CVPR Week 6: Hypoxemia Flashcards
1
Q
Objectives
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2
Q
describe O2 transport throughout the body
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3
Q
describe O2 transport throughout the body
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4
Q
Atmospheric gaseous composition
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5
Q
low PaO2 in the blood is
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arterial hypoxemia
6
Q
arterial hypoxemia is defined by?
A
low PaO2 in the blood
7
Q
arterial hypoxemia defect in?
2 listed
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- Breathing
- Pulmonary O2 diffusion
8
Q
inadequate blood flow
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hypoperfusion hypoxia
9
Q
hypoperfusion hypoxia is defined by?
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inadequate blood flow
10
Q
hypoperfusion hypoxia defect in
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circulatory O2 delivery
11
Q
Insufficient Hb
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Anemic hypoxia
12
Q
Anemic hypoxia is defined by?
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insufficient Hb
13
Q
Anemic hypoxia defect in?
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O2 carrying capacity
14
Q
Decreased cellular metabolism
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Histotoxic hypoxia
15
Q
Histotoxic hypoxia is defined by?
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decreased cellular metabolism
16
Q
Histotoxic hypoxia defect in?
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tissue O2 utilization
17
Q
defect in tissue O2 utilization
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histotoxic hypoxia
18
Q
defect in O2 carrying capacity
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anemic hypoxia
19
Q
Defect in circulatory O2 delivery
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hypoperfusion hypoxia
20
Q
Defect in pulmonary O2 diffusion
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arterial hypoxemia
21
Q
defect in breathing
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arterial hypoxemia
22
Q
arterial hypoxemia always results in?
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Low PaO2 in blood
23
Q
Identify
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24
Q
Identify
A
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Identify
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hypoperfusion hypoxia is a defect of
inadequate blood flow
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generalized hypoperfusion is referred to as?
Shock
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Shock is referred to as?
generalized hypoperfusion
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global decrease in blood flow is associated with?
decreases in MABP
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MAP =
CO X TPR = MAP
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Types of circulatory shock
3 listed
* Septic shock
* Anaphylactic shock
* neurogenic shock
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Neurogenic shock is caused by?
failure of the autonomic nervous system to control peripheral resistance
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Anaphylactic shock is caused by?
severe allergic reaction and massive cytokine release causing global vasodilation and massive pressure loss
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Septic shock cause
infection in the blood causes a massive immune response and cytokine release leading to massive global vasodilation and loss in pressure and resistance
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Causes of cardiogenic shock
* Arrhythmias
* Heart failure
* Autonomic failure
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CO =
SV x HR = CO
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Causes of hypovolemic shock
* hemorrhage
* dehydration
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Hypoperfusion hypoxia O2 values
* normal PaO2 because lungs are diffusing fine
* lower PvO2 because the tissues extract what they can
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Describe the O2 environment in Hypoperfusion hypoxia
* Normal PaO2
* Low PvO2
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Regional hypoperfusion is referred to as?
Ischemia
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Ischemia is?
regional hypoperfusion
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Explain this graph
if the autoregulatory mechanism is impaired somehow then this leads to subnormal flow and ischemia
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Anemic hypoxia is a defect in?
Insufficient hemoglobin or impaired hemoglobin
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Insufficient or impaired hemoglobin results in
reduced oxygen-carrying ability due to the loss of red blood cells (says the slide)
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O2 values of anemic hypoxia
* Normal PaO2
* Low CaO2
* Low PvO2
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Describe the O2 environment of anemic hypoxia
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Causes of Anemia
5 listed
* genetic
* hemorrhage
* autoimmune
* nutritional deficiency (iron, vit B12, folate)
* bone marrow destruction
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PO2 in the blood in
1. Polycythemia
2. Normal
3. Anemia
4. Carbon monoxide poisoning
* Doesn't change the PO2 in the blood but instead binds more or less O2 depending on the amount of Hb present
* It changes the total O2 content and not the PaO2
* Carbon monoxide poisoning binds to Hb with greater affinity than O2 does which lower the amount of Hb for O2 to bind to
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Histotoxic hypoxia is a defect involving
reduced cellular usage of O2
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Some causes of Histotoxic hypoxia
* Cyanide poisoning
* Sulfide poisoning
* Narcotics (barbiturates)
* Vitamin B, deficiency or Beriberi
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Histotoxic hypoxia O2 values
* Normal PaO2 because perfused normally
* High PvO2 because O2 isn't being used up by the tissues normally
* Low VO2 because
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Describe the O2 environment of Histotoxic hypoxia
* Normal PaO2
* High PvO2
* Low VO2
