B: Gas Laws and Dead Space Flashcards
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A: Boyle’s Law = (pressure:volume) = [V1•P1 = V2•P2] OR
[V = 1/P] as long as temp & mass are constant
B: Charle’s Law = ([Kelvin Temperature]:volume) = [V = T] at constant pressures
C: [GayLussac’s Law] = ([Kelvin Temperature]:pressure) =
[P = T] at constant volume
D: [COMBINED GAS LAW] = [V = (T/P)]
E: Avogadro’s law (volume:amount law) states that if amount of gas in a container INC, Volume INC
F: Ideal gas law: PV = nRT (R is universal gas constant)
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A: Dalton’s Law of Partial Pressures : Total Pressure = Sum of all individual non-reacting partial pressures
B: [Amagat’s Law of Partial Volumes] = same as Dalton’s but with Volume
C: [Henry’s Law of Gas Solubility] = Concentration of gas in a solution is DIRECTLY proportional to its partial pressure ABOVE the liquid solution
D: ºAtmospheric/barometric pressure @sea level = 760 mm Hg Ambient Air : -79% N2 = 563 mm Hg -21% O2 = 150 mm Hg -1% water vapor -0.04% CO2
E: When air enters respiratory SYSTEM it is filtered, warmed to body temp (37º C) and then humidified 100%. [Water Vapor pressure is 47 mmHg at 37ºC] so this “dilutes” the other gases being inhaled
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A: When tracheal air reaches Alveoli gas composition DRASTICALLY CHANGES—> since O2 is flowing into pulm blood and CO2 is flowing OUT pulm blood. BUT on average:
ºPaNitrogen = 563 mm Hg/constant because our body doesn’t produce nor consume it
ºPaO2 in alveoli “PAO2” = 102 mm Hg
*ALVEOLAR O2 GAS EQUATION
B: How do you calculate [Alveolar PaO2] from using [Alveolar PaCO2= 45 mm Hg] if you breath 100% O2??
1st. [Barometric - (water vapor p.)] x (% O2) = A
1st. [713] x (1) = (A)
2nd. (A) - [Alveolar PaCo2] / 0.8 = [Alveolar PaO2]
2nd: [(A) - 45] / 0.8 = [Alveolar PaO2]
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- Alveolar Co2 gas equation*
B: Normally [CO2 production] is about 250 mL/min and [alveolar ventilation] = 5L/min in order to keep [PACO2 at 40-45 mm Hg]. HYPERventilation : (10L/min) will DEC PACO2 to 20 mm Hg.
C: Distribution of inspired air into vertical lung is NOT UNIFORM and shunts MORE to LUNG BASE (near diaphragm). This is because:
- there are MORE alveoli at Lung bases to receive MORE air
- at FRC Lung base is more compliant-> so receives better volume changes during ventilation
D: [Intrapleural Pressure] & [TransPulmLung pressure] are Greater at APEX and this EFFECT is Amplified at RV, but disappears at TLC
E: [TransPulmLung pressure] at RV = low for both parts of lung but Apex is HIgher..and there is a GREATER DIFFERENCE between Apex & base
F: [TransPulmLung pressure] at TLC = HIGHER for both parts of lung and Apex is still HIgher..but here there is smaller difference between the two
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A: Rate at which Alveolar fills with depends on
ºResistance (INC Resistance = INC TC)
ºCompliance (DEC Compliance = DEC TC)
[R x C = (time constant) ] **HIGH (time constant) means alveoli are filling up & emptying out SLOWLY! **
C: [Single-Breath Nitrogen Washout Test] assess uniformity of ventilation and determine [ANATOMICAL dead space] = when we breathe in atmospheric air lung is 78% N2. If we were to exhale everything out and then inhale 100% O2 this would dilute the N2. (LUNG BASES SHOULD HAVE MORE DILUTION since they receive MORE VENTILATION) Once pt breaths out into a N2 meter at constant flow from TLC –>RV the N2 concentration is plotted and 4 parts results
Part 1) N2 remains fixed at zero as dead space filled with O2 empties first
Part 2) rapid Upswing in %N2 concentration as alveolar regions empty
Part 3) [Alveolar plateau] occurs as a result of equal emptying of ALL lung zones from base to apex
