Trigger - Fluid, Electrolyte, and Acid-Base Disorders Flashcards
Increased RAAS activity and SNS output is the body’s reaction to what
drop in osmotic pressure
also:
increased SNS output
increased RAAS activity
increased ADH levels
Increased thirst
decreased atrial natriuretic peptide (ANP)
decreased ADH levels and increased atrial natriuretic peptide is the body’s reaction to what
increase in osmotic pressure
also:
decreased SNS output
decreased RAAS activity
decreased ADH levels
decreased thirst
increased atrial natriuretic peptide (ANP)
etiologies include decreased PO intake, excessive fluid loss and third spacing
isotonic fluid volume deficit
s/s include AMS, weak pulse, hypotension, capillary refill of 2 seconds, and fatigue.
isotonic fluid volume deficit
Labs show:
high Uosm and Urine SG
increased Hct
isotonic fluid volume deficit
managed with admission of normal saline.
may also need Packed red blood cells or Inotropes
isotonic fluid volume deficit
when are inotropes indicated
poor cardiac output seen in isotonic fluid deficit
what is the cause of hyperchloremic metabolic acidosis. How do you treat this?
excess NS given for treatment of volume depletion
treat with bicarb solution (dextrose in H2O with HCO3)
when is mean arterial pressure used in the management of a patient
to assess the endpoint of treatment in patients being treated for isotonic fluid volume deficit
etiology includes over intake of salt such as during a state fair.
isotonic fluid volume excess
other etiologies include HF, renal failure and corticosteroids
etiologies include heart failure, renal failure, and corticosteroids
isotonic fluid volume excess
s/s are bloating, extremity edema, bulging neck veins, possible hypertension with full/bounding pulse.
isotonic fluid volume excess
general - decreased thirst, feeling bloated/swollen
CV - full, bounding pulse; distended neck veins, may see increased BP
High ECF - ascites, pulmonary edema, extremity edema
Labs:
abnormal renal labs
Low Uosm and Urine Sg
low Hct
isotonic fluid volume excess
labs:
abnormal renal labs
High Uosm and Urine sg
Low hct
isotonic fluid volume excess d/t inability to get rid of urine
Labs:
abnormal renal labs
Low Uosm and Urine sg
High Hct
Isotonic fluid volume deficit d/t renal fluid wasting
treatment plan includes:
restriction of fluid and sodium intake
furosemide (loops)
dialysis (if furosemide doesn’t work)
isotonic fluid volume excess
etiology includes impaired renal excretion of phospate
hyperphosphatemia
s/s include fatigue, SOB, N/V and +chvostek and trousseau’s
hyperphosphatemia
tx includes phosphate binders with meals and restoration of renal function
hyperphosphatemia, also obv limit intake of phosphate via processed foods
etiologies include:
use of diuretics, insulin, beta-agonists, or loops
OR
if patient is in alkalosis!
hypokalemia
also could be d/t intrinsic potassium wasting, metabolic acidosis, or hypomagnesemia
s/s include constipation, hypotension, palpitations, fatigue, cramps, dysrhythmias
hypokalemia
ECG shows flattened T waves -> prolonged QT -> U wave -> ST depression
hypokalemia
what is the management of acute severe hypokalemia
potassium replacement:
* oral or IV K chloride or K gluconate
* IV - 10-20mEq/hr max
* oral - 10-40 QD - QID
contributing factors include: hypomagnesemia and metabolic acidosis
hypokalemia
etiologies include: metabolic acidosis, adrenal insufficiency, hemolysis, cell damage and excessive/severe muscle contraction
hyperkalemia
causes include:
* Renal - inadequate excretion, metabolic acidosis
* Adrenal insufficiency
* Cellular breakdown - traumatic stick, hemolysis, crush injury
* Release from ICF - cell damage, excessive/severe muscle contraction
* Other causes - ACEI/ARB, beta-blockers, excess intake (usually IV)
etiologies include: traumatic stick, crush injury, or the use of ACEI/ARBs or BB
hyperkalemia
causes include:
* Renal - inadequate excretion, metabolic acidosis
* Adrenal insufficiency
* Cellular breakdown - traumatic stick, hemolysis, crush injury
* Release from ICF - cell damage, excessive/severe muscle contraction
* Other causes - ACEI/ARB, beta-blockers, excess intake (usually IV)
s/s include diarrhea, hypotension, palpitations, weakness, cramps, dysrhythmias, cardiac arrest
hyperkalemia
ECG - peaked T waves → loss of P waves → widened QRS → sine wave
hyperkalemia
what is the major difference in the s/s of hyperkalemia and hypokalemia
hyperkalemia presents with diarrhea, vomiting, cardiac arrest and no fatigue.
