Oxygen Therapy Flashcards
Oxygen Delivery Equation
DO2= CO x Arterial O2 content
Failure of O2 delivery can be d/t
hypotension
acidosis
coagulopathy
Oxygen Use equation
VO2=CO x O2a-O2v
Oxygen extraction ratio
normal 25%
heart has very high demand
Hypoxemia definition
deficiency of O2 in the blood
Hypoxia definition
O2 delivery to tissues not sufficient to meet metabolic demand
Anesthesia Oxygenation goal
maintain oxygenation and ventilation
Oxygen therapy is
the prevention and correction of hypoxemia and tissue hypoxia
Surgical patients are at an increase risk of
hypoxia/hypoxemia
Main causes of hypoxemia
V/Q mismatch (not enough blood flow or oxygen to the lungs)
R to L shunt (blood entering L side of heart w/o being oxygenated first
diffusion impairment (impaired movement of oxygen from the lungs into the bloodstream)
hypoventilation (shallow and ineffective breathing)
low environmental oxygen
Main causes of hypoxia
any condition or event that reduces O2 intake asthma lung disease heart disease anemia high altitudes carbon monoxide or cyanide poisoning
Hypoxic Hypoxia
pulmonary diffusion effect
Drug overdose, COPD, emphysema, asthma, ateletasis
Hypoxia d/t circulatory
reduced CO
CHF or MI
Hypoxia d/t Hemic
reduced hemoglobin content
carboxyhemoglobinemia, methemoglobinemia, anemia
Hypoxia d/t demand
increased O2 consumption
fever, seizure, shivering, mH
Hypoxia d/t histotoxic
inability of cells to utilize oxygen
cyanide toxicity
Hypoxia Signs and Symptoms
vasodilation tachycardia tachypnea cyanosis confusion lactic acidosis
Methods to improve oxygenation of MV patients
treatment needs to be tailored to cause increase Ve increase CO increase CaO2 optimize V/Q relationship increase FiO2
Supplemental O2 for non-intubated patients
nasal cannula
simple face mask
face mask with reservoirs
venturi masks
Nasal cannula
flow rates 1-6L/min
FiO2 increases about 4% per L/Min
Simple Face Mask
FiO2 40-60%
minimum 6L flow required to prevent rebreathing
Minimum is whatever patient’s Mventilation is
Face mask with reservoirs
FiO2 60-100%
Venturi Masks
more precise FiO2
24-50%
Oxygen Toxicity
High FiO2 over long periods can be harmful to lung tissue
What lung tissue damage is seen from O2 toxicity
decreased ciliary movement
alveolar epithelial damage
interstitial fibrosis
O2 toxicity is dependent on
FiO2, duration and patient susceptibility
safe vs toxic O2 therapy
Safe 100% O2 up to 10-20 hours
Toxic: 50-60% O2 for more than 24-72 hours
High Risk O2 Toxicity Patients
> 70 Ys
PMH: radiation to chest lunge
glicomyocin
S/S of Oxygen Toxicity
cough dyspnea rales hypoxia decrease diffusion increase in the arterial alveolar gradient
Absorption Atelectasis
nitrogen is replaced by oxygen
under ventilated alveoli have decreased volume
due to greater uptake of oxygen
increases pulmonary shunting
Induced Hypoventilation
chronic CO2 retainers rely on hypoxic drive
peripheral chemoreceptors are triggered by hypoxemia
increased O2 can lead to hypoventilation
Fire Hazard
O2 can support combusion
use extreme caution with head and neck cases
Retinopathy
O2 therapy in neonates can lead to vascular proliferation fibrosis retinal detachment and blindness
Population at risk for retinopathy
< 36 weeks gestational age
weight <1500gm
up to 44wks gestational age are considered high risk
safe O2 administration PaO2 60-80mmHg
hypercapnia
increased Co2 >45mmHG
Causes of hypercapnia
increased Co2 concentration
increased CO2 production
increased alveolar dead space
decreased alveolar ventilation
Increased alveolar dead space
decreased alveolar perfusion
interruptions in pulmonary circulation
pulmonary disease
Decreased alveolar ventilation
can be central or peripheral
respiratory depression most common cause in immediate postoperative period
Clinical manifestations of Hypercapnia
directly produces vasodilation of peripheral vessels
indirectly increase hR after catecholamine release
produces effects due to acidotic state
Nonspecific signs of hypercapnia
headache, N/V, sweating, flushing, shivering, restlessness
CNS Considerations for hypercapnia
regulation of ventilatory drive
cerebral blood flow
Cardiovascular considerations in hypercapnia
depression of smooth muscle and cardiac muscle
increased catecholamine release
vasodilation vs vasoconstriction
pulmonary consideration in hypercapnia
increased RR
increased pulmonary vascular resistance
right shift in Hgb dissociation curve
treatment of hypercapia
adjustment to the cause
increase minute ventilation
hypocapnia
CO2 less then 35mmHg
cause is usually iatrogenic
Manifestations of hypocapnia
decrease CBF
cardiovascular decrease in CO, coronary constriction
hypoxemia may result from hypoventilation
treatment of hypocapnia
decrease minute ventilation
