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PHYSIOLOGY > REGULATION OF ALVEOLAR VENTILATION high altitude vs acclimatization > Flashcards

REGULATION OF ALVEOLAR VENTILATION high altitude vs acclimatization Flashcards

1
Q

ALVEOLAR VENTILATION

A
  • mediated by
  • CENTRAL CHEMORECEPTORS
  • PERIPHERAL CHEMORECEPTORS
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2
Q

CENTRAL CHEMORECEPTORS

A
  • in the MEDULLA of the brain
  • MONITOR MAINLY ARTERIAL CARBON DIOXIDE
  • monitor hydrogen ions
  • main drive for alveolar ventilation
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3
Q

PERIPHERAL CHEMORECEPTORS

only ARTERIAL OXYGEN MAIN JOB

A
  • located in the CAROTID SINUS AND AORTIC ARCH
  • monitor arterial OXYGEN MAINLY
  • LEAST extent monitor arterial CO2
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4
Q

PERIPHERAL CHEMORECEPTORS
(only ARTERIAL OXYGEN MAIN JOB) takes over the job of CENTRAL CHEMORECEPTORS (only MONITOR MAINLY ARTERIAL CARBON DIOXIDE)

A
  • when there is dramatic fall in PaO2
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5
Q

arterial hydrogen ions

A
  • cannot cross the BBB area

- any H+ ions affecting or stimulating the central chemoreceptors come from INFECTION IN THE CSF (meningitis)

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6
Q

MENINGITIS

A
  • hyperventilation
  • due to excessive production of H+ ions in the CSF due to infection stimulating the central chemoreceptors
  • increase H+ in the blood it will not affect the chemical receptors because it will not cross the BBB
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7
Q

chronic hypoventilation

A
  • overdose of morphine and heroin
  • it will suppress the MEDULLA causing depression of ventilation causing hypoventilation
  • causing INCREASE IN CARBON DIOXIDE it will stimulate central receptors, in cases of overdose it blocks central receptors causing it not to control the increase in carbon dioxide
  • ## arterial oxygen DECREASES PaO2 stimulate peripheral receptors
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8
Q

treatment of DECREASE PaO2

A
  • dont correct the PaO2 to normal because we need to keep the peripheral receptor in play
  • correcting the O2 to normal is removing the ventilatory drive of the patient, can cause collapse
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9
Q

ANEMIA

A
  • decrease total O2 content
  • normal PaO2
  • normal PaCO2
  • no ventilatory changed
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10
Q

CASE: from room air to oxygen mask 21% (same as room air)

A
  • SAME/NORMAL ventilation

- central chemoreceptors

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11
Q

CASE: from room air to oxygen mask 100% for 15 mins.

A
  • SAME/NORMAL ventilation
  • central chemoreceptors
  • increasing O2 does not stimulate peripheral receptors and its just a waste in O2
  • decreasing O2 stimulates peripheral receptors
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12
Q

CASE: room air to 3% CO2 and 15% O2

normal CO2 in room air

A
  • hyperventilation by peripheral chemoreceptors

- due to decrease in O2

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13
Q

normal ventilation center

A
  • medulla
  • normal ventilatory rhythm EXPIRATION > INSPIRATION
  • MOST COMMONLY AFFECTED IN STROKE PATIENTS
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14
Q

ABNORMAL BREATHING PATTERNS

A
  • APNEUSTIC BREATHING
  • BIOT’S BREATHING
  • CHEYNE-STOKES BREATHING
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15
Q

APNEUSTIC BREATHING

A
  • prolonged inspiration alternating with short period of expiration
  • CAUDAL PONS LESION where pneumatic center is located (stroke)
  • I > E
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16
Q

BIOT’S BREATHING

A
  • irregular patterns of APNEA
  • seen in patients with INCREASED INTRACRANIAL PRESSURE
  • MIDBRAIN LESION
17
Q

