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Phys3 Acid/base phys
Phys3 Komar Acid/base Physiology I, II, & III
Question | Answer |
---|---|
ratio of HCO3- to PaCO2? | 20:1. **[HCO3-]: 24. PaCO2: 40x0.03 |
Assesing Acid/Base disorders: if change in pH and change in PCO2 are opposite? | RESPIRATORY |
Assesing Acid/Base disorders: if change in pH and change in [HCO3-] are in same direction? | METABOLIC |
Once Acid/base disorder is identified by initial change (change in either {HCO3-] or PCO2), what should occur with compensatory response? | the other should change in the same direction. **if opposite direction, suspect mixed disorder. |
Definition of Acid | Donates an H+ |
Definition of Base | Accepts H+ |
Important pH ranges for body fluids: Parietal gastric juice | < 1.0 |
Important pH ranges for body fluids: Mixed gastric secretions | 1-2 |
Important pH ranges for body fluids: Liver bile | 7.4-8 |
Important pH ranges for body fluids:Pancreatic juice | 7.4-8 |
Important pH ranges for body fluids: Jejunal fluid | 7.6-8.2 |
Important pH ranges for body fluids: Ileal fluid | 7.6-8.2 |
What handles volatile acids? | LUNGS. **ex: carbonic acid b/c it is converted to CO2. |
what handles fixed acids? | KIDNEYS. **ex: lactic, acetoacetic, sulfuric, phosphoric, B-hydroxybutyric. |
Main bodily processes producing H+ | 1.Metab of carbs, FA, aa's (urea & H2O excreted, CO2 blown off). 2.Anaerobic glycolysis. 3.FA metab (prod ketone bodies). 4.aa metab (prod sulfuric/hydrochloric acid). 5.Catabolism of phospholipids & nucleic acid (prod phosphor/uric acid) |
Main bodily processes consuming H+ | 1.Ox of lactic acid. 2.Lactic acid -> glucose. 3.Ox of ketone bodies. 4.Catabolism of aa's to ammonium. 5.Metab of citrate. |
Foods with acidifying effects | 1.Proteins. 2.Bezoic acid (Cranberries, plumes, prunes). 3.Oxalic acid (tea, cocoa) |
Foods with alkalizing effects | 1.Fruits: citrus & tomoatoes (despite acidic juice, metabolism produces alkalizing citrate). 2.Vegetables. |
Do buffers prevent changes in pH? | NO, they respond and MINIMIZE the changes that do occur in pH. |
When are buffers MOST effective | If pka is within +/- 1 of deisred pH. **Keep protein functioning at premium. |
4 main buffer systems in the body | 1.Bicarbonate/CO2 (primary system in ECF). 2.Inorganic/organic phosphates (primary system in ICF). 3.Proteins (as side chain components). 4.Bone (Formation produces H+, Resorption consumes H+). |
Could liver disease affect pH? | YES, albumin and proteins are important buffers. |
Buffer systems seen in plasma (ECF) | 1.Bicarb/CO2. 2.Protein. 3.Inorganic Phosphates (H2PO4/HPO4) |
Buffer systems seen in interstitial fluid (ECF) | 1.Bicarb/CO2. 2.Inorganic Phosphates (H2PO4/HPO4). |
Buffer system seen in intracellular fluid (ICF) | 1.Inorganic phosphates (H2PO4/HPO4). 2.Organic phosphates. 3.Protein. 4.Bicarb/CO2. |
Buffer system in RBC | 1.Hb protein. 2.Orgnaic phosphates. 3.Inorganic phosphates (H2PO4/HPO4). 4.Bicarb/CO2. |
Buffer system in Bone | 1.Hydroxyapatite. 2.Carbonate. |
Normal arterial PaCO2, HCO3-, and base excess ranges. | 1.PCO2: 35-45mmHg. 2.[HCO3-]: 21-28mEq/L. 3.Base excess: -2 - +2 mEq/L. |
