Fluid, Electrolyte and Acid/Bases Flashcards
body water content
- infants- 73% or more water (low body fat, low bone mass)
- adult males- 60% water
- adult females- 50% water (higher fat content, less skeletal muscle mass)
- water content declines to about 45% in old age
- daily recommended amount- 8 cups
total body water
- 40L - 60% body weight
- intracellular fluid- 25L- 40%
- interstitial fluid- 12L- 80 of ECF
- extracellular fluid- 15L- 20% body weight
- plasma- 3L- 20% ECF
extracellular and intracellular fluids
- each fluid compartment has a distinctive pattern of electrolytes
- ICF- major cation is K and major anion is HPO42-
- ECF- major cation is Na and major anion is Cl
fluid movement among compartments
- regulated by osmotic and hydrostatic pressures
- water moves freely by osmosis
- osmolarities of all body fluids are almost always equal
- change in solute concentration of any compartment leads to net water flow
- increase in ECF solate -> water moves out of cells
- decrease in ECF solate -> water moves into cells
regulation of water intake
- thirst mechanism is the driving force for water intake
- the hypothalamic thirst center osmoreceptors are stimulated by:
- increase in osmolality of 1-2% activates receptors
- angiotensin 2 or baroreceptor input
- dry mouth - less saliva
- substantial decrease in blood volume or pressure
regulation of water output
- obligatory water losses:
- insensible water loss- from lungs and skin
- feces
- minimum daily sensible water loss of 500 ml in urine to excrete wastes
- body water and Na content are regulated in tandem by mechanisms that maintain cardiovascular function and blood pressure
- thirst is not always a reliable indicator of need (the last straw)
regulation of water output: influence of ADH
- hypothalamic osmoreceptors trigger or inhibit ADH release (inc in ECF solute concentration)
- decrease in ADH -> dilute urine and decrease volume of body fluids
- increase ADH -> concentrated urine
- conserves water in body
- water reabsorption in collecting ducts is proportional to ADH release
- other factors may trigger ADH release via large changes in blood volume or pressure
electrolyte balance
- electrolytes are salt, acids, and bases
- salts enter the body by ingestion and are lost via perspiration, feces, and urine
- salts:
- controlling fluid movement, osmotic relations between cells
- excitability; neuromuscular excitability
- secretory activity
- membrane permeability
- eat a meal high in salt will cause a temporary increase in blood volume
- electrolyte balance usually refers only to salt balance
central role of sodium
- most abundant cation in the ECF (90-95%)
- highest in blood plasma
- exerts the most significant osmotic pressure
- regulation of sodium linked to BP
- sodium is a water magnet
- aldosterone regulates salt
regulation of sodium balance: aldosterone
- if blood volume and BP is low then aldosterone is released
- renin-angiotensin mechanism is the main trigger for aldosterone release
- granular cells of JGA secrete renin in response to:
- sympathetic nervous system stimulation
- decrease filtration osmolality
- decrease stretch (due to decreased blood pressure)
regulation of sodium balance: ANP atrial natriuretic peptide
- released by atrial cells in response to stretch (if BP is high)
- decrease BP and blood volume:
- decrease ADH, renin and aldosterone production
- increase excretion of sodium and water
- promotes vasodilation
cardiovascular system baroreceptors
- if an increase in blood volume and pressure:
- baroreceptors alert the cardiovascular centers in brain
- sympathetic nervous system impulses to the kidneys decline
- afferent arterioles dilate
- GFR increases
- Na and water output increase (less reabsorption)
- blood volume and pressure decrease
- baroreceptors provide information on the fullness or volume of the circulation that is critical for maintaining CV homeostasis
regulation of potassium balance
- importance of potassium:
- affects RMP (resting metabolic potential) in neurons and muscle cells (especially cardiac muscle)
- K balance is controlled by the kidney
- over 80% of K is reabsorbed at the prox tubule
- potassium is part of bodys buffer system
- shift of H+ shift in and out of cells induce corresponding shifts in K in the opposite direction to maintain cation balance
- Na is reabsorbed at collecting ducts never excreted, K can be excreted at ducts
- the collecting ducts control the amount of K secreted back into filtrate
- ***high K content of ECF favors secretion of K
