Term
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Definition
For all gases, equal # molecules with same vol. and @ same Temp. will exert equal gas pressure (i.e. colligative property, not dpendent on quantum features) |
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Term
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Definition
Hypoxia = low O2 in air Hypoxemia = arterial blood |
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Term
All the -pneas: Eu- Hyper- Hypo- Dys- Tachy- A- |
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Definition
Eupnea=normal (at rest) Hyperpnea=increased vol./time
Hypopnea=decreased vol./time
Dyspnea=awareness (pathological) Tachypnea=increased rate Apnea=cessation |
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Term
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Definition
Increased pCO2 in alveolar space and/or arterial blood |
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Term
Hyperventilation vs. hypoventilation |
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Definition
Determine ventilation status based on: pCO2 Defined as breathing IN EXCESS OF/DEFICIENT FOR metabolic requirements |
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Term
Example: Hyperventilation vs. hyperpnea vs. tachypnea |
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Definition
Hyperventilation=decreased pCO2 (not always increased pO2 due to other factors) Hyperpnea=increased ventilation/time (not in excess of metabolic needs) Tachypnea=increased breathing RATE (not necessarily hyperpnea or hyperventilation)
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Term
Ideal Gas Law (IGL) Other laws based on it: Charle's law Boyle's law Avogadro's hypothesis |
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Definition
PV=nRT R=gas constant (only constant in eq.) Charle's: if V=constant, P is proportional to T Boyle's: as gas is compressed, its vol. increases proportionally (P1V1=P2V2) Avogadro's: if n=constant, T=constant and V=constant, than P will be also constant (duh) |
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Term
1 mole of any gas under ideal gas conditions @ 0 C, 760 mmHg: 1. volume 2. number of molecules |
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Definition
1. 22.4 L 2. 6 x 1023 (Avogadro's #) |
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Term
4 stages of respiration: which use energy? |
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Definition
1. Ventilation (air from atm into lungs) 2. Pulm. gas exchange 3. Gas transport 4. Periph. gas exchange 1, 3 use energy (metabolic; circulation, pump mm.) |
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Term
Major point: What determines arterial blood gas pressures? |
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Definition
Respiratory system dynamics, NOT Hb! Ex: case of anemia (arterial gases at normal levels; see difference only in mixed venous blood) |
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Term
Lung equilibrium volume vs. Pleural cavity equilibrium volume |
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Definition
0% vs. 60% Net=functional residual capacity (FRC) ~37% FRC cannot be measured by spirometry b/c it includes residual volume |
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Term
Respiratory muscles: 1. inhalation 2. exhalation 3. during exercise or pathology |
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Definition
1. diaphragm 2. passive (except for laryngeal mm. resisting a bit) 3. Inspiration: SCM, scalenes, external intercostals Expiration: internal intercostals, abdominals
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Term
3 important pressures to know: |
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Definition
1. PTP=transpulmonary (only fluctuares a little)
2. Palv=alveolar (fluctuates btw. + and - 1 mmHg)
3. Ppl=pleural (fluctuates the most, always NEGATIVE; diaphragm)
PTP=Palv - Ppl
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Term
1. What (pressure) causes ventilation? 2. During breathing, why does P alv change LESS THAN P pl? 3. Situation btw. inspiration and expiration=? 4. What happens when P pl EXCEEDS P TP? |
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Definition
1. Palv (- @ inspiration, + @ expiration) 2. Energy dissipated in stretching alveoli (elastic recoil energy that is dissipated in expiration (passive)). 3. Palv=0, so Ppl=PTP (Ppl represents lung elastic recoil force-i.e. PTP-in this case) 4. Palv must be negative, so inspiration happens.
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Term
How to calculate airway resistance |
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Definition
1. There must be airflow for there to be resistance... R=Palv/airflow (Palv calculated from Ppl and PTP) |
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Term
Lung volume vs. 1. P pl 2. P TP |
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Definition
1. As Ppl decreases (becomes more -), LV increases, and decreases as Ppl increases (becomes less -). 2. As PTP increases, LV increases, and vice-a-versa. |
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Term
Possible values for: P pl PTP |
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Definition
Ppl is negative under normal conditions, but it can become + under FORCED expiration. PTP is ALWAYS + (even under forced exhalation conditions, b/c Palv becomes + enough to compensate for the + Ppl
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Term
Saline-filled lung vs. air-filled |
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Definition
1. Saline-filled lung will have no surface tension to overcome (air-liquid interface eliminated), so only tissue forces need to be overcome (simple inv. parabolic) 2. Air-filled: surface tension AND tissue forces must be overcome, so the curve represents hysteresis (not simple parabolic, but sigmoidal)
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Term
Lung compliance in normal px, emphysema and pulm. fibrosis |
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Definition
Normal, at 60% VC, 10 cm H2O (collapsing force) Emphysema: greater compliance, larger vol. - lungs filled, but no fresh air ciirculates much Pulm. fibrosis: lower compliance, smaller vol. Ex: Farmer's lung, Coal Miner's disease (increased PA O2, decreased PaO2 and MV O2; decreased pCO2) |
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Term
Chest wall elastic characteristics: 1. at rest 2. @ 0% VC 3.@ 100% VC 4. at equilibrium with lungs (physiological) |
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Definition
1. 60% VC, no pressure 2. at 0%, exerts -40 cm H2O filling pressure 3. at 100%, exerts, +15 cm H2O recoiling pressure 4. At physiological equilibrium: 40% VC, ~-5 cm H2O
