Body Compartments PDF

*Renal physiology, fluids and electrolytes* Renal function - Receives 20-25% CO - Ultrafiltrate: 180L daily - Reabsorption: 1-2L - Functions: - maintains osmotic pressure - electrolytes - glucose reabsorption - removes nitrogenous waste - others: RBC p...

*Renal physiology, fluids and electrolytes* Renal function - Receives 20-25% CO - Ultrafiltrate: 180L daily - Reabsorption: 1-2L - Functions: - maintains osmotic pressure - electrolytes - glucose reabsorption - removes nitrogenous waste - others: RBC production (EPO), hormones, calcium/phosphorus metabolism, secretes hormones Renal anatomy (see pictures) - Located below the diaphragm in the RP space - Renal artery, vein and ureter align = hilum - Renal calyx (holds urine): congregates to the renal pelvis - The hilum leads into the ureter - Renal cortex is on the outside (shell), renal medulla is inside (core) - Nephron is the functional unit of the kidney (count around 1 million) - Have a capillary bed (which is the glomerulus) - There are juxtamedullary nephrons and cortical nephrons - Glomerulus: network of capillaries (group of small blood vessels) - Bowman's capsule: double-walled capsule that encases the glomerulus - "Glomerular capsule" - Comprised of epithelial cells - Is continuous with a long tubule that collects filtrate - Drains into the renal pelvis, specifically per the picture the proximal convoluted tubule - Glomerular capillaries are positioned between afferent and efferent arterioles - Afferent arterioles carry blood INTO the glomerulus - Efferent arterioles carry blood OUT of the glomerulus - Pressure in the glomerular capillaries is a function of them BOTH - Fluid, amino acids, ions (small particles) are RAPIDLY filtered - Higher molecular weight proteins and RBCs are retained in capillary, SLOWLY (if at all) filtered - Filtration rate is influenced by MAP, CO, and the SYMPATHETIC nervous system Renal blood flow - Cortex receives 94% renal blood flow (\@1L/min) - **The cortex RATHER than the medulla receives more blood flow** - This is because the cortex's man purpose is filtration, while the medulla's main purpose is to concentrate urine. - **Autoregulation** occurs at MAP 80-180 mmHg (how the kidney modifies GFR and RBF) - Changes and stabilization - [Afferent glomerular arterioles CHANGE] (respond to BP changes) - They carry blood into the glomerulus - [GFR and RBF remain STABLE] (over a wide range of perfusion pressures) Macula densa - Regulates tubuloglomerular feedback (TGF) to maintain GFR (again homeostasis) - Changes the rate of filtration by reflex vasoconstriction or dilation of the **AFFERENT** arteriole - Vasoconstriction ---\> high flow rates ---\> increased solute delivery - Vasodilation ---\> low flow rates ---\> decreased solute delivery Kidneys and blood fluid regulation - Primary role in regulation (blood, ECFV \[AVP, ANP, RAAS\], osmolarity, plasma concentration of ions/urea) - All these systems (AVP, ANP, RAAS) adjust to maintain homeostasis - In addition to filtration, reabsorption, excretion Renal tubules - Proximal tubule comes off the glomerulus ---\> LOH ---\> medulla ---\> dDCT - *Picture this*: Capsule/head and capillaries are in the cortex, loop is in the medulla - **Nephron loops in the medulla, osmolarity is concentrated** - **HYPERTONIC, urine is concentrated** - Cortex osmolarity: 300 mOsm (more dilute) - Medulla osmolarity: 1200 mOSm (more concentrated) - ⅔ of reabsorption and secretion occurs in the proximal tubule - Collecting system receives urine from nephrons RAAS (renin-angiotensin-aldosterone system) - **Stimulus**: decrease in renal perfusion (at the juxtaglomerular apparatus), renal hypoperfusion - Kidneys secrete renin and renin triggers → - Liver releases angiotensinogen - Which is converted into angiotensin I - ACE from the lungs converts angiotensin I to angiotensin II - Angiotensin II stimulates the release of aldosterone - Net