BRTP04 Theory of Oxygen Administration Flashcards

1
Q

PICO2

A

Partial pressure of inspired carbon dioxide

Normal value
0.23 mmHg

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2
Q

PIO2

A

Partial pressure of inspired oxygen

Normal value 159 mmHg

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3
Q

PAO2

A

Partial pressure of oxygen in the alveoli

99-100 mmHg

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4
Q

PaO2

A

Partial pressure if oxygen in arterial blood

80-100 mmHg

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5
Q

PvO2

A

Partial pressure of oxygen mixed in venous blood

40-45mmHg

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6
Q

SaO2

A

Oxygen saturation of Hemoglobin in arterial blood

95-97.5%

(Found when blood is drawn ABG)

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7
Q

SvO2

A

Oxygen saturation of hemoglobin in mixed venous blood

75%

(Found w pulse oximeter)

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8
Q

PvCO2

A

Partial pressure of carbon dioxide in mixed venous blood

45 mmHg

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9
Q

PACO2

A

Partial pressure of carbon dioxide in the Alveoli.

40 mmHg

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10
Q

PaCO2

A

Partial pressure of carbon dioxide in arterial blood

35-45 mmHg

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11
Q

CaO2

A

20.4%

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12
Q

Respiration has 3 basic processes

A
  1. Ventilation
  2. External respiration- happens at AC membrane
  3. Internal respiration- gas exchange at tissue
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13
Q

Aerobic metabolism

A

Sustains life, Metabolism that occurs IN THE PRESENCE OF OXYGEN

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14
Q

Anaerobic metabolism

A

Functions WITHOUT AIR OR OXYGEN

In the cytoplasm

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15
Q

Oxygen definitions

A

Colorless, tasteless, transparent gas

In atmosphere 21%
Density 1.429 g/L
Supports combustion

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16
Q

Hypoxia

A

Lack of oxygen at the tissue level; doesn’t meet cells metabolic needs

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17
Q

Hypoxemia

A

Lack of oxygen in the arterial blood (decreased PaO2)

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18
Q

Hyperoxia

A

Increased levels of oxygen to the tissues usually due to the use of supplemental O2.

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19
Q

Hypocapnea or hypocarbia

A

Decrease in CO2 in the blood

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20
Q

Hypercapnea or hypercarbia

A

Increase in CO2 in the blood

Remember this is associated with abnormal drowsiness

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21
Q

Secondary polycythemia

A

Increased production of red blood cells. A compensatory mechanism of the body to decreased levels of oxygen in the blood (PaO2). More RBCS available to carry oxygen to the tissues.

Remember it’s always a secondary issue, a separate issue has to exist for this one to begin.

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22
Q

Cyanosis

A

Cyanosis is visible bluish tinge if the skin and mucous membranes.

Visible when you have 5gm/100ml or 5gms% of blood of dissociated hemoglobin. (Most important part of this definition)

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23
Q

Time limits to diffusion

A

Pulmonary blood is normally exposed to alveolar gas for 0.75 seconds during exercise it may fall to 0.25 seconds.