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Term
1. What determines airway resistance? 2. What component of the airway has highest resistance? Why? 3. How does lung elasticity counteract airway resistance? |
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Definition
1. MAJOR: airway diameter (under physiological control; effected by most pathology) Minor: airway length, gas density 2. Highest=least cross-sectional area (bronchioles) 3. As alveoli fill, there is a large rediction in surface tension, which acts on surrounding alveoli to expand these (+ feedback loop basically) |
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Term
Airway cellular characteristics based on generation 0-16 17-23 |
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Definition
0=trachea-->16 (bronchioles) "conducting zone"
Have ciliated columnar epithelium, cartilage, SMCs, and Goblet cells 17-23: "respiratory zone"; respiratory bronchioles, alveoli Have cuboidal-->squamous epithelium (no cilia)
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Term
What is the relationship btw. expiratory flow and lung volume? |
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Definition
As lung volume decreases, so does expiratory flow rate: 1. lung elastic recoil decreases with decreased volume 2. lung elastic recoil pressure/PTP decreases during expiration - Net: exp. airflow is greatest at max. lung volume - Calculate: airflow=PTP/R |
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Term
Note: at 40% VC, how does exp. airflow rate depend on effort? *Equal pressure point effect |
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Definition
It does not; effort-independent. Equal pressure point: where PA=Ppl (any increase in effort (Ppl) is offset by increased compression of airway, which increases R, so airflow doesn't increase) |
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Term
Max expiratory flow rates in disease: Emphysema Pulmonary fibrosis Exercise vs. rest |
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Definition
Both=lower max exp. rate Emphysema: decreased PA, increased RA (F=P/R) Fibrosis: same, but DECREASED volume (opposite)
Exercise vs. rest: During exercise, inspiratory reserve is favored (b/c RA is lower at greater VolumeA)
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Term
Calculating elastic work and flow resistive work: from vol. vs. pressure graph CC examples of increased RA How would V vs. P graph change is upper airways were reduced in diameter 90%? |
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Definition
Elastic is area above/L of lung compliance line, while flow work is to R/below. If UR airways were decreased in diameter, the inspiratory line below lung compliance line would bow out more (more work). This is an example of an asthma attack Other examples of increased RA: emphysema, bronchitis, sleep apnea
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Term
1. What is the alveolar filling "time constant"? 2. Implications in tachypnea |
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Definition
1. Def=rate of alveolar filling when a pressure change is applied Uneven filling of alveoli
2. at low freq. of breathing, different time constants (and therefore uneven filling) is of no consequence but at high freq., pendelluft can occur (gas x-change btw. adjacent alveoli instead of common airway) Effect: reduced alv-cap gas exchange |
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Term
Graphic/clinical example: Ratio of dynamic compliance over static vs. respiration freq. (Normal vs. asthmatic people) 1. How will the ratio change with freq. for each population? |
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Definition
1. Ratio decreases sharply with increased freq. in asthmatics (100-->20), while remaining stable for normal individuals see pg. 642 of notes |
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Term
1. FRC 2. RV 3. TLC Definitions and values. |
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Definition
1. Functional residual vol=vol. of lungs after expiration with NO RESP. MUSCLE activity (40% TLC=2400mL) 2. residual volume=maximal expiratory muscle contraction (limited by chest wall elasticity) 20% TLC=1200mL 3. total lung capacity=maximal inspiratory muscle activity (100%=~6 L) |
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Term
Difference between and how to calculate: 1. Dead space ventilation (VD) 2. Alveolar ventilation (VA) 3. Pulmonary (Inspiratory) ventilation (VI) 4. Expiratory ventilation (VE) Note: there should be dots over the Vs in these symbols, indicating 1 minute as time dimension/unit |
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Definition
1. Volume of airways =VT x [PaCO2 - PeCO2]/PaCO2
2. Volume of fresh air reaching lungs =[VT - VD] x resp. rate (breaths/min.)
3. Total vol. of air reaching lungs in 1 min. =VT x breaths/min.
4. Total vol. of air exiting lungs in 1 min. =effectively equal, but actually slightly LESS THAN VI (b/c of the 10:8 O2:CO2 usage/production ratio)
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Term
Respiratory Quotient (RQ): 1. What does it approximate? 2. Equation |
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Definition
1. Approximates the metabolic rate (CO2 production over O2 consumption) 2. RQ=VECO2/VIO2
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Term
Difference btw: 1. Anatomical VD (Bohr equation)
2. Physiologic VD
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Definition
1. VD calculated from Bohr Eq. (VD=VT x [PaCO2-PeCO2]/PaCO2)-->vol. of conductive resp. structures
2. Physiologic VD=Anatomical VD + Alveolar VD(dead space of underperfused alveoli...a fxnal definition of VD) Vol. of conductive + unperfused alveolar resp. structures
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Term
Alveolar hyperventilation vs. hypoventilation (define with examples)
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Definition
Hyper: increase in PaCO2 Ex: decr. breathing w/o decr. in metabolic need Hypo: decreased PaCO2 Ex: VA incr. w/o incr. in metabolic rate Concept: "ventilation" status depends upon metabolic needs
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Term
Calculating alveolar gas concentrations using the respiratory quotient (RQ): 1. PaCO2=? 2. PaO2=? 3. How does RQ fit in? What does it mean? How does it vary for different caloric sources (diet)? |
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Definition
1. =VCO2/[VA x (PAtm-47)]...so basically a ratio of metabolism (VCO2) to metabolic rate (VA) 2. "Alveolar gas equation" (Wikipedia): PaO2=PIO2 - PaCO2/RQ RQ used to calc. alv. O2 pressure (based on metabolic rate). RQ for fats=0.7-ish (varies) RQ for CHOs=1.0 RQ for proteins/AAs=varies 0.7-1.0 RQs >1.0 mean energy being stored (ex: hibernating bear) or misused (pathological, etc.)