hypokalemia presents with fatigue, constipation and no cardiac arrest.
both present with cramps, hypotension, palpitations, dysrhythmias, and weakness. both present with ECG DIFFERENT ECG changes
what are the three steps to managing hyperkalemia
immediate clocking of cardiac effects
rapid reduction in plasma K+
removal of potassium
what is IV calcium gluconate used for?
reducing cardiac excitability in hyperkalemia.
IV calcium - reduced cardiac excitability
10mL of 10% calcium gluconate IV over 2-3 minutes w monitoring
repeat if ECG changes do not improve or recur in 1-3 minutes
may not be needed if there are no cardiac s/s or arrhythmias present
what interacts with IV calcium gluconate? How do we treat these pateitns?
digoxin!
patients taking digoxin are at risk for cardiac toxicity when given IV ca Gluconate.
give a SLOWER infusion of IV ca Gluconate to patients on digoxin.
when is insulin used in this lecture?
used alongside H2O and dextrose to reduce plasma volume of K+ in hyperkalemi.
can also add albuterol!
What should be cautioned in CHF patients and is not an effective treatment in ESRD patients?
Albuterol and insulin + glucose in hyperkalemia to reduce plasma K+
exchanges Na+ for K+ in GI tract which increases fecal excretion of K+
GI cation exchangers
SE include hypernatremia, intestinal necrosis, constipation and fecal impaction
GI cation exchangers
DDI with sorbitol and digitalis
GI cation exchanegrs
DDI with Lithium, LT4 and metformin
GI exchangers
DDI with antacids or laxatives with Al or Mg
Gi exchangers
Avoid in post op patients or patients with a hx of renal transplant
GI cation exchangers
also wth hx of bowel obstruction, slow intestinal transit, or ischemic bowel disease
A patient is hypervolemic with good renal function and hyperkalemia. what is the tx?
loop or thiazide diuretics
could use GI exchanger i think but i think the loops or thiazides are first line
low Na with normal serum osmolality.
isotonic hyponatremia
caused by extra molecules in the blood like protein and lipids
isotonic hyponatremia
low Na with high serum osmolality
hypertonic hyponatremia
caused by other molecules present in the blood such as glucose, radiocontrast, mannitol
hypertonic hyponatremia
etiologies include burns, diuretics, intrinsic renal salt wasting
hypovolemic hyponatremia
also:
GI loss (N/V)
burns
dehydration
ACEi
diuretics
mineralocorticoid deficiency
intrinsic renal salt wasting
etiologies include: N/V, dehydration, ACEI, mineralocorticoid deficiency
hypovolemic hyponatremia
GI loss (N/V)
burns
dehydration
ACEi
diuretics
mineralocorticoid deficiency
intrinsic renal salt wasting
sodium is retained but water retention is disproportionately larger than Na retention
hypervolemic hyponatremia
etiologies include:
nephrotic syndrome, liver disease, HF and intrinsic renal fluid retention
hypervolemic hyponatremia
etiologies include hypothyroidism, psychogenic polydipsia, beer potomania, SIADH
euvolemic hyponatremia
UNa+ and Uosm are used to assess what
ADH activity
s/s include NV, HA, confusion and lethargy
early hyponatremia
s/s include seizures, coma, brainstem herniation and death
late hyponatremia
most s/s d/t cerebral edema
hypoatremia
IV rehydration with isotonic .95 NS
tx for non severe hypovolemic hyponatremia.
