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Acid, Base, Electrolytes
Balance and Alterations
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Fluid Compartments
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Fluid Compartments: 20 – 40 – 60 Rule
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Fluid Movement
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Water and Electrolyte Balance
Input = output Hormones Na+ / K+ Renin Aldosterone ANP Reproductive Hormones GCC Ca++ / Mg++ Calcitonin PTH H2O ADH Anions follows passively Cl- HCO3- PO4=
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Water Intake Loss Osmosis Hormonal control Capillary Dynamics Normal
Abnormal Osmosis Hormonal control Capillary Dynamics CHP COP IHP IOP
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Osmosis
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Capillary Dynamics
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Capillary Pressures
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Fluid Shift to third space
Edema Effusion Transudate Low cell Low protein Exudate Types: Nonseptic, Septic Contents High cell High protein
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Edema Causes Vessels Types Obstruction Overload Inflammation
hypoalbuminemia Vessels Angioedema Lymphedema Types Localized Pitting Weeping Dependent Generalized
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Pulmonary Edema
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Pleural Effusion
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Terminology Isotonic Hypertonic Hypotonic Hypovolemia Hypervolemia
Hyperosmolar Hypotonic Hypo-osmolar
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Functions of electrolytes
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Electrolyte Fluid Composition
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Hormones that regulate Electrolytes
Aldosterone ANP PTH Cacitriol Calcitonin
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Cations + charge Location Function Hormonal Controls Alterations Hypo-
Hyper-
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Hyponatremia < 135 mEq/L Etiology Clinical Signs H20 shift to ICF
Decreased Na+ (diet) Increased H20 Diuretics Hiridosis Addison’s Disease DM Diarrhea CRF Clinical Signs H20 shift to ICF Cells swell CNS sensitive V/D Lethargy Confusion Seizures Muscle weakness
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Hyponatremia
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Hypernatremia > 147 mEq/l Etiology Clinical Signs Osmotic shrinkage
Excessive intake Hyperaldosteronism Drowning (salt water) H20 loss DI Renal Fever / Sweat Burns Diarrhea Clinical Signs Osmotic shrinkage CNS sensitive Lethargy Irritability Hemorrhage Seizures Coma Muscle weakness
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Hypokalemia < 3.5 mEq/l Etiology Clinical Signs Decreased RMP
Decreased intake ANS V/D Diuretic Sweating Digitalis Insulin excess Clinical Signs Decreased RMP Heart dysrhythmia Bradycardia AV blocks PVCs Sphincter weakness Delayed cardiac repolarization ST segment depression T decreased/inverted
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Hyperkalemia > 5.5 mEq/l Etiology Clinical Signs
Increased intake Insulin deficiency Hemolysis Hypoxia CRF Diuretics Burns Extensive surgeries Clinical Signs Inactivate Na+ channels Muscle weakness Muscle paralysis paralysis Cardiac dysrhythmia Peaked T wave Widened QRS
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Hypocalcemia < 8.5 mg/dL Etiology Clinical Signs NMJ irritability
Nutritional deficiency Osteoblastic metastasis PTH deficiency Hyperphosphatemia Increased protein binding Chelation therapy Clinical Signs NMJ irritability Muscle Spasm Dyspnea Seizures Colic Tetany Cardiac Dysrhythmia
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Hypercalcemia > 10.5 mg/dL Etiology Clinical Signs NMJ decreased
Cancer Hyperparathyroidism Bone remodeling Increased reanal filtering Clinical Signs NMJ decreased Fatigue Lethargy Weakness Cardiac dysrhythmia Bone loss Urolithiasis
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Hypomagnesemia < 1.5 mEq/l Seen with hypokalemia and hypocalcemia
Etiology Decreased dietary intake GI loss Malabsorption Maldigestion Diarrhea CRF Clinical Signs Decreased threshold Tetany Vertigo Nystagmus Muscle spasms hyperreflexia Seizures Cardiac Dysrhythmia
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Hypermagnesemia > 2.5 mEq/l Etiology Clinical Signs
Excess intake (antacids) Decreased renal excretion CRF Adrenal insufficiency Clinical Signs Increased threshold for depolarization Muscle weakness Decreased reflexes Hypotension Decrease Na+ current Cardiac dysrhythmia Bradycardia
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Anions Chloride ECF Alterations Phosphate ICF, stored in bones
Hypochloremia < 95 mEq/L Accompanies hyponatremia Severe vomiting Diuretics Hyperchloremia > 103 mEq/L Accompanies hypernatremia Phosphate ICF, stored in bones Alterations Hypophosphatemia < 2.7 mg/dL Antacid use Prolonged decrease cam cause Rickets/’Osteomalacia Hyperphosphatemia > 4.5 mg/dL Renal failure Overuse of laxatives Hypoxia
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Acid Base Terms Define pH Acid Base Salt Buffer Strong Weak
Volatile : CO2 from CH20 and Fat Metabolism Nonvolatile: H2SO4, H2PO4 from protein metabolism Base Salt Buffer
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Acid Sources