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Term
Difference in pressures due to gravity within the lungs: 1. Implications on filling
2. Where does air tend to go after RV at FRC and above? Why? 3. Summarize concisely these results |
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Definition
1. Upright ONLY: upper lung expanded (higher compliance), lower lung compressed (by weight of lung)-->upper lungs at higher compliance; fill with more air than lower 2. Will go to lower lung more b/c upper lung is already filled with air (at higher compliance), making lower lung compliance greater at larger lung volumes) 3. @ RV, lung weight compresses lower lung, making upper lung compliance greater (air goes to upper), while above RV (FRC and above), the lower lung get more air b/c it is at higher compliance Upper lung is filled with air and at low compliance under normal resp. contitions |
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Term
N2 measurement experiment: 1. Desribe the 4 phases of N2 exhalation observed 2. How does this example reveal the difference in lung compliances from top to bottom of lung in normal and maximal expiration respiration? |
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Definition
Phase I: VD contains no N2 Phase II: VD transitioning to VA ([N2] rises quickly) Phase III: [N2] stable (rising slightly); emptying normal breathing lung vol. Phase IV: below FRC (to RV), N2 is high b/c it is coming from upper lung that only ejects air at maximal expirations, so it would've had more time to increase its [N2], so we see the sharp rise again) 2. The 100% O2 went to the lower lung more
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Term
Closing Volume (CV) of airways in emphysema: 1. How is it changed from normal? |
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Definition
In emphysema, the CV occurs at a greater lung volume due to the increased tendency for the airways to collapse in emphysema (reduced elasticity-->increased RA-->collapse incr.) |
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Term
Differences btw. pulmonary & systemic vasculature: 1. wall thickness 2. compliance 3. pressure (quantitative examples)
4. blood volume |
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Definition
Referring to pulmonary vessels: 1. thinner walls==> 2. greater compliance 3. lower pressures RV=20/0 vs. LV=120/5 Pulmonary aa.=20/5 vs. aorta=120/80
4. 10% of blood volume |
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Term
Visualize graph (p. 649) of pressures in pulm. aa., pulm. capillaries & LA: 1. What are these pressures? How do they change? 2. Graph of LA pressure vs. Pulm. aa. pressure? How does LA affect pulm. aa.? |
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Definition
1. Pulm. aa.=25/8 right after RV, then this pulse pressure decreases to a constant ~7 mmHg @ the pulm. capillaries, then decr. to LA=5 mmHg (or incr. to LA=10 mmHg, depending; LA=5-10 mmHg range of normal) 2. As PLA incr., so does Ppulm aa. (exponentially!). W/in normal ranges (5-10) for LA, pulm. aa. pressure remains relatively constant, but at higher pressures, it incr. MORE rapidly (exponential)
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Term
Effect of Palv on blood flow in adjacent pulm. capillaries: (3 zones) |
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Definition
Zone 1 (upper)=no flow Zone 2 (middle)=intermittent (Psys intermittently exceeds Palv=flow)
Zone 3 (lower)=continuous |
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Term
Pulmonary vasculature resistance vs. lung volume: 1. Define: alveolar vessels & extraalveolar vessels 2. How does resistance change in each with lung vol.? 3. Graph: which other graph does this graph resemble?
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Definition
Alveolar=pulm. capillaries Extraalveolar=pulm. arterioles & venules 2. During inspiration (lung expansion): Alveolar R incr. + extraalveolar R decr. @ RV, Ralv is low & Rextraalv is high, and the reverse at TLC is true. Equilib. in middle 3. Resembles equilibrium graph of breathing freq. vs. elastic+flow resistive work (p. 640 vs. 650)
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Term
Graph of blood flow vs. lung region (p. 651): 1. During exercise, what is flow like? 2. What is the abrupt decrease in flow at the very bottom of the lung attributed to? 3. At rest, what % (approx.) of blood flow goes where within the lung? |
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Definition
1. During exercise,the whole lung=Zone 3 b/c the pulm. pressure is always higher than Palv 2. May be due to weight of the lung compressing pulm. vessels there (this could be tested while patient lies down, but apparently it has not been done) 3. At rest, ~80% flow goes to bottom, while only ~20% goes to top |
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Term
1. Is gravity the sole determinant of regional blood flow in the lungs? 2. What is the effect of alveolar hypoxia on pulm. regional blood flow? |
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Definition
1. Gravity is only secondary. "sequential branching of pulm. vessels" is one hypothesized primary factor 2. With incr. hypoxia (lower pO2 in alveoli), pulm. vascular resistance (PVR) actually increases. This is exaggerated by decreased pH...seems like a pretty bad call on biology's part...
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Term
1. During incr. pulm. bloof flow, what occurs to maintain a long pulm. transit time (of blood)? 2. What is the major factor determining rate of equilibration of gases btw. alveoli & pulm. capillaries? |
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Definition
1. Pulm. capillaries expand (incr. total of pulm. vasculature), so blood units stay in lungs for longer 2. Binding to protein in blood: Gases that are not bound (freely circulate) will reach equilibrium rapidly. Ex: N2O (anesthetic)
Gases that are bound will take much longer (b/c bound gases do not contribute to blood partial pressure of that gas) Ex: O2, CO
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Term
1. What is the (quantitative) balance of hydrostatic and osmotic forces that keep the lungs dry? 2. Why does pulm. edema not occur until LA pressure exceeds 25 mmHg?
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Definition
1. Pc=+7 (lower than systemic's +17.3) πp=-28 (same as systemic) Pif=-8 (less than systemic's -3) πif=-14 (WAY less than systemic's +8!) Favoring filtration: Pc, Pif, πif (+7 - (-8 - 14))=29 Favoring retention: πp=28 Net: +1 mmHg favoring filtration (which is cleaned up by pulm. lymphatics (@-5 mmHg) and a very small amt. evaporates thru alveolar surfaces) 2. Lung vasculature HIGH compliance prevents Pc from becoming too high and favoring filtration enough to cause edema...up to a point, which=25 mmHg
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Term
1. Why is it ideal for every alveolar-capilary unit to receive the same amount of VA and cardiac output (Qc)? 2. Describe what the V/Q ratio means from 0 to ∞. What will pO2 and pCO2 be under these conditions? 3. What is the term for the volume occupied by an alveolus that is not ventilated? |
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Definition
1. If each unit is not receiving the same relative amt. of VA and Q, then there exists areas of over and under ventilation & perfusion. VA adn Q are matched under ideal conditions.
2. VA/Q ratio is another measure of metabolism/metabolic rate. When V=0, V/Q=0 (alveolus=atmospheric air pressures) PAO2=PaO2=40 mmHg, PACO2=PaCO2=45 mmHg When Q=0, V/Q=∞ (alveolus=mixed venous blood pressure) PAO2=PBO2=150 mmHg, PACO2=PBCO2=0 mmHg
When V/Q=1, perfect match (ideal): PAO2=100 (PBO2=150, PaO2=40), PACO2=40 (PaCO2=45) 3. Alveolar dead space (adds into physiological VD)
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Term
1. What is the term for venous blood exiting the pulm. capillaries that was not ventilated? (p. 655)
2. How do VA/Q ratios compare regionally w/in the lung? (p. 655)
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Definition
1. Venous admixture (gas pressures=mixed venous) 2. See graph p. 655: Bottom: Q > VA =0.7 (minimum) Middle: Q & V lines intersect=1.0 (ideal) at about the level of rib #3 Top: Q < VA = greater than 1.0 (up to ~4.0) Note: over a large portion of the lung, there exists a good VA/Q necessary for gas exchange!
