Acid-Base Abnormalities PDF
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This document provides an overview of acid-base abnormalities, including pH control mechanisms, volatile acids, non-volatile acids, and physiological buffers. It covers different types of acid-base imbalances, such as acidosis and alkalosis, and their causes and clinical considerations.
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ACID-BASE ABNORMALITIES Normal pH (7.35–7.45) H+ must be neutralized by the retention of bicarbonate or excreted. Lungs, and kidneys are major organs involved in the regulation of acid-base balance. pH below 6.8 = death pH above 7.8 = death Carbonic System / Equation: CO2 + H2O ➔ H2CO3 ➔ HCO3- +...
ACID-BASE ABNORMALITIES Normal pH (7.35–7.45) H+ must be neutralized by the retention of bicarbonate or excreted. Lungs, and kidneys are major organs involved in the regulation of acid-base balance. pH below 6.8 = death pH above 7.8 = death Carbonic System / Equation: CO2 + H2O ➔ H2CO3 ➔ HCO3- + H+ - Carbonic system is exchange of carbon dioxide & water to form carbonic acid that dissociates into bicarbonate and hydrogen ions - CO2 & H2O are eliminated by lungs - Bicarb are produced and either retained or eliminated & H+ eliminated via kidneys - Maintain homeostasis pH Control Mechanisms Kidneys: Bicarb ○ Metabolic acidosis or alkalosis determined by amount of bicarb produced or reabsorbed through kidneys Lungs: CO2 Chemical buffers ○ Buffering systems usually plasma proteins and the carbonic acid equation ○ Carbonic acid is a buffer so we don't have H+ circulating all over ○ RBC binds to H+ ions as well and serves as a buffer Volatile Acids in Body Carbonic acid (H2CO3) Can be eliminated as CO2 gas via the lungs *Definition: acid that can associate and dissociate When you’re sick, you retain organic acids - inc H+ ions in body and become more acidotic dt ineffective elimination of the organic acids Non-volatile Acids in Body Sulfuric, phosphoric, and other metabolic acids Eliminated by the renal tubules w/ the regulation of HCO- Physiological Buffers Binds excessive H+ or OH− without significant change in pH Located in ICF and ECF [intracellular and extracellular environments] ○ Consist of a buffering pair: weak acid/conjugate base. ○ Most important plasma buffering systems: carbonic acid-bicarbonate system and hemoglobin Associate and dissociate instantaneously ○ Notes: buffers allow for binding to avoid constant fluctuations to help maintain normal pH (7.35-7.45) Response to Acid-Base Imbalance 4 Categories of Acid-Base Imbalances Metabolic Acidosis (dt renal portion off balance w/ not eliminating enough H+ or not producing or retaining enough bicarb) ○ Compensation w/ Lungs kick in -> inc RR -> elim CO2 & H2O via respiration ○ Compensation w/ kidneys: retain bicarb & elim H+ via urine Metabolic Alkalosis (dt too much bicarb or excessive loss of H+) Respiratory Acidosis (pt stops breathing) ○ Can be dt lung damage - retaining CO2, becoming acidotic, or hypoventilation ○ Compensation w/ kidneys: Takes hours to days Respiratory Alkalosis (hyperventilation) Lung Response is QUICK -- Renal (Kidney) Response is SLOW Bicarb is represented by CO2 in an electrolyte panel pH HCO PCO2 3 ⬇️ Acidosis ⬇️ ⬇️ Metabolic Metabolic Acidosis pH LOW [7.45] HCO3- HIGH Bicarbonate concentration is increased, usually from excessive loss of metabolic acids (Cl −) Causes: - Excessive loss of chloride - Excessive bicarbonate intake or reabsorption Examples - Prolonged vomiting - Gastric suctioning - Hyperaldosteronism w/ hypokalemia - Diuretic therapy Symptoms of metabolic alkalosis ⬇️ Acidosis ⬆️ ⬆️ Respirator y Respiratory Acidosis pH LOW [7.45] pCO2 LOW [ 48 hours If sodium been that way over 48h, body has started to adjust If acute, need to think how many mmol/hr to correct it to avoid complications Risk in Addressing Sodium Abnormalities Rapid shift to HYPOTONIC environment -- CEREBRAL EDEMA ○ You can give NaCl 0.9% will be relatively hypotonic if the cell is very dry so the cell will suck in water from that fluid -> cerebral edema ○ Water intoxication w/ free water (overhydration) – overwhelm astrocytes – enter CNS to cause cerebral edema, lysis, and even death ○ *Issue with correcting dehydration too fast Rapid correction of sodium -- ACUTE DEMYELINATION SYNDROME ○ Sucks water out of sell – paralysis, weakness, acute demyelination ○ *Issue w/ correcting overhydration via sodium intake too fast HYPERNATREMIA [Na+ >145 mmol/L] Causes: ○ Free water deficit (or access to it) ○ Excessive salt intake Bicarb during resuscitation! ○ Symptoms: thirst, lethargy, confusion, weakness HYPOVOLEMIC Hypernatremia [LOW volume, HIGH Sodium] ○ Loss or inaccessibility to free water Loop diuretics (decreased sodium reabsorption, increased water loss) Osmotic diuretics DKA, Diabetes insipidus (DI) >>loop diuretics – distal tubule – dec sodium reabsorption >>osmotic diuretics – renal tubules – water sucked in (e.g. mannitol) - cause diuresis >>Causes osmotic pull (e.g. DKA, DI [don't produce ADH or vasopressin so we have so much sodium (It's osmolar that pulls water with it) so we're pouring out water (polyuria) --> low vol so cause sodium to be high] EUVOLEMIC Hypernatremia [NORMAL volume. HIGH Sodium; compensatory mechs or chronic conditions] ○ Sweating (sweat is hypotonic) ○ Altered thirst mechanisms (age, CNS abnormalities) Sweat is hypertonic (has kits of water in it) - lose water/volume from sweat but sodium stays in the body Older person: doesn’t have a thirst drive,but not always dehydration (same w/ CNS abnormalities), altered thirst mechanisms – hold onto more water (euvolemic) but sodium inc in relation to the amount of fluid they have HYPERVOLEMIC Hypernatremia [HIGH volume, HIGH sodium] ○ Admin of hypertonic saline, bicarbonate Free Water Deficit - Euvolemic, Hypovolemic - (0.6 x kg) x (Na/140-1) - Correct by