PGY 412 Fluid and Electrolyte Disorders + Respiratory Disorders

60

percent body weight accounted for by water of an average adult man

Percent Water Weight Determining Factors

build (fat is hydrophobic and adipose tissue contains very little water); sex (estrogen encourages fat storage); age (changes in muscle mass and fat storage especially in puberty/elderly)

Homeostasis

the tendency of a system to maintain internal stability, owing to the coordinated response of its parts to any stimulus that would tend to disturb its normal condition

Water Input Sources

ingested fluids; ingested food; metabolism from oxidative phosphorylation

Total Water Input and Output in Steady State

2400-3200 mL

Water Output Sources

urine; feces; sweat/skin evaporation; exhaled air

Urine Output

can be as great as 20 L per day (body fluid excess) or as little as 0.5 L per day (body fluid deficit) to balance alterations in total body water

Urobilin

a waste product of hemoglobin metabolism that is produced in a fixed quantity each day; its concentration depends only on the amount of urine generated

Near-Zero Content of Urine

glucose, amino acids, protein

Potential Toxins in Urine

metabolic wastes (potassium and urea); K+; H+

Intracellular Fluid (ICF)

cytosol

Plasma

extracellular fluid in rapid circulation that supplies cell nutrients and removes cell waste; aka intravascular fluid

Interstitial Fluid (IF)

extracellular fluid that bathes cells; transmits nutrients between ICF and plasma

60:40:20 Rule of Water Distribution

total body water is 60% of body weight (42 L); ICF is 40% of body weight (28 L); ECF is 20% of body weight (14 L) with IF being 15% and plasma being 5%

Pathologies in ICF Fluid Distribution

cels burst or shrink; neurological disorders

Pathologies in Plasma Distribution

blood pressure disturbances; cardiovascular events; majority of fluid disturbances

Pathologies in IF Distribution

edema; insufficient perfusion/lymph failure

Major Components of Fluid Composition

sodium, potassium, bicarbonate, chloride

Determinants of Blood Pressure

plasma volume, salt concentration

Blood Pressure

the result of the forces that blood and the vessels exert on each other

Hypertension

can be caused by vascular contraction (with normal plasma volume) or by an increase in plasma volume (with normal or contracted vascular tone)

Salt in the Plasma

encourages body water retention

High Salt Diet

can in the short term result in bloating and high blood pressure; kidneys eventually adjust to encourage salt excretion signaled by the high blood pressure sensors

Hypovolemia

too little plasma; risk of blood pressure being too low; tissues are not adequately perfused; symptoms include dizziness when standing, low or no urine output

Hypervolemia

too much plasma; risk of blood pressure being too high; mechanical stress on tissues and organs; symptoms include edema and high urine output; risk for stroke, vision loss, heart failure, and heart attack

Homeostatic Loop to Increased Plasma Volume (ex: excessive infusion with saline)

rise in blood pressure → sensing cells in the atria of the heart release atrial natriuretic peptide (ANP) → ANP acts on the kidneys to increase urine output → plasma volume falls, blood pressure returned to normal, signaling stops

Homeostatic Loop to Decreased Plasma Volume (ex: internal bleeding)

decrease in blood pressure → sensing cells in the renal vasculature release renin, triggering ANGII production in lungs and ALDO release from adrenal glands; sensing cells in general circulation activate the vagus nerve which leads to ADH release from pituitary → decrease urine output, increase thirst drive/fluid input, preserve blood pressure

Angiotensin II (ANGII)

produced in blood vessels of the lungs; acts on kidneys to decrease urine output; acts on the brain to increase thirst drive and fluid input; acts on the vascular system to contract vessels and preserve BP; causes constriction of afferent arteriole

Aldosterone (ALDO)

released from adrenal glands; acts on kidneys to decrease urine output; increases sodium permeability of the nephron peritubular capillaries

Antidiuretic Hormone (ADH)

released from the pituitary; acts on kidneys to decrease urine output; increases water permeability of the nephron peritubular capillaries

Atrial Natriuretic Peptide (ANP)

released from the atria of the heart; acts in the kidneys to increase urine output; inhibits ANGII production; causes constriction of efferent arteriole

Nephroms

functional unit of the kidney; 1 to 1.5 million of them in one kidney

Peritubular Capillaries

reabsorption and secretion center of the kidney; valuable components of plasma are reabsorbed into it

Two Major Control Points that Affect Urine Volume

flow into the nephron (glomerular capillaries → bowman’s capsule) and reabsorption from the nephron (peritubular capillaries)

Nephron Factors that Lower Urine Output

restricting through flow/afferent arteriole and increasing reabsorption

Nephron Factors that Raise Urine Output

diverting through flow/restricting efferent arteriole and decreasing reabsorption