C2: This test determines [ANATOMICAL dead space (using Fowler’s method)] by looking at [Part 2 first Upswing]. The Volume up to the Vertical meeting point between A and B is dead space. A and B are markings of when the curve starts to shift into different part
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A: [Ventilation = (Freq. of breathing) x TV] = 7500 mL/min]
A2: [Tidal Volume] fills Dead Space FIRST and then alveolar space smh —> Ventilation consist of dead space and “life space” ventilation
B: dead space Ventilation = (Freq. of breathing) x (Ventilation of dead space only)
C: ALVEOLAR VENTILATION =[ (Freq. of breathing) x (TV - (Dead Space VOLUME) ]
D: [Physiological Dead Space] is Total Volume that does NOT participate in gas eXchange =( [Anatomical Dead Space] + [Ventilated Alveoli but not perfused] ). It is identical to [alveolar PCO2]
D2: Normal ratio [Dead Space]/[Tital Volume] ratio is 0.2-0.35 and Anatomical & Physiological Dead Space are usually the same
D3: Lung Dz pt have a HIGHER Physiological Dead Space #
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A: alveolar ventilation is less than [Pulmonary Tidal Ventilation]. INC TV is MORE EFFECTIVE at increasing [Alveolar ventilation] (and DEC Dead space ratio) than increasing respiratory rate
B: INC [Pulmonary tidal volume]—-> DEC [dead space ventilation
C: [Pulmonary Tidal VENtilation] is comprised of air going to [Dead Space] AND air going to [actual alveolar ventilation]
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A: 3 Factors facilitate gas diffusion
1) LARGE Alveolar Surface Area
2) Short Distances for gas to travel
3) Use of gases w/advantageous diffusion properties
B: [Capillary diameter = less than 10 µm] vs. [Erythrocyte= 7µm diameter]. Erythrocytes pass thru capillaries in SINGLE FILE in less than 1 sec.
C: Fick’s Law states [amount of gas transferred] is ººproportional to area / Diffusion constant / [∆ partial pressure]
ºººINVERSE to THICKNESS
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D: [Graham’s Law] –> {Gas DIFFUSION RATE = [Solubility coefficient] / [√molecular weight] }
D2: CO2 Diffuses across alveolar membrane 20x FASTER than O2 due to its Higher [Solubility coefficient]
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A: N20 / O2 / CO2 are all [PERFUSION LIMITED] = their partial pressures end up having enough time to equilibrate with alveolar pressure first BEFORE leaving the Capillary. This is because they are less soluble and don’t combine chemically w/proteins.
A2: O2 can be converted into [diffusion limited] uptake in 3 ways: at low alveolar PO2 (i.e. high altitudes) and during Exercise becuz it’ll start being taken up by Hgb/perfusing much more rapidly and then only need to worry about [diffusion rate].
•(This convert also occurs from a [Thickened Blood-Gas Barrier]**
••*RBC that spend less than 0.25 sec in capillary bed will induce [diffusion limited] conversion
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vs.
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B: CO which is [diffusion limited] = it NEVER has the time to reach equilibrium with alveolar pressure once in capillaries becuz it’s taken up RAPIDLY by Hgb AS SOON as it diffuses over = [perfusion UNlimited]
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A: driving Pressure in the pulmonary circuit is 6 mm Hg vs. in the Body 87 mm Hg. Resistance to flow in lungs is less than 10% of Resistance to flow in the Body!
B: [pulmonary arteries] have thin walls with minimal smooth muscle. They are easily distended and 7 x MORE COMPLIANT than Systemic Arteries with low pressure circulations
C: [Pulm Vascular Resistance] = [∆ Pressure] / [Blood Flow (Q)] . [PVR] INC at very low OR VERY HIGH lung volumes.
