Fluids and Electrolytes Flashcards
Water makes up ___% of total body weight
Water makes up 45 – 60% of total body weight
The intracellular water makes up __% of total body water.
The intracellular water compartment makes up 66% of total body water.
The extracellular water compartment makes up __% of total body water.
The extracellular water compartment makes up 34% of total body water.
The intravascular (plasma) compartment and interstitial compartments are found in the:
extracellular water compartment.
Remember that the hydrostatic pressure in capillary microcirculation drives
Remember that the hydrostatic pressure in capillary microcirculation drives fluid into the interstitium and fluid returns to plasma via LYMPHATICS
Na, Cl & HCO3 make up __% of the active osmoles in the ECW
Na, Cl & HCO3 make up 90% of the active osmoles in the ECW
the resting membrane potential is
the resting membrane potential is NEGATIVE and is essential for cell function/nerve conduct
60 – 70% of filtered Na and H2O is absorbed in the
60 – 70% of filtered Na and H2O is absorbed in the PROXIMAL CONVOLUTED TUBULE
The electrolytes absorbed and secreted at the distal convoluted tubule includes:
Sodium is absorbed, potassium & hydrogen is secreted.
The substance absorbed at the collecting duct is:
water is absorbed at the collecting duct.
PTH, angiotensin, and endothelin ALL influence function of the ___.
PTH, angiotensin, and endothelin ALL influence function of the PCT
Prostaglandins, glucagon, calcitonin and epinephrine work at the:
Loop of Henle
Aldosterone, natriuretic peptides and sympathetic tone all work at the:
distal collecting tubule.
during shock, fluid shifts from
during shock, fluid shifts from INTRAcellular water to EXTRAcellular water.
Shock results in expanded ECW, which is restored to normal volume via
is expanded ECW, which is restored to normal volume via renal function (natriuretic peptides such as ANP, BNP and CNP).
AVP increases the ECW in shock, as hypotension is a strong stimulus. AVP is an increase in response to:
AVP is an increase in response to plasma osmolarity > 280 mOsm/kg.
During shock, the function of ANP and BNP is:
ANP and BNP vasodilate and increase microvascular permeability.
The normal pH is 7.40. Daily metabolism provides
The normal pH is 7.40. Daily metabolism provides increase Hydrogen ions, making a positive daily balance. The excess is excreted in urine
- Low rates of survival: pH
- Low rates of survival: pH > 7.70 or < 7.00
Shock is defined as a:
Shock: rapid accumulation of H+ in ICW and ECW. The cell membrane is not readily permeable to H+ and the kidney cannot compensate for a sudden rapid increase.
CO2 is cleared from the body via the
CO2 is cleared from the body via the pulmonary system.
A major ECW & ICW buffer is:
(1) HCO3
(2) Proteins
(3) inorganic phosphate
(4) oxidative phosphorylation.
(1) HCO3 is a major ECW and ICW buffer.
Proteins are:
ICW buffers.
**HCO3 is absorbed and H+ is excreted, as well as production of ammonium in tubular filtrate in the nephron at the:
The distal convoluted tubule is essential for acidic urine.HCO3 is absorbed and H+ is excreted, as well as production of ammonium in tubular filtrate.
Which of the following is TRUE?
- A low GFR enhances the DCT’s ability to keep up with H+.
- Aldosterone: retains Na and HCO3, even if the pH is 7.40.
- Malnutrition: glutamine deficiency accelerates NH4+ excretion.
Aldosterone: retains Na and HCO3, even if the pH is 7.40.
Metabolic acidemia is defined as:
Metabolic acidemia: An abrupt addition of sufficient protons to reduce bicarbonate buffer by 50%.
Respiratory acidemia is defined as:
Respiratory acidemia: a sudden reduction in alveolar ventilation causes an increase in PaCO2 to 50 torr.
Metabolic alkalemia is defined as:
Metabolic alkalemia: an abrupt addition of sufficient bicarbonate to increase the buffer concentration to 30 mEq/L.