Diuretics

can be useful to treat hypervolemia; block renal tubular fluid reabsorption; encourages the loss of salt and water as urine; no effect on efferent arterioles

Diuretic Targets

ALDO receptors, salt reabsorbing channels and transporters, ADH receptors, water reabsorbing channels

Diuretic Side Effects

dehydration, constipation, excessive sodium and potassium loss

Ethanol as a Diuretic

inhibits ADH secretion; increases urinary output for up to 24 hours

Plasma and IF

the same solution distributed across the capillary wall, which is freely permeable to salts, solutes, and water

Interstitial Fluid Steady State

rate of fluid exit from capillary = rate of fluid drainage into lymphatic vessels

Starling Forces

hydrostatic pressure and oncotic pressure; determine the distribution of ECF (plasma and IF)

Hydrostatic Pressure

blood pressure squeezing plasma out of the capillaries into the IF space

Oncotic Pressure

force exerted specifically by blood plasma proteins on water movement

Plasma Proteins

act as osmolytes; cannot leave the capillaries (albumin)

Positive Net Filtration Pressure

fluid is flowing from capillary to the interstitial space; higher hydrostatic pressure

Negative Net Filtration Pressure

fluid is flowing from the interstitial space to the capillary; higher oncotic pressure

Volume Homeostatic Feedback Loop

deals with the change in plasma volume

Beyond Primary Homeostatic Control

changes in extracellular fluid volume outside of the circulation; cannot be sensed

Edema

interstitial fluid build up in tissue outside of circulation; increases the diffusion distance over which nutrients, oxygen, and wastes must travel to and from circulation; insufficient perfusion can cause cell injury, death, and lead to necrosis

Localized Edema

contained ot a specific site (sprained finger) or organ (pulmonary edema)

Generalized Edema

more uniform distribution of fluid in interstitial spaces

Dependent/Pitting Generalized Edema

a manifestation of an edema hat is gravity-dependent (fluid accumulates in lowest part of the body, which depends on position)

Causes of Edema

increased capillary hydrostatic pressure, decreased capillary oncotic pressure, lymphedema

Causes of Increased Capillary Hydrostatic Pressure

increased plasma volume (Na+, water retention); local accumulation of fluid (prolonged standing, congestive heart failure); decreased vascular volume (tight clothing, inflammation of veins)

Causes of Decreased Capillary Oncotic Pressure

loss of plasma proteins into urine (kidney disease); loss of plasma proteins into IF (increased capillary permeability, burns, allergic reaction); decreased production of plasma proteins (liver cirrhosis, malnutrition)

Lymphedema

blockade of the lymphatic ducts that drain IF

Causes of Lymphedema

surgical removal (secondary: cancer treatment); physical block (secondary: tumor or injury); rare genetic condition (primary)

Treatment of Generalized Edema

lowering capillary hydrostatic pressure (promotes fluid movement from IF back into circulation where additional volume can be sensed and corrected); lower dietary salt intake; treat with diuretics to increase urine output and lower plasma volume

Treatment of Dependent Edema

compression stocking to increase IF hydrostatic pressure; pushes excess ECF back into circulation

Kwashiorkor

affects children from 1-5 years old; characterized by dependent edema (feet, abdomen) and malnutrition fueled by a diet composed almost entirely by carbohydrates (low protein → low albumin → low capillary oncotic pressure); hyporvolemia exacerbates edema

Kwashiorkor Causes of Death

secondary complications (infection/sepsis, hypovolemic shock/heart failure)

Kwashiorkor Treatment

correcting electrolyte imbalance, hypoglycemia, and macro/micronutrient deficiency

Osmolality

measurable property of a solution based on the amount of dissolved particles it contains

Tonicity

the ability of a solution to draw water out of or into cells

Iso-osmotic/Isotonic

ECF and ICF have the same osmolality; ECF solution that does not cause cells to alter volume

Hyper-osmotic/Hypertonic

plasma osmolality rises above 294; ECF solution that causes cells to shrink

Hypo-osmotic/Hypotonic

plasma osmolality falls below 280; ECF solution that causes cells to swell

Sodium (Na+)

the major osmotically active/water attracting particle in ECF; accounts for 85% of plasma osmolality; the only ECF component abundant enough that small percentage changes can substantially alter osmolality

Swollen Cells

occlude circulation and lymph drainage; can release cytotoxins when burst; due to a decrease in Na in the ECF (water drawn in)

Shrunken Cells

can release potassium; hyperpolarizing cells (makes them harder to excite); due to increase in Na in the ECF (water drawn out)

