BRTP04 Theory of Oxygen Administration Flashcards
PICO2
Partial pressure of inspired carbon dioxide
Normal value
0.23 mmHg
PIO2
Partial pressure of inspired oxygen
Normal value 159 mmHg
PAO2
Partial pressure of oxygen in the alveoli
99-100 mmHg
PaO2
Partial pressure if oxygen in arterial blood
80-100 mmHg
PvO2
Partial pressure of oxygen mixed in venous blood
40-45mmHg
SaO2
Oxygen saturation of Hemoglobin in arterial blood
95-97.5%
(Found when blood is drawn ABG)
SvO2
Oxygen saturation of hemoglobin in mixed venous blood
75%
(Found w pulse oximeter)
PvCO2
Partial pressure of carbon dioxide in mixed venous blood
45 mmHg
PACO2
Partial pressure of carbon dioxide in the Alveoli.
40 mmHg
PaCO2
Partial pressure of carbon dioxide in arterial blood
35-45 mmHg
CaO2
20.4%
Respiration has 3 basic processes
- Ventilation
- External respiration- happens at AC membrane
- Internal respiration- gas exchange at tissue
Aerobic metabolism
Sustains life, Metabolism that occurs IN THE PRESENCE OF OXYGEN
Anaerobic metabolism
Functions WITHOUT AIR OR OXYGEN
In the cytoplasm
Oxygen definitions
Colorless, tasteless, transparent gas
In atmosphere 21%
Density 1.429 g/L
Supports combustion
Hypoxia
Lack of oxygen at the tissue level; doesn’t meet cells metabolic needs
Hypoxemia
Lack of oxygen in the arterial blood (decreased PaO2)
Hyperoxia
Increased levels of oxygen to the tissues usually due to the use of supplemental O2.
Hypocapnea or hypocarbia
Decrease in CO2 in the blood
Hypercapnea or hypercarbia
Increase in CO2 in the blood
Remember this is associated with abnormal drowsiness
Secondary polycythemia
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.
Cyanosis
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)
Time limits to diffusion
Pulmonary blood is normally exposed to alveolar gas for 0.75 seconds during exercise it may fall to 0.25 seconds.
Atmospheric pressure at sea level
14.7 psi
Dead space
Air present with no blood flow
Shunt
Blood flow with no airflow
4 types of tissue hypoxia
- Hypoxemia aka hypoxic hypoxia
- Anemic hypoxia
- Circulatory hypoxia
- Histotoxic hypoxia (dysoxia)
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)
Causes of hypoxemia
Hypoventilation, high altitude, shunt (atelectasis), V/Q mismatch (under ventilated alveolar lung regions) diffusion
Anemic hypoxia
A hemoglobin deficiency. Low amounts of hemoglobin (Hb) in the blood
Common in blood loss.
Responds well to oxygen therapy
Causes of anemic hypoxia
Loss of Hb, decreased Hb production, abnormal Hb, or impaired chemical combinations of Hb with O2 (carbon monoxide poisoning)
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)
Causes of circulatory hypoxia
Sufficient blood flow is not reaching the tissue and therefore oxygen is not being delivered.
(Cardiac pump failure, CHF, shock)
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
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
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
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)
What ranges indicate hypoxemia (need for oxygen use)
PaO2 less than 60 mmHg
SaO2 less than 90%
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
Oxygen toxicity
Can I occur as a result of an increased FiO2.
FiO2 greater than 50% for longer than 24-48 hours.
Oxygen toxicity early phase
Tachypnea Fatigue Anxiety Irritation of trachea Mild cough Pain in inspiration Decreased vital capacity
(Acute issues)
Oxygen toxicity late phase
Atelectasis Consolidation Lung fibrous Pulmonary congestion Pulmonary edema Inflammation Fibrin formation
(Chronic issues)
2 types of chemical receptors
Central: (found in brain) responds to HIGH CO2
Peripheral: mainly responds to HIGH PaO2 (PaO2 less than 60 mmHg)
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.
Knocking out hypoxic drive
Can occur as a result of an increased PaO2
Hypoxic drive with COPD patients
COPD patients don’t always respond to CO2 levels and will only respond to low PaO2z
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
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
O2 induced hypoventilation
High PaO2
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.
Normal oxygen content (CaO2)
Total content of arterial O2
CaO2= (Hb x 1.34x SaO2) + (PaO2 x .003)
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
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
Diffusion
Done across the AC membrane
Perfusion
Done across tissue
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
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
O2 dissociation curve
Left shift
Shifts LEFT creates an INCREASED affinity
Oxygen transferred to the blood and Hb
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
A/C membrane has 3 main barriers
Alveolar epithelium
Interstitial Space and it’s structures
Capillary endothelium