D: [LUNG PERFUSION] is influenced by
- [Pulm Vascular Resistance]
- Gravity
- Alveolar pressure
- [Arterial-venous pressure gradient]
E: In the lungs, INC [Arterial or venous Pressure]/[Cardiac Output]—->DEC [Pulmonary Vascular Resistance] . This is due to [Alveolar CAPILLARY RECRUITMENT] which involve opening up normally UNavailable capillaries AND distending already-perfused capillaries
F: changes in [Pulm vascular resistance] during INhalation form a U-shaped curve with [nadir trough] at FRC. This is becuz during INhalation extra-alveolar vessels DEC resistance but [alveolar vessels INC resistance]
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A: There are 2 reasons blood flow is HIGHER in LUNG BASES
1. Bases have More [Lung tissue & capillaries] due to triangular shape of vertical lung
- Blood is more massive than air so GRAVITY pulls blood into Base more easily
B: [R Ventricle] and Gravity work together to overcome [Pulmonary Vascular resistance] and push blood “up hill”. There are 3 Zones Blood Flows thru in Lungs
Zone 1 =
º “NO FLOW ZONE” . Blood can nOT reach this part because R Vt is not that strong :-( AND [Atmospheric ALVEOLAR] pressures are greater than BOTH arterial and venous in this zone.
ºThis is a pathological zone due to low R Vt [Cardiac Output], hypOtension or [Mechanical Positive Pressure Ventilation].
ºDue to [pulmonary arterial pressures] this zone exist only above the shoulders normally and does not exist in regular lungs!
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[R Ventricle] and Gravity work together to overcome [Pulmonary Vascular resistance] and push blood “up hill”. There are 3 Zones Blood Flows thru in Lungs:
Zone 2 = “COMPRESSIVE WATERFALL ZONE” = top/mid lung. [Pulmonary ARTERIAL pressure] is HIGHER than [Atmospheric Alveolar] pressure but since venous pressure is still lower than [Atmospheric Alveolar pressure] blood tends to “FALL DOWN” thru the capillaries to zones where venous is higher and UNobstructed
ºWorks like a Starling resistor where [Atmospheric Alveolar pressure] controls flow! (not pressure gradient between [Pulmonary ARTERIAL] and vein)
º[Atmospheric Alveolar] pressure COMPRESSES the vessels and INC their [Vascular Resistance] during inhalation
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[R Ventricle] and Gravity work together to overcome [Pulmonary Vascular resistance] and push blood “up hill”. There are 3 Zones Blood Flows thru in Lungs:
Zone 3 = “Normal Zone” = Lung Base. [Pulmonary Arterial Pressure] AND [Venous Pressure] are GREATER than [atmospheric alveolar] pressures here —->[atmospheric alveolar pressure] has NO EFFECT ON VASCULAR RESISTANCE here
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A: [Hypoxic Vasoconstriction] is determined by [Alveolar PO2 gas only]. It shifts blood AWAY from hypoxic areas to well-perfused areas. (Local vasoconstrictors/vasoDilators also help but are short-lived and only important in pathological conditions) [Hypoxic Vasoconstriction] is important at birth!
B: Water Balance inside & Outside Lung vessels depends on [Starling forces = Hydrostatic vs. oncotic pressures]. Normally there is a net OUTWARD force pushing fluids into interstitium and then collected by lympathics.. In the lungs…
- Plasma water is filtered from PULMONARY capillaries into alveolar walls and then picked up by lymphatics. Excessive Filtration–>[Alveolar wall Engorgement] AND [Alveolar flooding/internal drowning].
