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Acid Base Phys 2
| Question | Answer |
|---|---|
| What is the main characteristic of acid-base disorders? | abnormal H+ conc. in blood; abnormal pH |
| What is acidemia? | Increased H+ concentration in blood; decreased pH |
| What is alkalemia? | Decreased H+ concentration in blood; increase pH |
| What pathophysiological process is acidemia caused by? | Acidosis |
| What pathophysiological process is alkalemia caused by? | Alkalosis |
| What causes metabolic acidosis? What does it lead to? | decrease bicarb concentration, leads to decrease in blood pH (acidemia) |
| What causes metabolic alkalosis? What does it lead to? | increase in bicarb concentration, leads to increase in pH |
| What causes respiratory acidosis | hypoventilation (memory tip: hypo = low, low pH = acid) |
| What causes respiratory alkalosis | hyperventilation (memory tip: hyper = high, high pH = alkaline) = xs loss of CO2 |
| What is the first line of defense to an acid-base disturbance? | buffering in ECF/ICF |
| Two additional types of compensatory responses to acid-base disturbances | respiratory compensation, renal compensation |
| Compensatory response to metabolic acid-base disturbance? | respiratory - modulate PCO2 |
| Compensatory response to respiratory acid-base disturbance? | renal - modulate conc of bicarb |
| The compensatory response is always____as the original disturbance | in the same direction. (in metabolic acidosis, concentration of bicarb decreases, in respiratory acidosis, PCO2 increases) |
| What do the renal rules predict for metabolic disorders? | expected compensatory change in PCO2 (respiratory compensation) for a given change in bicarb concentration |
| What to the renal rules predict for respiratory disorders? | expected compensatory change in bicarb concentration (metabolic/renal compensation) for a given change in PCO2 |
| Situations that can cause metabolic acidosis | 1. Increased production of fixed acids 2. Ingestion of fixed acids 3. Inability of kidneys to excrete fixed acids 4. Loss of bicarb via kidneys or GI tract |
| Ways we gain fixed acid (H+) that can lead to metabolic acidosis | increased production or ingestion of fixed acid decreased excretion of fixed acids |
| Ways excess fixed acid is buffered in the ICF and ECF | ICF - proteins, organic phosphates ECF - H+ buffered by HCO3- (decreasing bicarb conc.) |
| Mechanism of respiratory compensation in metabolic acidosis | - decreased arterial pH stimulates peripheral chemoreceptors in the carotid bodies - causes hyperventilation in response - hyperventilation causes decrease in PCO2 |
| Mechanism of renal correction in metabolic acidosis | -buffering and compensation happen quickly - ultimate correction takes several days |
| Cause of metabolic alkalosis | Increase in bicarb conc. in blood, mainly loss of fixed acid from body (vomiting) |
| Gastric parietal cells use carbon dioxide and water to produce what? Where do these products go? | H+ and HCO3- ; H+ goes into stomach lumen. HCO3- goes into blood stream. |
| Describe ICF buffering in metabolic alkalosis | H+ leaves the cell in exchange for K+. This leads to hypokalemia. |
| What is the respiratory compensation for metabolic alkalosis? | - increase in arterial pH inhibits peripheral chemoreceptors - hypoventilation response |
| Three secondary effects cause by ECF volume contraction in metabolic alkalosis. | -metabolic alkalosis (loss of fixed H+) -metabolic alkalosis (RAAS -induced increase in bicarb reabsorption, H+ secretion) -hypokalemia (RAAS-induced inccrease in K+ secretion) |
| What does hypoventilation cause? | retention of CO2, increase in PCO2 |
| Causes of CO2 retention | -inhibition of medullary respiratory center (opioids) - paralysis of respiratory muscles - airway obstruction - CO2 exchange failure in alveoli (eg COPD) |
| Relationship between PCO2 and pH | inversely related |
| Relationship between PCO2 and [HCO3-] | directly related by mass action |
| where does buffering of CO2 occur? | ICF - especially RBCs |
| renal compensation for respiratory acidosis | - increase in H+ excretion as NH4+ - increase in HCO3- synthesis and reabsorption |
| describe acute respiratory acidosis | pH quite low, no renal compensation yet |
| describe chronic respiratory acidosis | renal compensation increases bicarb conc, tends to normalize ratio of bicarb to CO2 and pH |
| Causes of hyperventilation | -direct stimulation of medullary respiratory center - hypoxemia -mechanical ventilation - PE - high altitude |
| What is the primary disturbance in respiratory alkalosis? | Decrease in PCO2 |
| where does buffering occur in respiratory alkalosis? | ONLY in ICF - RBCs |
| renal compensation for respiratory alkalosis | -decrease in H+ excretion as NH4+ -decrease in HCO3- synthesis and reabsorption |
| describe acute respiratory alkalosis | -renal compensation hasn't happened yet -pH still quite high |
| describe chronic respiratory alkalosis | renal compensation decreases bicarb conc, normalizes ratio of bicarb to CO2 and pH |
Created by:
rhumes
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