Respiratory alkalemia is defined as:
Respiratory alkalemia: a sudden increase in alveolar ventilation causes a decrease in PaCO2 to 20 torr.
- Hypoxia causes
- Hypoxia causes a rapid rise in ICW H+ and little change in ECW pH
T/F: in hypoxia, . Rapid infusion of HCO3 can worsen ICW pH (increased CO2).
True.
The result of lactic acidosis is:
anaerobic glycoslysis
Etiologies of lactic acidosis include:
hemorrhage, MI, alcholism and septic shock.
A patient presents with dilutional metabolic acidosis. There is a decreased anion gap. Treatment of this is:
renal correction via ammonium chloride excretion.
A patient with diarrhea experiences metabolic acidosis, which presents as reduciton in HCO3, Na and K. Treatment is:
IV fluids with NaCl and KCl
Treatment of metabolic acidosis involves:
Sodium bicarbonate SLOWLY infused, especially if the pH < 7.2
Diabetic ketoacidosis results in:
(1) Increased metabolism and insulin levels.
(2) An increase in beta-hydroxybutyric acid and acetoacetic acid.
(3) decreased anion gap and low hydrogen protons.
(2) An increase in beta-hydroxybutyric acid and acetoacetic acid.
Kussmaul’s respirations are seen in patients with diabetic ketoacidosis when PaCO2 is:
PaCO2 < 20 mmHg.
T/F: Ketoacidosis does occur in alcoholics due to decreased glucose intake.
False.
A patient presents with renal failure. They have a low GFR and an inability to clear extracellular water protons. The results is:
metabolic acidosis.
Renal tubular acidosis causes metabolic acidosis. Treatment is:
bicarbonate and dialysis.
Metabolic alkalosis occurs as a result of:
excess ECW HCO3.
Sodium bicarbonate perfusion can result in:
mechanical ventilation in hypoventilation syndrome.
Gastric outlet obstruciton causes metabolic alkalosis that has characteristics of:
hypochloremia, hypokalemic metabolic alkalosis.
Increased use of loop diuretics is associated with:
metabolic alkalosis and an increase in aldosterone.
Respiratory alkalosis occurs due to:
acute hypoxia and hyperventilation.
Respiratory acidosis results from:
Decreased alveolar ventilation.
T/F: giving supplemental oxygen to a patient in respiratory acidosis can suppress respiratory drive and cause death.
True.
T/F: Sodium only makes up 5% of the osmolarity of extracellular water compartment.
False.
Moderate hyponatremia is defined as:
(1) 120 meq/L
(2) 120 - 130 meq/L
(3) 130 - 138 meq/L
Moderate hyponatremia is defined as (2) 120 - 130 meq/L.
Severe hyponatremia results in
Severe hyponatremia results in seizures and coma, with < 110 meq/L causing death from cerebral edema.
Acute hyponatremia causes:
Na and H2O are lost and replaced by hypoosmotic fluid
Acute hyponatremia can be resuscitated with
Dilutional: resuscitation of losses with HYPOTONIC solution
Desalination in acute hyponatremia refers to
Desalination: an increase in AVP (due to stress, pain or anxiety) causes water retention despite isotonic resuscitation
The type of diuretics that cause obligatory sodium loss (and acute hyponatremia) are:
Furosemide and mannitol
Diabetic ketoacidosis is a cause of:
(1) acute hyponatremia
(2) chronic hyponatremia
Diabetic ketoacidosis is a cause of (1) acute hyponatremia.
Cerebral salt wasting is associated with:
acute hyponatremia
Cerebral salt wasting is treated via:
Check 24 hour urine sodium levels and treat with daily sodium replacement.
Chronic hyponatremia is associated with:
(1) Diabetes insipidus
(2) SIADH
(3) Diabetic ketoacidosis
Chronic hyponatremia is associated with (2) SIADH
AVP secreting tumors that are seen in carcinoid and small lung cancer are associated with:
chronic hyponatremia.
