Fluid, Electrolyte, and Acid-Base Balance Flashcards
Review slide 6 and 7 for a good overview video and flowchart of fluid balance
Does water rely on active transport for movement between body compartments?
No, water moves freely from one body water compartment to another according to osmolar gradient
Do electrolytes (Na+, K+, Cl-, PO4-) rely on active transport for movement between body water components?
Yes, their movement between intracellular and extracellular compartments requires active transport
What ions maintain osmolality in extracellular fluid (ECF)?
Primarily by Na+, but also by chloride and bicarbonate anions
What ions maintain osmolality in intracellular fluid (ICF)?
Primarily by K+ (cations), but also by anion proteins and phosphate
Do proteins like albumin contribute to osmolality?
Yes, but are only found in intracellular fluid and within blood vessels
Proteins are not found in interstititial ECF
This lack of proteins in the interstitial ECF helps maintain osmotic gradient between the interstitial fluid and blood vessels (if pt has low serum albumin, it can cause edema due to loss of osmotic gradient towards vessels)
What causes low albumin states to result in edema?
If pt has low serum albumin, it can cause edema due to loss of osmotic gradient towards vessels. More fluid remains in the interstitial space
Review oncotic pressure
What is the severe consequence of plasma hyperosomolality?
Brain cell shrinkage (water moves into plasma from cell)
This results in somnolence, confusion -> if
severe enough -> cerebral
bleeding, death
What is plasma osmolality?
concentration of effective solutes in plasma (relative to water)
What is the severe consequence of plasma hyo-osmolality?
Brain cell swelling ->
headache, N+V, gait
instability -> seizures,
coma, death
What are osmoreceptors?
Specialized cells that recognize changes in plasma osmolality and initiate corrective actions by the release of hormones, etc.
When is vasopressin/ADH released by osmoreceptors?
Released in response to increased plasma osmolality (as sensed by osmoreceptors
ex. increased Na+ after salty meal
Also released in response to non-osmotic stimuli when osmoreceptors in the brain detect ↓ circulating
blood volume or ↓ blood pressure
ex. diarrhea, poor kidney perfusion, extreme blood loss
What are the corrective actions associated with vasopressin/ADH when increased osmolality is detected by osmoreceptors?
Stimulates water reabsorption in the distal tubule/collecting duct of the kidney (↓ diuresis) -> excretion of a
more concentrated urine (hold on to more fluid)
Also stimulates thirst (increase fluid intake)
What corrective actions are associated with vasopressin/ADH in response to lower blood volume?
Water conservation restores circulating blood volume at the expense of decreased serum osmolality
-> dilutional hyponatremia
What stimulates release of aldosterone?
- ↓ blood volume or ↓ blood pressure activates Renin-Angiotensin-Aldosterone System (RAAS) ->stimulates
release of aldosterone - ↑ serum K+ or ↓ serum Na+ can also stimulate aldosterone release
What is the role of aldosterone on fluid balance?
Stimulates reabsorption of sodium from the distal convoluted tubule of the kidney -> ↑ serum Na+ (and
therefore water because water follows sodium) and ↓ serum K+ (risk of hypokalemia)
What stimulates the release of natriuretic peptides?
Released by the atria/ventricles of the heart in response to ↑ blood pressure and/or ↑ blood volume
What is the role of natriuretic peptides on fluid balance?
Inhibit the activity of aldosterone by reducing sympathetic nervous system activity (↓ RAAS activation) and also increases vasodilation
Oppose the effects of ADH and aldosterone
What is the role of the kidney in maintaining fluid balance?
Kidney regulates water excretion to keep serum osmolality relatively constant (275-290 mOsm/kg) despite variability in water intake
What determines serum osmolality?
Primarily determined by sodium concentration
- ~90% of the body’s sodium is extracellular
- Sodium is the predominant solute in the ECF
Also affected by glucose and urea concentrations
Serum osmolality = (2 x serum Na+) + serum glucose + serum urea
What is included in supplemental fluid therapy?
Water
Electrolytes (usually 75-175 mEq Na+ and 20-60 mEq K+ per day)
Dextrose (100-150g/day to prevent catabolism and starvation ketoacidosis)
Review slide 19
What are some mechanisms by which the body looses water?
Fluid loss in urine + fluid loss in stool + insensible fluid loss from skin, respiratory tract
Minimum amount of fluids needed per day ~ 1400 mL (or 60mL/hr) to recover losses
What are the primary causes of hypovolemia?
