Chapter 6 Flashcards
(160 cards)
1
Q
RBC
A
Made by bone marrow, Adult Male: 4.7-6.1 million RBC per microliter, Adult Female 4.2-5.4 Million/ uL
2
Q
Anemia
A
low RBC or low HCT (hematocrit)
3
Q
Polycythemia
A
high RBC, Altitude may increase hgb, when PaO2 decreases - hgb increases
4
Q
Hematocrit
A
Percentage of RBCs in blood volume
5
Q
Hematocrit normal ranges
A
Adult males 42%-52%, adult females 37-47%
6
Q
Polycethymia
A
high hematocrit
7
Q
pH normal ranges
A
arterial 7.35-7.45, venous 7.30-7.40
8
Q
PCO2 normal ranges
A
Arterial 35-45 mmHg, Venous 42-48mmHg!!
9
Q
HCO2
A
Arterial 22-28 mEq/L, Venous 24-30 mEq/L
10
Q
PO2
A
arterial 80-100 mmHg, venous 35-45 mmHg!!
11
Q
Hemoglobin
A
Oxygen carrying component of RBC’s (report as weight / 100ml of blood
12
Q
Hemoglobin
A
Oxygen carrying component of RBC’s (report as weight / 100ml of blood.) about 280 milion hgb, pigmented portion of RBC’s (red, significant in SaO2 measurement)
13
Q
each RBC contains how many heme groups
A
4 that can each carry 1 molecule of O2
14
Q
What combines with the O2
A
FE++ contains about 280 milion hgb, pigmented portion of RBC’s (red, significant in SaO2 measurement)
15
Q
What combines with the O2
A
FE++ contains
16
Q
Each gram of hbg can carry how much O2
A
1.34 = 20.1 vol %O2
17
Q
PaO2 of 100=
A
0.3 mL, 100x0.003= 0.3mL
18
Q
Oxyhemoglobin Dissociation Curve
A
percent of O2 attached to hbg in reference to PaO2 and O2 content
19
Q
Steep Portion of curve
A
PaO2 of 40-70 mmHg
20
Q
Upper Plateau of curve
A
> 70 mmHg
21
Q
Lower Plateau of curve
A
anaerobic, in deep do-do!
22
Q
Reference point on curve
A
is PaO2 at 50% hemoglobin saturation (P50), done by tonometery, not clinically practical
23
Q
Right shifts
A
O2 readily releases
24
Q
left shift
A
impairs O2 release
25
Oxygenation
1. O2 Transport- dependant on O2 content (CaO2), cardiac output (CO or QT), Oxyhemoglobin dissociation curve 2. PaO2 normally drawn from? 3.PAO2 4. SaO2 5. A-aDO2 6. PaO2/PAO2 ratio 7. PaO2/FiO2 ratio
26
PaO2 drawn from
Measured from ABG sample, normal adult range 80-100mmHg, Clinically acceptable to keep in 60-80% range, higher then 125mmHg can reduce blood flow to brain and kidneys, O2 toxicity,
27
Higher than what mmHg PaO2 can cause what damage
125mmHg can reduce blood flow to brain and kidneys
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PAO2 equation
(Pb-47) x FiO2 - (PaCO2/ 0.8), Partial pressure of alveolar O2
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SaO2
Functional (oximetry), fractional (includes CoHbg, MetHbg, ect), Carbon Monoxide affinity for hbg is 210x that of O2
30
A-aDO2 or P(A-a)O2
indicates gas exchange efficiency
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PaO2/PAO2 ratio
helpful in predicting FiO2 for desired PaO2
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PaO2/FiO2 ratio
Ratio> then 200 indicate an ability to reduce FiO2 or PEEP
33
Tissue Oxygenation
1. Oxygen Content % 2. Arterial-Venous Oxygen Content Difference 3. Shunt Equation 4. Oxygen Deliver 5. Oxygen Consumption 6. Oxygen Consumption index 7. Oxygen extraction ratio
34
Oxygen Content
Report as %. -Arterial O2 Content (CaO2) -Venous O2 Content (CvO2) - Pulmonary Capillary O2 Content (CcO2)
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Arterial O2 Content (CaO2)
CaO2= (Hbg x 1.34 x SaO2) + (PaO2 x 0.003). Normal is about 20%. Hbg plays the biggest role in O2 number
36
Venous O2 content (CvO2)
CvO2= (Hbg x 1.34 x SvO2) + (PvO2 x 0.003). Normal is about 15%. Blood obtained from pulmonary artery. PaO2 = 45%, Sat = 75%, Tissue use = 5%
37
Pulmonary Capillary O2 content (CcO2)
CcO2= (Hbg x 1.34) + (PAO2 x 0.003) assuming its 100% saturated
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Arterial- Venous Oxygen Content difference
amount of blood used by cells. CaO2-CvO2. Normal is about 5% (or apporoximately 250mL of O2)
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C(a-v)O2=
CaO2 (left heart)- CvO2 (back to heart)
40
Shunt Equation
Qs/Qt= CcO2-CaO2/ CcO2 - CvO2. Calculates amount of blood that goes through lungs without picking up O2. Normal Range is below 10%. 20-30% Critical. >30% life threatening
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Diffusion
from alveoli to capillary, hbg picks up O2 to tissue, creating CO2
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1st sign of hypoxia
increase HR
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Hemoglobin increases to
help O2 Sats (transfussion)
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Oxygen Delivery
Amount of O2 delivered peripheral tissues (capillaries/cells), CO x CaO2 x 10. normal range is 550-650 ml/min/m3. decreased with low PaO2, Hbg, or cardiac output. normal response is increase in CO or increase in Hbg (exercise, high altitude)
45
Oxygen consumption
amount of O2 used by cells. VO2= COx (CaO2-CvO2) x 10. normal range is 2.86-4.29 ml/min/kg
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Oxygen Consumption Index
VO2/BSA (body surface area). Clinically more accurate in determining O2 consumption
47
Oxygen Extraction Ratio (O2ER)
Amount of O2 Extracted by cells vs. amount avaliable. O2ER= CaO2 -CvO2/ CaO2. report as %. Normal range is approx 25%
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Tissue Hypoxia
Hypoxic Hypoxia, Anemic Hypoxia, Circulatory Hypoxia, Histotoic Hypoxia
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Oxygen is carried in two forms
Dissolved in plasma, bound to hbg
50
Dissolved in plasma