Normal venous electrolyte values of Na+, K+, CO2 content and Cl- | 1.Na+: 135-145 mEq/L. 2.K+: 3.5-5mEq/L. 3.Cl-: 95-105mEq/L. 4.CO2 content: 21-29mEq/L |
How can henderson-hasselbach find BL pH using HCO3- and PCO2? | pH = pK + log[A-]/[HA]. 1.pK @ normal body temp: 6.1. 2.[A-]: [HCO3-]. 3.[HA]: [PCO2 x 0.03]. **0.03 is the solubility of CO2. |
Difference b/w Acidosis/Alkalosis Vs. Acidemia/Alkalemia? | Osis: relates to disturbances in acid/base balance. Emia: relates specifically to BL pH. |
What is a Primary Acid/Base disturbance? | either resipiratory or metabolic. |
Difference b/w Simple Vs. Mixed Disorder? | 1.Simple: Only one primary acid/base disturbance. 2.Mixed: 2 or more primary disturbances in acid/base balance. |
Can pH be normal AND have an acid/base disturbance? | YES. with mixed alkalosis/acidosis this can happen. **need to analyze both [HCO3-] & PCO2 levels. |
Which has a greater capacity to regulate pH: Kidneys or Lungs? | KIDNEYS. **if either are compromised, acid/base disturbances will result. |
Are buffer systems compensatory mechanisms? | NO!! only the lungs & Kidneys: 1.Lungs: regulate removal of CO2. 2.Kidneys: regulate excretion/reabsorption of H+/HCO3- |
Compensation for metabolic acidosis (Dec HCO3-) | Dec PCO2 (hyperventilation) |
Compensation for metaboic alkalosis (Inc HCO3-) | Inc PCO2 (hypoventilation). |
Acute response to respiratory acidosis? | Buffering systems: 1.Hb. 2.Serum proteins (carbaminos). 3.Phosphates. |
Chronic response to respiratory acidosis? | Kidneys: 1.Inc excretion of titratable acids. 2.Inc generation of HCO3-. **this occurs w/in hours and is complete in days. |
Causes of respiratory acidosis? | 1.COPD. 2.Obstructive disease (asthma, bronchitis, emphysema). 3.CNS disease affecting respiration. 4.Drug inhibition of respiration. 5.Disease of respiratory muscles. |
Acute response to respiratory Alkalosis | Buffer systems; 1.H+ moves from cells to plasma. 2.Hb combines with HCO3-. 3.Inc lactic acid due Dec O2 delivery. |
Chronic response to respiratory Alkalosis | Kidneys: 1.Dec H+ excretion. 2.Dec HCO3- reabsorption. |
Causes of respiratory Alkalosis | 1.Psychogenic Hyperventilation. 2.Altitude. 3.Improper ventilator use. 4.Drugs (aspirin). 5.Fever. |
Differentiate b/w acute or chronic respiratory acidosis | Chronic will have Inc ammonium (NH4) levels in urine. |
Differentiate b/w acute or chronic respiratory alkalosis | Chronic will have Inc HCO3- levels in urine and Dec ammonium (NH4) levels. |
What is the Anion Gap | Change of [Anion] (conjugate base) after introduction of an acid. **Anion Gap=[Na+]-([Cl-]+[HCO3-]) |
Using the Anion Gap to distinguish metabolic acidosis | 1.Normal Anion Gap + Hyperchloremic: Inc [Cl-], Dec [HCO3-], normal [unmeasured anions]. 2.Inc Anion Gap + normochloremic: Normal [Cl-], Dec [HCO3-], Inc [unmeasured anions]. |
Normal anion gap values | Anion Gap: 9-16mEq/L. **Anion Gap=[136]-([100]+[24]) |
What is the Anion Gap | |
Using the Anion Gap to distinguish metabolic acidosis | 1.Normal Anion Gap + Hyperchloremic: Inc [Cl-], Dec [HCO3-], normal [unmeasured anions]. 2.Inc Anion Gap + normochloremic: Normal [Cl-], Dec [HCO3-], Inc [unmeasured anions]. |
Normal anion gap values | Anion Gap: 9-16mEq/L. **Anion Gap=[136]-([100]+[24]) |
