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CFRN > Oxygen Dynamics > Flashcards

Oxygen Dynamics Flashcards

1
Q

Minute ventilation

A

minute ventilation = 4-8 L/min (~5/min ave)
cardiac output = 4-8L/min (~5.5/min ave)
V = minute ventilation
Q = cardiac output.
Ideally V = Q
V/Q mismatch is a problem

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2
Q

V/Q Mismatch

A

Venous admixture: minute ventilation issue - not moving gas across alveolar membrane
Signs = tachypnea,

Areas with high V/Q ratio have low perfusion, whereas areas with low V/Q ratio have high perfusion.

Will respond to O2 therapy

V/Q mismatch is most common cause of hypoxemia (PNA, PE, COPD, fibrosis, asthma)

Deadspace ventilation: no perfusion (heart problem)
ie PE, cariogenic shock (poor circulation). In PE, blood flow to an area of lungs is blocked (no perfusion = high V/Q), meaning low O2 saturation blood flow increases to all other areas. As a result, everywhere else has a low V/Q (decreased O2 in blood).

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3
Q

Ventilation issues (examples)

A

COPD - inspiratory and expiratory problem
Asthma - similar to copd. Narrowed, diseased airways. Need ventilation help.

PNA - Trouble getting O2 to red blood cell (need oxygenation help)
ARDS - need oxygenation help, getting O2 where it needs to go
Pulmonary edema -

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4
Q

Cardiac Output issues (perfusion issues)

A

Trauma - deadspace ventilation issues
Tension Pneumo -
Cardiac tamponade -
Cardiogenic shock -

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5
Q

Tension Pneumothorax

A

Air enters pleural space and can’t leave
Increased pressure on lungs, trachea, heart
Decreased cardiac output due to collapse of blood vessels that drain into the heart
Decreased cardiac output leads to decreased perfusion.
Chest pain, sob, tachypnea, bulging neck vein

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6
Q

Cardiac Tamponade

A

blood, pus, or air builds up in pericardial space, increasing pressure and compressing the heart’s chambers
the increased pressure limits the amount of blood the heart can pump, thereby leading to decreased perfusion
sob, chest pain, pale skin

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7
Q

Cardiogenic shock

A

decreased cardiac output and therefore decreased perfusion because of hypotension.
chest pain/pressure, rapid/weak pulse, sob, pale cool skin

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8
Q

venous admixture

A

inability to move gas across alveolar membrane
(not ventilating properly)

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9
Q

shunt

A

where blood flows past alveoli with no gas exchange occurring
PaO2 falls, PaCO2 falls - hyperventilation
Will respond to O2 therapy
Main causes of shunting are: atelectasis (collapsed alveoli), pulmonary edema, small airway closure

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10
Q

respiratory alkalosis

A

caused by low CO2 (hyperventilating)
high pH, over 7.45 (abg test)
PaCO2 (resp system) below 35 mm Hg (abg test)
HCO3 (bicarb - metabolic system)
…if HCO3 is normal (22-26), metabolic system is not trying to compensate.
if HCO3 is under 22, metabolic system is trying to compensate
Will respond to O2 therapy

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11
Q

respiratory acidosis

A

When the body can’t remove enough CO2 through breathing. High CO2 = acid buildup
low pH (under 7.35) (abg test)
PCO2 above 45 (abg test)
HCO3 over 30

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12
Q

Q (cardiac output)

A

4-8 LPM range
5.5-6 LPM average for adults
SV x HR (SV = stroke volume)

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13
Q

Deadspace ventilation

A

no perfusion
Could be small part of lungs
Could be complete block of blood to lungs (ie saddle embolus)
Could be due to cariogenic shock (bradycardia or left ventricle not working due to high external pressure and vascular resistance)
Tension pneumo
cardiac tamponade

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14
Q

Aerobic respiration

A

Process in which food glucose is converted to energy in the presence of oxygen
Biproducts = CO2 and H2O
Production of ATP
Lack of glucose or O2 alters ATP production, with lactic acid as byproduct
peds and elderly have limited glycogen stores
(Oxygen dynamics part 2)

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15
Q

Glycolysis

A

1st stage of ATP production
Conversion of glucose to pyruvate
+2 ATP net change
Sympathetic NS stimulates B1 (heart rate) and B2 receptors (skeletal muscles, liver, lungs - bronchodilation).
Release of glycogen
(Oxygen dynamics part 2)

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16
Q

Lactate

A

Indication of STRESS
Lactate is a byproduct of glycolysis
Elevated lactate in the absence of activity is an indication of stress
Formed with and without oxygen (aerobic and anaerobic respiration)
NOT and indication of tissue hypoxia
(Oxygen dynamics part 2)

