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55 Cards in this Set

  • Front
  • Back
What does extracellular fluid consist of?
Intravascular fluid
Interstitial fluid
What is the most abundant extracellular ion?
Na+
What is the most abundant intracellular ion?
K+
What is the key to osmotic pressure?
Na+
What is the key to hydrostatic pressure?
plasma proteins (albumin)
What fluids and/or electrolytes are related to the RAA/Aldosterone system?
fluid, Na+ & K+
What fluids and/or electrolytes are related to the Atrial Natriuretic Peptide system?
fluid
Na+
What fluids and/or electrolytes are related to fluid shifts?
fluid
Na+
What fluids and/or electrolytes are related to Thirst?
Fluid, Na+
What fluids and/or electrolytes are related to kidney function?
fluid
Na+
K+
What is hypervolemia?
too much fluid in the intravascular space
What causes hypervolemia?
1. decreased kidney function
2. too much IV solution (increased osmolarity)
What are the signs and symptoms of hypervolemia?
1. increased BP - BP = HR x Vol X PVR
2. increased JVD
3. bounding pulse --> increased vol = increased CO --> arteries are "full"
4. Weight Gain
What is the compensation for hypervolemia?
fluid shift - IV --> IS (THIRD SPACING)
What fluids and/or electrolytes are related to the ADH (antidiuretic hormone) system?
Fluid
What is "third spacing"?
it is when the fluid is pushed from the intravascular space to the interstitial space. this will cause edema
How is hypervolemia corrected?
increased renal output **it's the only correction!
What is hypovolemia?
not enough fluid in intravascular space
What causes hypovolemia?
- not enough fluid intake
- increased clearance of fluids because of impaired tubules
What are the signs and symptoms of hypovolemia?
- decreased BP
- INCREASED HR (HPA)
- Weight loss
- weak pulse
How does the body compensate for hypovolemia?
- fluid shift (from IC or IS --> IV)
How does the body correct hypovolemia?
- increasing thirst
- decreasing urine output by ADH & RAA
What signs and symptoms occur after compensation fluid shift?
intracellular dehydration:
- dry skin
- poor skin turgor
- dry mucous membrane
- confusion (brain cells dehydrated)
Explain the MOA for thirst.
hyperosmolarity (hypovolemia) --> triggers osmoreceptors --> stimulates "thirst center" (hypothalamus) --> increased thirst --> increased fluid intake
What triggers thirst?
- increased osmolarity
- decreased blood volume (hypovolemia)
- dryness of muscous membranes of mouth
What is the MOA for ADH (anti-diuretic hormone)?
hyperosmolarity (hypovolemia)
--> stimulates osmoreceptors --> stimulates "thirst center" (hypothalamus) --> posterior pituitary --> ADH --> adds pores to renal tubules which increases permeability to water --> water is reabsorbed and results in decreased urine output
What is the MOA for RAA (renin-angiotensin-aldosterone) and how does it help correct hypovolemia?
- acts to reabsorb Na+
- renin is produced in the juxtaglomerular cells in the kidney and it stimulates formation of angiotensin I (inactive form) --> ACE (angiotensin converting enzyme) converts this to its activate form which is angiotensin II --> stimulates the secretion of aldosterone which increases Na+ reabsorption. H2O is passively reabsorbed by osmotic pressure. ***Angiotensin II also causes vasoconstriction in blood vessels which leads to increased BP & angiotensin II can lead to vascular remodelling
What is hyponatremia?
low sodium levels
What causes hyponatremia? (list 3)
- decreased Na+ intake (rare)
- increased Na+ loss (burns, N/V, diuretics)
- dilution of Na+ (sweating --> stimulates thirst; kidney dysfuntion - impaired excretion of H2O; replaced fluid losses with D5W)
What does N/V result in?
loss of Na+
loss of fluid
loss of acid
What are the signs and symptoms of hyponatremia?
- edema - swelling (fluid in interstitial space)
- vascular hypovolemia - osmotic pressure will move fluid to interstitial space
- decreased BP
- increased HR (HPA)

- behavioural/neurological changes - lethargy, confusion, seizures AND less Na+ to DEPOLARIZE cells
How does the body compensate for hyponatremia?
fluid shift (from IV - IS)
How does the body correct hyponatremia?
