surface for gas exchange
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Type I pneumocytes
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Produce SURFACTANT
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Type II pneumocytes
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Nasopharynx communicates with nasal cavity through _
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Choanae
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Abducts vocal folds
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Posterior cricoarytenoid
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Adducts vocal fold
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Lateral cricoarytenoid
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Tenses vocal fold
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Cricothyroid
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Relaxes vocal fold
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Thyroarytenoid (including vocalis)
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Opens laryngeal inlet
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Thyroepiglotticus
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Closes laryngeal inlet
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Aryepiglotticus
Oblique and transverse arytenoids |
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The only laryngeal muscle that is innervated by external laryngeal nerve - branch of superior laryngeal branch of vagus
All other intrinsic muscles of larynx are innervated by _ |
Cricothyroid
Recurrent laryngeal nerve |
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Divided by oblique and horizontal fissures into three lobes
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Right lung
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Has only one fissure - oblique
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Left lung
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Superficial drainage of lungs is to _ nodes from there to _
Deep drainage to _ from there to _ Bronchomediastinal lymph trunks drain to the _ |
Bronchopulmonary - tracheobronchial
Pulmonary - bronchopulmonary Right lymphatic and thoracic ducts |
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Air inspired and expired in normal breathing
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Tidal volume
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Volume in lungs with maximal inspiration
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Total lung capacity
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Volume in lungs at end of quiet passive expiration, the equilibrium point of the system
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FRC
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Volume at the end of maximal forced expiration
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Residual volume
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Volume expired from maximal inspiration to maximal expiration
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Vital capacity
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The volume inspired with maximal inspiratory effort in excess of tidal volume
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IRV
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The volume expelled with active respiratory effort after passive expiration
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ERV
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The volume of air inspired with maximal inspiratory effort after passive expiration
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Inspiratory capacity
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Cannot be measured with spirometry
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FRC
RV |
