C: Diving / High Altitudes Flashcards
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A: Once DEC PaO2 in arteries stimulate [Peripheral chemoreceptors] to activate HYPERventilation —> [Respiratory Alkalosis] which is fixed by Kidneys eliminating excess HCO3. Even with the Renal fix, people at high altitudes will STILL have mild [Respiratory Alkalosis] BUT this is OK :-) because it INC Hgb affinity for O2 and enhances their O2 loading! [LEFTWARD SHIFT]
B: High-altitude natives have HIGHER [oxygen carrying capacity] likely due to polycythemia which develops after long exposures to High-altitudes. Erythropoietin from Kidneys stimulate Bone Marrow to make RBC and this normalizes O2 concentration! This process takes longer so this is why acclimatization takes a while
B2: Acclimatization also includes LARGER LUNGS which develop in from-birth High-altitude natives and gives them more alveolar surface area
C: Even with this..at Higher altitudes [Oxygen diffusion] across alveolar-capillary membrane is limited! and there will be a larger [AaDO2]. Exercise and Lung dz that thickens alveoli membrane will Worsen this!
D: HYPERventilation ALSO DEC PaCO2 in Alveoli so that partial pressure of O2 will INC 5-Fold in Alveoli. Inspite of lower inspired PO2, [High-Altitude Natives] have mixed venous blood that is only 7 mmHg lower than us!
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A: As a person ASCENDS from earth’s surface [Pulmonary HTN] INCREASES due to [hypoxic pulmonary vasoconstriction] which occurs when ALVEOLAR PaO2 is low. This can lead to [PULMONARY EDEMA]
B:[low-landers] can develop [Cheynes-Stokes Respiration] with apneic periods of 15 sec long during first few days of high altitude
C1: [Acute Mountain Sickness] = Sx lowlanders get during first 6-12 hours of being in High altitudes. Sx include: [HA / fatigue / nausea/ loss of appetite and insomnia] . Sx are SEVERE on 2nd/3rd day BUT Acclimatization completes by 5th day for improvement.
C2: [AMS] is Typically associated with Pulmonary, Cerebral and Peripheral Edema—>Fluid imbalance! Younger people are more at risk and sometimes the only tx is to return to low altitude.
- *AMS might be caused by
1. hypoxia paired with
2. hypocapnia,
3. [Fluid imbalance] and
4. [respiratory alkalosis]
D: [Pulmonary Edema] from AMS may be caused by pulmonary vasoconstriction OR INC permeability of pulmonary capillaries at High altitudes. Best tx = rapid descent & O2 therapy
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A: [Monge’s Chronic Mountain Sickness] is seen in LONG-TERM resident of High-Atltitude and is characterized by somnolence, loss of mental acuity, [marked polycythemia] and SEVERE HYPOXEMIA—->cyanotic appearance and HIGH hematocrit! R Ventricular Hypertrophy is also common
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A: For every 33 Feet you travel UNDER you INC barometric pressure by [1 atm]. So at 33 Feet below surface = [2 atm]
B: As a Diver goes BELOW surface, the lung is COMPRESSED according to [Boyle’s law]: P1V1 = P2V2] where
P1= Pressure prior to Dive
V1= Lung VOLUME prior to Dive
P2= Pressure created in Diver's Lungs at specific water depth (Will INC) V2= Resulting Lung Volume at that water depth (will DEC)
C: During Diving A [CO2-O2 paradox] can occur
C1: As the subject Dives DOWNWARD CO2 will move from Alveoli BACKWARDS into [Pulmonary capillary blood] because [Pulmonary Alveoli CO2] becomes greater than [pulmonary venous CO2]
C1: AS SUBJECT RETURNS UPWARD TO SURFACE, alveolar air expands and this causes PaCO2 to DEC. —>CO2 will now from [Pulmonary capillary blood] into Alveoli again like normal
D: Same thing happens to O2 during descent but when ASCENDING if [Pulmonary venous O2] becomes GREATER than the [alveolar PaO2] than Oxygen will start to move backwards into the Alveoli during Ascent = [O2 Paradox] = [hypoxia of ascent]
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A: INC Atltitude = DEC Barometric pressure AND [PaO2] of inspired air
B: Mount Everest (at 29029 ft) has a Barometric pressure of 255 mmHg and PO2 of 54 mmHg {.21 x 255}.