also used to treat isotonic fluid deficit but with that you can also give PRBC and inotropes
may co admin a loop to avoid volume overload and/or desmopressin to avoid osmotic demyelination syndrome
addition to treatment for severe hyponatremia
what is treatment for severe hypovolemic hyponatremia
- achieve 44-6mEq/L increase in sodium ASAP
- repeat 1-2x at 10 min intervals if serum Na or s/s do not improve
- monitor tx by measuring Na every 2 hours
- may co admin a loop to avoid volume overload and/or desmopressin to avoid osmotic demyelination syndrome
treatment includes hypertonic saline, salt tablets or fluid restriction
hypervolemic hyponatremia
when do you use conivaptan or tolvaptan
nonemergent hyponatremia
(vasopressin receptor antagonists)
CI for fluid restriction
vasopressin receptor antagonists
Major SE hepatotoxicity. do not use for more than 30 days
vasopressin receptor antagonists
monitor LFT, renal function and electrolytes with this treatment
vasopressin receptor antagonists (becasue hepatotoxicity)
etiology is excessive water loss through renal or non renal sources
hypernatremia with normal Uosm
etiology is neurogenic or nephrogenic DI
hypernatremia with low Uosm
S/s include delirium, thirst, weak pulse, low BP, seizures
hypernatremia
Neuro - Increased thirst, HA, agitation, delirium, seizures, coma, death
CV - low BP, high HR, weak/thready pulse, dry mucous membranes, low skin turgor
Labs:
Increased Hct
could be Hypernatremia
(would see abnormal Uosm, Urine SG, and renal labs)
could also be
isotonic fluid volume deficit
tx: correction with fluid replacement within 24 hours to avoid CNS damage
hypernatremia present for less than 24 hours
correction with fluid replacement gradually at 6-12 mEq/L per 24 hours
hypernatremia present for more than 48 hours
etiologies include: hypokalemia, vomiting and gastric suction
metabolic alkalosis
also:
hypochloremia
hypokalemia
vomiting
Gastric suction
admin of bicarb/alkaline sol
diuretics
“perfect combo”
etiologies include: hypochloremia and diuretics
metabolic alkalosis
also:
hypochloremia
hypokalemia
vomiting
Gastric suction
admin of bicarb/alkaline sol
diuretics
“perfect combo”
etiology includes the combination of hypovolemia, hypochloremia, hypokalemia and reduced GFR
perfect setting for metabolic alkalosis
s/s include dysrhthmias, dizziness, panic, lightheadedness, seizures.
metabolic alkalosis
may also see NV, abdominal pain and hx of GI suctioning
etiology includes ketoacidosis and lactic acidosis
metabolic acidosis
also includes:
severe diarrhea
urine exposed to GI mucosa
distal or proximal tubular renal acidosis
ketoacidosis
lactic acidosis
decreased GFR
etiology includes: severe diarrhea and urine exposed to GI mucosa
metabolic acidosis
etiologies: decreased GFR
metabolic Acidosis
s/s include vasodilation (flushing), constipation, confusion, weakness, drowsiness
metabolic acidosis
Neuro - decreased neuronal excitability - confusion, weakness, drowsiness
CV - vasodilation (flushing), dysrhythmias
GI - Abdominal pain, NVD, constipation
pulm - increased depth and rate of respiration
bone - decreased density with chronic
decreased protein binding to calcium d/t decreased neuronal excitability
metabolic acidosis with hypercalcemia!
s/s include muscle weakness, increased thirst and nephrolithiasis
metabolic acidosis with functional hypercalcemia
tx includes decrease intake of animal content, especially proteins
chronic metabolic acidosis (main tx is HCO3 replacement
etiology includes CKD, GI loss, renal tubular acidosis
CHRONIC metabolic acidosis
how do you treat AKI with metabolic acidosis
dialysis and bicarb