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Term
1. How does emphysema affect VA/Q? 2. What factors contribute to NORMAL and abnormal physiological shunting of blood (avoiding ventilation) (4)? |
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Definition
1. There is non-uniform time constants distributed unevenly throughout the lung-->uneven ventilation = variable ratio 2. 1. Thebesian circulation (to L ventricle-->coronary sinus-->RA) 2. Bronchial circ. (emties into pulm. veins) "venous admixture"
3. Atelectatic/collapsed alveoli (alveolar dead space) 4. Congenital defects (causing L-R mixing)=abnormal
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Term
1. Equation: calculate vol. of a cardiac shunt (away from pulm./ventilation) (Qshunt & QTotal)
2. Why is it that once the cardiac shunt reaches ~50% CO (to lungs portion), increasing resp./PAO2 has little if any effect on PaO2? (p. 657)
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Definition
1.Qshunt=[O2]end pulm.cap - [O2]arterial QTotal=[O2]end pulm.cap - [O2]venous 2. When breathing 100% O2, every 1% of shunt=20 mmHg decr. PAO2-->PaO2. Why? Math unsure... |
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1. What determines gas diffusion btw. two compartments? Depends on phase? 2. Calculate partial pressures of gases in a mixture. What are %s of N2, O2, CO2 and H2 in air? 3. Calculate concentrations of gases dissolved in a liquid. (All p. 658) |
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Definition
1. Pressure gradient (magnitude of difference in gas pressure) determines diffusion rate 2. Partial pressure=PB x % comp. N2=0.8 O2=0.21 CO2=0.003 (0.3%) (H2<0.5%) 3. Henry's Law: (Gas pressure @ 760 mmHg; sea level is std.; ex: for O2=150 mmHg) Conc.=Gas pressure x Solubility coefficient (mmHg-1 =units)
Solubility coeff. for N2=.012, O2=.003, CO2=.072 CO2 is 6x more soluble than N2 and 24x more soluble than O2. |
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Term
Name the 2 processes determining lung diffusion rate. |
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Definition
"Diffusion capacity of lung"=DL 1. Diffusion of gas: D=ΔP A S/d √MW ΔP=pressure gradient A=surface area S=solubility d=diffusion distance (thru various tissue layers) MW=molec.weight (CO2=44, O2=32) 2. Vmax for Hb binding to O2 (sigmoidal, cooperative, 4/molecule)
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Term
1. How is diffusion capacity determined in the lab? 2. How does diffusion limit O2 vs. CO2 in the pulm. capillaries? (p. 661)
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Definition
1. Diffusion (D)=VA/[PA-Pcaps] (D=total gas x-change/mean capillary gradient) Note: difficult to measure Pcaps for O2, CO2, but can approx. for CO b/c Hb reacts with it so readily that it basically =0, so DCO=VCO/PA, CO) 2. O2 equilibriates faster, but is MORE affected by a reduction in the rate of diffusion w/in the lung. CO2 equilibriates slower (due to complex chemical rxns involving it in the blood), but is LESS affected by diffusion rate limitations. |
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Term
How do the following affect lung diffusion capacity? 1. Hypoxia
2. Exercise
3. Emphysema 4. Fibrosis 5. High-altitude RESIDENCE |
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Definition
THINK: D=ΔP A S/d √MW 1. Hypoxia: D=decr. b/c ΔP decr. 2. Exercise: D=incr. b/c A incr. (pulm. cap. dilation) 3. Emphysema: D=decr. b/c A decr. (alveolar coalesce) 4. Fibrosis: D=decr. b/c d=decr. (alveolar membranes thickened by inflammation) |
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Term
1. Calculate amt. of dissolved (free) and bound O2 in the blood. What is the total (in mL/dL)?
- Amount of Hb in blood (g/dL) - Arterial vs. mixed venous PO2 normal values and % Hb saturation values. - What does P50 signify?
2. Calculate total O2 content of blood (CaO2).
3. What is the difference btw. gas partial pressure & gas content/conc. (in blood)?
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Definition
Dissolved O2=PaO2 x S (S=0.003 for O2 in blood @ 37 C, 760 mmHg) Bound O2=[Hb]blood x 1.34 x - [Hb]blood=15 g/dL - NORMAL: PaO2= 98 (98), PmvO2=40 (75) mmHg (% Hb sat.; SaO2) P50 = PaO2 at which 50% Hb is saturated (or 50% total O2 binding spots are sat.)
2. Bound O2=15 x 1.34 x 0.98=19.7 mL/dL Dissolved O2= CaO2=bound + dissolved=20 mL/dL 3. Pp reflects the Ekinetic of dissolved gas (free) in blood, while CaO2 is total amt. of gas in blood (mL). So arterial pO2 means that O2 at a conc. of 20 mL/dL will exert a pressure of ~98 mmHg on the arterial walls if Hb releases all its O2 into blood (free).
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Term
1. Stuff that affects Hb affinity for O2: - Shift direction 2. How is P50 correlated with Hb affinity for O2?
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Definition
1. Shift curve R=unload O2 (lower affinity, P50 incr.) CO2, H+(lower pH <7.35), raised temp., 2,3-DPG
Shift curve L=retain O2 (higher affinity, P50 decr.)
pH high (>7.45), low CO2, low 2,3-DPG, low temp. 2. P50 (PaO2 @ which Hb sat.=50%) is inversely correlated with Hb affinity for O2. Example: @ a higher P50, MORE O2 is req. to saturate Hb to 50%
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Term
1. What efect do CO poisoning and anemia have on PaO2 and CaO2? *effective Hb binding curve shifts* 2. Is Hb affinity for O2 affected in either situation? |
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Definition
1. Both conditions decrease O2 content of blood. SHIFT=R (p. 666) 2. When CO binds Hb, it actually increases Hb affinity for O2, resulting in even lower tissue pO2 req. for diffusion of O2 blood-->tissue. PaO2 must decr. to lower values in order to release the same (required=5 mL/dL) amt. of O2 to the tissue.
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Term
1. What factors affect pO2 in systemic capillaries? How do these factors change during EXERCISE? 2. How is CO2 transported in the blood (%s)?