B2: The PiO2(O2 of actual INSPIRED AIR) = 44 mmHg because you have to subtract 47 mmHg {.21 x (255-47)} of water vapor pressure.
C: People who haven’t acclimatized will be unconscious in 45 seconds and DEAD IN 4-6 MINUTES. [High-Altitude Natives] typically have PaCO2 of 33 mmHg (vs. 40)]
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A: During Breath hold diving challenges ability to survive depends on
1) duration of breath hold
2) ability to withstand water pressure
3) exposures to high gas pressures
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B: Diving response is detectable in all air breathing vertebrates and is activated by APNEA. It Includes
1. Peripheral vasoconstriction from sympathetics to shunt blood to vital organs
2. Initial HTN
3. Vagally-induced BRADYCARDIA and [Cardiac Output] DEC
4. Splenic contraction—>enhances Hgb concentration in blood
PREVENTABLE DIVING MISHAPS
C: Hypoxic [Loss of Consciousness] occurs at PO2 of 20-25 mmHg. Divers will die sometimes because HYPERventilating before the dive DEC [CO2 Drive-To-Breath] and can result in LOC without warning if there’s a weak Voluntary override of this inhalation impairment
D: During Ascent hypoxia may occur when DEC in water & gas pressure also causes DEC PO2 within the Alveoli —->[O2 paradox] where O2 travels BACKWARDS from [pulm. capillaries] into Alveoli because there’s more O2 in [pulm. capillaries] at tht point—>[pulm capillary PaO2 of less than 25 mmHg] during ascent —> [Hypoxia of Ascent]
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A: It’s bad to not eat well before Diving due to [Carbohydrate depletion]! —> you’ll have less CO2 production and use more O2 Faster! This will DEC ur urge to inhale and if Diver doesn’t voluntarily override inhalation impairment (like if they’re passed out from hypoxia) —> DEATH from DROWNING!
B: [Barotrauma of Descent]
1.Diver inhales to TLC and [Vital Capacity] represents part of lung that can be used to pressure equilibrate. Blood is translocated from [Extrathoracic blood volume] —> [intrathroacic blood volume] in the vascular bed & heart.
- At Greater depth limits of compression of chest wall and stretching of diaphragm is reached beauty can still compress lung air and maintain pressure equilibrium by redistributing a large amount of blood from ETBV–>ITBV.
- With EVEN FURTHER descent, underpressure develops in the lung relative to ambient water and therefore leads to extravasation of fluid (pulm edema) from ITBV and bleeding due to capillary rupture
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A: [Decompression Sickness] occurs when Nitrogen gas reaches its solubility during ASCENT TOO FAST (during RAPID ASCENT) and is transported from tissues as BUBBLES instead of liquid-soluble form. –>depending on where bubble formation occurs this can cause
- The Bends = Joint Pain
- The Chokes = Chest pain and cough
- Paresthesia
- Vertigo / nausea / fatigue / LOC
- Skin Rash
- Paralysis / Abd pain / Bladder Dysfunction
B: [Decompression Sickness] can be treated with [Hyperbaric Oxygenation]
C: [Inert Gas Narcosis] = at [6 x atmospheric pressure/50 m] under water Nitrogen causes euphoria! And at even deeper levels —> [Loss of coordination] or Coma!
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A: Oxygen Toxicity can occur and is damaging to both Lung and CNS. At Higher Barometric pressures you have a higher PO2 inhaled and if [FiO2 > 0.5] in lungs =
- endothelial cell of pulmonary capillary damage
- Substernal pain during breathing
- impaired gas exchange
- DEC in Vital Capacity
- Atelectasis
- Retrolental fibroplasia in premature infants
A2: In the CNS, it'll cause: Confusion, seizures and coma at 4 atm in 30 minutes but otherwise -vomiting -dizziness -vision/hearing impairment
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A: Dissolved Oxygen is a SMALL % of total O2 & measured clinically as PaO2 (via blood gas analysis). Amount dissolved is dependent on [Henry’s Law] –> Concentration of gas in solution is proportional and equal to partial pressure above gas x [constant] : {Concentration = P x [constant] }
C: Adult Hgb has 4 polypeptide chains (2 alpha & 2 beta) with 4 heme groups that each bind 1 O2 molecule.
