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Phys3 Acid/base phys

Phys3 Komar Acid/base Physiology I, II, & III

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.
Created by: WeeG



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