Outline

Chapter 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 per hour in dry hot climate

- 30-50 mEq/L Na

- Thirst is primary compensation for this

- Sweat sodium losses can result in hypovolemia

- Burns and exudative skin losses changes the nature of fluid losses resulting in fluid losses more similar to plasma with a variable amount of protein

- Bronchorrhea

- Sequestration into a third space

- Volume Deficiency produced by the loss of interstitial and intravascular fluid into a third space that is not in equilibrium with the extracellular fluid.

- Hip fracture 1500-2000 into tissues adjacent to fxr

- Intestinal obstruction, severe pancreatitis, crush injury, bleeding, peritonitis, obstruction of a major venous system

- Difference between 3rd space and cirrhosis ascities

- Rate of accumulation, if the rate is slow enough there is time for renal sodium and water compensation to maintain balance.

- So cirrhotics get edema from salt retension and do not act as hypovolemia

- Hemodynamic response to volume depletion

- Initial volume deficit reduced venous return to heart

- Detected by cardiopulmonary receptors in atria and pulmonary veins leading to sympathetic vasoconstriction in skin and skeletal muscle.

- More marked depletion will result in decreased cardiac output and decrease in BP

- This drop in BP is now detected by carotid and aortic arch baroreceptors resulting in splanchnic and renal circulation vasoconstriction

- This maintains cardiac and cerebral circulation

- Returns BP toward normal

- Increase in BP due to increased venous return

- Increased cardiac contractility and heart rate

- Increased vascular resistance

- Sympathetic tone

- Renin leading to Ang2

- These can compensate for 500 ml