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Definition
1.) 1. Metabolic rate (+ during exercise) 2. Hb affinity for O2 (- during exercise)
3. Blood flow (+ during exercise)
4. PaO2 (NO CHANGE during exercise)
Net: end capillary pO2 is decreased. 2. 70% HCO3 25% bound to Hb 5% free
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Term
1. What is the Haldane effect? 2. What is the chloride shift (in the blood)? 3. What is the importance of carbonic anhydrase in RBCs? What are the effects if this dysfxns? |
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Definition
1. As Hb becomes more bound to O2 (incr. PaO2), Hb binding to CO2 and H+ is decreased. 2. The exchange of Cl- in plasma, for HCO3- in RBCs (purpose: drives CO2 + H2O rxn by carbonic anhydrase w/in RBCs) 3. CA converts CO2 into H2CO3 and then HCO3. If this does not happen, PvCO2 and free CO2 in blood INCREASE.
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Term
Blood gas values to know: 1. for O2: PaO2, PvO2, SaO2, SvO2, [Hb], dissolved, bound and total/content [O2]a and [O2]v 2. for CO2: PaCO2, PvCO2, dissolved and total/content [CO2]a & v
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Definition
PaO2=95, PvO2=40 SaO2=98, SvO2=75 dissolved [O2]a=0.3, dissolved [O2]v=0.1 bound [O2]a=19.7, bound [O2]v=15.1 Total content: CaO2=20.0, CvO2=15.2 PaCO2=40, PvCO2=45 dissolved [CO2]a=2.52, dissolved [CO2]v=2.84 Total content: CaCO2=48, CvCO2=52 |
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Term
1. Why doesn't the difference CaO2-CvO2 = CvCO2-CaCO2 (difference in gas contents)
-Respiratory quotient -Metabolism vs. metabolic rate (difference btw. them) 2. What accounts for the difference btw. pO2 and pCO2 btw. arterial and venous systems (difference btw. gas pressures)?
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Definition
1. This difference reflects the respiratory quotient (R) (CO2produced/O2 utilized). When R=1.0, only CHOs are being metabolized. When R=0.7, only fats are being metabolized (metabolism > metabolic rate; ex: ) When 0.7<R<1.0, protein, fat & CHOs metabolized. Summary: diff. in CONTENT=diff. in metabolic utilization ratio 2. Difference has to do with the different affinities Hb has for O2 (preferred substrate) vs. CO2. A gas no longer exerts pressure when it is bound to Hb.
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Term
1. What are effective ways to increase O2 delivered to cells (in normal individual)? 2. Explain observed differences in PaO2, SaO2 and CaO2 btw. COPD, anemia and CO poisoning clinical examples. |
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Definition
1. Increase either [Hb] or blood flow. 2. COPD: decr. CaO2 (only slight w/in Hb sat. curve that has a small slope (60-100 mmHg), decr. PaO2, decr. SaO2. Anemia: [Hb] decr.-->CaO2 decr. A LOT, but SaO2 and PaO2 REMAIN ~CONSTANT b/c O2 is getting in and binding normally, but there is less Hb to carry it around in the blood/unit vol. CO poisoning: everything normal ([Hb], PaO2, SaO2) except CaO2 (b/c CO is taking up spots on all Hb, creating a "virtual anemia" effect, just with normal [Hb]blood). |
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Term
1. What are the most common Sx of COPD, CO poisoning and anemia mentioned in lecture? 2. How would administration of 100% O2 affect the COPD, CO and anemia patients?
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Definition
1. COPD=exertional dyspnea (CaO2 not decr. that much b/c CO poisoning=headaches, confusion (low CaO2 only abnormal blood gas property) Anemia=fatigue, low work tolerance (more severe than in COPD, depending on [Hb], extent of obstr.) 2. This treatment would help most in the CO poisoning case (incr. [O2] would aid in comp. inhibition @ Hb by CO)...it would help the LEAST for the anemic patient b/c the problem is not with O2, but with having enough Hb to carry it.
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Term
1. What CNS structure(s) exert(s) control over the respiratory muscles? 2. What are the branstem nuclei that control respiration? Where are they located relative to other structures? 3. What are the targets of each of these nuclei?
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Definition
1. The cerebrum controls the resp. muscles (thru brainstem intermediate) 2. (1) NPBL (Nuc. parabrachialis)/pneumotaxic ctr. Located dorsal BS, inf/medial to Inf. Colliculi
(2) DRG (dorsal resp. group) Dorsal, in rostral medulla (level of CN XII)
(3) VRG (ventral resp. group) Ventral, in rostral medulla (level of CN XII) Note: all resp. nuclei are paired structures.
3. DRG-->Intercostals & DIAPHRAGM (+) VRG-->Intercostals (+)
NPBL-->DRG (-)
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Term
1. Resp. control nuclei lesions & brainstem transsections: what the spirometer graph looks like. |
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Definition
Vagus sets rhythm, cerebrum (-) regulates (slows rate and deepens by resp. mm. ctrl.) 1. Lesions: NPBL-->loss of resp. mm. inhibition=one big breath VRG and/or DRG-->no resp. b/c all resp. muscle ctrl. is removed Vagus N.-->resp. rate SLOWS down & deepens Transsections: 1. midbrain (elim. cerebral ctrl.)= 2. ponto-medullary jxn (elim. cerebrum & pons)=no regular rhythm anymore 3. caudal medulla (cerebrum + whole BS elim.)=no resp. AT ALL |
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Term
1. Def: respiratory neuron 2. Use the 2 categorization criteria to classify all respiratory neurons into __ groups.
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Definition
1. Any neuron that is active during any phase of the respiratory cycle. 2. 3 categories based on phase timing: (1) inspiration (2) late inspiration (3) expiration 2 more categories based on firing pattern: (4) incremental (increasing) (5) decremental (decreasing) Total classification combos=6 (2 x 3)
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Term
1. Difference btw. resp. RHYTHM generator and resp. PATTERN generator(s)? What is the current hypothesis about what these structures are?
