The cellular environment: fluids, and electrolytes, acids, and bases

Capillary hydrostatic pressure

• Pushes water OUT of the capillary

• Increased venous pressure in heart failure—> increase capillary hydrostatic pressure —> more fluid leaves capillaries —> edema

Capillary oncotic pressure

Pulls water into capillary

albumin holds water in the blood stream

Interstitial hydrostatic pressure

Pushes water into the capillary

Interstitial oncotic pressure

Pulls water OUT into the interstitial space

plasma albumin decreases ?

decrease albumin —> decrease capillary oncotic pressure —>less water pulled into capillaries—> fluid remains in the interstitial space —> edema

example : liver disease - decrease albumin production which leads to edema/ ascites

What is filtration

movement of fluids from the capillary to interstitial space

think: capillary to tissue

reabsorption ?

Movement of fluid from the interstitial space to capillary

Think: tissue to capillary

why does heart failure cause peripheral edema

venous congestion → increase capillary hydrostatic pressure → increased filtration of fluid from capillaries into tissue → edema

HF= pressure pushes fluid out

Natriuretic peptides

• ANP (atrial natriuretic peptide)

• BNP (brain natriuretic peptide) → Heart Failure

What do ANP and BNP ultimately try to accomplish?

Get rid of Na+ and water, decreasing blood volume and blood pressure

what happens when ANP/BNP are released

increase Na+ excretion → increase water exretion → decrease blood volume → decrease bp

How do RAAS and natriuretic peptides differ?

• RAAS → SAVE Na+ and water → increase volume/BP

• ANP/BNP → DUMP Na+ and water → decrease volume/BP

What happens when plasma osmolality increases

increase osmolality → increase ADH → increase water retention

what does increased plasma osmolality mean

plasma is too concentrated — too much solute, needs more WATER

What happens to cells in an ISOTONIC solution?

water moves in and out equally

example: 0.9% saline

What happens to cells in a HYPERTONIC solution

Water moves out of the cell → cell SHRINKS

high solute outside → H20 goes out →cell shrinks

What happens to cells in a HYPOTONIC solution?

water moves INTO the cell → cell SWELLS

low solute outside → H20 goes into cell → cell SWELLS

What causes a hypertonic/hyperosmolar imbalance?

• water loss

• solute gain

What causes a hypotonic/ hypoosmolar imbalance?

• water gain

• solute loss

What does isotonic fluid LOSS cause

Hypovolemia

what happens to cells in hypernatremia?

The high sodium concentration makes the ECF hypertonic → water moves OUT of cells into the ECF → cells shrink/dehydrate

Why are neurologic symptoms especially important in hypernatremia?

• water leaves brain cells, causing them to shrink and become dehydrated

• symptoms:

  • weakness

  • lethargy

  • confusion

  • muscle twitching

  • hyperreflexia

  • seizures

  • coma

Diabetes Insipidus

decrease ADH effect → increase free water loss → serum Na+

What happens to cells in hyponatremia

decrease Na+ in ECF → decrease ECF osmoality → water moves from ECF to ICF → cell SWELL

Why are neurologic symptoms the biggest concern with hyponatremia?

• water moves into brain cells, causing cerebral swelling

  • headache

  • lethargy

  • confusion

  • apprehension

  • seizures

  • coma

SIADH

excess ADH → excessive water retention → sodium becomes diluted

SIADH= save inappropriate amounts of H20

What factors move K+ INTO cells?

• Insulin

• Epinephrine

• Alkalosis

K+ goes into cells → serum K+ decrease

What factors move K+ OUT of cells?

• insulin deficiency

• aldosterone deficiency

• some forms of acidosis

• cell lysis

• strenuous exercise

K+ moves OUT → serum K+ increases

WHat does insulin do to serum K+?