Volume depletion generally results from decreased total body sodium due to renal or extrarenal sodium loss from the ECF
How is sodium lost renally?
- Increase diuresis (on TZDs)
- Salt-wasting nephropathies
- Mineralocorticoid deficiencies (reduced ability to release aldosterone)
How is sodium lost extrarenally?
- Fluid loss from the GI tract (vomiting, diarrhea)
- Skin losses (burns)
- Hemorrhage
- Increased capillary permeability (sodium moves into interstitial space, “third-spacing”)
Why is water loss not a common primary cause of hypovolemia?
We have to lose a lot of free water to cause volume depletion, because most of our water is in the intracellular fluid.
The intravascular space (blood) only accounts for 8.5% of total body water
What are some signs and symptoms associated with hypovolemia?
Mild volume depletion may be asymptomatic
Severe volume depletion may lead to mental status changes, renal failure, and hypovolemic shock
Symptoms: thirst, fatigue, muscle cramps, orthostatic dizziness
Signs: Reduced JVP, postural hypotension and tachycardia, reduced sweat
How is hypovolemia treated?
Mild hypovolemia can be corrected orally (soup contains fluid and Na+)
Symptomatic fluid loss and intolerance to oral administration necessitates IV therapy (use Na+ based isotonic solutions, normal saline preferred, since same Na+ concentration as blood the fluid will stay in the ECF)
Why can we not just administer water IV to correct hypovolemia?
Water on its own will flow out of the ECF into interstitial space due to osmotic gradient
What are the primary causes of hypervolemia?
Surplus total body sodium (disorder of renal sodium retention)
Also may result from decreased effective circulating volume (body compensates by reducing excretion of fluid)
What is the clinical presentation of hypervolemia?
Expansion of the interstitial fluid compartments of the ECF may result in peripheral edema, ascites, and pleural effusions
Expansion of the intravascular component of the ECF may result in increased JVP, pulmonary crackling, S3 heart sound, and elevated blood pressure
What are some symptoms associated with hypervolemia?
Dyspnea, orthopnea, leg swelling, abdominal distention
Lab values tend to be unremarkable
Chest X-rays can help detect pleural effusions or edema
Symptoms only appear until 3-4L of fluid retention has occurred (rapid weight gain is the earliest way to detect someone is retaining fluid)
What are some potential underlying causes of hypervolemia?
HF, liver disease, or kidney disease
How can sodium excess be managed in patients with hypervolemia?
Dietary sodium restriction
Diuretics (TZDs, loop diuretics, K+ sparing)
What is the impact of TZDs on Na+, K+, Mg2+, and Ca2+?
All electrolytes except Ca+ is reduced
Na+ is reduced
K+ is reduced
Mg2+ is reduced
Ca2+ is increased (higher rates of kidney stones)
What is the impact of Loop diuretics on Na+, K+, Mg2+, Ca2+?
All electrolytes except Na+ is reduced
Na+ is no change
K+ is decreased
Mg2+ is decreased
Ca2+ is decreased
What is the impact of Potassium-sparing diuretics on Na+, K+, Mg2+, & Ca2+?
All electrolytes except K+ is no change
Na+ is no change
K+ is increased
Mg2+ is no change
Ca2+ is no change
What is the most common electrolyte abnormality?
Hyponatremia
What are the consequences of ingesting too much “free” water?
Rare, need to consume a LOT of water (deliberate) to overwhelm the kidney’s ability to excrete all of it (seen in patients with solute-poor diet)
Psychogenic polydipsia (rare presentation, but pt has compulsive water drinking, seen with schizophrenia)
Beer potomia (excessive alcohol, and poor dietary intake of solutes)
What is hyperosmolar hyponatremia?
Occurs when an osmotically active agent other than Na+ accumulates in the ECF, drawing water into the ECF and diluting sodium
Sodium content is normal, but concentration is low due to dilutional effect
Commonly caused by hyperglycemia (over 30mmol/L)
Excessive blood glucose draws from ICF -> ECF
What is hypovolemic hyponatremia?
Results from net sodium loss
TZD (block Na+ reabsorption in distal tubule, increased Na+ and water loss, lower blood volume, ADH released to capture more water, more sodium than water lost)
Hyponatremia develops within 2 weeks of starting therapy or increasing dosages
Uncommon with loop diuretics due to MOA and target
What is hypervolemic hyponatremia?