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17
Q

CO2

A

biproduct of cellular respiration
generated during Krebs cycle
(6 CO2 per 2 pyruvates moving into Krebs cycle)
we make about 150L CO2 daily
(Oxygen dynamics part 3)

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18
Q

Niacin

A

NAD+
bind with hydrogen ions to become NAD+H (+6 during Krebs cycle)
(Oxygen dynamics part 3)

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19
Q

Riboflavin

A

FAD+
Bind with hydrogen ions to become FADH2
(+2 during Krebs cycle)
(Oxygen dynamics part 3)

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20
Q

Krebs cycle

A

purpose: transport energy source that will be used to generate ATP (hydrogen)
(Oxygen dynamics part 3)

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21
Q

Hydrogen

A

acids, protons
(Oxygen dynamics part 3)

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22
Q

oxidative phosphorylation (electron transport chain)

A

formation of ATP
formation of water (H2O) from NADH
(Oxygen dynamics part 3)

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23
Q

Uncoupler of oxidative phosphorylation

A

Inhibits production of H2O during oxidative phosphorylation. Therefore decreased ATP production. Hydrogen is acidic, so acid accumulates in cell.
ie cyanide
ie CO (carbon monoxide)
ie Aspirin
(Oxygen dynamics part 3)

24
Q

ATP production (totals)

A

net per glucose molecule = +36 ATP
gross + 38 ATP per glucose molecule
(2 from glycolysis, 2 from Krebs cycle, and 34 from electron transport chain) minus 2 ATP burned during 1st phase
(Oxygen dynamics part 3)

25
Q

How many ATP are formed in aerobic/ cellular respiration? ***

A

36 (net total)
(Oxygen dynamics part 3)

26
Q

cyanide

A

Inhibits cytochrome c oxidase, which prevents electrons from passing through the enzyme and being transferred to oxygen.
Ultimately, reduces the generation of ATP
antidote is a b-vitamin (hydroxocobalamin (HCO)
Blocks the cells ability to use oxygen
(Oxygen dynamics part 3)

27
Q

P (in the beginning of a formula)

A

P stands for partial pressure
PO2: partial pressure of oxygen in the given environment (80-100 mmHg)
PaO2: partial pressure of dissolved oxygen in the blood (little ‘a’ refers to arterial blood) (80-100 mmHg).
PAO2: partial pressure of alveolar oxygen (80-100 mmHg)
(Oxygen dynamics part 4)

28
Q

S (in the beginning of a formula)

A

S stands for saturation
SaO2: the amount of total Hgb in the blood that is saturated (93-98%)
SpO2: total saturation of oxygen bound to one Hgb (93-98%)
SvO2: Mixed venous oxygen saturation (measured from pulmonary artery (60-80% w/healthy adult usually around 80%). Only using 20% of available O2
ScvO2: Central venous oxygen saturation (measured from central line w/distal tip at top of right atrium. So reads 5-8% higher than actual) (normal = 70-80%).
(Oxygen dynamics part 4)

29
Q

hgb

A

12-15 g/dL

30
Q

CaO2

A

total content of oxygen bound to Hgb (16-22 mL/O2/dL)
Total content of arterial oxygen
CaO2 = (1.34 x Hgb x SaO2)

example: an adult male patient with a Hgb level of 15 g/dL and an SaO2 of 100%. We would calculate the CaO2 as follows:

(1.34 x 15.0 x 1.0) = 20mL O2/dL of blood
Hgb is the biggest factor

Imagine if this patient had a Hgb level of 6 g/dL:
(1.34 x 6.0 x 0.98) = 7.87mL O2/dL of blood
That reduced the content of O2 by 60%.

31
Q

DO2

A

DO2 = Q x CaO2
delivery of oxygen each minute (900-1100 mL/kg/min). Based on body surface, average adult = 550 mL/min

32
Q

Sinus tach

A

220 - age
Must rule out 3 H’s before labeling SVT (ie 22yo male with HR 200 could be sinus tach)
Hypoxia - can lead to sympathetic response (could be tachycardia)
Hyperthermia (fever can induce tachy)
Hypotension

(Oxygen dynamics part 5)

33
Q

SV (stroke volume)

A

Volume of blood pumped from the ventricle per beat.
3 components of stroke volume:
preload, afterload, contractility

34
Q

Preload

A

resistance that right ventricle has to contract against
amt of volume entering right atrium
can give volume, raise legs, lower head, etc to improve preload

35
Q

afterload

A

left ventricular end diastolic pressure
(pressure at rest)
systemic vascular resistance
normal 800-1200 dynes/sec
high afterload states (high diastolic pressure) = restrictive cardiomyopathies
backup of blood against mitral valve leads to pulmonary edema
dobutamine reduces systemic vascular resistance and therefore reduce afterload/LVEDP. Increases contractility
milrinone works on calcium channels to optimize afterload reduction.
(Oxygen dynamics part 5)