2. Where does the "respiratory rhythmogenesis" originate from? |
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Definition
1. Rhythm generator(s) (RRGs)="trigger" pattern generators Pattern generator(s) (RPGs)=provide proper sequential activation of resp. pump & LMNs Rhythm generators= 1. preBotzinger Complex (rostral tip of VRG) 2. another more rostral structure **These reciprocally coupled and activate the RPG centers together** |
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Term
1. Where/how are breathing and other behaviors coordinated? 2. What is the difference btw. the 2 competing theories of the model of respiratory rhythmogenesis? |
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Definition
1. First, a "trigger" (RRG) activates a master pattern generator that provides the proper sequence of activations to achieve the required behavior (ex: sneezing, yawning, vomiting, coughing) 2. (1) Pacemaker: spont. depolarizing neurons reside w/in the pre-Botzinger Complex (2) Network: through reciprocal inhibition w/in a network of resp. neurons in the CNS
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Term
1. Components of the carotid body (4). 2. Innervation of the carotid body (2). 3. Defs: chemoreceptor, respiratory chemoreceptor
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Definition
1. chemoreceptor cells (w/ synaptic vescicles in cytoplasm), sustentacular cells (support), capillaries, and sensory neuron dendrites/nerve endings 2. (1) sensory neurons in petrosal ganglion (CN IX) sending fibers via the carotid sinus n. (2) Sup. cervical ganglion via ganglioglomerular nn. (p. 679)
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Term
1. Which "chemicals" does the carotid body respond to? 2. Effect of surgical removal of carotid body. 3. Roles of carotid body in resp. regulation/ctrl (5). |
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Definition
1. Responds to hypoxia (stronger) and hypercapnia (weaker response). 2. (1) transient hypoventilation, then (2) attenuated sensitivity to CO2. 3. (1) O2 chemoreceptors, (2) CO2 chemoreceptors (3) stabilize/regularize resp. (to elim. variations in pO2 and pCO2 breath-to-breath) (4) tonic excitatory input to medullary neurons (5) high-alt. acclimatization |
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Term
1. Medullary neurons' chemoreceptors: sensitive to what "chemicals", relative sensitivity? Which causes the greater (+) ventilatory response: resp. acidosis/hypercapnia or metabolic acidosis? Why? |
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Definition
1. Have BOTH CO2-H+ and O2 chemoreceptors. Respond stronger to resp. acidosis and hypercapnia than to metabolic acidosis So...theory is that medullary neurons' chemoreceptors must be responding to intracellular rise in CO2/H+ (b/c metabolic is just H+ in intercellular spaces, while resp. acidosis "carries H+ into cells" via CO2 diffusion...same for hypercapnia). |
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Term
1. Experiment: cooling (temp.) medullary neurons in anesthetized and awake goats: 2. Experiment: cooling VRG neurons in goats with intact or removed carotid bodies. What are the results and implications of these experiments? |
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Definition
1. After cooling, anesthetized goats exhibited sustained apnea (awake recovered firing after decrease in freq.) 2. Cooling in both cases caused a reduction in freq. of firing from VRG (reflecting decreased resp.). This decr. was accentuated in carotid body-lacking goats. Meaning: (1) VRG neurons--> (+) respiration (2) Not only CO2-H+ chemoRs, but ALSO carotid body chemoreceptors influence VRG neurons (+) (3) VRG lies w/in the rostral medulla-->rostral spinal cord (caudal terminal) |
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Term
1. There are at least 3 (+)/excitatory inputs into the respiratory control center: name them. Importance? 2. Clinical conditions that are relevant to this concept. |
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Definition
1. Carotid chemoreceptors 2. Ventrolateral medullary neurons (likely part of the RTN; retrotrapezoidal nuc.) 3. Wakefulness centers (?) Importance: when all 3 inputs (-), the RG-RG system is non-functional.
CC: relevance to conditions like sleep apnea, Sudden Infant Death Syndrome & Cong. Central Alveolar Hypoventilation. |
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Term
1. Relative to norma, how do PCO2 and PO2 change in (1) hypercapnia (inspiring CO2-rich air) and (2) hypoxia (inspiring O2-poor air)? Why? 2. What undelies the observed incr. in ventilation (both situations)? |
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Definition
1. Breathing CO2: incr. PCO2 (due to air), incr. PO2 (due to hyperventilation) Breathing O2-poor air: PO2 decr. (due to air), PCO2 decr. (due to hyperventilation reducing relative proportion of CO2 to all gases in alveoli) 2. carotid chemoRs (quick rxn), intracranial chemoRs (have a more latent rxn/effect on VE (p. 686) Major point: both hypoxia & hypercapnia incr. ventilation/min. This hyperventilation (resp. in excess of metabolic need) causes an incr. in PO2 and a decr. in PCO2 (effect of taking in more air). |
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Term
1. What are some similarities btw. hypercapnia and COPD? 2. How would you characterize [H+] status in the case of hypercapnia or hypoxia (quantitative measure)?
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Definition
1. Really, only the hypercapnia (incr. PACO2). 2. In resp. acidosis, every +1 mmHg of CO2 translates roughly into a decrease in pH of ~0.01. hypercapnia=resp. acidosis hypoxia=resp. alkalosis (acute) (b/c PCO2 decr.)
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Term
1. Why is VE incr. MORE in hypercapnia than hypoxia? 2. What happens in CHRONIC alveolar hypoventilation? |
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Definition
1. CO2 is more important of a controller of resp. in eupneic breathing than O2 (diff. in sensitivities of the 2 sets of chemoRs). 2. Kidneys make more HCO3- (to compensate for incr. H+), CO2-H+ chemoRs become desensitized, pH is almost returned to normal (by kidney comp.). |
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Term
1. Phases of resp. adaptation in chronic hypoxia. 2. From these phases, what is the major coping mechanism for prolonged hypoxia? 3. What is the major mechanism for altitude acclimatization in humans (which phase represents)? 4. What phase represents those living at high altitude? |
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Definition
1. I: initial hyperpnea (carotid O2 chemoR activation) II: return to normal (CO2-H+ chemoR attenuation + hypoxic brain depression) III: second period of hyperpnea (incr. carotid chemoRs) IV: return to normal (carotid chemoR attenuation) 2. chemoR desensitization/attenuation (CO2-H 1st) 3. Phase 3: carotid chemoRs incr. sensitivity 4. Phase 4: attenuated carotid chemoRs (this only occurs in high alt. residents)
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Term
1. Def: hypoxic brain depression 2. How are SIDS and hypoxic brain depression possibly related? |
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Definition
1. the direct depressant effect of low [O2] on neuron excitability (lowered). 2. Decr. excitability of resp. neurons is one of the postulated causes of Sudden Infant Death Syndrome (SIDS); esp. RRG neurons.
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Term
1. Name the hypothesized causes of SIDS (7). 2. Name the symptoms of CCAH (3) and treatment (also, 3 physiologically normal processes).
