Q=Cardiac output ave
CaO2= total content O2 bound to Hgb.
DO2=amt of o2 delivered each min.
O2ER Extraction ratio
CVO2 central venous= mixed oxygenation= mixed venous 02sats
Q=4-8l/min. Ave adult 5.5/m
CaO2=16-22ml/02/dL every min.
D02-ave adult is 550 ml
O2ER- 3ml/kg/min.
Minute Ventilation average
4-8lt/min (Ave adult 5l/min)
V/Q mismatch
V=ventilation/ Q= co
Ventilation issue not moving gas from alveoli to capillaries. S&s pt hypoxic,tachypnic,COPD,asthma,pna uncompensated resp alkalosis .try PT on o2 Shunting block. Qshunt p.e. or no pump tension pnuemo,co issues
O2-Hgb Disassociation curve
Relationship between partial pressure of O2(Pao2)& the saturation of hgb w o2(SaO2) . Shift to right= still aerobic, shift to left hgb holds onto o2 and doesn’t release it to tissues=anaerobic
LEFT SHIFT=LOWER (increased affinity to bind o2=unloading more difficult.)
Where: lungs
Causes: Decreased CO2,
Dec. Acidosis(inc. ph/alkalosis, Dec. 2,3DPG, Dec temp. Fetal hemoglobin(want baby to have lots o2)
Can have an excellent SaO2(&spo2) in L shift but a poor PaO2( tissue Hypoxia resp alkalosis
R shift can have lower than normal SaO2&spo2 but normal pao2. Hgb has less affinity for O2= unload easier(more available to use)
RIGHT SHIFT=RAISED
WHERE: muscles,tissue,placenta
Increased CO2
Acidosis (pH lo)
2,3Dpg
Temperature
Hypoxemia
Insufficient oxygenation of the blood will lead to hypoxic state. =Anaerobic metabolism
Bohr Effect
When CO2 rises or pH drops, Hgb releases more O2 to tissues. This will cause a High PaO2 and a lowe SaO2
“RAISED TEMP
ACID
2,3-DPG
PaO2
Right Shift on O2 diss curve
LOW TEMP
ACID
2,3-DPG
PaO2
Left Shift
Haldane Effect
Refers to the effect of O2 on CO2&H+ binding to Hgb. As O2 binds w Hgb, it causes a state of cooperativity, causing the release of CO2&H+,
Oxyhgb curve graph
Decrease by 4 for every drop in sats for first 10, then decrease by 1.5 for every drop in sats.
ie:
Sats 86% what’s your PAo2?
100-40-(1.5 x4 )= 54
Calculation to identify the content of Arterial O2(CaO2 total content of O2 bound to Hgb (16-22ml/O2/dL) every minute (amt of O2 delivered to bodya tissue every min)
D02=Q x CaO2
DO2 is amt O2 del each min Ave 550
Q=C.O. (SV, preload,afterld contract)
CaO2=total amt of O2 bound to Hgb 16-22ml/O2/dL every minute
CaO2=Hgb x Sao2 x 1.34
(1.34 fixed #)= O2 carrying capacity
i.e. sats=98%xHgb 10 x 1.34= 13.3ml/O2/dl
SaO2
SpO2
SvO2
Scvo2
Sao2- the Amt of Hgb in blood that is saturated w o2
Spo2-(pulse ox) -the % of Hgb in blood that is carrying O2 93-98%
Svo2- pulm art line mixed venous normal healthy adult 60-80%(if we are 80 we are only using 20% of our 02 so have leftovers
Scvo2- central venous mixed normal is 70-80% (5-8%higher than SvO2)
PO2-
Pao2
PAo2
Po2- partial pressure of O2 in given environment 80-100mmhg(Daltons Law)
Pao2- partial pressure of o2 dissolved in blood 80-100mmhg
PAo2- partial Alveolar pp of O2 80-100mmhg
Aerobic Respirations
Glycolysis> Krebs cycle>
Oxidative phosphorylation (Net 36 ATP)
- normal CO2 production (150ml/day)
Krebs cyclye
Glycolysis (glucose to pyruvate=2atp) NADH, FADH(B12) RESULTS IN CO2 AND NET 36ATP
Krebs cycle but no oxidative phosphorylation step. Excess CO2 production, Lactate productions, ethonal production. Met only 2 Atp
Anaerobic resperations
Cyanide poisening
It blocks the oxidative phosphorylation, pt is well oxygenated but cell death is happening= pt acidemia.
Treat hydroxocobalmin which is a form of vitamin b-12
I:E ratio for intubated asthmatic in resp failure
1:4
OI oxygen index formula
Fio2 x 100 x map/PaO2
In neo w PPHN IF > 25= severe hypoxemic resp failure