36
Q

dobutamine

A

reduces systemic vascular resistance and therefore reduce afterload/left ventricular end diastolic pressure. Increases contractility
(Oxygen dynamics part 5)

37
Q

milrinone

A

works on calcium channels to optimize afterload reduction.
(Oxygen dynamics part 5)

38
Q

lazy river example (cardiac output)

A

rafts = oxygen molucules
slow river = low cardiac output
if the river (cardiac output) is slow, it doesn’t matter how many rafts (oxygen molecules) you have…it’ll take a long time for them to reach their destination
(Oxygen dynamics part 5)

39
Q

Delivery of O2 to tissues

A

DO2 = Q x CaO2

DO2 : delivery of oxygen to tissue
Q : SV x HR
CaO2 : {1.34 x Hgb x (SaO2)} + (PaO2 x 0.003)

Q = cardiac output
CaO2 = O2 content of arterial blood

{1.34 x Hgb x (SaO2)} is the formula that measures amt of O2 bound to Hgb (98%)

(PaO2 x 0.003) is a measurement of what’s dissolved in plasma

1.34: for every 1g/dL of Hgb, we carry 1.34mL of O2

(Oxygen dynamics part 5)

40
Q

O2ER

A

Measurement of how much oxygen is removed from hgb to tissues. Oxygen consumption-extraction = 3mL/kg/min.
Oxygen extraction (average = 561mL O2/min)
O2ER = (CaO2 - CvO2)/CaO2

Normal BMI = 1.7m2
VO2 = 200-250 mL O2/min (consumption)
VO2I = 120-150mL O2/min/1.7m2

O2ER = (0.95-0.75)/0.95 = 21%
(0.95 = SaO2, 0.75 = SvO2 (from ABG)

(Oxygen dynamics part 5/6)

41
Q

Debt to income ratio example of O2ER

A

$561/min earnings (average O2 delivery grabbed by Hgb and stored for later)

How much could we spend per min?
Say debt to income ratio of 20% (normal SvO2 for healthy adult = 80% (80% left over after consumption)

561 x .2 = 112.2 mL consumed, 448.8 mL/min left over (savings)

If our body starts using more O2, debt to income ratio increases.
>30% is concerning
Approaching anaerobic threshold at 40%

(Oxygen dynamics part 6)

42
Q

Anaerobic respiration

A

In oxygen deprivation state (high debt to income ratio), nothing happens after glycolysis. Oxidative phosphorylation doesn’t happen. Niacin and riboflavin don’t bind with hydrogen, hydrogen (acid) accumulates, ATP production decreases dramatically (34 of the 36 ATP are in oxidative phosphorylation). Only +2 instead of +36 ATP per glucose to glycogen conversion.
(Oxygen dynamics part 6)

43
Q

Identifiable Causes (of anaerobic respiration)

A

Hypoxic hypoxia: deficiency in alveolar O2 exchange (venous admixture), or CO poisoning. Problem of getting O2 to Hgb

Hypemic hypoxia: reduction in the O2 carrying capacity in the blood due to hemorrhage, anemia, or certain drugs

Stagnant hypoxia: obstructive shock, reduced cardiac output or pooling of blood such as heart failure, PE, or shock states

Histotoxic hypoxia: a result of poisoning or metabolic disorders such as cyanide poisoning or ETOH
(Oxygen dynamics part 6)

44
Q

PaO2

A

Measurement of the amount of O2 dissolved in the blood (but NOT bound to Hgb). Measured in PaO2.
For every mmHg of pressure, each 100mL of blood can contain 0.003mL of O2 dissolved in plasma, which is approximately 2-3% of the total oxygen stores.
(Oxygen dynamics part 6)

45
Q

EtCO2 vs PaCO2

A
  1. EtCO2 will always be the lower value. EtCO2 can never exceed or equal PaCO2. (PaCO2 will always be 3-5 mmHg higher)
    When EtCO2 is higher than normal (>45 mmHg, hypercapnia. COPD, asthma. Low minute ventilation.
    When EtCO2 is lower than 35;3Ps of EtCO2
    (Oxygen dynamics part 7)
46
Q

3 P’s of EtCO2

A

Pulse: is there a pulse and is it enough to perfuse?
Perfusion: check MAP (is it enough to perfuse (>65)?
pH: partial compensation of metabolic acidosis?