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Definition
1. (1) low CO2-H+, (2) carotid hypoxic chemoR sensitivity, (3) hypoxic brain depression (esp. resp. ctrs.), (4) failure of sleep arousal mechanisms, (5) airway obstruction, (6) airwayR inhibition of resp. 2. Congenital Central Alveolar Hypoventilation (CCAH): (1) absent CO2-H & (2) carotid hypoxic chemoRs, (3) central sleep apnea Normal: exercise hyperpnea, airway reflexes & resp. mechanics Tx=diahragm pacing, mechanical vent. during sleep (these px have constant dyspnea, i.e. they need to consciously think about resp. or they will not do it)
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Term
1. Name the stages of sleep (5). Include SWS, periodic breathing and regular breathing in descrip. 2. What is RIP? How does it work?
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Definition
1. Non-REM: 4 stages 1-2=periodic breathing (fluctuates regularly) 3-4=slow wave sleep (SWS); regular breathing REM=5th stage ...then arousal. 2. Resp. Inductance Plethysmography (RIP): non-invasive way to measure resp. (elastic band inductance measured-->stretch changes inductance in band around abdomen/chest)
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Term
1. How does breathing change during REM? 2. How does overall ventilation compare btw. the different stages of sleep? 3. What is paradoxical thoracoabdominal movement?
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Definition
1. Breathing is irregular in timing and amplitude during REM. 2. VE is highest during wakefullnes, lowest during NREM (SWS esp.), and intermediate during REM. 3. When abdominal and thoracic movements are opposite (abd. incr. in diameter, while chest decreases, for example) |
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Term
1. What is central apnea? How is it defined? 2. What is obstructive sleep apnea? What differentiates this from central sleep apnea syndrome (CSAS)? |
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Definition
1. Failure of RRG mechanisms manifested in a lack of thoracic & abdominal motion/resp. mm. inactivity. "Central Sleep Apnea Syndrome" 2. Cessation of airflow despite continued resp. pump muscle activity. Paradoxical thoracoabdominal wall movements noted as well (p. 693).
Notes: SaO2 decreases in apnea |
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Term
1. 2 primary locations of obstruction in sleep apnea. 2. What causes these obstructions? 3. Statistics of OSA in the U.S. 4. Symptoms of OSA (6) and treatments. |
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Definition
1. retropalatal=soft palate retroglossal=back of tongue 2. Loss of rhythmic & tonic genioglossal m. activity, or anatomical abnormalities, loss of protective resp. reflexes 3. 15% of adults in the USA! 4. Sx: hypoxemia, psychiatric disorders, hypertension, daytime somnolence, incr. symp. nerve activity Tx: surgery, tracheotomy, + pressure breathing, oral mechanical devices |
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Term
1. What is Cheyne-Stokes respiration? 2. What might cause it? Under what conditions does this type of resp. occur in normal and diseased px? |
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Definition
1. Periodic breathing: (longer) phases of hyperpnea and apnea. 2. Might be caused by increased gain of carotid chemoRs resulting in PaO2 "over corrections" When: high alt. (first few days), CHF, unstable sleep states |
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Term
1. Lung defense mechanisms: (1) in conductive resp. system, (2) in respiratory system (x-change area). 2. What is the primary surface tension-reducing component of surfactant? 3. Of the protein component of surfactant, which have immune fxn and which have surface tension-reducing fxns? |
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Definition
In conductive: ciliated eipthelium (mucociliary clearance), coughing, sneezing, etc. In resp. part: Type II alveolar cells (secrete surfactant; 90 lipids/10 protein). Type I cells form structure of alveoli. Neutrophils and alveolar macrophages (dust cells) also protect. Opsonins (immunoglobulins). 2. Dipalmitoylphosphatidylcholine (DPPG) (50% of 90% lipids=45% surfactant) 3. Surfactant proteins (SPs): SP-A, SP-D=collectin family of immune proteins that have CHO recognition sites-->promote phago by coating viruses & bacteria SP-B, SP-C=essential to fxn of surfactant (incr. rate of spreading over alveolar surface)
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Term
Airway reflexes: which ones cause which responses: 1. epipharyngeal 2. laryngeal 3. pharyngeal 4. nasal Which reflexes utilize (1) slowly adapting, (2) rapidly adapting and/or (3) c-fiber neurons? |
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Definition
1. Epipharyngeal=aspiration reflex (indicated by brief incr. in phrenic n. activity) 2. Laryngeal=apnea reflex (water injected into larynx=no phrenic n. activity (apnea/prolonged expiration; "clearing airway") 3. swallowing 4. sneezing, "diving reflex" Slow: bronchodilation, tachycardia
Rapid + C-fiber: bronchoconstriction, mucus secretion, pulm. chemoreflex, bradycardia |
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Term
1. Are the "lung irritant receptors" slowly or rapidly adapting receptors? 2. Compare: Hering-Breuer deflation vs. inflation reflexes
(1) types of fibers carrying signals (2) function |
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Definition
1. rapidly adapting 2. H-B reflexes use stretch receptors in lung smooth muscle to prevent overinflation and over-deflation of the lungs. Deflation reflex: (1) BOTH slow & rapidly adapting receptors (stretch and other proprioceptor receptors in lungs)
(2) prevents over-deflation Inflation reflex: (1) slowly adapting receptors (stretch)
(2) prevents over-inflation |
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Term
CNS pathway for resp. reflexes/neural control of respiration/lung volumes: 1. nerve carrying signals 2. CNS target(s) 3. descending controller(s) |
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Definition
1. Stretch receptor afferents in vagus n.
2. Vagus n. afferents (incr.)-->excites pontine apneustic resp. ctrl. center (in NTS). 3. NTS (once excited) inhibits Nuc. ambiguus 4. Nuc. ambiguus is responsible for tonic inhibition of heart rate (its efferents also carried by vagus n.)