- when K levels are low, the kidneys conserve K by reducing its excretion
influence of aldosterone on potassium balance
- stimulates K secretion (and Na reabsorption)
- increased K in the adrenal cortex causes:
- release of aldosterone
- potassium secretion
- amount of K in ECF determines how much will be secreted in kidney
regulation of caclium
- calcium role in ECF- neuromuscular excitability, blood clotting, cell membrane permeability, secretory activities
- hypocalcemia -> causes muscle tetany
- hypercalcemia -> increase heart rate and contractility but very high calcium levels may cause heart arrhythmias
- calcium balance is controlled by parathyroid hormone (PTH) and calcitonin
influence of PTH parathyroid hormone on calcium
- bones are the largest reservoir for Ca and phosphates
- PTH promotes increase in calcium levels in blood by targeting bones, kidneys, and small intestine (indirectly through vitamin D)
- calcium reabsorption and phosphate excretion go hand in hand
regulation of anions
- Cl- is the major anion in the ECF
- helps maintain the osmotic pressure of the blood
- follows Na ions out of filtrate
an increase in the ECF solute content causes ______
- water to move into the cell
- solute to move out of the cell
- water to move out of the cell*
- both a and b
you would expect blood levels of ANP to increase when _____
- blood pressure is increased
- there is an increase in preload
- the walls of the atria are stretched
- all of the above occur*
- a and c only
acid-base balance
- pH affects all functional proteins and biochemical reactions
- normal pH of body fluids:
- arterial blood- pH 7.4
- venous blood- pH 7.35
- alkalosis or alkalemia- arterial blood pH > 7.45
- acidosis or acidemia- arterial pH < 7.35
most H+ is produced by metabolism
- phosphoric acid from breakdown of phosphorus containing proteins in ECF
- lactic acid from anaerobic respiration of glucose
- fatty acids and ketone bodies from fat metabolism
- H+ liberated when CO2 is converted to HCO3- in blood
concentration of hydrogen ions is regulated sequentially by:
- chemical buffer systems- rapid- first line of defense
- brain stem respiratory centers- act within 1-3 min
- renal mechanisms- most potent, but require hours to days to effect pH changes
strong acids
- dissociate completely in water (liberate their H+)
- can dramatically affect pH
weak acids
- dissociate partially in water
- are efficient at preventing pH changes
- act as chemical buffers
strong bases
- dissociate easily in water
- quickly tie up H+
weak bases
-accept H+ more slowly
acidity of solution reflects the free hydrogen ions
true
chemical buffer
- system of one or more compo9unds that act to resist pH changes when strong acid or base is added
- binds to H+ when pH drops and releases them when pH rises
- bicarbonate buffer system- most effective in ECF
- phosphate buffer system most effective in urine and ICF
- protein buffer system- in plasma and cells
bicarbonate buffer system: if strong acid is added
- if strong acid is added:
- pH decreases only slightly, unless all available HCO3- (alkaline reserve) is used up then buffer system is ineffective and pH will drop
- HCO3- concentration is closely regulated by the kidneys
- HCl + NaHCO3 (sodium bicarb) -> H2CO3 (carbonic acid) + NaCl
- strong acid + weak base -> to weak acid + salt
bicarbonate buffer system is strong base is added
- pH rises only slightly
- H2CO3 (carbonic acid) supply is almost limitless (from CO2 released by respiration) and is subject to respiratory controls
- NaoH (sodium hydroxide) + H2CO3 -> NaHCO3 + H2O
- strong base + weak acid -> to weak base + water
- weak base replaces strong base to prevent change in pH
physiological buffer systems
- respiratory and renal systems
- act more slowly than chemical buffer systems
- have greater buffering power than chemical buffer systems
respiratory regulation of H+
- respiratory system eliminates CO2
- a reversible equilibrium exists in the blood
- CO2 + H2O -> H2CO3 -> H+ HCO3- (bicarbonate ion)
- during CO2 unloading the reaction shifts to the left (and H+ is incorporated into H2O) LUNGS
- during CO2 loading the reaction shifts to the right (and H+ is buffered by proteins) TISSUES
respiratory regulation of H+ acidosis
- hypercapnia activates medullary chemoreceptors
- response -> increase RR
- rising plasma H+ activates peripheral chemoreceptors
- response -> increase RR
- more CO2 is removed from the blood
- H+ concentration is reduced
respiratory regulation of H+ alkalosis