Increased AVP secretion is seen in cerebral injuries, tumors and infections. This is associated with:
chronic hyponatremia.
T/F: renal disease presents with a chornic impaired ability to retain sodium.
True.
Adrenal infarct, hemorrage, tumor or adrenalitis are associated with:
chronic hyponatremia.
Central pontine myelinolysis is characterized by no symptoms and sudden contraction. To avoid this and chronic hyponatremia, treatment is:
Fluid restriction and slow replacement of Na (no more than 0.25 meq/L).
A patient presents with central pontine myelinolysis and chronic hyponatremia. In order to replenish sodium, treatment should involve:
give sodium AND potassium.
Severe hypernatremia is:
(1) 146 - 159 meq/L.
(2) > 160 meq/L
Severe hypernatremia is (2) > 160 meq/L
Hypernatremia results in dehydration of
dehydration in BOTH ECW and ICW compartments.
A severe symptom of hypernatremia is
The brain can shrink, resulting in neurologic symptoms – lethargy, insomnia, central pontine myelinolysis or coma
Hypernatremia is treated when the kidneys increase urine sodium output. This is initiated by:
• The hypothalamus releases AVP, increasing TBW
Hypernatremia is treated when the kidneys increase urine sodium output. This is initiated by:• The hypothalamus releases AVP, increasing TBW. AVP release is inhibited by:
Alcohol
Which of the following is a common cause of hypernatremia?
(1) Endocrine syndromes
(2) Overreaction of renal tubular cells to respond to ADH.
(3) Decreased salt intake and increased water intake
(4) SIADH
(1) Endocrine syndromes (ADH synthesis or release fails) are a common cause of hypernatremia.
Diabetes insipidus is a common cause of:
hypernatremia
Diabetes insipidus: results from a lack of
Diabetes insipidus: results from a lack of ADH or response to ADH.
post decompressive obstructive uropathy, sickle cell disease, medullary cystic kidney disease or medications (Lithium, glyburide, amphotericin B, demeclocycline) are all causes of hypernatremia secondary to
diabetes insipidus
Treatment of diabetes insipidus is:
amiloride (5 - 10 mg daily).
Which of the following is an acute cause of hypernatremia?
(1) enteric fistulae, vomiting, diarrhea.
(2) mild burns
(3) hospitalized patients with normal mental status.
(1) Enteric fistulae, vomiting and diarrhea are acute causes of hypernatremia.
Treatment of hypernatremia is:
replace water.
Treatment of diabetes insipidus:
AVP (DDAVP).
Excess potassium is excreted via
Excess potassium is excreted via the distal collecting tubule into the urine**.
______ controls potassium excretion
Aldosterone controls potassium excretion
More bicarbonate in the filtrate
More bicarbonate in the filtrate FAVORS potassium excretion
Hyperkalemia of 6 mmol/L presents with EKG changes of:
ECG changes (T waves higher than R waves)
Hyperkalemia of 7 mmol/L presents with EKG changes of:
Decreased P waves, increased PR interval, widened QRS.
Hyperkalemia of 8 mmol/L presents with EKG changes of:
Asystole/Ventricular fibrillation/PEA
Drugs associated with hyperkalemia:
spironolactone, beta blockers, cyclosporine, FK506
Hyperkalemia is caused by succinylcholine. It is:
- Succinylcholine: depolarizing agent in patients with muscular atrophy. This is common in neurological disorders (paraplegics), rhabdomyolysis, burn patients and sustained reduction of RMP in myocytes (Potassium goes from the ICW to ECW).
Treatment of hyperkalemia:
- Treatment: IV Ca++ (affects ECW), IV HCO3 (affects ICW), glucose and insulin (affects ICW).
• 9alpha fludrocortisone: is used in patients with aldosterone deficiency.
• Dialysis.
• Kayexalate: cation exchange resin binds intestinal K+ (colonic mucus is high in K+).