Gaseous form of O2 in the plasma, moves around freely, partial pressure is how its measured, PaO2, Dependent on the partial pressure available and temp of blood.
51
how many ml of O2 in 100ml blood per 1mmhg
0.003. Very small amount of total oxygen content is in the form of dissolved
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Bound with hemoglobin
Oxygen diffuses into blood and combines with hbg.
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normal hbg
12-16 g/100ml
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Each heme/iron group can hold
4 oxygen molecules, when all 4 are full its 100% saturated
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Oxyhemoglobin=
hemoglobin with oxygen bound
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Deoxyhemoglobin =
hemoglbin without oxygen (reduced hemoglobin)
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Each g% carries how many ml of O2
1.34 ml. so to calculate amount of oxygen carried by hbg (1.34 x g%hbg) saturation %
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Total Oxygen Content equation
CaO2 = (1.34 x Hbg x O2 sat) + (PaO2 x 0.003)
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Oxygen Dissociation Curve y axis
hbg saturation (vertical)
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Curve X axis (horizontal)
PaO2
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SaO2 over what are in the 90% or greater saturation levels
60mmHg
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Curve Safety levels
PaO2 60, SaO2 90. below these levels the O2 content falls rapidly in relation to PaO2
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Anemic Hypoxia
hbg= 8.7
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Right Shift >
Decrease in pH, increase in Temp-CO2- 2,3 DBG
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Left Shift >
Increase in pH- Carbon Monoxide (Carboxyhemoglobin), Decrease in Temp-2,3 DPG
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A shift to the right...
enhances the unloading of O2 at the cellular level. Doesnt pick up at lungs, diffuses into tissue
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a shift to the left...
facilitates the loading of O2 onto the hbg in the lungs (clinically harmful). Picks up at lungs, holds at tissue
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DO2=
CO x (CaO2 x 10). delivery decreases with decrease in any one of the above
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arterial to venous difference
the difference in the O2 of the blood before and after it passes the cells
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normal CaO2 is
20 Vol%
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Normal CvO2 is
15 Vol%
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so what is extracted by cells (50ml/l blood)
5 vol%
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febrile -> increase temp -> increase metabolism -> increase CO2 -> decrease pH =
Right shift
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Oxygen Consumption
Amount of O2 extracted by the peripheral tissue in 1 min
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Over one minute 250ml
5L/min x 5 vol% x 10 (normal)
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VO2 Equation
VO2 = CO [(CaO2-CvO2) x 10). normal 250 ml
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What causes O2 consumption to go up
Exercise, seizures, shivering, hyperthermia, body size
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What causes O2 consumption to go down
Skeletal Muscle Relaxation - induced by drugs, Peripheral Shunting- sepsis, trauma, Certain Poisons- cyanide, Hypothermia
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Cyanide
Lack of O2 to tissues- brain)
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Oxygen Extraction Ratio
The Percent of O2 taken by cells. amount extracted/ total amount available. 5 vol%/ 20 vol% = 25%= O2ER
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Normal O2ER
25%
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the higher the oxygen consumption the
higher the ratio
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Mixed Venous Oxygen Saturation
SvO2 monitoring used to monitor CO. Must have stable saturations and hemoglobin levels
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If saturations and hemoglobin levels are stable
a decrease in SvO2, CvO2, or PvO2 means an increase in O2 consumption or decrease in CO
85
True Shunting
Doesnt respond to O2...Anatomic Shunts, Capillary shunts, absolute shunting
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Anatomic Shunts norm
2-5%
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Anatomic shunt veins
Bronchial, pleural, and thesbesian veins. Veins that feed the pulmonary system
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Anatomic shunt abnormalities
CHF, Intrapulmonary Fistula, Vascular Lung Tumors
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Capillary Shunts
Blood that goes through the lungs without exchanging gas
90
Capillary shunt examples
alveolar collapse/atelectasis, Alveolar fluid accumulation, alveolar consolidation
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Absolute shunting
is refractory to oxygen therapy
92
absolute shunting- increasing the FiO2 will
not increase the saturation in the blood that does come into contact with alveoli because it is already fully saturated.