- Plasma water filtered from systemic capillaries goes into pleural space and is eventually picked up by lymphatics. Excessive Filtration here–> [Pleural space Engorgement]—-> [Pleural Effusions] which DEC lung volume and FRC
C: When [Interstitial Drainage rates] EXCEED [Maximal Lymphatic Flow]—> interstitial AND then Alveolar Lung EDEMA Develop
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A: Alveolus and its capillary blood flow are the functional unit of Lung. [V/Q ratios] dictate amount of O2 put IN and amount of CO2 taken out from [pulmonary capillary blood]
B: [alveolar Pulmonary capillary blood] goes from [40 mm Hg/DEoxygenated] to [100 mm Hg/ONCE OXYGENATED] and CO2 levels in capillary blood DECREASES from
45—>40 once it passes the Alveolus
C: Although [alveolar Pulmonary capillary blood] ONCE OXYGENATED STARTS AT 100 mm Hg it DEC by 5 in the ARTERIES due to 3 things:
- mixing with Bronchiolar venous blood
- mixing with [thebesian veins tht drain myocardium]
- [V/Q] inequalities between Lung apex and BASE
D: The difference between [pulmonary capillary blood] PaO2 of ARTERIES and [pulmonary capillary blood] PaO2 of alveoli should be LESS THAN 15 but will INC with dz
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A1: [V/Q ratio] at the level of 1 alveoli compares [alveolar ventilation: capillary blood flow]
B1: [V/Q ratio] GREATER THAN 1 = VENTILATION IS GREATER THAN PERFUSION. THIS OCCURS AT LUNG APEX & WITH [DEAD SPACE ALVEOLUS] WHICH ARE VENTILATED BUT NOT PERFUSED {physiological dead space/OVER-VENTILATED}. ALVEOLAR PARTIAL PRESSURES HERE EQUAL ATMOSPHERIC PARTIAL PRESSURES BECAUSE NOTHING IS MOVING: PaO2(150MMHG) and PaCO2(0 MMHG)
C: Normal [V/Q ratio] = 0.8
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D: [v/q ratio] less than 1 = perfusion is GREATEr than ventilation and this occurs more commonly at lung bases & with [shunt alveolus] where [v/q ratio] = 0.
D2: In [shunt alveolus] alveolar pressures equal mixed venous blood pressures: PCO2(45mmHg) and PO2(40mmHg) and no gas exchange occurs
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A: LUNG BASE receives LARGEST % of VENTILATION ANND PERFUSION and apex the least.
A2: PERFUSION INCREASES more Vastly from apex–>BASE than ventilation does –> this is because gravity has STRONGER effects on [HIGH DENSITY BLOOD] than [low density air]
B: The [middle Lung] is the ONLY part where [Perfusion/Blood Flow] and ventilation are ideally matched LUNG BASE has MORE BLOOD FLOW than Ventilation–> DEC [V/Q ratio}
C: Lung BASE has turnover of alveolar gas with fresh air that is less frequent—> “over-perfusion” –>gives even more time for O2 to leave and CO2 to enter
D: Due to V/Q inequality between apex and BASE, MOST of Oxygenated Blood comes from BASE.
[apex alveolar PaO2 of 132 mm Hg] + [BASE ALVEOLAR PaO2 of 89] —> [Arterial PaO2 of 97 mm Hg]
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A: Difference between PaO2 INSIDE ALVEOLI and actually inside Arteries should be less than 15 mmHg but INC by 4 every 10 years = [AaDO2] = used to determine causes of [Hypoxemia]
B: There is a Difference of PaO2 between these two places because:
1) [V/Q] inequalities between Lung apex and BASE
2) [Anatomical Shunts (Thebesian vessels / [bronchial venous dumping into pulm veins] )
C:[AaDO2] can be determined by finding [alveolar PaO2] with the [Alveolar Gas equation].
C2: And then find [ARTERIAL PaO2] with Blood Gas Analysis
C3: = (150 mm Hg - 40 mm Hg / 0.8) - 95 = 5 mm Hg Difference! 150 = room air 40= PaCO2 from [Blood Gas Analysis] 95= Arterial PaO2 from [Blood Gas Analysis]
0.8 = [respiratory quotient] = constant = [excreted CO2/O2 taken up]
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A: [Tissue hypoxia] is usually due to to low of vascular routes and too high of tissue demands. [Tissue hypoxia] can become [TISSUE ANOXIA/NO O2 AT ALL] during clot formation.