CHEYNE-STOKES BREATHING

A
  • cycles gradually INCREASING IN DEPTH AND FREQUENCY followed by a GRADUAL DECREASE IN DEPTH AND FREQUENCY between periods of apnea
  • lesion in the MIDBRAIN
  • INFANTS
  • during sleep in high altitude
18
Q

unusual environment

A
  • increase altitude

- increase pressure

19
Q

INCREASE ALTITUDE

A
  • O2 content is equal to PaO2 + HgB saturation + HgB concentration
20
Q

FACTORS DETERMINING HIGH ALTITUDE

PaO2 is determined by

A
  • PAO2
21
Q

FACTORS DETERMINING HIGH ALTITUDE

PAO2 is determined by

A
  • Patm

- fO2

22
Q

FACTORS DETERMINING HIGH ALTITUDE

HgB concentration is determined by

A
  • O2 release by erythropoietin by the kidney
23
Q

FACTORS DETERMINING HIGH ALTITUDE

HgB saturation is determined by

A
  • alveolar O2 (PAO2)

Patm and fO2

24
Q

HIGH ALTITUDE

Acute changes

A

1 - decrease Patm

#2 - decrease PaO2 and decrease PAO2 due to #1
- decrease PaCO2 and decrease PACO2 due to #2 peripheral chemoreceptors take place
- increase peripheral ventilation, increase systemic arterial pH CAUSING RESPIRATORY ALKALOSIS
- HYPERVENTILATION due to #2
- decrease HgB saturation due to #1 and # 2
- decrease O2 content
- no change HgB concentration

25
Q

alkalosis

A
  • increase blood pH > 7.45
26
Q

alkalemia

A
  • increase arterial blood pH > 7.45
27
Q

RESPIRATORY ALKALOSIS may be produced as a result of medical treatment (iatrogenically) during excessive mechanical ventilation.

A

Other causes include:

  • psychiatric causes: anxiety, hysteria and stress
  • CNS causes: stroke, subarachnoid haemorrhage, meningitis
  • drug use: doxapram, aspirin, caffeine and coffee abuse
  • moving into high altitude areas, where the low atmospheric pressure of oxygen stimulates increased ventilation
  • lung disease such as pneumonia, where a hypoxic drive governs breathing more than CO2 levels (the normal determinant)
  • fever, which stimulates the respiratory centre in the brainstem
  • pregnancy
  • high levels of NH4+ leading to brain swelling and decreased blood flow to the brain
  • vocal cord paralysis, compensation for loss of vocal volume results in over-breathing and breathlessness
28
Q

HIGH ALTITUDE

acclimatization 3-4 weeks the pH returned to NORMAL vs adaptation physiologic comes into play

A

1 - decrease Patm

#2 - decrease PaO2 and decrease PAO2 due to #1
- decrease PaCO2 and decrease PACO2 due to #2 peripheral chemoreceptors take place causing
- increase in ventilation HYPERVENTILATION
- SYSTEMIC arterial pH decrease to normal via renal compensation by decreasing production of HCO3
- increase HgB CONCENTRATION due to increase production of erythropoietin by the kidney
- decrease HgB SATURATION due to #1 and # 2
- increase O2 content back to normal
- POLYCYTHEMIA
- INCREASED MITOCHONDRIA
- ANGIOGENESIS
- decrease PaO2 is due to increased cellular oxidative enzymes

29
Q

VENTILATION IS

A
  • INVERSE TO CO2
30
Q

O2

A
  • 21%

- side effects O2 toxicity

31
Q

nitrogen

A
  • 79% of breath insoluble at sea level, it cannot dissolve or diffuse
  • dissolved in the plasma
  • nitrogen narcosis
  • caissons disease
32
Q

caissons disease (bends)

A
  • breathing high pressure nitrogen for prolonged period
  • sudden decompression- nitrogen bubbles due to undissolving of nitrogen in plasma nitrogen narcosis same as air embolism
33
Q

treatment caissons disease (bends)

A
  • repressurized

- redissolved the nitrogen to slowly release pressure

34
Q

decompression sickness

A
  • gas bubbles blocking blood vessels

PHYSIOLOGY (40 decks)

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