- alkalosis depresses the respiratory center
- respiratory rate and depth decrease
- CO2 and H+ concentration increases
acid-base imbalances
- respiratory system impairment causes acid-base imbalances
- hypoventilation -> respiratory acidosis
- hyperventilation -> respiratory alkalosis
renal mechanisms of acid-base balance
- most important renal mechanisms
- conserving (reabsorbing) or generating new HCO3- (bicarbonate ions) will lose H+ and increase pH
- excreting HCO3- will acidify blood and decrease pH
- generating or reabsorbing one HCO3- is the same as increasing pH
- H2CO3 (carbonic acid) -> H+ + HCO3- (bicarbonate ion)
abnormalities of acid-base balance
- respiratory acidosis and alkalosis- failure of respiratory system to perform its normal pH balancing role
- metabolic acidosis and alkalosis- all abnormalities of acid-base imbalances except those caused by too much or too little CO2
respiratory acidosis
- the most important indicator of adequacy of respiratory function is PCO2 level (normally 35-45mmHg)
- PCO2 above 45 -> respiratory acidosis
- most common cause of acid base imbalances
- due to decrease in ventilation or gas exchange- hypoventilation
- characterized by falling blood pH and rising PCO2
- common causes- pneumonia, emphysema, bronchitis
respiratory alkalosis
- PCO2 below 35 mmHg -> respiratory alkalosis
- a common result of hyperventilation due to stress or pain
- panic attack
- not common
metabolic acidosis and alkalosis
- any pH imbalance not caused by abnormal blood CO2 levels
- indicated by abnormal HCO3- levels
- lowered HCO3- (free H+) - acidosis
- elevated HCO3- alkalosis
- normal bicarbonate levels - 22-26 mEg/L
causes of metabolic acidosis
- ingestion of too much alcohol ( -> acetic acid)
- excessive loss of HCO3- (persistent diarrhea)
- accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure
metabolic alkalosis causes
- much less common
- indicated by rising blood pH and HCO3-
- caused by vomiting of the acid contents of the stomach or by intake of excess base (antacids)
effects of acidosis and alkalosis
- blood pH below 7 -> depression of CNS -> coma > death
- blood pH above 7.8 -> excitation of nervous system -> muscle tetany, extreme nervousness, convulsions, respiratory arrest
respiratory compensation in metabolic acidosis
- high H+ levels stimulate the respiratory centers
- rate and depth of breathing are elevated
- respiratory system tries to correct
- blood pH is below 7.35 and HCO3- level is low
- as CO2 is eliminated by the respiratory system, PCO2 falls below normal
respiratory compensation for metabolic alkalosis
- revealed by:
- slow, shallow breathing, allowing CO2 accumulation in the blood
- high pH (over 7.45) and elevated HCO3- levels
renal compensation
- hypoventilation causes elevated PCO2
- respiratory acidosis- renal compensation is indicated by high HCO3- levels
- respiratory alkalosis exhibits low PCO2 and high pH
- renal compensation is indicated by decreasing HCO3- levels
holy grail guide
- respiratory acidosis- pH < 7.35; PCO2 > 45; HCO3- > 26 IF compensating
- respiratory alkalosis- pH > 7.45; PCO2 < 35; HCO3- < 22 IF compensating
- metabolic acidosis- pH < 7.35; PCO2 < 35 if compensating; HCO3- decreased
- metabolic alkalosis- pH > 7.45; PCO2 > 45 if compensating ; HCO3- elevated
- easy way to remember:
- if the pH and PCO2 are moving in the reverse direction than it is a REspiratory issue
- if the pH and PCO2 are moving in the same direction than it is a MEetabolic issue
- decreased pH = acidosis
- elevated pH = alkalosis
- RE = reverse
- ME = same
a falling blood pH and a rising partial pressure of carbon dioxide due to pneumonia or emphysema indicates ________
- respiratory acidosis*
- respiratory alkalosis
- metabolic acidosis
- metabolic alkalosis
which of the following is the initial H+ regulatory mechanism in the body
- renal excretion
- chemical buffers*
- brain stem respiratory centers
- lactic acid production
a patients test results show PCO2 > 45 mmHg, HCO3- level of 24 mEg/L, and pH < 7.35. These indicate ____
- metabolic acidosis
- metabolic alkalosis
- respiratory acidosis*
- respiratory alkalosis
test results: pH 7.48; PCO2 is 46 mmHg; HCO3+ 33 m/Eg/L. Patient is breathing slow and shallow
- metabolic acidosis
- metabolic alkalosis*
- respiratory acidosis
- respiratory alkalosis
a patient is breathing rapidly, and blood pH analysis indicates an abnormally low value, what is the likely diagnosis
- respiratory acidosis*
- metabolic acidosis
- metabolic alkalosis
- respiratory alkalosis