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Classifications of hypoxemia
3 listed
* Mild 60-80 mmHg or \>95% SaO2
* Moderate 46-60 mmHB or 75-90% SaO2
* Severe \< 40 mmHg or \< 75% SaO2
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Mild hypoxemia symptoms
* May be unnoticeable
* increased pulse and breathing rate
* impaired thinking and attention
* reduced coordination
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Mild hypoxemia lab values
* 60 - 80 mmHg
* 90 - 94% SaO2
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Moderate hypoxemia symptoms
5 listed
* Drowsiness
* headache
* mental and muscle fatigue
* faulty coordination
* poor judgement
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Moderate hypoxemia lab values
* 40 - 60 mmHg PO2
* 75 - 90% SaO2
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Severe hypoxemia symptoms
5 listed
* seizure and muscle twitching
* very poor judgement and coordination
* impaired respiration
* nausea
* vomiting
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Severe hypoxemia lab values
* PO2 \< 40 mmHg down around 30 pass out, down around 20 basically dead
* SaO2 \< 75%
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what is the interpretation of V/Q
the balance between O2 delivery to alveoli (V) and the O2 removal by the blood (Q)
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Ideal V/Q vs Healthy Actual V/Q
Ideal V/Q = 1
Actual V/Q = 0.8
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V/Q =
ventilation / perfusion
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Normal PO2s and PCO2s in pulmonary arteries capillaries veins alveoli and environmental air
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A-a gradient =
equation
A-a gradient = PAO2 - PaO2
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typical A-a gradient
100 PAO2 to - 92 PaO2
usually about 5 to 10 mmHg difference
increases as you age
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A-a gradient interpretations relative to the cause of hypoxemia
* if A-a gradient = 5-10 mmHg then the cause is usually due to high altitude or hypoventilation
* If A-a gradient = increased then this is due to at least on or a combination of V/Q mismatch, impaired diffusion, and/or shunt
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Increased A-a gradient causes
3 listed
at least one of these or a combination of them V/Q mismatch, impaired diffusion, and/or shunt
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How to measure alveolar PAO2
the alveolar gas equation
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Alveolar gas equation
FiO2 (Patm - PH2O) - [PaCO2/RQ]
PH2O is the water vapor pressure from the humidifying of the air while breathing it in
FiO2 = the atmospheric PO2
so FiO2(Patm - PH2O) = inspired air
so
inspired air - perfused air going out
PaCO2 is the arterial blood gas pressure
RQ = respiratory quotient
70
The typical difference between Air and alveolar PO2 is about?
~ 10 mmHg
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RQ =`
respiratory quotient explained
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RQ interpretation
the respiratory quotient
typically = 0.8
interpreted as
for every 8 molecules of CO2 made it took 10 molecules of O2 to make it
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PaCO2 / RQ =
basically O2 in the pulmonary capillaries / tissue usage
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How altitude effects PAO2
the only thing that changes is the atmospheric PO2 which thereby reduces PAO2
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Adaptation to high altitude and PAO2
since we are highly adapted to high elevation the PCO2 is a little bit lower and so the PAO2 os actually a little bit higher
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sensors of low PaO2
carotid body chemoreceptors
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Effects of low PaO2
4 listed
* increase HR
* increases ventilation
* constricts pulmonary arteries
* dilates systemic arteries to attempt to deliver as much oxygen as possible
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Acute Protective mechanisms against hypoxemia
4 listed
* increase HR
* increases ventilation
* constricts pulmonary arteries
* dilates systemic arteries to attempt to deliver as much oxygen as possible
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how is increasing ventilation protective against hypoxemia
* you would have reduced resistance to hypoxemia with lower atmospheric O2
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Ventilation effects on PAO2 and PAO2
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Increasing PACO2 does what to PAO2
the amount of CO2 reduces the amount of O2 can be in there at one time
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Usual causes of hypoventilation
4 listed
* Depressed CNS (drug overdose or CNS lesion)
* Nerve conduction defects (Guillain-Barre, spinal cord injury or phrenic nerve paralysis)
* Lung disease (sleep apnea, obesity)
* Respiratory Muscle weakness (muscular dystrophy, myasthenia gravis or hypothyroidism)
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Typical CNS causes of hypoventilation
2 listed
* drug overdose
* CNS lesion
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Typical causes of nerve conduction defects resulting in hypoventilation
3 listed
* Guillian-Barre
* spinal cord injury
* phrenic nerve paralysis
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Typical causes of lung disease defects resulting in hypoventilation
2 listed
* sleep apnea
* obesity
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Typical causes of muscle weakness defects resulting in hypoventilation
3 listed
* Muscular dystrophy
* myasthenia gravis
* hypothyroidism
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Identify
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Identify
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A-a gradient of hypoventilation
Hypoventilation results in a normal A-a gradient because there's nothing wrong with the amount of atmospheric oxygen or its ability to perfuse the problem lies in the amount and frequency of ventilation
However, there is CO2 dilution from the reduced ventilation but this doesn't affect the A-a gradient because the CO2 will be in the PACO2
90
How can hypoventilation or high altitude hypoxemia be corrected?