Compensation for hyperchloremic metabolic acidosis? | 1.Hyperventilation. 2.Inc acid excretion (except with RTA) |
Metabolic acidosis with NORMAL anion gap? | Hyperchloremic metabolic acidosis. **Dec [HCO3-]. **Inc [Cl-] |
Metabolic acidosis with WIDE anion gap? | Normochloremic metabolic acidosis. **Dec [HCO3-]. **Normal [Cl-] |
Causes of hyperchloremic metabolic acidosis | 1.Diarrhea. 2.Type I,II,IV Renal Tubular Acidosis. 3.Drugs (acetazolamide for glaucoma). 4.Ammonium Chloride ingestion. |
Compensation for hyperchloremic metabolic acidosis? | 1.Hyperventilation. 2.Inc acid excretion (except with RTA) |
Metabolic acidosis with WIDE anion gap? | Normochloremic metabolic acidosis. **Dec [HCO3-]. **Normal [Cl-] |
Causes of Normochloremic metabolic acidosis | ELMPARK MUDPILES KULT |
compensation for normochloremic metabolic acidosis | 1.Hyperventilation. 2.Kidney increases acid excretion. |
Delta Ratio | Used to determine if a mixed acid/base disorder is present. DR = change in anion gap/ change in [HCO3-] |
When do you use the delta ratio? | when there is a high anion gap with metabolic acidosis. |
Delta ratio values | 1.Normal: ~1-2 (no mixed disorder). 2. < 1: simultaneous normal anion gap acidosis. 3.> 2: simultaneous metabolic alkalosis OR compensatory chronic respiratory acidosis |
Why does a Delta ratio > 2 indicate simultaneous metabolic alkalosis or compensatory chronic respiratory acidosis? | B/c there is a lesser Dec in [HCO3-] than expected in metabolic acidosis. **therefore something else is going on to slightly Inc the [HCO3-]. |
What is metabolic alkalosis ALWAYS associated with? | Renal impairment. Causes Inc [HCO3-] in plasma. |
Causes of metabolic alkalosis | 1.vomiting. 2.nasogastric suction. 3.posthypercapneic alkalosis). 4.Rapid infusion of bicard, lactate, or citrate. |
compensation for metabolic alkalosis | 1.Hypoventilation. 2.Kidneys excrete excess bicarb. |
Acidosis effects of respiration | 1.Hyperventilation. 2.Right shift of Oxygen dissociation curve. 3.Dec 2,3 BPG. |
Acidosis effects on CV system | 1.Dec inotropy. 2.Inc SNS outflow. 3.resistance to catecholamines. 4.Venoconstriction. 5.Vasoconstriction of pulmonary arteries. |
Acidosis effects on CNS | 1.Vasodilation (Inc intracranial pressure) |
Acidosis effects on bone, K+, and ECF phosphate? | 1.Inc bone resorption (consumes H+). 2.Shifts K+ out of cell: Hyperkalemia. 3.Inc ECF phosphate. |
Alkalosis effects on respiration | 1.Hypoventilation (due to inhibition of respiratory drive via central & peripheral chemoreceptors). 2.Left shift of oxygen dissociation curve. 3.Inc 2,3 BPG |
Alkalosis effects on CV system | 1.Dec Inotropy. 2.Arrhythmias |
Alkalosis effects on CNS | 1.Vasoconstriction (leads to confusion, seazures, unconciousness). 2.Inc neuromuscular excitability. |
Alkalosis effects on K+ | Since H+ out of cells, leads to hypokalemia. |
K+ changes with pH changes | 1.Alkalosis: H+ moves out of cell, so K+ moves in causing HYPOkalemia. 2.Acidosis: H+ moves into cell, so K+ moves out causing HYPERkalemia. |
Ca+ changes with pH changes | 1.Alkalosis: anionic proteins more neg, so more Ca+ is bound cuasing HYPOcalcemia. 2.Acidosis: anionic proteins are less negative, so less Ca+ is bound causing HYPERcalcemia. |