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pH Define Water Dissociation Scale Blood values Abnormal Values
pH = log (1/[H+]) pH = -log [H3O+] Water Dissociation H2O + H2O H3O+ + OH- Scale Blood values Venous Arterial Abnormal Values Acidemia Alkalemia
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pH formula and scale
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Acid Base Chart
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pH of Solutions
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Acid Base Regulation for Balance
Systems Chemical Buffer Systems Respiratory System Renal Time Seconds to Minutes Minutes to Hours Hours to Days / Weeks Strength Problems (reference 7.4 as normal average): + / changes result in respiratory rate changes + / to 0.3 changes result in CV and Nervous changes + / to 0.5 changes result in death
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Chemical Buffer Systems
Define 3 types Name of System Buffer formula or name of chemical Location Effectiveness [pKa buffer = pH location] Why important
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pH changes with/without buffers
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Bicarbonate Chemical Buffer
H2CO3, HCO3- Plasma buffer pK = 6.1 Important: Can measure components pCO2 = 40 mmHg HCO3- = 24 mM Can adjust concentration / ratio of components kidneys lungs Recalculate pH of buffer system in ECF using Henderson-Hasselbach pH = log(24 / 0.03x40) pH = log (20/1) pH = 7.4
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Bicarbonate Buffer System
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Phosphate Chemical Buffer
H2PO4-, HPO4= ICF, Urine pK = 6.8 Important Intracellular buffer ICF pH = ~ 6.5 – 6.8 Renal Tubular Fluids Urine pH ranges 6.0 – 7.0
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Protein Chemical Buffer
Proteins With Histadine: AA contain imidazole ring, pKa = 7.0 R-COOH R-COO- + H+ R-NH2 R-NH3+ ICF (hemoglobin), ECF pK = 7.4 Important Most numerous chemicals Most powerful chemical buffer
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Proteins in acid base
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Hemoglobin
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CO2 transport and RBC buffer
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Respiratory for A/B Balance
Occurs in minutes CO2 only Rate changes
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Respiratory Controls for Acid /Base balance
Volatile Acid: CO2 pH changes in CSF Respiratory Rate Pons Medulla Oblongata Chemoreceptors pCO2 pO2
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CO2 and pH Increase CO2 Decrease CO2 Increase H+ Decrease H+
Decrease pH Decrease CO2 Decrease H+ Increase pH
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Renal Control for Long Term Acid / Base Balance
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Renal processes in A/B balance
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Renal Physiology Filtration Reabsorption Secretion
Remove metabolic acids: Ketones, Uric acid Filter Base [HCO3-] @ Renal Filtration Membrane Reabsorption PCT Reverse CO2 equation to create HCO3- Secretion PCT, late DCT and Cortical CD CO2 equation to create H+ for secretion
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Renal Mechanisms for A/B
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Renal Ion Exchanges Na+ / K+ antiporter Na+ / H+ antiporter
Na+ / HCO3- cotrans H+ / K+ ATPase H+ ATPase Cl- / HCO3- exchanger
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Renal Buffer Mechanisms
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Normal Acid Base Values
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Respiratory and Renal Balance
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Acid-Base Problems Acidosis Acidemia Alkalosis Alkalemia
State of excess H+ Acidemia Blood pH < 7.35 Alkalosis State of excess HCO3- Alkalemia Blood pH >7.45
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Classifying Respiratory Acid Base Problems (pCO2 changes)
Respiratory Acidosis Respiratory Rate Decreases Any Respiratory Disease Obstruction Pneumonia Gas exchange / transport problems Respiratory Membrane RBC / Hemoglobin Respiratory Alkalosis Respiratory Rate Increases
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Classifying Metabolic Acid Base Balance Problems (H+/ HCO3-)
Systems Renal Endocrine GI Cardiovascular / Fluid administration Metabolic Acidosis Retain Acid Lose Base Metabolic Alkalosis Retain Base Lose Acid
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Other System diseases in Metabolic Acid/Base Problems
GI Vomiting Diarrhea Medications : Antacids Endocrine DM Hyperaldosteronism Metabolism Increase acid production
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Ketones
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Compensation
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Adjustments for Acid/Base Balance
Imbalance Respiratory Acidosis Incr pCO2 Respiratory Alkalosis Decr pCO2 Metabolic Acidosis Decr HCO3- Incr H+ Metabolic Alkalosis Incr HCO3- Decr H+ Compensation Increase renal acid excretion, Incr HCO3- Decrease renal acid excretion, decr HCO3- Hyperventilate to lower pCO2 Hypoventilate to increase pCO2
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Summary for A/B Balance
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Questions? Water and electrolytes
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