A1: [Hypoxemia] occurs when O2 CONCENTRATION IN ARTERIAL BLOOD ITSELF is too low. It’s defined as [ARTERIAL PaO2 of less than 80 mm Hg] at sea level.
- 4 things cause Hypoxemia at room air*:
1. [hypOventilation]
2. [Diffusion limitation]
3. SHUNT [Anatomical vs. Physiological]
4. [V/Q inequality] = MOST FREQUENT CAUSE
B2: When hypOventilation causes [Hypoxemia] [AaDO2] is likely still normal because BOTH alveoli AND Arteries will be receiving less O2 due to LESS VENTILATION–> INC Arterial PaCO2
B3: {[Hypoxemia] 2º to hypOventilation} can be caused by [morphine/heroin/barbiturates/Anesthesia] which centrally depress breathing drives AND
B4: can be corrected by giving Additional O2
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A1: [Hypoxemia] occurs when O2 CONCENTRATION IN ARTERIAL BLOOD ITSELF is too low. It’s defined as [ARTERIAL PaO2 of less than 80 mm Hg] at sea level.
- 4 things cause Hypoxemia at room air*:
1. [hypOventilation]
2. [Diffusion limitation]
3. SHUNT [Anatomical vs. Physiological]
4. [V/Q inequality] = MOST FREQUENT CAUSE
A2: {[Hypoxemia] 2º to [Diffusion limitation]} will cause [AaDO2] to INC because there’ll be more O2 in alveoli and LESS O2 IN ARTERIES BECAUSE LESS DIFFUSED ACROSS “Fick’s Law” .
A3: {[Hypoxemia] 2º to [Diffusion limitation]} can be caused by [Lung Edema] / Fibrosis / [Alveolar capillary Block]
A4: {[Hypoxemia] 2º to [Diffusion limitation]} can be CORRECTED by giving Additional O2
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A1: [Hypoxemia] occurs when O2 CONCENTRATION IN ARTERIAL BLOOD ITSELF is too low. It’s defined as [ARTERIAL PaO2 of less than 80 mm Hg] at sea level.
- 4 things cause Hypoxemia at room air*:
1. [hypOventilation]
2. [Diffusion limitation]
3. SHUNT [Anatomical vs. Physiological]
4. [V/Q inequality] = MOST FREQUENT CAUSE
A2: {[Hypoxemia] 2º to SHUNT [Anatomical vs. Physiological]} will cause [AaDO2] to INC.
ºAnatomical Shunt shits [DEoxygenated Venous Blood] from [pulmonary artery], BYPASSES Alveoli ,and directly to [Pulmonary Veins] where it mixes with Oxygenated blood.
ººº Physiological Shunts are mostly caused by Atelectasis (collapse & closure of Lung —> DEC or NO gas exchange! )
A3: SHUNT [Anatomical AND Physiological] IS THE ONLY CAUSE IN WHICH Giving Additional O2 WILL NOT HELP!
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A1: [Hypoxemia] occurs when O2 CONCENTRATION IN ARTERIAL BLOOD ITSELF is too low. It’s defined as [ARTERIAL PaO2 of less than 80 mm Hg] at sea level.
- 4 things cause Hypoxemia at room air*:
1. [hypOventilation]
2. [Diffusion limitation]
3. SHUNT [Anatomical vs. Physiological]
4. [V/Q inequality] = MOST FREQUENT CAUSE
A2: {[Hypoxemia] 2º to [V/Q inequality] IS THE MOST COMMON HYPOXEMIA IN PT WITH RESPIRATORY DZ! [AaDO2] is INC in this situation.
A3: This Condition CAN be improved by giving Additional O2
B: [V/Q inequality] DEC gas exchange efficacy for all gases!