increasing FiO2
so basically increase the oxygen concentration of the air to be inspired FiO2
an easy way to do this is using supplemental O2
However, with hypoventilation, the hypercapnia will still persist due to the reduced breathing rate so the reduced ability to dump CO2
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Increasing FiO2 in hypoventilation
the PAO2 will rise however the hypercapnia will remain because of the reduced ventilation so PACO2 will remain high
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The normal A-a gradient is due to
some amount of natural V/Q mismatch that occurs and some degree of shunt which will account for the 5-10 mmHg gradient
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Natural V/Q mismatch
gravity is a cause because blood and air are not equally distributed throughout the lung
* Zone 1 is the superior apex of the lung where more ventilation than perfusion occurs
* in Zone 2
* In Zone 3
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Zone 1 of the lung
more V than Q
↑V/↓Q = ↑1
PA\>Pa\>Pv
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Zone 2 of the lung
V and Q are pretty equally matched
so
V/Q = ~ 1
Pa\>PA\>Pv
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Zone 3 of the lung
Less V and more Q
↓V/↑Q = ↓1
Pa\>Pv\>PA
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The effect of V/Q mismatching on PAO2 and PACO2
**Low V/Q** =
↓ PAO2
↑PACO2
**High V/Q** =
↑PAO2
↓PACO2
98
When V/Q = 0
referred to as R-L shunt
and the concentrations of PACO2 and PAO2 will be very close to mixed venous blood
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When V/Q = ∞
referred to as Deadspace
and the concentrations of PACO2 and PAO2 will be very close to inspired air
100
Compensatory mechanisms for V/Q mismatch
2 listed
* Vasoconstriction
* Bronchiolar constriction
101
Bronchial constriction airways in response to V/Q mismatching
↑PO2 but ↓ PCO2 and an ↑pH around smooth muscle in the bronchials causes contriction of airflow to better perfused areas
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Response of bronchials to reduced perfusion
↓ blood flow causes type II pneumocytes to produce less surfactant causing ↓ compliance and ventilation so the alveoli shrink
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Vasoconstriction in response to V/Q mismatching
in response to local alveolar hypoxia, the arterioles feeding the alveoli constrict (hypoxic vasoconstriction) diverting blood to better-ventilated areas
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Increased V/Q mismatch interpretation
When V/Q = \> 1
blockade of perfusion but increased ventilation
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Decreased V/Q mismatch interpretation
* when V/Q = \< 1
* Reduced ventilation but increased perfusion
106
Increased V/Q mismatch compensation
2 listed
↑PO2 but ↓ PCO2 and an ↑pH around smooth muscle in the bronchials causes contriction of airflow to better perfused areas
also
↓ blood flow causes type II pneumocytes to produce less surfactant causing ↓ compliance and ventilation so the alveoli shrink
107
Decreased V/Q mismatch compensation
in response to local alveolar hypoxia, the arterioles feeding the alveoli constrict (hypoxic vasoconstriction) diverting blood to better-ventilated areas
108
Types of R to L shunts
2 listed
* Anatomical shunts
* Intrapulmonary shunts
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Anatomical shunt description
blood that does not traverse the pulmonary capillaries
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Normal anatomical shunts
**coronary circulation**
blood goes from the left heart to the coronary circulation and back into the left heart
**Bronchial circulation**
Actually part of the systemic circulation and carries blood that supplies the lung with O2 and gets dumped back into the lung through the bronchial vein past the pulmonary arteries so it is not oxygenated by the alveoli directly
111
Identify
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Intrapulmonary shunt description
blood traverses pulmonary capillaries that are adjacent to unventilated or poorly ventilated alveoli
113
Absolute or true intrapulmonary shunt
V/Q = 0
114
Shunt-like intrapulmonary shunt
Low V/Q
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Normal shunts account for how much of the cardiac output?
2 - 5 % of the CO
116
A-a gradient genesis
* anatomical shunts (pulmonary and bronchial circulations)
* Gravity (non-uniform ventilation and perfusion distribution)
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Shunt-like effects are usually due to?
Diffusional impairment or diffusional limitations where Fick's law of diffusion is manipulated
118
Examples of causes of diffusional impairment
6 listed
* Atelectasis/Pneumothorax
* Emphysema alveolar-capillary destruction
* Interstitial edema fluid accumulation
* Alveolar fibrosis thickening of the alveolar wall
* Pneumonia alveolar inflammation
* Pulmonary edema fluid accumulation
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Emphysema shunt-like state
destruction of alveoli and capillaries reducing the surface area available for diffusion
120
Alveolar fibrosis cause of shunt-like state
thickening of the alveolar wall which decreases diffusion
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Pneumonia cause of shunt-like state
alveolar inflammation or edema interfering with diffusion
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Interstitial edema cause of shunt-like state
fluid accumulation in between the capillary and the alveoli interfering with diffusion
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Atelectasis cause of shunt-like state
the collapse of alveoli reduces ventilation and therefore diffusion capabilities
124
Pneumothorax cause of shunt-like state
collapse of the lung prevents alveolar filling and therefore interferes with diffusion
125
How are shunts graded?
the degree of shunts is determined by the effectiveness of supplementary O2
126
What is the cut-off for supplemental O2 effectiveness for shunts?
~30% anything more than that and supplemental O2 will not be effective
127
Exercise and the identification of diffusional limitations
* A-a gradient can seem normal at baseline resting conditions but exercise can unmask diffusional limitations
* Reduced perfusion time in the capillaries as a result of exercise may expose diffusional limitations that might otherwise go unnoticed
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exercise diffusional limitations
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Summary I
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Summary 2
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Question
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Question
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Question
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