Flashcards in REGULATION OF ALVEOLAR VENTILATION high altitude vs acclimatization Deck (34)
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1
ALVEOLAR VENTILATION
- mediated by
- CENTRAL CHEMORECEPTORS
- PERIPHERAL CHEMORECEPTORS
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CENTRAL CHEMORECEPTORS
- in the MEDULLA of the brain
- MONITOR MAINLY ARTERIAL CARBON DIOXIDE
- monitor hydrogen ions
- main drive for alveolar ventilation
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PERIPHERAL CHEMORECEPTORS
only ARTERIAL OXYGEN MAIN JOB
- located in the CAROTID SINUS AND AORTIC ARCH
- monitor arterial OXYGEN MAINLY
- LEAST extent monitor arterial CO2
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PERIPHERAL CHEMORECEPTORS
(only ARTERIAL OXYGEN MAIN JOB) takes over the job of CENTRAL CHEMORECEPTORS (only MONITOR MAINLY ARTERIAL CARBON DIOXIDE)
- when there is dramatic fall in PaO2
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arterial hydrogen ions
- 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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MENINGITIS
- 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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chronic hypoventilation
- 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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treatment of DECREASE PaO2
- 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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ANEMIA
- decrease total O2 content
- normal PaO2
- normal PaCO2
- no ventilatory changed
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CASE: from room air to oxygen mask 21% (same as room air)
- SAME/NORMAL ventilation
- central chemoreceptors
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CASE: from room air to oxygen mask 100% for 15 mins.
- 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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CASE: room air to 3% CO2 and 15% O2
normal CO2 in room air
- hyperventilation by peripheral chemoreceptors
- due to decrease in O2
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normal ventilation center
- medulla
- normal ventilatory rhythm EXPIRATION > INSPIRATION
- MOST COMMONLY AFFECTED IN STROKE PATIENTS
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ABNORMAL BREATHING PATTERNS
- APNEUSTIC BREATHING
- BIOT'S BREATHING
- CHEYNE-STOKES BREATHING
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APNEUSTIC BREATHING
- prolonged inspiration alternating with short period of expiration
- CAUDAL PONS LESION where pneumatic center is located (stroke)
- I > E
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BIOT'S BREATHING
- irregular patterns of APNEA
- seen in patients with INCREASED INTRACRANIAL PRESSURE
- MIDBRAIN LESION
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CHEYNE-STOKES BREATHING
- 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
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unusual environment
- increase altitude
- increase pressure
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INCREASE ALTITUDE
- O2 content is equal to PaO2 + HgB saturation + HgB concentration
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FACTORS DETERMINING HIGH ALTITUDE
PaO2 is determined by
- PAO2
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FACTORS DETERMINING HIGH ALTITUDE
PAO2 is determined by
- Patm
- fO2
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FACTORS DETERMINING HIGH ALTITUDE
HgB concentration is determined by
- O2 release by erythropoietin by the kidney
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FACTORS DETERMINING HIGH ALTITUDE
HgB saturation is determined by
- alveolar O2 (PAO2)
Patm and fO2
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HIGH ALTITUDE
Acute changes
#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
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alkalosis
- increase blood pH > 7.45
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alkalemia
- increase arterial blood pH > 7.45
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RESPIRATORY ALKALOSIS may be produced as a result of medical treatment (iatrogenically) during excessive mechanical ventilation.
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
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HIGH ALTITUDE
acclimatization 3-4 weeks the pH returned to NORMAL vs adaptation physiologic comes into play
#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
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VENTILATION IS
- INVERSE TO CO2
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O2
- 21%
- side effects O2 toxicity
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nitrogen
- 79% of breath insoluble at sea level, it cannot dissolve or diffuse
- dissolved in the plasma
- nitrogen narcosis
- caissons disease
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caissons disease (bends)
- breathing high pressure nitrogen for prolonged period
- sudden decompression- nitrogen bubbles due to undissolving of nitrogen in plasma nitrogen narcosis same as air embolism
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treatment caissons disease (bends)
- repressurized
- redissolved the nitrogen to slowly release pressure
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