effect: - Circulating volume increases - Juxtaglomerular apparatus perfusion increases - Increased NaCL and H2O reabsorption (water and salt retention) - Increased BP - Increased K+ secretion - Increased ADH secretion Measuring kidney function - GFR and SCr are commonly used - GFR is based on age, race, gender, muscle (normal: 75-115) - Expect a higher GFR in younger, male patients because they have MORE muscle mass - SCr is LESS sensitive (normal 0.5-1.2) - See a decrease in GFR BEFORE we see an increase in SCr - ***Test question: Which one is the better indicator of kidney function? GFR*** Acute kidney injury (AKI) - 3 major classifications: Prerenal, intrarenal, postrenal - Prerenal: "what happens before we hit the kidney" - Can see azotemia - HIGH concentrations of nitrogen-containing substances (urea) in the blood - MAIN CAUSE: hypoperfusion - Common causes: dehydration, septic shock, heart & liver failure, HD changes, medications - Medications include diuretics, NSAIDs, ACEIs, ARBs, cyclosporine - Prerenal azotemia (hypoperfusion) can lead to acute tubular necrosis (ATN) - Treatment: correct the underlying circulation problem - Intrarenal: "what happens in the kidney" - MAIN CAUSE: acute tubular necrosis - Caused by ischemia or nephrotic agents (iodine, ABX, atheroembolism) - Most common peri operative cause (secondary to renal medullary ischemia) - **More common in major operations with significant blood loss and hypotension** - Cardiac surgery, valve surgeries, vascular procedures with aortic cross clamp, aortic surgeries, procedures on CPB, intrapersonal procedures (with fluid shifts) - Overarching causes: ischemia, sepsis, infection, nephrotoxins (exogenous: contrast, antibiotics; endogenous: hemolysis, rhabdomyolysis, myeloma, crystals) - Postrenal: "what happens after the kidney" - Also known as OBSTRUCTIVE nephropathy - See impedance/hinderance to urine flow - Causes: renal stones, prostatic hypertrophy, mechanical obstruction by catheters - **Diagnosis** (do not need to memorize, need to know for clinical) - RIFLE - Risk of renal dysfunction: SCr 1.5x, UOP x 0.5 ml/kg x 6 hours - Injury to kidney: SCr 2x, UOP \ low H2O - Down its concentration gradient - This is a PASSIVE process Oncotic pressure - Part of osmotic pressure - Pressure exerted by colloids (albumin, globulin, fibrinogen) aka colloid osmotic pressure **Pressure and capillaries** - Arteriole: oncotic pressure \> osmotic pressure (H2O and nutrients move OUT) - Venule: osmotic pressure \> oncotic pressure (H2O and nutrients move IN) **Starling\'s law of the capillary** - Capillary oncotic pressure: inward pressure in capillaries (generated by proteins) - Capillary hydrostatic pressure: outward movement of fluid - Interstitial oncotic pressure: fluid drawn out of the capillaries (normally this is ZERO) - Interstitial hydrostatic pressure: inward movement of fluid (normally this is LOW) Capillary permeability - Brain: tight junctions limit passage of only small molecules - Liver: wide channels allow almost all molecules to pass - Kidneys: fenestrae allow large volume of small molecules to pass Daily water needs (based on size and surface area for water requirements ONLY) - First 10 kg = 4 ml/kg/hr = 100 ml/kg/day - Next 10 kg = 2 ml/kg/hr = 50 ml/kg/day - 20+ kg = 1 ml/kg/hr = 20 ml/kg/day - For example: 70 kg would be 110 cc/hr Volume losses - As osmolarity increases, vasopressin increases - Vasopressin holds onto fluid to increase blood pressure - At about 290 mOSm we get thirsty (normal: 275-295 mOsm) - Insensible: 500-1000 mL/day (½ respiratory, ½ skin) - GI: 100-200 mL/day - Urinary: 1000 mL/day - Third space: shift from intravascular to interstitial space - Seen after abdominal, bowel obstruction, peritonitis, pancreatitis, sepsis, trauma - No real way to measure this, just an estimate - Surgical third space (very broad strategy) - **Replacement** (depends on the level of trauma (minor, moderate, extreme) - Minor: 