C: Even though CO2 elimination is still impaired by [V/Q inequality] you can improve this by INC [alveolar ventilation] due to its dissociation abilities.
C2: [V/Q inequality] causes Hypoxemia which (DURING [V/Q inequality]) CAN NOT BE FIXED BY INC [alveolar ventilation]
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A: [Carbon MONOxide] has 200x STRONGER AFFINITY for Hgb than O2 and only needs partial pressure of [1 mm Hg] b4 FULLY SATURATING Hgb/preventing O2 from hopping on. It forms [Carboxyhemoglobin] which is EVEN MORE RED IN COLOR!
B: [Pulse Oximeter] of 97% Hgb Saturation = Normal. Pulse Ox of 90% corresponds to PaO2 of [60 mm Hg] which is DANGEROUS but normal for pt with COPD.
C: Hgb SATURATION is INDEPENDENT of Hgb Concentration
D: 1 gram of Hgb binds to 1.34 mL of O2 = [O2 capacity]. Normal blood has 15g Hgb/100 mL = [20.1 mL O2 bound/100 mL = SO2 100%]
E: There is [4.4 mL O2 / 100 mL] EXTRACTED from blood during “drop off” to tissues
E2: Anemic Pts only have 7.5g Hgb/100 mL = [10.1 mL O2 bound / 100 mL = SO2 100%]. This means in order for THEM to extract 4.4 mL of O2 they’ll have to go down to a SO2 of 54% from 97% (vs. the normal of 75% post drop-off)
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A: Breathing has 3 phases
1) Inspiratory airflow
2) expiratory airflow
3) expiratory APnea (DEC during exercise)
C: Breathing is BOTH Automatic and Voluntary. [Medullary Respiratory Centers] AUTOMATICALLY GENERATE nerve impulses to [Spinal Cord]—> [Respiratory Muscles] for control. These muscles expand lung and chest wall which
1. via [mechanoreceptors] feed back to [Medullary Respiratory Centers] AND
- via changes in Blood pH after diffusion feed back to [Medullary Respiratory Centers] as well via [Central&Peripheral Chemoreceptors]
D: The Cerebral Cortex allows VOLUNTARY respiratory control using [Corticospinal tracts]
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A: [Medullary Respiratory Centers] consist of
1. [Dorsal Respiratory Group-NST] = generates inspiratory m.
- ## [ventral respiratory group -Nc. paraambiguus]B: [Medullary Respiratory Centers] are “controlled” by [PONTINE Respiratory Groups] which are the
-[Apneustic Center] = EXCITES DRG by blocking Pneumotaxic –> generates inspiratory m.
and
-[Pneumotaxic center] = STOPS DRG from stimulating inspiratory m. & controls breathing pattern = BLOCKS INSPIRATION from occur
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A: [CENTRAL CHEMORECEPTORS] that feedback to [Medullary Respiratory Centers] are found on the ventrolateral surface of the Medulla and are sensitive to changes in CSF pH! THESE ARE THE MAIN [CHEMORECEPTOR VENTOREGULATORS]
B: [Blood Brain Barrier] is normally impermeable to [H+ and HCO3], soo…PCO2 is the only factor that stimulates [CENTRAL CHEMORECEPTORS] and this occurs WITHIN MINUTES of PaCO2 changes. THEY DO NOT RESPOND TO PO2 CHANGES!
C: [Blood Brain Barrier] can BECOME partly permeable to H+ when Arterial pH is realllly low smh
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A: [peripheral chemoreceptors] in the [aortic arch] and [Carotid Bodies] also feedback to [Medullary Respiratory Centers] and are the ONLY chemoreceptors that respond to [High PCO2] AND [low PO2 dude]! They’re responsible for 20-40% of ventilatory responses to CO2.