Hypokalemia may result from
digoxin toxicity (arrhythmias), GI tract or renal losses, and urine K+ < 20 mmol/L.
Flaccid paralysis and respiratory compromise
are seen when potassium levels are
K+ < 2.0
Fatigue weakness, ileus
are seen when potassium levels are:
K+ < 3.5
Hypokalemia is seen in
in CHF and can be treated with diuretics
increased aldosterone and catecholamines
increased aldosterone and catecholamines increase renal tubule excretion
EKG findings of hypokalemia
decreased T waves and onset of U waves; patient presents with atrial tachycardia/AV dissociation/Ventricular tachycardia and ventricular fibrillation
- Primary aldosteronism adenoma or hyperplasia: results in
hypokalemia, HTN and mild alkalosis.
Treatment of hypokalemia
REPLACE K+. In cardiac patients, keep K+ ABOVE 4.0 mmol/L
Treatment of hypokalemia in cardiac patients involves addition of:
also note that MAGNESIUM may also be needed, it decreases the risk of arrhythmias.
If a patient has hypokalemia with acidosis, treatment is:
If a patient has ACIDOSIS, first correct K+ and then pH.
Treatment of diabetic ketoacidosis can result in:
hypokalemia of the intracellular water.
80% of calcium is bound to ____, and is diffusible when bound to ions
80% of calcium is bound to albumin, and is diffusible when bound to ions
Calcium is regulated by
Calcium is regulated by PTH, calcitonin and vitamin D
THE EXTRACELLULAR CONCENTRATION OF CALCIUM IS
THE EXTRACELLULAR CONCENTRATION OF CALCIUM IS GREATER THAN THE INTRACELLULAR CONCENTRATION [ECW] > [ICW]**.
The symptoms associated with calcium levels > 9 - 11 mg/dL
nephrolithiasis
(2) weakness/stupor/CNS dysfunction.
The symptoms associated with calcium > 17 mg/dL
Tachyarrhythmias
(2) coma
(3) ARF/ileus
Hyperparathyroidism with a 85% solitary adenoma as well as SECONDARY hyperparathyroidism cause
hypercalcemia
(myeloma/hematologic malignancies, bone malignancies (osteoclastic activity IL-1, TNF-alpha, IL-6). Thiazides, vitamin A&D overdose and immobility are also etiologies of
hypercalcemia
Treatment of hypercalcemia is:
treat the underlying problem (i.e., fluids, diuretics, hemodialysis, bisphosphonates)
T/F: Acute hypocalcemia is life threatening as it impairs membrane depolarization!!
True
Chvostek’s and Trousseau’s sign are associated with:
acute hypocalcemia
chemotherapy applied to solid tumors and LYMPHOMAS is associated with
acute hypocalcemia
Saponification of fat in pancreatitis.
*Citrate chelation from blood product transfusion.
are both associated with
acute hypocalcemia
Chronic hypocalcemia is a result of
PARATHYROID DYSFUNCTION
Etiologies of chronic hypocalcemia
Vitamin D deficiency/short gut syndrome/fat malabsorption.
- Renal and liver disease.
- Extensive osteoblastic skeletal metastases (such as from prostate and breast cancers).
- Chemotherapy, including cisplatin, 5-fluorouracil and leucovorin, mediated through hypomagnesemia.
Treatment of chronic hypocalcemia
calcium and vitamin D
Etiology of hypermagnesemia
- Hypermagnesemia: renal failure OR oral antacid use
The result of hypermagnesemia
The result is calcium is blocked, myocardial cells are affected and heart failure results.
The result of hypomagnesemia
diarrhea/diuretic use/heavy EtOH use. This is more common in diabetics with osmotic diuretics and equilibration is slow.
- If a patient presents with both hypocalcemia and hypomagnesemia,
REPLACE BOTH CONCURRENTLY.
Which of the following is associated with cell energy failure?