• insulin stimulates the Na+/K+ ATPase, causing K+ to move:

Blood → INTO cells

therefore: Insuline decreases serum K+

insulin can be used to temporarily treat severe hyperkalemia

What hormone increases K+ excretion by the kidneys

aldosterone → increase renal K+ excretion → decrease serum K+

What does hypercalcemia do to membrane excitability

increase Ca++ decreases excitability

“calms”

What does hypocalcemia do to membrane excitability

decrease Ca++ increases excitability

Cardiac effects on hypokalemia

• dysrhythmias

• ST depression

LOW K = LOW/FLAT T + U

Hypokalemia

everything gets slow and weak

decrease membrane excitability

Insulin and Alkalosis = K+ into cells

How does acidosis affect potassium

H+ → INTO cell

K+ → OUT of cells

Serum K+ increases = hyperkalemia

ECG of hyperkalemia

HIGH K = HIGH/PEAKED T

digoxin and hypokalemia

Hypokalemia increases the risk of digoxin toxicity and dysrhythmias

K+ and digoxin fight for the same receptors → not enough K+, more room for digoxin = toxicity

Hyperkalemia

• Renal failure

• Acidosis → K+ out of cells

• cell destruction K+ is released

treatment for hyperkalemia

• protect heart →calcium

• Shift K+ into cells → insulin

• Remove K+ → diuretic / GI potassium binder/dialysis

What stimulates parathyroid hormone release

• low serum ca++ → increase PTH

• PTH saves calcium and pees phosphate

PTH saves calcium, dumps phosphate, and activates Vitamin D

causes of hypocalcemia

• hypoparathyroidism - decrease PTH

• vit d deficiency

• chronic kidney disease

• massive blood transfusion

why can chronic kidney disease cause hypocalcemia

kidney failure → decrease activation of vit d → decrease intestinal ca++ absorption → decrease serum ca++

Neuromuscular activity in hypocalcemia

it increases

low calcium = nerves and muscles GO

muscle spasms

Chvostek sign

facial muscle twitch - checking for hypocalcemia

trousseau sign

inflate BP cuff above systolic pressure for several minutes → carpal spasm occurs = hypocalcemia

causes of hypercalcemia

• hyperparathyroidism

• bone metastasis

• excess vit d

• immobilization

• acidosis

• sarcoidosis

neuromuscular excitability in hypercalcemia

• it decreases

• weakness

PTH and phosphate

• increase PTH → decreases phosphate

• PTH saves Ca++ and pees phosphate

hypophosphatemia results from

• malnutrition/malabsorption

• vit d deficiency

• hyperparathyroidism

• renal phosphate loss

why can severe hypophosphatemia be dangerous

• phosphate is essential for ATP/energy production

• muscle weakness

• respiratory muscle weakness

• neurologic changes

• cardiac dysfunction

no phosphate → trouble making ATP - > cells lose energy

hyperphosphatemia associated with:

renal failure

Why can hyperphosphatemia lead to hypocalcemia?

excess phosphate binds to calcium

PTH releases calcium from where when it is needed:

• bone (releases)

• kidney (retains)

• vit d (activation increase → GI calcium absorption increase)

• phosphate (excretion)

hypomagnesemia

• from malabsorption

increase excitability - tremors hyperreflexia, muscle cramps, tetany, seizures

Hypermagnesemia

• renal failure and magneisum intake

decrease excitability - decrease deep tendon reflexes, muscle weakness, lethargy, hypotension, bradycarida

normal arterial blood pH

7.35-7.45

<acid

>alkaline

components that control acid-base balance

lungs - CO2

kidney - H+ and HCO3

3 major buffering systems in the body

• bicarbonate buffer system

• protein buffer system

• phosphate buffer system

What ratio of bicarbonate to carbonic acid maintains a normal pH

20 parts base : 1 part acid

7.40 / 40 / 24

cause of metabolic acidosis

• hyperventilate to get pH normal

so cause

• lactic acidosis - gain acid

• renal failure - cant excrete H

• diabetic ketoacidosis

• diarrhea - lose bicarb

cause of metabolic alkalosis

• vomiting - acid

• gastic suction

• excess bicarbonate

• some diruretics