Ventilation Perfusion Inequality And Hypoxemia Flashcards
What is dead space?
Volume of inhaled air that does not participate in gas exchange
Regions 9f no gas exchange
Conducting airways -anatomical dead space(150 ml)
Alveoli with no perfusion (alveolar dead space)
What are shunts?
Imperfect matching of lungs airflow and blood flow
Two causes for physiological shunt (total venous admixture)
- I) 50% comes from anatomical shunt (right to left shunt) (bronchial circulation, thebesian veins)
- II) 50% from low VA/Q e.g. at the base of the lung, partially obstructed airway
What is “wasted air” and “wasted blood”?
- All of the inspired air does not participate in gas exchange, resulting in some “wasted air”- physiologic dead space
- All of the blood entering the lung is not fully oxygenated, leading to some “wasted blood”-physiologic shunt
The lung is a …
Slinky
Top-has most of the weight of the rest of the slinky pulling it down on it- therefore the coils are apart
Middle- has half of the mass of the rest of the slinky pulling down in it - therefore the coils are tighter together than at the top
Bottom- has very little weight of the slinky pulling down on it - therefore the coils are tighter together than at the top
In addition the lung is resting on the contents of the abdomen
What is the pressure volume at FRC?
- The apex of the lung is less compliant than the base
- At rest the lung apex is approximately 70% distended
- At rest the lung base is 15% distended
Describe pressure volume changes during inspiration
During inspiration the change in volume at the apex is significantly less than at the base
The ventilation gradient is aligned with gravity
Summarize regional differences in perfusion
- Pulmonary circulation is a high-flow, low-pressure, low-resistance system
- Since upward flow runs against hydrostatic pressure there is more resistance to blood flow toward the apex of the lung (no hydrostatic pressure to overcome in blood flowing down)
Alveolar pressure also affects pulmonary perfusion- high alveolar volume in the apex reduces blood flow (this restriction is not present when alveolar pressure falls below pulmonary arterial pressure)
What are the ventilation regional differences?
At the top
Intrapleural pressure more negative
Greater transmural pressure gradient, alveoli larger, less compliant
Less ventilation
At the bottom Intrapleural pressure less negative Smaller transmural pressure gradient Alveoli smaller, more compliant More ventilation
What are the perfusion regional differences?
At the top
Lower intra vascular pressures
Less recruitment , distention
Higher resistance, low blood flow
At the bottom Greater vascular pressures More recruitment, distention Lower resistance Greater blood flow
What is the ventilation perfusion ratio gradient?
Ventilation and blood flow are both gravity dependent
Blood flow is proportionally greater than ventilation at the base and vice versa at the apex
Ventilation-perfusion ratio decreases down the lung
Gas exchange is more efficient at the apex of the lung as compared to the base
What is hypoxic vasoconstriction?
For low V/Q ratio (lots of blood or too little ventilation); causes the blood coming into the area to be directed to other parts of the lung
What is bronchoconstriction?
For high V/Q ratio, the bronchi will construct slightly to increase the resistance and decrease the amount of ventilation coming into an area that is not well perfused thus limiting the amount of alveolar dead space
Increases V/Q
What is the effect of embolism and dead space on V/Q?
Perfusion is low in well ventilated areas (embolism) or in the extreme case-perfusion is absent in ventilated areas (dead space-e.g. trachea/bronchi)
What is the effect of a shunt on V/Q ratio?
Shunt- blood is passing through unventilated or poorly areas e.g. COPD
How is A-a O2 gradient measured?
PAO2 without diffusion problems or VA/Q mismatch should ideally be equal to the PaO2
Normal value 5-15 mmHg, this increases with age
A-a O2 gradient= PAO2-PaO2
What is the effect of diffusion block on A-a O2 gradient?
Increase
What is the effect of generalized hypoventilation on A-a O2 gradient
None
What is the effect of anatomical Shunt on A-a O2 gradient?
increase
What is the effect of Reginal low VA/Q ratio (90%) on A-a O2 gradient?
Increase
What are the respiratory causes of hypoxemia?
Reginal low VA/Q ratio
Anatomical. Shunt
Generalized hypoventilation
Diffusion shock
What is acclimatization?
Called acclimation is the process in which an individual organism adjusts to a change in its environment. Such responses are often reversible should environmental conditions revert to an earlier state
What altitudes are considered in altitude physiology?
Typically focuses on people above 2500m; about 8,000 ft
Very high altitude (3500-5500 m; about 11,500-18,000 ft
Extreme altitude (above 5500m; 18,000 ft)
How does altitude affect hypoxemia?
-With high altitude, there is increased hypoxemia
With high altitude alveolar PO2 decreases which results in decreased arterial PO2 (hypoxemia)
-Ventilation is stimulated by the hypoxemia experienced by carotid/aortic bodies
Minute alveolar ventilation increases in an attempt to restore blood oxygen levels
Acclimatization results in restoration of oxygen delivery towards sea level values.
What are the causes when hypoxia in terms of no or short term acclimatization ?
One possibility:
Extreme short term exposure:
-flight
-driving an alpine pass
-work in hypoxic chambers/rooms for fire protection
-Coach for altitude training (also simulated altitude)
-Alpine skiing
Another possibility: Limited exposure: -Business trip -Vacation/holidays -Special military missions
What can lead to hypoxia as well as adaptation ?
Expatriates:
- Work for several months or years at altitude (families often included)
- Immigrants (originally lowlanders)
High altitude population:
- Sherpa
- tibetian
- qetchan
- Ethiopia
What can rapid altitude increase result in?
Rapid accent to high altitude can result in:
- Transient headache (high-altitude headache or [HAH])
- Acute mountain sickness (AMS) and HAH
- High-altitude cerebral edema(HACE)
- High-altitude pulmonary edema (HAPE)
Chronic mountain sickness (CMS) and right ventricular hypertrophy develop CAN over months to years
what happens in rapid altitude increase?
Hypodemia-stimulated ventilation
PCO2 declines producing resp. Alkalosis
These tend to counter the increase in ventilation due to hypoxia
Over 2-3 days - blood pH is corrected (acidified) by renal excretion of HCO3^-. CSF also returns to normal with HCO3^- excretion
Full hypoxic ventilatory drive is then restored
Immediate rise in cardiac output
What are the long term methods acclimation ?
Polycythemia- low PO2 of kidney stimulates the release of erythropoietin- which in turn stimulates bone marrow to increase RBC production
Hypoxemia- induces a higher RBC count per unit volume- I.e. more Hb/dL, I.e. greater carrying capacity for oxygen for a given PO
Blood viscosity is greatly increased
2,3-DPB levels rise resulting therefore in increased oxygen unloading
Explain the pulmonary effects of mountain effects
-The pulmonary hypoxic vasoconstriction increases pulmonary vascular resistance- increasing hydrostatic pressure in the pulmonary circulation
Cardiac output is also increased- increased sympathetic stimulation due to arterial chemoreceptor stimulation
These factors favor pulmonary edema
Analysis of pulmonary exudate demonstrates high protein levels- I.e. capillary permeability is increased
Explain the cerebral effects of mountain sickness
- Cerebral circulation is sensitive to hypocapnia - it is a strong cerebral vasoconstrictor
- At altitude the brain receives blood flow with low PO2 this may be compounded by reduced blood flow due to cerebral hypocapnic vasoconstriction
- Headaches, mental confusion etc. common symptom of altitude sickness
Ultimately though- low PO2 leads to cerebral vessel vasodilation and hyper perfusion of the vessels
Increases the likelihood of cerebral edema