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Alveolar collapse or atelectasis example
CHF
94
Alveolar Consolidation example
pneumonia
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Shunt-Like effect (relative shunt)
Responds to O2. Perfusion is in excess of ventilation. easily corrected by O2 therapy
96
Shunt like effect caused by
hypoventilation, uneven distribution of ventilation, Alveolar- capillary diffusion defects.
97
During shunt like effect the alveoli are in contact with blood so
an increase in FiO2 will cause more O2 in blood.
98
Alvolar-capillary diffusion defects
lose surface area
99
Uneven distrubution of ventilation examples
chronic emphysema, bronchitis, asthma
100
Normal Shunt %
10% or less
101
Abnormal but usually not clinical significant shunt %
10-20%
102
shunt that needs aggressive cardiopulmonary support (life threatening) %
30%
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Tissue Hypoxia
1. Hypoxic Hypoxia 2. Anemic Hypoxia 3. Circulatory Hypoxia 4. Histotoxic Hypoxia
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Hypoxic Hypoxia
Inadequate O2 at the tissue cells caused by low arterial O2 tension (Low PAO2), Diffusion Impairment, Ventilation/ Perfusion mismatch (shunt-like effect), Pulmonary shunting
105
Hypoxic hypoxia/ Low PAO2 caused by
hypoventilation, high altitude, FiO2 less than 21%
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Hypoxemia
low oxygen in the blood (arterial blood tension)
107
Hypoxia
low oxygen in tissue cells
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Anemic Hypoxia
"think hbg" ..Low RBC=Low Hbg, 8.7, CaO2 low, PaO2 is norm, but the O2-carrying capacity of the hbg is inadequate. Decreased hbg concentration= anemia, hemorrhage. abnormal hbg= carboxyhbg, methbg
109
Circulatory Hypoxia
Stagnant hypoxia or hypoperfusion, Slow blood flow to cells/ decrease CO. thus O2 is not adequate to meet tissue needs. caused by slow or stagnant (pooling) peripheral blood flow and arterial-venous shunts
110
Histotoxic Hypoxia
impaired ability of the tissue cells to metabolized O2- cells cannot use O2, Cyanide poisoning, Norm blood values, Increase CvO2 because cells not using O2
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Cyanosis
Central and Peripheral cynosis (blood gas)
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Central Cyanosis
5 g% reduced hemoglobin (un-oxygenated), causes blue-grey discoloration of the mucus memranes and nailbeds
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Peripheral Cyanosis (acrocyanosis)
Poor perfusion (cold hands) can cause the nailbeds to look cyanotic
114
Polycythemia
adaptive mechanism designed to increase the O2 carrying capacity of the blood
115
Polycythemia does what
increase RBC that means more Hbg (and Hematocrit) to carry more O2
116
What causes polycythemia
chronic hypoxemia (COPD, CHF, and high altitude), increased viscosity of blood with increased work to the heart
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Carbon Monoxide Transport
Carried 6 ways
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Cells consume about how much O2 and produce how much CO2
Cells consume about 250mL of O2 and produce 200mL of CO2
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CO2 transport, plasma-
1% attached to carbamino protein, 5% forms bicarbonate, 5% dissolved (whats measured in an ABG)
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CO2 transport, RBC-
5% dissolved in cell intracellular fluid, 21% combines with Hbg, 63% forms bicarbonate intracellular. Forms faster in cell due to carbonic anhydrase
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CO2 does what to move out CO2
equalizes in reverse at alveoli
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Haldane Effect
More oxygen less CO2, this is what helps CO2 off load at lungs and on load at cells
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H+ + HCO3 ->
H2CO3 -> H20 + CO2
124
H+ does what to pH
goes down, more acidic
125
Hypoxemia (Norm, mild, moderate, severe)
Norm 80-100 mmHg, Mild 60-80 mmHg, Moderate 40-80 mmHg, Severe <40mmHg
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O2 carry
50ml
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question 30
a
128
Importance of starting CPR within the first 4 min
Total oxygen delivery (DO2)- the O2 supply system equation- illustrates that about 1000ml of O2 are transported to the tissue cells each min.. VO2- the O2 demand equation- illustrates that of this 1000ml, about 250ml of O2 are consumed by the tissue cells in the course of the metabolic process. 4 min= total 1000ml O2 (250ml a min)
129
What happens following cardiac arrest
immediate stoppage of the O2 delivery system- leads to anaerobic metabolism and lactic acidosis, the sudden stoppage of transporting the tissue CO2 to the lungs for eliminatin- rapid accumulation of CO2, the abrupt drop in pH.