Homeostasis of ECF Tonicity

rise in plasma causes hypertonic ECF; sensing cells in the hypothalamus activate the pituitary to release ADH; ADH increases water retention; plasma is diluted to isotonic set point (any consequent volume disturbance is handled by volume homeostatic feedback loop)

Darrow-Yanet Diagrams

device for visualizing changes in osmolality and volume in ICF + ECF; can be used to depict all six classic types of fluid disturbance; osmolality on y axis and volume on x axis

Types of Fluid Disturbance

pure water loss, ECF loss, salt loss, salt excess, ECF excess, pure water excess

Hypertonic Fluid Disturbance

pure water loss and salt excess; changes in ECF volume with increases in ECF tonicity → ICF shrinkage

Isotonic Fluid Disturbance

ECF loss and ECF excess; therefore no effect on ICF

Hypotonic Fluid Disturbance

salt loss and pure water excess; changes in ECF volume with a decrease in ECF tonicity → ICF swelling

Isotonic Hypovolemia

fluid loss; caused by hemorrhage, excessive sweating, vomiting, diarrhea; signs are weight loss, dryness of skin and mucous membranes, decreased urine output, maybe decreased BP; resolved by oral or IV administration of electrolytes and glucose solution/correction of underlying cause

Isotonic Hypervolemia

fluid excess; cauased by excessive administration of IV fluids, hypersecretion of aldosterone; signs are weight gain, distended neck veins, increased bp, diluted hematocrit/protein/edema, pulmonary edema, heart failure; resolved by diuretics and correction of underlying cause

Hypersecretion of Aldosterone

may be caused by a tumor in the adrenal glands; decreases urine output by promoting Na+ reabsorption, water is reabsorbed along the osmotic gradient; treatment includes surgical removal of the adenoma or K+ sparing diuretics

Spironolactone

competitive inhibitor of the aldosterone receptor; K+ sparing

Hypernatremia/Pure Water Deficit

causes are increased Na (dietary, infusion of hypertonic saline) and decreased H2O (rare, impaired water access or intake, excess water loss via hyperventilation, fever, diabetes insipidus); ECF signs are hypo or hypervolemia depending on cause; ICF signs are cell shrinkage which causes twitching, convulsions, coma

Risk of Hypotonic Infusion

red blood cell lysis and cerebral edema

Diabetes Insipidus

characterized by dilute urine production and intense thirst; loss of ADH secretion (head injury, autoimmune disease, AVP gene mutations); aquaporins are not mobilized into nephron tubule; untreated can lead to severe hydration, electrolyte imbalance (seizures, permanent brain damage, death)

Diabetes Insipidus Treatment

consuming water to match urine output and desmopressin

Hypernatremia Treatment

infusion with salt free isotonic (5% glucose) fluid/correction of underlying cause

Hyponatremia/Pure Water Excess

caused by loss of Na (dietary, vomiting, diarrhea, diuretic treatment, dilutional following infusion with 5% glucose saline) and increased H2O (water intoxication, SIADH); ECF signs include hyper and hypovolemia (water excess/salt loss); ICF signs include cell swelling altering Vm of neurons, muscle lethargy, confusion, seizures, coma

Hyponatremia Treatment

hypertonic (3% salt) fluid replacement, but slowly to prevent osmotic demyelination syndrome; correction of underlying cause

Water Intoxication

cerebral edema; outpaces the filtration rate of the kidney (~1L of plasma/hour); altered excitability and pressure; can cause brain damage, coma, and death; symptoms include confusion, headache, muscle weakness, drowsiness, nausea/vomiting, bloated stomach

7.35-7.45

physiological range of plasma and interstitial fluid pH; [H+] = 9.2e-9

pH Influences

many processes; namely enzyme activity and neuronal excitability

Alkalosis Imbalance

pH > 7.45; confusion, vomiting, muscle spasms

Acidosis Imbalance

susceptibility to osteoporosis and chronic kidney disease; weakness, nausea, vision loss, coma; pH < 7.35

The Daily Acid Load

70 mmoles H+/day; metabolism, diet, alkali loss, disease

Buffering Power

the ability of a solution to resist pH

Buffering Power of Blood

80 mmol/L/pH-unit

CO2/HCO3-

major blood buffer system; the remaining 1/3 of plasma buffering power comes from proteins and phosphate

Henderson-Hasselbalch for Whole Body pH Balance

6.1 + log [HCO3-/CO2]

Kidney’s Role in Maintaining Acid-Base Status

reclaim filtered HCO3- (to prevent plasma HCO3 being lost in urine); generate new HCO3 and excrete H+ (to replace plasma HCO3 lost to acid neutralization and get rid of the acid)