RAA/Aldosterone
decreased [Na+] & decreased blood volume stimulate the release of renin which is a hormone produced by juxtaglomerular cells in the kidney --> it converts angiotensin to angiotensin I (inactive form) --> ACE (angiotensin converting enzyme) converts angiotensin I to angiotensin II (active form) --> the effects are release of aldosterone from the adrenal cortex --> causes Na+ reabsorption followed by H2O reabsorption. Angiotensin II also causes vasoconstriction which increases BP. And lastly, it causes vascular remodelling
What is aldosterone?
- a mineral corticoid
- secreted from adrenal cortex
- secreted when Na+ levels are low or K+ levels are high
- increases reabsorption of Na+
- increases excretion of K+ from distal tubule of kidney
- increases passive H2O reabsorption
What is hypernatremia?
too much sodium
What causes hypernatremia?
- food intake (rare)
- inappropriate administration of saline solution (D5 NS)
- over-secretion of ALDOSTERONE (Cushing's)
- Renal failure
- altered Na+ loss in relation to H2O loss (Diabetes insipidus, ADH, DM, polyuria, profuse sweating, diarrhea)
How does the body compensate for hypernatremia?
fluid shift from IC & IS --> IV
What are the signs and symptoms of hypernatremia?
- intracellular dehydration
- dry skin
- poor skin turgor
- dry mucous membranes
- thirst
- restlessness
- hypervolemia
- wt. gain, increased BP, increased HR, bounding pulse
How does the body correct hypernatremia?
ANP (Atrial Natriuretic Peptide)
- increased blood volume causes the heart to stretch which causes the atrium cells within the heart to release ANP --> this increases GFR decreases Na+ reabsorption and increases Na+ excretion. it also inhibits the release of RAA
Why is K+ important?
it is needed for CELLULAR function
* sudden increases can be fatal but body can adapt to small increases
What is hypokalemia?
low K+ levels
What causes hypokalemia?
- decreased intake
- elderly, alcoholism, anorexia nervosa
- loss of K+
- renal disorders
- GI disorders (diarrhea)
- vomiting/NG suctioning
- diuretic use - inhibits reabsorption of Na+ and increases secretion of K+
What are the signs and symptoms of hypokalemia?
- mild losses - no symptoms
- severe losses - neuromuscular excitability decreased (skeletal muscle weakness, smooth muscle atony (lacking tone), and cardiac dysrhythmias
- cardiac dysrhythmias are also due to changes in membrane excitability (EKG changes)
What is hyperkalemia?
too much K+
What causes hyperkalemia?
- increased intake (rare)
- shift of K+ from cells to ECF
- cell trauma (burns)
- insulin deficiency (insulin promotes entry of K+)
- hypoxia
- decreased renal secretion
- K+ sparing diuretics
What are the signs and symptoms of hyperkalemia?
- muscles: early - hyperactivity
late - weakness and flaccid paralysis
- cardiac - decreased cardiac conduction (cardiac arrest) and more rapid depolarization
- kidney - oliguria (abnormally small urine output)
What does the body do in response to hyperkalemia? (this mechanism is not sufficient for correction).
high K+ causes release of aldosterone from the adrenal cortex --> aldosterone speeds up ATPase to get 2 K+ out for each Na+ reabsorbed
How can you manage fluid shifts?
1. observe signs & symptoms
2. check serum electrolyte levels
3. measure intake and output (considering insensible loss of approx. 600 mL/day) *should not balance exactly
What are some hypotonic solutions?
ex. 0.45% NS or 0.33% NS (not usually given to people with low BP cause it will further drop)
What are some isotonic solutions you could give for maintenance?
NS, R/L
What are some hypertonic solutions?
D5W R/L, D5W 0.45% NS
What is the main cause for the release of ADH?
low blood volume or hyperosmolarity
- result: in increased water reabsorption
What is the main cause for the release of RAA?
low sodium levels (hyponatremia) or low blood volume
- result: Na+ reabsorption (primary)
H2O reabsorption (secondary)
What is the main cause for the release of aldosterone?
- low Na+, high K+ or low blood volume
- release is stimulated by angiotensin II from the RAA system
- result: Na+ reabsorption (increases)
H2O reabsorption (secondary)
What is the main cause for the release of ANP (atrial natriuretic peptide)?
- triggers by stretching of the heart because of increased blood volume and hypernatremia
- result: increases GFR which in turn decreases Na+ reabsorption (Na+ is excreted)