- Adult Hgb is 50% Saturated with O2 at PO2 of 27 mmHg
- Hgb is 90% Saturated with O2 at PO2 of 60 mmHg and
- Hgb is 98% Saturated at PO2 of 100 mmHg
D: AT PaO2 LESS than 60 mmHg, small changes in pressure—>LARGE RELEASES of O2 from Hgb = DANGER
E: O2 saturation = [Amount O2 combined with Hgb] / [O2 capacity]
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A: RIGHTWARD Bohr shift {i.e. exercise} INCREASES P50 (point at which Hgb is 50% saturated) = Hgb needs a higher PO2 in order to be 50% saturated because it’s unloading faster/Affinity has DECREASED!
B: RIGHTWARD Bohr shift causes : ºINC Temp ºINC PCO2 ºINC [2,3 DPG] ºINC H+
(is the exact opposite for leftward bohr shift causes)
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A: [Carbon DIOXIDE] is carried in the blood 3 ways
1st) As Bicarbonate in [RBC:MOST COMMON vs plasma]
2nd) As [CarbaminoHgB compound] with proteins
3rd) Dissolved in plasma
B: Dissolved CO2 is measured clinically as PaCO2 (via blood gas analysis). Amount dissolved is dependent on [Henry’s Law] –> Concentration of gas in solution is proportional and EQUAL to partial pressure above gas x [constant] : {Concentration = P x [constant] }
C: Per 1 mmHg of PCO2 there is [0.067 mL CO2/100 mL of blood] which 20 x MORE THAN O2! IN Plasma most CO2 stays as CO2 since there is a slow conversion to carbonic acid. In RBC, [CARBONIC ANHYDRASE] SPEEDS UP CONVERSION AND INC HCO3
D: Most important protein is globin of hemoglobin—->Caraminohemoglobin
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A: [Chloride Shift] = occurs when intracellular H+ and HCO3 INC so HCO3 diffuses Out IN EXCHANGE for Cl- diffusing IN to maintain electrical neutrality. This allows us to obtain Plasma Buffers when we need them!
C: [Haldane Shift Effect]= when Hgb is bound to Oxygen it releases CO2 more easily. This Is great when Hgb picks up O2 in Alveoli becuz this effect will help to release CO2 to alveoli. INC PO2 shifts [CO2 dissociation curve] to the RIGHT and causes Hgb affinity for CO2 to DECREASE!
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D: Opposite of [Haldane Shift Effect] is the [BOHR SHIFT] in which HIGH PCO2 environment will actually DEC Hgb affinity for OXYGEN and help to release O2 in the tissues!
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A: [Tissue hypoxia] = when there is insufficient O2 available to maintain adequate aerobic metabolism. THERE ARE 4 TYPES. º[Hypoxic Hypoxia] º[Stagnate Circulatory Hypoxia] º[Anemic Hypemic hypoxia] º[Histotoxic Hypoxia]
B: In [Hypoxic Hypoxia], DEC PaO2 leads to insufficient O2 delivery to tissues and often CYANOSIS due to INC DeOxyhemoglobin (at least 6 g/DL of DOxyHGb required).
C: [Hypoxic Hypoxia] is common during Suffocation, COPD and [Pulmonary Fibrosis]
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A: [Tissue hypoxia] = when there is insufficient O2 available to maintain aerobic metabolism. THERE ARE 4 TYPES.
º[Hypoxic Hypoxia]
º[Stagnate Circulatory Hypoxia]
º[Anemic Hypemic hypoxia]
º[Histotoxic Hypoxia]
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B: [Stagnate Circulatory Hypoxia] = DEC Blood FLOW to tissues such as in [Vascular Dz] and [Cardiac insufficiency]
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C: [Anemic Hypemic Hypoxia] = Inability of Blood To CARRY OXYGEN like in anemia or [Carbon monoxide poisoning]
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D: [Histotoxic Hypoxia] = Inability of Tissue to USE delivered Oxygen. Occurs in [Cyanide or Sodium Azide poisoning]
E: [Oxygen content] and [Blood Flow] are the 2 factors that Determine Oxygen delivery to Tissues!