••[Carotid Body peripheral chemoreceptors] respond to low pH THAT MAY COME FROM RENAL OR METABOLIC ACIDOSIS. ••
C: [Hering-Breuer Reflex] = DEEP inflation activates [Pulmonary Stretch receptors] found in [Visceral pleura] & [large airway smooth m.] & INHIBITS FURTHER INSPIRATION by sending inhibitory signals to the DRG via Vagus nerve (AND VICE VERSA FOR DEFLATION–>INITIATES inspiratory m. and blocks vagus n. )
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D: [Irritant receptors] lie between epithelial cells of our airway and are stimulated by [noxious gases], [cigarette smoke], dust & [COLD AIR]. They send impulses thru the Vagus Nerve and play a role in ASTHMA!
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E: [Juxtacapillary receptors & bronchial-c fibers] respond to chemical injected into PULMONARY (J RECEPTORS) and bronchial (c fibers) circulation
F: Other receptors involved in breathing control include
1) Nose/Upper airway irritant receptors
2) Joint/Muscle receptors
3) Pain/Temp Receptors
4) Arterial Baroreceptors
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A: At normal PaO2, ventilation INC 3 L/min for each 1 mmHg INC in PaCO2. IF PaO2 is LOWERED under [100 mmHg] DURING HIGH PaCO2—> This response becomes MORE STEEP and ventilation INCREASES MORE RAPIDLY from PaCO2 Increase!
**PaO2 HAS to be LOWER than 60 mmHg in order to get LARGE COMPENSATORY RESPONSE **
A2: At low or normal PaCO2, PaO2 can be decreased to
[50-70 mmHg] WITHOUT ANY CHANGE in Ventilation
B: HIGH PaCO2 will make you want to breathe MORE FREQUENTLY/HYPERVENTILATE (and vice versa). A lowered PaO2 will make this response more sensitive
C: [PaCO2 Ventilatory Response] is LESS sensitive (doesn’t respond as quickly to PaCO2 increase) during…
*sleep
*aging
*[Athletes or Divers]
*[Morphine/ BARBITURATES / (ELEVATED WOB FROM COPD) ]
*[Anesthetics] = [RESPONSE BARELY WORKS AT ALL]
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D: [Metabolic Acidosis] makes [PaCO2 Ventilatory Response] MORE SENSITIVE to Increases in PaCO2
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B: [Metabolic Acidosis] from [uncontrolled DM] and [Renal Failure] INC ventilation despite low PaCO2. This occurs because [Carotid Body peripheral chemoreceptors] sense low pH.
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A:During exercise, TV is able to INC by accessing IRV and ERV. Ventilation INC 15x the resting level with O2 consumption of 4L/min and Ventilation of 120L/min
B: During “moderate” Exercise PaO2, PCO2 and pH do NOT change that much …so it is NOT understood why ventilation actually Increases during “moderate” exercise lol
C: SEVERE Exercise causes [lactic acid] release which DEC pH and eventually stimulates [anaerobic threshold] –> which is the point variables like [O2 consumption] and [Ventilation rate] change
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A: 30% of normal people have brief episodes of apnea or hypOventilation during sleep and this does NOT effect blood gas levels
B: MOST CLINICALY IMPORTANT breathing syndrome is Sleep Apnea { [Obstructive/OSA] vs. [Central Alveolar hypOventilation/Ondine’s Curse] }
- [Kussmaul breathing] = INCREASED DEPTH of breathing and HYPERventilation characteristic of [Diabetic KetoAcidosis]
- ————————————————————————————- - [Biot’s respiration] = Are SUPER DEEP inhalations and exhalations followed by long pauses inbetween. Pt exhibit this near death from neuronal damage.
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[Apneustic respiration] = Sustained periods of INhalation followed by brief exhalation. Is caused by NO input from the [PONTINE pneumotaxic center] and Vagus n. to inhibit inspiratory m. Usually is associated with brain damage or intoxication
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[Cheyne-Stokes Ventilation] comes from brain injury with INC [intracranial pressure] from tumors & encephalopathy. It is fast inhalation and exhalation with long pauses inbetween.