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24
Q

Atmospheric pressure at sea level

A

14.7 psi

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25
Dead space
Air present with no blood flow
26
Shunt
Blood flow with no airflow
27
4 types of tissue hypoxia
1. Hypoxemia aka hypoxic hypoxia 2. Anemic hypoxia 3. Circulatory hypoxia 4. Histotoxic hypoxia (dysoxia)
28
Hypoxemia
Also known as hypoxic hypoxia Inadequate delivery of oxygen to the lung or “from the lung to the blood”. Responds well to oxygen therapy (except shunts)
29
Causes of hypoxemia
Hypoventilation, high altitude, shunt (atelectasis), V/Q mismatch (under ventilated alveolar lung regions) diffusion
30
Anemic hypoxia
A hemoglobin deficiency. Low amounts of hemoglobin (Hb) in the blood Common in blood loss. Responds well to oxygen therapy
31
Causes of anemic hypoxia
Loss of Hb, decreased Hb production, abnormal Hb, or impaired chemical combinations of Hb with O2 (carbon monoxide poisoning)
32
Circulatory hypoxia
Stagnant or hypoperfusion or LOW BLOOD FLOW. Associated with ischemia (tissue death) Oxygen therapy limited (other actions need to be to be taken for oxygen to effective)
33
Causes of circulatory hypoxia
Sufficient blood flow is not reaching the tissue and therefore oxygen is not being delivered. (Cardiac pump failure, CHF, shock)
34
Histotoxic hypoxia (dysoxia)
Poisoning of the cellular oxygen utilization mechanism has occurred. The cell is not able to accept O2 from the blood. Cyanide poisoning is the most common example Does not respond to O2 therapy at all Antidote is the only cure
35
Acute vs chronic
Acute is effects felt currently, usually can be resolved quickly Chronic is progressive, non curable and dealt with longer than 3 months
36
Acute hypoxia signs and symptoms (try to know as many as you can)
Tachypnea, increase RR, increased depth of RR tachycardia, hypertension, increased Cardiac output, arrhythmia Confusion, lethargy, restlessness, loss of muscle coordination Liver damage kidney damage
37
Chronic hypoxia signs and symptoms
``` Persistent mental and physical fatigue Decrease in physical activity Barrel chest (increase AP diameter) Clubbing of fingernails Secondary polycythemia Increase in size of heart (right sided heart failure) (for pulmonale) Jugular vein distention (JVD) ```
38
What ranges indicate hypoxemia (need for oxygen use)
PaO2 less than 60 mmHg SaO2 less than 90%
39
When is Hypoxia suspected
Increase work of breathing Increase work of heart Severe trauma (traumatic brain injury) Acute myocardial infarction (heart attack) Short term therapy, post anesthesia recovery
40
Oxygen toxicity
Can I occur as a result of an increased FiO2. FiO2 greater than 50% for longer than 24-48 hours.
41
Oxygen toxicity early phase
``` Tachypnea Fatigue Anxiety Irritation of trachea Mild cough Pain in inspiration Decreased vital capacity ``` (Acute issues)
42
Oxygen toxicity late phase
``` Atelectasis Consolidation Lung fibrous Pulmonary congestion Pulmonary edema Inflammation Fibrin formation ``` (Chronic issues)
43
2 types of chemical receptors
Central: (found in brain) responds to HIGH CO2 Peripheral: mainly responds to HIGH PaO2 (PaO2 less than 60 mmHg)
44
Hypoxic drive
Chronic CO2 retainers breathe due to a lack of oxygen in the blood The body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate respiratory cycle.
45
Knocking out hypoxic drive
Can occur as a result of an increased PaO2
46
Hypoxic drive with COPD patients
COPD patients don’t always respond to CO2 levels and will only respond to low PaO2z
47
Bronchopulmonary dysplasia (BPD)
Fibrotic tissue damage caused by the exposure of high levels of inhaled oxygen (FiO2) to immature lung tissue of a premature baby. *HIGH FiO2*
48
Retinopathy of prematurity (ROP)
ROP occurs as a result of increased PaO2 greater than 80 mmHg Irreversible damage to the retina if an infant due to exposure to high levels in the arterial blood *HIGH PaO2*
49
O2 induced hypoventilation
High PaO2
50
Absorption Atelectasis
Collapse if alveoli as the result of high levels of oxygen (increase FiO2) in the inhaled air causing elimination of nitrogen from lung Increased FiO2 collapses alveoli. Lack of nitrogen met with increased O2 causes this.
51
Normal oxygen content (CaO2)
Total content of arterial O2 CaO2= (Hb x 1.34x SaO2) + (PaO2 x .003)
52
Alveolar air equation
PAO2=[(Pb-47) FiO2] - (PaCO2 x 1.25) If FiO2 is 60% or more, then don’t include the factor of 1.25 Typical Pb will be 760
53
P(A-a) gradient
P(A-a) gradient= PAO2-PaO2 Normal (A-a) gradient is 5-10 mmHg No more than 65mmHg on 100% oxygen
54
Diffusion
Done across the AC membrane
55
Perfusion
Done across tissue
56
O2 dissociation curve Right shift
Shifts to the RIGHT decrease affinity (decreased attraction to O2) Releases to tissue but won’t be picked up by lungs
57
Causes of a right shift
Decrease in pH (increase in hydrogen ions) Increase in temp Increase 2,3 DPG Increase in PaCO2 Increased PaCO2 causes acidosis
58
O2 dissociation curve Left shift
Shifts LEFT creates an INCREASED affinity | Oxygen transferred to the blood and Hb
59
Left shift causes
Increase in pH (decrease in Hydrogen ions) Decrease in temperature Decrease 2,3 DPG Decrease in PaCO2 Low PaCO2 is associated with alkalosis
60
A/C membrane has 3 main barriers
Alveolar epithelium Interstitial Space and it’s structures Capillary endothelium