Ventilation Perfusion Inequality And Hypoxemia Flashcards

1
Q

What is dead space?

A

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)

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2
Q

What are shunts?

A

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
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3
Q

What is “wasted air” and “wasted blood”?

A
  • 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
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4
Q

The lung is a …

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

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5
Q

What is the pressure volume at FRC?

A
  • 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
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6
Q

Describe pressure volume changes during inspiration

A

During inspiration the change in volume at the apex is significantly less than at the base

The ventilation gradient is aligned with gravity

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7
Q

Summarize regional differences in perfusion

A
  • 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)

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8
Q

What are the ventilation regional differences?

A

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
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9
Q

What are the perfusion regional differences?

A

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
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10
Q

What is the ventilation perfusion ratio gradient?

A

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

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11
Q

What is hypoxic vasoconstriction?

A

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

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12
Q

What is bronchoconstriction?

A

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

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13
Q

What is the effect of embolism and dead space on V/Q?

A

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)

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14
Q

What is the effect of a shunt on V/Q ratio?

A

Shunt- blood is passing through unventilated or poorly areas e.g. COPD

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15
Q

How is A-a O2 gradient measured?

A

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

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16
Q

What is the effect of diffusion block on A-a O2 gradient?

A

Increase

17
Q

What is the effect of generalized hypoventilation on A-a O2 gradient

A

None

18
Q

What is the effect of anatomical Shunt on A-a O2 gradient?

A

increase

19
Q

What is the effect of Reginal low VA/Q ratio (90%) on A-a O2 gradient?

A

Increase

20
Q

What are the respiratory causes of hypoxemia?

A

Reginal low VA/Q ratio

Anatomical. Shunt

Generalized hypoventilation

Diffusion shock

21
Q

What is acclimatization?

A

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

22
Q

What altitudes are considered in altitude physiology?

A

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)

23
Q

How does altitude affect hypoxemia?

A

-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.

24
Q

What are the causes when hypoxia in terms of no or short term acclimatization ?

A

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
25
Q

What can lead to hypoxia as well as adaptation ?

A

Expatriates:

  • Work for several months or years at altitude (families often included)
  • Immigrants (originally lowlanders)

High altitude population:

  • Sherpa
  • tibetian
  • qetchan
  • Ethiopia
26
Q

What can rapid altitude increase result in?

A

Rapid accent to high altitude can result in:

  1. Transient headache (high-altitude headache or [HAH])
  2. Acute mountain sickness (AMS) and HAH
  3. High-altitude cerebral edema(HACE)
  4. High-altitude pulmonary edema (HAPE)

Chronic mountain sickness (CMS) and right ventricular hypertrophy develop CAN over months to years

27
Q

what happens in rapid altitude increase?

A

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

28
Q

What are the long term methods acclimation ?

A

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

29
Q

Explain the pulmonary effects of mountain effects

A

-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

30
Q

Explain the cerebral effects of mountain sickness

A
  • 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