(1) DKA
(2) Thiamine deficiency (alcoholism)
(3) Acute anoxia (i.e., CO poisoning or drowning)
(4) All of these
(4) All of these
According to Blalock: all acute injuries result in
changes in fluid and electrolyte metabolism
Hypovolemic shock: hypovolemic shock results form
inadequate oxygen deliver due to decreased intravascular volume
Hemorrhagic shock is due to
bleeding, whether form the GI tract, wounds or fractures
Compensated hemorrhagic shock presents with:
SVR adjustment - perfusion suboptimal.
Critical organs perfused at the expense of others.
Uncompensated hemorrhagic shock presents with:
Hypotensive 20 - 40% loss of EBV
Vasoconstriction mechanism unable to compensate.
Hemorraghic shock (lethal exsanguination) is associated with:
> 40% EBV, syncope and cardiac arrest.
Fluid shifts seen in DKA, burns and accompanying GI losses as in SBO or c. difficile colitis can cause
hypovolemic shock.
**The surgeon’s most effective intervention for hypovolemic shock is
HEMOSTASIS
Phase 1 of hypovolemic shock is characterized by:
Hypovolemia/vasoconstriction/acidemia
Transfuse for EBL > 30% of estimated blood volume (EBV).
Ptaients experience minimal shock during this phase.
Phase 2 of hypovolemic shock is characterized by:
Duration and magnitude is proportional to severity of injury.
Weight gain/edema (i.e., abdominal viscera).
Phase 3 of hypovolemic shock is characterized by:
Occurs within 2 - 4 days of phase 1.
If there is a failure of phase 3 onset, complications occur (CHF or sepsis).
Anaphylactic shock: this is a shift of plasma fluid into the
interstitium
Lab values of septic shock
INCREASED lactate, HR, CVP, CO and DECREASED blood pressure and SVR
Cardiogenic shock: results when
the cardiac output of the left ventricle is inadequate.
Lab values of cardiogenic shock:
INCREASED heart rate, CVP, PCWP and SVR; DECREASED BP and CO.
If a patient with cardiac shock is under anesthesia, EKG presents with:
If the patient is under anesthesia, the EKG shows decreased ST segments, Q waves and LBBB, as well as signs of hypotension and arrhythmia. Serum troponin elevation is present.
If a patient with cardiac shock is conscious, they present with:
chest pain followed by shock 6 - 12 hours later.
Etiologies of cardiac shock:
(1) Cardiac contusion
(2) Cardiac tamponade
(3) Massive pulmonary embolism
Treatment of cardiogenic shock:
: O2, nitroglycerin, morphine or aspirin. If a patient has an arrhythmia, use cardioversion to sinus rhythm.
Primary adrenal insufficiency: is pathology of the
GLAND and includes adrenalectomy, hemorrhage and infarction.
Iatrogenic causes of primary adrenal insufficiency:
post-operative in patients with antiphospholipid antibody syndrome and heparin induced thrombocytopenia (HIT).
Secondary adrenal insufficiency: is a disease of the
pituitary and hypothalamus. There is DECREASED release of ACTH and AVP.
Etiology of secondary adrenal insufficiency
Sheehan’s syndrome
Treatment of secondary adrenal insufficiency
hydrocortisone 100 mg IV Q8Hrs
: in this condition, there is LIMITED cortisol production when stressed
Relative adrenal insufficiency
Etiology of relative adrenal insufficiency
autoimmune/adrenalitis (lymphocyte mediated), TB, patients on LONG TERM STEROID TREATMENT (causes reduction in ACTH), atrophy of the adrenal cortex.
Treatment of relative adrenal insufficiency
- Treatment: requires steroid supplementation in PERIOPERATIVE PERIOD. Low doses of glucocorticoids and minaeralocorticoids may be beneficial
Treatment of relative adrenal insufficiency
: look for sepsis and test with IV corticotrophin. Serum cortisol levels are also affected – if there is little to no elevation in serum cortisol, the odds of mortality increase.
