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Chapter Fourteen, part 1.  Hypovolemic States

Chapter Fourteen, part 1. Hypovolemic States

FromChannel Your Enthusiasm


Chapter Fourteen, part 1. Hypovolemic States

FromChannel Your Enthusiasm

ratings:
Length:
106 minutes
Released:
Jan 29, 2024
Format:
Podcast episode

Description

OutlineChapter 14- Hypovolemic States- Etiology - True volume depletion occurs when fluid is lost from from the extracellular fluid at a rate exceeding intake - Can come the GI tract - Lungs - Urine - Sequestration in the body in a “third space” that is not in equilibrium with the extracellular fluid. - When losses occur two responses ameliorate them - Our intake of Na and fluid is way above basal needs - This is not the case with anorexia or vomiting - The kidney responds by minimizing further urinary losses - This adaptive response is why diuretics do not cause progressive volume depletion - Initial volume loss stimulates RAAS, and possibly other compensatory mechanisms, resulting increased proximal and collecting tubule Na reabsorption. - This balances the diuretic effect resulting in a new steady state in 1-2weeks - New steady state means Na in = Na out - GI Losses - Stomach, pancreas, GB, and intestines secretes 3-6 liters a day. - Almost all is reabsorbed with only loss of 100-200 ml in stool a day - Volume depletion can result from surgical drainage or failure of reabsorption - Acid base disturbances with GI losses - Stomach losses cause metabolic alkalosis - Intestinal, pancreatic and biliary secretions are alkalotic so losing them causes metabolic acidosis - Fistulas, laxative abuse, diarrhea, ostomies, tube drainage - High content of potassium so associated with hypokalemia - [This is a mistake for stomach losses] - Bleeding from the GI tract can also cause volume depletion - No electrolyte disorders from this unless lactic acidosis - Renal losses - 130-180 liters filtered every day - 98-99% reabsorbed - Urine output of 1-2 liters - A small 1-2% decrease in reabsorption can lead to 2-4 liter increase in Na and Water excretion - 4 liters of urine output is the goal of therapeutic diuresis which means a reduction of fluid reabsorption of only 2% - Diuretics - Osmotic diuretics - Severe hyperglycemia can contribute to a fluid deficit of 8-10 Iiters - CKD with GFR < 25 are poor Na conservers - Obligate sodium losses of 10 to 40 mEq/day - Normal people can reduce obligate Na losses down to 5 mEq/day - Usually not a problem because most people eat way more than 10-40 mEq of Na a day. - Salt wasting nephropathies - Water losses of 2 liters a day - 100 mEq of Na a day - Tubular and interstitial diseases - Medullary cystic kidney - Mechanism - Increased urea can be an osmotic diuretic - Damage to tubular epithelium can make it aldo resistant - Inability to shut off natriuretic hormone (ANP?) - The decreased nephro number means they need to be able to decrease sodium reabsorption per nephron. This may not be able to be shut down acutely. - Experiment, salt wasters can stay in balance if sodium intake is slowly decreased. (Think weeks) - Talks about post obstruction diuresis - Says it is usually appropriate rather than inappropriate physiology. - Usually catch up solute and water clearance after releasing obstruction - Recommends 50-75/hr of half normal saline - Talks briefly about DI - Skin and respiratory losses - 700-1000 ml of water lost daily by evaporation, insensible losses (not sweat) - Can rise to 1-2 liters
Released:
Jan 29, 2024
Format:
Podcast episode

Titles in the series (19)

A chapter by chapter recap of Burton Rose’s classic, The Clinical Physiology of Acid Base and Electrolyte Disorders, a kidney physiology book for nephrologists, fellows, residents and medical students.