130
Anatomic shunt exists when
blood frows from the right side of the heart to the left side without coming in contact with an alveolus for gas exchange. Norm 3%.
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CHF
certain congenital defects permit blood flow directly from the right side of the heart to the left side without going through the alveolar capillary system for gas exchange.
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Intrapulmonary Fistula in anatomic shunting
a right to left flow of pulm blood does not pass through the alveolar capillary system.
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Vascular Lung tumors
Some lung tumors can become very vascular. some permit pulmonary arterial blood to move through the tumor mass and into the pulm veins without passing through the alveolar capillary system
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Capillary shunt is commonly caused by
1. alveolar collapse or atelectasis 2. alveolar fluid accumulation or 3. alveolar consolidation
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The sum of the anatomic shunt and capillary shunt is referred to as the
absolute or true shunt
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Clinically patients with absolute shunting respond
poorly to O2 therapy, because alveolar oxygen doesnt come in contact with the shunted blood.
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Absolute shunting is what to O2 therapy
refractory, that is , the reduced arterial O2 level produced by this form of pulm shunting cannot be treated simply by increasing the concentration of inspired O2
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When pulmonary capillary perfusion is in excess of alveolar ventilation a what is said to exist
relative shunt or shunt like effect.
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common causes of relative shunt include
1. hypoventilation 2. Ventilation/ perfusion mismatch (chronic emphysema, bronchitis, asthma, secretions) and 3. alveolar-capillary diffusion defects (alveolar fibrosis or alveolar edema)
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End result of pulmonary shunting is
venous admixture
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venous admixture is the
mixing of shunted, non-reoxygenated blood with reoxygenated blood distal to the alveoli. losing oxygen molecules
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Venous admixture continues until
1. the PO2 throughout all the plasma of the newly mixed blood is in equillibrium and 2. all of the hbg molecules carry the same number of O2 molecules. resulting in reduced PaO2 and CaO2 returning to the left side of the heart
143
Hypoxemia is frequently associated with
hypoxia
144
Hypoxia is characterized by
tachycardia, hypertension, peripheral constriction, dizziness, and mental confusion
145
Hypoventilation caused by
chronic obstructive pulm disease, central nervous system depressants, head trauma, and neuromuscular disorders
146
High altitude can cause what to develop
hypoxic hypoxia
147
Diffusion impairment examples
Interstitual fibrosis, lung disease, pulmonary edema, pneumonconiosis
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In plasma
carbamino compound (bound to protein), Bicarbonate, Dissolved CO2
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In RBC
dissolved CO2, Carbamino-Hbg, Bicarbonate
150
Dissolved CO2 in the intracellular fluid of the RBC accounts for what percent of the total CO2 released at the lungs
5%
151
Carbamino-hbg
21% of the CO2 combined with hemoglobin
152
When the blood pH decreases, the oxyhemoglobin dissociation curve shifts
right and the P50 increases
153
When shunted, non reoxygenated blood mixes with reoxygenated blood distal to the alveoli (venous admixture) the
PO2 of the nonreoxygenated blood increases and the CaO2 of the reoxygenated blood decreases
154
Normal arterial HCO3 range is
22-28 mEq/L
155
The normal calculated anatomic shunt is about
2-5 percent
156
in which of the following types of hypoxia is the O2 pressure of the arterial blood (PaO2) usually normal
Anemic hypoxia, circulatory hypoxia, histotoxic hypoxia
157
If the patient normally has 12g% hbg, cyanosis will likely appear when
7g% hbg is saturated with O2
158
The advantages of polycythemia begin to be offest by the increased blood viscosity when the hematocrit reaches about
55-60 Percent
159
Assuming everything else remains the same, when an indiv CO decreases the
C(a-v)O2 increases and the SVO2 decreases
160
Under norm conditions the O2ER is about
25 %
