ANP140 Chapter 24 Water, electrolyte, and acid-base balance

Intercellular fluid

65% of water

Fluid inside cells

Extra cellular fluid

35% of water

fluid outside cells

-tissue fluid 25%

-bloodstream and lymph 10%

Water intake / output

2500 ml/day

water intake

200ml metabolic water

700ml food

1600ml drinking

water output

200ml feces (increase with diarrhea)

300ml Expired air (increase w cold) (insensible water loss)

400ml cutaneous transpiration (insensible water loss)

100ml sweat (increase w temperature)

1500ml urine

urine output

Only way the body can regulate change in h20 balance

- Must have at least 400ml per day to get rid of metabolic waste

Regulation of water intake

increase blood osmolarity

stimulate hypothalamic osmoreceptors

increase ADH

ingestion of h20

ingestion of Water

1.) cools and moisten mouth

2.) distend stomach

- Short term inhibition, don't drink to much ~ 30 min

- Long term inhibition of thirst

3.) Rehydration of blood

Increase firing of osmoreceptors

increase thirst

osmoreceptor-ADH mechanism

This mechanism helps regulate water output. Osmoreceptors in the hypothalamus detect high osmolarity, triggering production of ADH as you become thirsty. This causes changes in water permeability in the distal convoluted tubules and collecting ducts so that water is minimized. If low osmolarity is detected (proper hydration), ADH is not secreted in high levels, so water can be lost through urination as the distal convoluted tubule and collecting duct are not permeable to water now

Regulation of plasma osmolarity

ex.) Dehydration

Increase plasma osmolarity

increase osmoreceptors

increase ADH

Increase h20 reabsorption in CD

decrease h20 excretion

- increase urine osmolarity

- decrease plasma osmolarity

Water imbalance

can lead to circulatory shock or neuro dysfunction from decrease BV/BP or dehydration

Hypovolemia

decreased blood volume

ex.) hemorrage

Hypovolemia osmolarity

normal

Hypovolemia causes

loosing h20 and na+ in even amounts

Dehydration

Lack of drinking h20

dehydration osmolarity

increase osmolarity

dehydration casues

More h20 loss then Na+

Dehydration changes cells

cells shrink because h20 leaves

Fluid Deficiency

water out > water in

fluid excess

water in > water out

(less common bc kidneys are good at removing excess)

volume excess

extra h20 and Na+ in even amounts

ex.) renal failure

volume excess osmolarity

Normal

Hypotonic hydration

More h20 the Na+

ex.) drinking lots of water

hypotonic hydration osmolarity

decrease osmolarity

hypotonic hydration cells

swell up

volume excess and hypotonic hydration cause

edema because of increase BP/BV

Pulmonary + cerebral edema

ECF

Na+ and Cl

ICF

K+ and phosphates

electrolyte balance

ECF and ICF should be 300 m0ms/L

Sodium (Na+)

Only need 0.5 g/day

Hypernatremia

high sodium in the blood plasma

- dehydration

Hyponatremia

low sodium in the blood plasma

- excess h20 consumption

sodium imbalances

CNS dysfunction, edema, Increase BP

Potassium (K+)

Small changes in ECF K+ can be deadly due to effect on excitable tissues

Hyperkalemia

excessive potassium in the blood plasma

Cells more excitable, increase RMP

K+ diffuse into cell making it positive

Ex.) Crush injury, cardiac arrest

Hypokalemia

Low potassium levels in the blood plasma

Cells less excitable, decrease RMP

K+ diffuse out of cell making it negative

ex.) Muscle weakness, arrhythmia, vomiting, diarrhea

Normokalemia

A normal level of potassium in the blood

Normal resting membrane potential -70mv

Aldosterone regulates

Na+ and K+ concentrations

Hypercalcemia

increase plasma calcium

Hypercalcemia effects

muscle weakness, arrhythmia

(Hypoparathyroidism (increase PTH))

hypocalcemia

decrease plasma calcium

hypocalcemia effects

cramps, seizures, tetanus, heart failure, asphyxiation

(vitamin d deficiency)

Calcium

reabsorption regulated by PTH

Absorption increases with vitamin D

Acids

release H+ into solutions

bases

accepts h+

Buffors

stabilize pH by removing H+ or adding H+

strong acids

HCl

Fully ionize into H+ + Cl-

weak acids

H2CO3

Can go between H2CO3 and HCO3- + H+

Balanced pH

H+ equal HCO3-

increasing acidic

decrease pH

Increase H+

increase basic

Increase pH

decrease H+

sources of gaining H+

increase CO2

metabolism of proteins

decrease HCO3- (diarrhea, urine)

sources of losing H+

decrease CO2

metabolism

decrease H+ (vomiting, urine)

High protein diet

excess H+ ions so urine is acidic

buffer system ICF

1.Phosphates

H2PO4- <--> HPO4- + H+

Buffer system ECF

2.) Bicarbonate

CO2 + H2O <--> H2CO3 <--> HCO3- + H+

protein buffer system

Primary ICF buffer (hemoglobin)

Also buffers ECF (plasma protein)

3/4 buffer capacity

-COOH <--> - COO + H+

-NH3+ <--> -NH2 + H+

mechanisms to maintain acid base balance

buffers, respiratory, renal

1.) Buffers

first line of defense

short term

fast/speedy - (msec-sec)

Low buffering capacity

2. Respiratory

Change H+ levels by changing ventilation to alter CO2

intermediate Buffer capacity

intermediate speed - (sec-min)

3.) renal

Excrete excess H+ and HCO3-

longer term

high buffer capacity

slow speed (hours to days)

Renal Control of pH

Kidneys filter HCO3- but cannot reabsorb directly

- Filtered HCO3- is recycled into new HCO3- then reabsorbed

excess HCO3- (alkalosis)

-HCO3 > H+

Excess HCO3 has no H+ to combine with and is excreted

excess H+ (acidosis)

H+ > HCO3-

1.) secreted H+ combine with phosphates and are excreted

2.) amino acid catabolism increases when pH decrease, Excess H+ is excreted as ammonium (NH4+)