4 ml/kg/hr (laparoscopic, head, neck, hernia) - Moderate: 6 ml/kg/hr (major ortho, colon resection, thoracic, off-pump CABG) - Extreme: 8 ml/kg/hr (open AAA, CPB) Colloid and crystalloid difference - Crystalloid: electrolyte solutions composed of inorganic salts (NaCl) - Colloids: large molecules (60,000 Daltons) - *Imagine the image* - Colloids fill the plasma (intravascular) more (hold) - Crystalloid fill the extra-vascular more (go straight through) Changes in plasma volume with different fluids - From highest to lowest: Albumin, NaCl, D5W Changes in interstitial volume with different fluids - From highest to lowest: NaCl, albumin + D5W (the same) Closest pH, osmolality and electrolyte composition as plasma = normosol, plasmalyte, isolyte ("PIN") **Osmolality versus osmolarity (often used interchangeably)** - Osmo**[lal]**ity: \# of moles of dissolved particles per **kg** **solvent** (mOsm/**kg**, **[direct]**, weight) - Osmo**[lar]**ity: \# of dissolved particles per **L of** **solution** (mOsm/**L**, **[indirect]** or calculated, volume) Osmolarity - Lower osmolarity = lower solutes - Higher osmolality = higher solutes (water moves towards higher solute side) - Expressed in osmoles (Osm), mEq = mOsm - Monovalent ions (ex: NaCl 0.9% = 154 mEq Na + 154 mEq Cl = **308 mOsm/L NaCl** - Close to plasma osmolarity (290 mOsm), so is LR but issue is calcium and potassium - Hypertonic: water moves out, cells shrink - Hypotonic: water moves in, cells swell - Isotonic = net water movement, cell stays the same Isotonic saline (NS) - Chosen because it is isotonic, net water moving in and out - Not so great after all (high Na+ and high Cl) - Has a lower pH (5.5) (normal: 7.4) - Risk: Hyperchloremic acidosis (with large volumes) - Mainly due to high Cl level and lack of buffer Lactated ringer's ("Hartman's solution") - Contains **potassium and calcium** - 4 mEq of potassium; 3 mEq of calcium - Also contains **LACTATE** to reduce Cl concentration and increase the pH (6.5) - The problem with this solution specifically is the CALCIUM - Calcium makes it incompatible with blood products (**NEVER use with RBCs**) - Calcium also binds to citrate and depletes these levels - Lactate load is actually pretty small (main concern is with patient with existing lactic acidosis and/or liver disease, anyone with impaired clearance of lactate) Balanced salt solutions ("PIN") - Acetate and gluconate buffers added to increase pH to 7.4 - ECF composition: potassium, sodium, magnesium - Normosol, isolyte, plasmalyte (contains phosphate 1 mEq/L) Dextrose - 5% dextrose (50 g of dextrose per L) - Usually in hypertonic solutions can use D5 ½ NS - Infused at 125 mL/hr for 3L/day and 500 kcal/day enough to spare protein catabolism in starvation, therefore has a **protein sparing effect** - Dextrose can be metabolized ---\> free water ---\> hypotonic solution now ---\> can result in swelling - Problems with dextrose: osmolarity similar to plasma, remains in intravascular space, can result in cellular swelling, enhanced lactate production (in tissue hypoperfusion, glucose ---\> lactate), INCREASED lactate levels, hyperglycemia - Research shows trickle feeds are preferred Colloid - Osmotic pressure of plasma = 20-25 mmHg, produced by plasma proteins - The oncotic pressure of 5% albumin is the MOST similar at 20 - The MOST dominant plasma protein is albumin - Weight (highest to lowest): hetastarch ---\> albumin ---\> dextran - Duration of effect (highest to lowest): hetastarch ---\> albumin ---\> dextran - Oncotic pressure (highest to lowest): albumin (25%) ---\> dextran ---\> hetastarch ---\> albumin (5%) Albumin - The most abundant plasma protein - Given to expand intravascular volume - Produced by the liver (10g/day) - Normal level 3.5-5 gm/dL - Functions: transport proteins, buffer, 75% plasma osmotic pressure, antioxidant - BEWARE of administration to Jehovah's Witness - BEWARE can cause