Net result: increased pulm. stretch-->incr. HR (Deflation reflex is just decr. vagal n. afferents from lungs)
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Term
Mechanism whereby ventilation increases during work is still unknown. 5 observations regarding work-induced hyperpnea: 1. temporal pattern of VA 2. blood gases 3. temporal pattern of Resp. Quotient (R) 4. electrically-induced exercise 5. paraplegic subject + electrically-induced exercise |
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Definition
1. VA exhibits (1) sharp initial increase, (2) slower increase to strady state by ~90 sec 2. blood gas homeostasis until about 60% maximal exertion 3. R constant until ~60% maximal exertion (then increases due to hyperventilation; mechanism unknown) 4. ventilatory response does not differ btw. voluntaryelectrically-induced exercise (not central ctrl.-dependent) and 5. paraplegics exhibit same ventilatory response as patients in #4 Implications: 1. fast & slow components 2. hyperpnea not a result of incr. chemoR activation 3. hyperventilation above 60% max exertion 4. ventilation not dependent on central ctrl. 5. ventilation not dependent on spinal afferents
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Term
1. Whatvalue determines if VA has been changed? 2. In a patient with low PaCO2 and high PaO2 (hyperoxia), what is then driving respiration if not chemoRs? |
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Definition
1. PaCO2 (Normal a=40, mv=45) 2. This would describe a case of hyperventilation (VA/VCO2 elevated relative to normal). Stress or a brainstem lesion (BSL) could be driving resp. |
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Term
1. Importance of maintaining a relatively constant [H+] 2. What is "physical-chemical H+ buffering"? 3. What are the primary buffering systems in the ECF vs. the ICF? |
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Definition
1. optimal enzyme fxn/protein stability CC: high [H+]=decr. neuron excitability (membrane channels)=coma (vs. low [H+]=seizures) 2. Fancy term for buffering 3. ECF=HCO3-, H2PO4, proteins(+) ICF=proteins, H2PO4
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Term
1. How to distinguish btw. resp. and metabolic acidosis 2. What is the "isohydric principle"? 3. |
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Definition
1. Given low pH (acidosis), if CO2 is also elevated, then it is most likely respiratory. 2. Concept that all buffer pairs existing within body fluid compartments are in equilibrium with the same pH (same compartment) and bind H+ according to their pKa. When [H+] is altered, so to will be all the buffer pairs in sol'n.
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Term
1. What determines buffering capacity for a given buffer pair? 2. When is a buffer at optimal buffering capacity (relative to pH of sol'n)? 3. What is "physiological buffering"? |
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Definition
1. (1) buffer concentration, (2) difference btw. pH of sol'n and pKa of buffer 2. When sol'n pH=pKa of buffer (equal amt. of A/B in solution) 3. Physiological buffering is the body's ability to generate buffer pairs from existing chemicals within the body fluids. |
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Term
1. Plasma [H+] regulation mechanisms: (1) transmembrane: ECF-ICF (2) pulm. ventilation (3) physiological buffering |
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Definition
1. (1) ICF has lost of buffers, ECF has less, so H+ is exchanged for either Na+ or K+ from inside cell. (2) Excess acid (H+) can be eliminated via conversion to H2CO3-->H2O + CO2. (3) Generation of HCO3 from Gln in the kidney and excretion of acid using NH3 as a buffer (ammonia excretion)
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Term
1. The body makes strong organic acids daily. What limits the body's ability to buffer these acids? 2. During acidosis, what role does the BBB play in regulating CSF pH? How effective? |
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Definition
1. The amt. of HCO3 available to buffer the H+ made by the body...hence, the kidney's ability to make HCO3 from Gln (primarily; brain also can do this) and then excrete the by-product ammonia. 2. The BBB limits passage of medium-sized uncharged and all charged particles (like H+), so the change in pH in the CSF is only 10% of the change in pH seen systemically.
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Term
1. The BBB is an ineffective barrier against resp. acidosis & alkalosis (gases are membrane-permeable). What does the brain do to regulate its pH in these situations? 2. Given a strong acid IV injection, what buffer systems will handle this (temporal sequence)? |
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Definition
1. During resp. acidosis: glial cells make NH3 During alkalosis: they make lactic acid 2. First 30 min.=HCO3 in plasma (depleted) After couple hours=H+/Na, K ECF-ICF exchange (transmembrane exchange now compromised) Days=kidneys will make more HCO3 to restore equilibrium, transmembrane gradients, and buffering capacity of blood to normal. kidney=ultimate corrector of A/B disturbances
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Term
1. What is normal [HCO3-] in mM/L? How would a decreased [HCO3] affect pH? 2. An elevated or lowered pH would cause mental confusion/lethargy? 3. What is the cause of posthypercapnic alkalosis?
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Definition
1. Normal=20-24 mM/L. Decreased [HCO3] would result in decreased pH (b/c it is buffering H+). 2. Lowered CSF pH=mental lethargy (decr. neuron excitability). 3. Renal compensation for resp. acidosis by increasing [HCO3].
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Term
1. What is cor pulminale? What can it be a complication of (a resp. disease)? What are other common comorbidities of this disease?
2. What are the symptoms of acute vs. chronic bronchitis? 3. |
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Definition
1. Cor pulmonale=R-sided heart failure (common w/ COPD). Also: URTI/URIs (upper resp. tract infections) and bronchitis. 2. acute=days-wks., chronic=persistent, productive sputum for at least 3 mo. or a 2 yr. period |
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Term
CC: COPD patient 1. Why elevated HCO3? 2. Why hypercapnia after admin. O2 supplement air? 3. Why the transient decrease in blood pH? 4. What is the alveolar-arterial oxygen gradient, and what does it indicate? |
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Definition
1. Renal compensation for chronic resp. acidosis. 2. Unknown: possible mechanisms include incr. Hb O2 sat. shifting CO2 from Hb to dissolved in blood (decr. pH; Haldane effect), suppressed hypoxic ventilatory reflex/reduced tidal vol./incr. dead space vol. (shallower breathing), etc. 3. due to the hypercapnia 4. Indicates how effectively O2 is diffusing from air into blood (indicates diffusion capability of lungs). |
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Term
1. What is status asthmaticus? What is typical presentation and treatment? 2. Lung fxn tests: COPD vs. restrictive lung disease
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Definition
1. Asthma attack that has failed to respond to bronchodilator admin. in outpatient setting (puff-puff no work). low pH, A-a mismatch (alv-arterial gradient) due to bronchoconstriction, hyperventilation and hypocapnia. Tx: corticosteriods, O2 supplemented air, intubation an option. 2. COPD=elevated TLC, RV, FRC RLD=reduced TLC, FRC, RV |
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Term
1. OSA and Pickwickian syndrome (Sx, etc). |
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Definition
1. OSA can cause hypertension, hypersomnolence (daytime), and stress-related comorbidities (incr. weight, asthma, etc.) Pickwickian syndrome=OSA + alveolar hypoventilation Pulm. hypertension-->RV hypertrophy, sleep-disordered breathing, nocturnal Hb O2 desat...
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