If perfusion status is low, EtCO2 is a reflection of that. Fix the perfusion problem and EtCO2 will be corrected.
(Oxygen dynamics part 7)

47
Q

** Bohr Effect **

A

RIGHT SHIFT OF OXYHEMOGLOBIN CURVE WHERE UP TO 68% OF O2 STORED IN HGB IS RELEASED, AND HGB HAS HIGH AFFINITY FOR CO2 AND H+.

defines right shift of oxyhemoglobin curve
Hemoglobin’s oxygen binding affinity is inversely related to both acidity and carbon dioxide concentration.
(CO2 and H+ are affecting the affinity of Hgb for O2…O2 released to tissue [up to 68%] and CO2 and H+ are bound to Hgb to be removed).
An increase in CO2 results in a decrease in blood pH, resulting in hemoglobin proteins releasing more of their oxygen (more O2 available to use).
Conversely, a decrease in CO2 provokes an increase in pH, which results in hemoglobin picking up more oxygen.
Where? muscle (‘CO2 factory,’ account for much of body heat), end tissue, placenta
Exercise: muscles need more O2

RAISED temp: muscles account for much of body heat
RAISED acid: muscles are CO2 factories bc it is a byproduct of cellular respiration
RAISED 2,3-DPG: causes O2 to release more easily from Hgb for tissues to use.
(Oxygen dynamics part 8)

48
Q

Right shift: rest

A

Arterial blood: PaO2 100 –> SpO2 98%
Venous blood: PaO2 40 –> SpO2 60%
Arterial/Venous difference: 38%
(Oxygen dynamics part 8)

49
Q

Right shift: exercise

A

Arterial blood: PaO2 100 –> SpO2 98%
Venous blood: PaO2 25 –> SpO2 30%
Arterial/Venous difference: 68%

(Oxygen dynamics part 8, -19:32)

50
Q

Right shift - patho

A

Raised temp
Raised acid (high hydrogen and/or CO2)
Raised 2,3 DPG (molecule attached to every RBC that facilitates offloading of O2 from Hgb (COPD). Blood doping increases this.
= Raised PaO2
Reduced affinity for oxygen on Hgb (more O2 available to use)
Right shift = right for the patient.
(Oxygen dynamics part 8)

51
Q

** Haldane Effect **

A

LEFT SHIFT OF OXYHEMOGLOBIN CURVE WHERE ONLY UP TO 8% OF O2 STORED IN HGB IS RELEASED (HIGH AFFINITY), BUT HGB HAS LOW AFFINITY FOR CO2 AND H+ SO IT IS RELEASED FOR REMOVAL FROM BODY.

defines left shift of oxyhemoglobin curve
The effect of oxygen on CO2 and H+ binding to Hgb. As O2 binds with Hgb, it causes a state of cooperatively, causing a release of CO2 and H+ (thereby decreasing acidity).
(O2 is affecting the affinity of Hgb for CO2/H+…Hgb doesn’t want to release O2 (only 8%) but it DOES want to release CO2 and H+).
Where: Lungs

LOW temp: cool inhaled air
LOW acid: lungs are alkalotic because they offload CO2 and H+ to be exhaled
LOW 2,3-DPG so Hgb in lungs can pick up O2
LOW PaO2: deoxygenated blood returning to lungs has PaO2 ~ 40mmHg. PaO2 in environment ~ 100mmHg, so diffusion will happen (Graham’s Law).
(Oxygen dynamics part 8)

52
Q

Left shift (lungs)

A

Arterial blood: PaO2 100 –> SpO2 98%
Venous blood: PaO2 40 –> SpO2 83%
Arterial/Venous difference: 15%

(Oxygen dynamics part 8)

53
Q

left shift - patho

A

Hgb has increased affinity to bind O2, meaning less O2 is available to use.
Low: temp
Low: acid (metabolic alkalosis)
Low: 2,3 DPG (massive transfusion of PRBCs)

54
Q

allosteric interaction (cooperativity)

A

the binding of oxygen molecules on one site on a hemoglobin molecule influences the binding affinity of oxygen molecules on other sites on the same protein. Ie after the first oxygen molecule binds, the other 3 bind more quickly.

55
Q

SPO2

A

Amount of oxygen that is bound to hemoglobin.
Measured with pulse ox (spO2) or sat from abg/vbg.
Each RBC contains about 270 million hemoglobin.
Each Hgb can carry 4 O2 molecules.
If each Hgb has 3 of 4 sites bound with O2, O2 sat = 75%

56
Q

shunt

A

Shunt: a block inhibiting gas exchange. Blood going to lungs gets NO ventilation and therefore no perfusion.
Does NOT respond to 100% O2 tx
Examples: Right to left shunting (congenital), ARDS (fluid leaks into alveolus)

PaO2 falls, PaCO2 falls - hyperventilation

CFRN (3 decks)

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