anaphylaxis - 5% albumin - 5g/dL or 50 g/L in NS - Colloid osmotic pressure = 20 mmHg, \*isotonic - 25% albumin - Shifts water intravascularly - Hyperoncotic (oncotic pressure = 70 mmHg) HES (hetastarch) - *Chemically modified (6% solution in NS), 450,000 Daltons* - Elimination: amylase, RES, renal - Similar to 5% albumin as volume expander - **Can be allergenic** because made from starchy plants - Ideal for JH patients - Problems with hetastarch: hemostasis ([impaired platelet adhesives], inhibits VIII (and von Willebrand), **[AKI]**, hyperamylasemia (lab finding not clinically relevant), anaphylaxis (0.0006%), hextend: 6% hetastarch with electrolytes Dextrans - 10% dextran: anticoagulant effect useful (to help prevent clotting) - 6% dextran: volume expander useful - Problems: [bleeding] (impaired platelet aggregation, this makes sense because has an anticoagulant effect), i[nterfere with cross match, renal failure], **anaphylaxis (uncommon)** Hypertonic saline - Thought to decrease cerebral edema - Pulls water out of cells an into blood vessels - Used to increase intravascular volume - Useful in brain injury (alternative to mannitol) - Treatment for hyponatremia but still controversial - Be careful with administration because can be caustic to vessels - *Would need more isotonic NS because not directional (versus hypertonic)* Crystalloid versus colloid - Crystalloid preferred over colloid (just as effective and less expensive) - BEST to use the fluid that matches the patient's physiologic need Electrolytes Plasma osmolality equation (see slide 57) *Osmolality calculated by summing major solutes, sodium concentration doubled to account for chloride, glucose and BUN measured in mg/L so must be divided by atomic weights (Answer: 290 mOsm)* - Electrolyte needs - Sodium: 75 mEq per day - Potassium: 45 mEq/day plus at least 10 mEq/L of urine - Consider losses in bodily fluids Osmolal gap - **Measured --- calculated (subtraction)** - The measured minus the calculated - Measured serum osmolality minus calculated serum osmolality - May be increased in situations in which other solutes are increased in plasma - Toxins such as ethanol, methanol, ethylene glycol (if gap is 10+) - Renal failure and high anion gap metabolic acidosis (Lactic and ketoacidosis) - **THE PRIMARY CAUSE OF high osmolal gap is [ethanol] ingestion** **Hypertonic syndromes** - Serum osmolarity tightly regulated - Too high: ADH will reduce UOP, lowers osmolarity - Too low: ADH will raise UOP, increases osmolality - *More about ADH* - **RAS system:** useful in hypovolemia and shock; when ECV is low it triggers the juxtomegular apparatus + baroreceptors to release renin from kidneys, renin converts angiotensinogen (from the liver) to angiotensin 1, the lungs then convert angiotensin 1 to angiotensin 2, angiotensin 2 then stimulates aldosterone to be released from kidneys which increases water + sodium absorption; end result = increased BP, increased sodium, decreased UOP - **Where water reabsorption takes place:** proximal tubule +/- loop of Henle - **ADH:** antidiuretic hormone, it's in the name "anti-diuretic" so it prevents diuresis, kidneys hold onto water + sodium - **SIADH:** too much ADH secretion from the PP of the hypothalamus, result is water + salt retention (hyponatremia + decreased UOP + seizures), causes: oat cell carcinoma, head problems, treatment: hypertonic fluids (D5NS, D51/2NS, 3% NS), fluid restriction - **DI:** too little ADH secretion from the PP of the hypothalamus to the kidneys, result is water+salt excretion (hypernatremia + increased UOP (dilute)), causes: head problems, dilantin, treatment: hypotonic (D5W) or isotonic fluids, ADH (vasopressin, DDAVP) - **Hyperosmolarity without hypernatremia may be seen with marked hyperglycemia** Sodium concentration in body fluids - From highest to lowest: small bowel, pancreases, furosemide, sweat, gastric, diarrhea, urine Hyponatremia - Plasma sodium \