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28 Cards in this Set
- Front
- Back
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What happens to alveolar ventilation at the onset of exercise? How about by 90 seconds of exercise?
What does this mean about the signal for hyperpnea during exercise? |
Alveolar ventillation dramatically increases within seconds of the onset of exercise. It then has a slower increase to a steady state, reached by 90 seconds. Hyperpnea must have a fast and slow component.
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At 60% of maximal exercise capacity, what two states are observed?
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Hyperventillation
and lactacidosis. You get HYPERPNEA right away when you exercise but HYPERVENTILLATION only occurs beyond 60% |
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Homeostasis of alveolar and arterial blood gasses exists until about what percent of maximal exercise capacity? What does this mean for the signal for hyperpnea.
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60%. This means that the signal for hyperpnea cannot be from increased stimulation of carotid and intracranial chemoreceptors. This is because you start breathing faster in exercise even before gas levels in your blood change.
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How can one predict the relationship between metabolic rate and alveolar ventillation?
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Look at arterial blood gas levels. Because there is homeostasis up to 60% of maximal breathing, this means alveolar ventillation is increasing in proportion to metabolic rate. At >60% maximal intensity, Va is increasing more than metabolic rate. We know this because PCO2 levels are dropping (hyperventillation).
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Is exercise hyperpnea dependent critically on central command. Is the ventillatory response dependent critically on spinal afferents
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No, exercise is not dependent on central command.The ventillatory response does not differ between voluntary and electrically induced exercise. Exercise hyperpnea not critically dependent on SC afferents since paraplegics have similar responses to normal individuals.
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What are some of the theories on the mechanism of exercise hyperpnea?
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Humoral (blood borne) theories include carotid chemoreceptors/ CO2 sensors in the lung/sensors in the heart.
Neural mechanisms include brain control or spinal afferent control. |
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Which theory of exercise hyperpnea does forster believe in most?
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Spinal Afferent theory (group 3 and 4 afferents)
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Why maintain a narrow range of H+ in organisms? What happens in DECREASED H+ in humans? What happens in INCREASED H+ in humans.
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Maintaining optimal pH is important for enzyme function. Too little H+ - seizures
Too much H+ - comma. |
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What is physical chemical buffering?
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PCB - compounds in blood minimize changes in pH when strong acids/bases are added. ie In physical chemical breathing you replace a strong acid with a weak acid to minimize changes in pH.
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How does physical chemical buffering work for the addition of HCl?
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HCl dissociates into H+ and Cl. The Cl gets with an Na to form NaCl. The H+ gets with a bicarbonate to form carbonic acid, a weaker acid.
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How does physical chemical buffering work for adding NaOH?
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NaOH dissociates into Na and OH. The Na gets with bicarbonate to form a NaHCO3. The OH gets with an H+ to form water.
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What are the primary H+ buffers in the extracellular fluid?
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ECF - Bicarb, H2PO3, proteins
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What are the primary H+ buffers in intracellular fluid?
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ICF- H2PO3, proteins.
Remember the bicarb gets pumped out of the cell. |
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How to determine what kind of acidosis?
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First look at blood pH; if pH <7.4, acidosis. If the acidosis is due to low bicarbonate (<24) this is a metabolic acidosis with respiratory compensation (PCO2<40). If the acidosis is caused by an elevated PCO2 (>40), this is respiratory acidosis with renal compensation HCO3 >24.
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How to determine what kind of alkalosis?
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If pH >7.4, alkalosis state.
If alkalosis is caused due to elevated HCO3>24, metabolic alkalosis with respiratory compensation PCO2>40. If alkalosis caused by PCO2<40, respiratory alkalosis with renal compensation (HCO3 <24). |
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What is the isohydric principle?
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When H+ is altered, ALL buffer pairs in a solution are altered.
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What are the 2 determinants for H+ buffering capacity?
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1) concentration of the buffer.
2) pK of the buffer relative to the pH of the solution. closer pk is to pH, the better the buffer. |
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What is physiological buffering?
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Physiological buffering is the processes in the body that alter the amount of physical chemical buffers.
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How is plasma H+ regulated by transmembrane exchange?
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During respiratory acidosis, buffering of the ECF occurs by moving H+ into the cells in response for Na+ or K+.
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How is plasma H+ regulated by pulmonary ventilation?
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During metabolic acidosis, lactic acid -> lactate + H+ -> H+ and HCO3 -> H2CO3 -> H20 + CO2. The CO2 is then eliminated.
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How is plasma H+ regulated by acid/base production?
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The brain can make lactic acid to buffer a respiratory alkalosis. If strong acid production is occuring in the body, we REABSORB more HCO3 and GENERATE more HCO3.
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Regeneration of HCO3 involves the production of what molecule
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NH3. Ammonia.
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When tissues make sulfuric acid, phosphoric acid, lactic acid etc, what happens to plasma HCO3 levels.
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The H+ combines with the HCO3 to form carbonic acid which is then eliminated through breathing as CO2.
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During METABOLIC acidosis/alkalosis, does brain H+ levels change?
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No, only 10% change in brain H+ levels as compared to blood.
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During RESPIRATORY alkalosis/acidosis, does brain H+ levels change?
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Yes, BB barrier cannot buffer respiratory acidosis/alkalosis, so you get increased NH3 production in the brain to compensate for acidosis and increased lactic acid in alkalosis.
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Describe what happens when a large dose of acid is infused into the blood, bringing down the pH to 7.
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1st 30 min- 40% of infused acid buffered by HCO3.
1st hours- H+ exchange for Na or K+ in intracellular fluid. After a few hours, plasma H+ is near normal. The kidney will work over the next days to eliminate the added H+. |
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What is the anion gap?
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In a normal cell, anions and cations are equal to maintain electric neutrality. The Anion gap only concerns 3 ions though.
The formula is Anion - Cation Na - (Cl + HCO3) |
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What does an increased anion gap mean. Why
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An increased anion gap means acidosis. This is because your bicarb levels are decreased.
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