Occurs during fluid-overloaded states such as HF, cirrhosis with ascites, and severe nephrotic syndrome
Fluid shifts from the intravascular to the interstitial space (dilutional hyponatremia)
What is euvolemic hyponatremia?
Activation of ADH in the absence of osmotic or volume-related stimuli
SIADH (Syndrome of Inappropriate Antidiuretic Hormone secretion) is the most common form
What are some causes of SIADH?
Non-physiological release of ADH from the pituitary or an ectopic source
- Neurological and psychiatric disorders (stroke, head trauma, acute psychosis)
- Pulmonary diseases (pneumonia, TB, acute resp. failure)
- Malignant tumours (most commonly small cell lung cancer)
- Drugs (SSRIs (get empiric sodium levels when starting SSRIs or SNRIs), antipsychotics, narcotics, NSAIDS)
What is the clinical presentation of hyponatremia?
Relatively asymptomatic (due to compensatory mechanisms)
Often detected on routine bloodwork
Associated with impaired attention, concentration, and gait (increased fall risk)
Symptoms are primarily neurological (proportional to the magnitude and speed of sodium decline)
What are normal sodium values?
135-145 mEq/L
What does acute hyponatremia (developing over 48h) present like?
Symptoms may appear below 125 mEq/L (nausea, malaise, heachache)
If Na+ continues to reduce, symptoms progress lethargy, headaches)
Seizures, coma if Na+ if less than 115 mEq/L
What does chronic hyponatremia present like?
Over 3 days of duration
Adaptive mechanisms kick in and help defend against cellular swelling, which minimizes symptoms
How is hyponatremia officially diagnosed?
Plasma osmolality (if it is over 275 mOsm/L, then the patient has hyperosmolar hyponatremia)
Urine osmolality (if it is over 100 mOsm/L, then suggests impaired free water excretion due to SIADH)
Urine sodium concentration (if it is under 20mEq/L, then hyponatremia)
What are some treatment pearls for hyponatremia?
It is important to correct hyponatreamia slowly (if too fast, can cause rapid cell swelling and brain damage)
Total daily sodium correction should not exceed 8mEq/L per day
How is symptomatic hyponatremia treated?
Hypertonic saline should be used to correct by 4-6mEq/L in the first 6h, max of 8mEq/L in the first 24 hours
Given as 100mL IV boluses (up to 3x in a day, PRN) or as IV infusion (calculate conservative infusion rate)
Frequent Na+ rechecks to ensure appropriate correction, and adjust strategy as needed
How is asymptomatic hypovolemic hyponatremia treated?
Hypovolemic hyponatremia: Use isotonic (0.9%) saline to restore intravascular volume (reduced renal water retention, turn off ADH –> normalize serum sodium concentration
How is hypervolemic hyponatremia treated?
Associated with HF and cirrhosis (manage underlying condition)
Restrict water intake (less than 1-1.2L/per day) and salt intake (1-2g/day)
Loop diuretics may help reduce hypervolemia
How is euvolemic hyponatremia (SIADH) treated?
Identify and correct underlying cause (usually drugs)
If not effective, try water restriction (less than 1-1.2L/day) and salt tablets to encourage water excretion
Loop diuretics may also help with water excretion without much Na+ loss
Refractory treatment options:
- Vasopressin antagonists (oppose the action of ADH, but risk of overcorrection)
Review slide 45 and 46 for diagrams of the different types of hyponatremia
What are the plasma sodium levels for hypernatremia?
Over 145mEq/L
What are some characteristics associated with hypernatremia?
State of hyperosmolality (cellular dehydration)
Usually caused by a water deficit, rather than net sodium gain
Hyperosmolar state stimulates thirst and excretion of a maximally concentrated urine
For hypernatremia to persist, the patient must have either an impaired thirst response or water loss in excess of electrolyte loss
What are some causes of impaired thirst response?
Limited access to water (infants and small children, institutionalized or intubated patients, delirium, dementia)
What are some causes of hypernatremia due to water loss in excess of electrolyte loss?
- Non-renal water loss is most commonly due to significant diarrhea
- Renal water loss from osmotic diuresis or diabetes insipidus (lack of secretion or response to ADH)
What is the clinical presentation of hypernatremia?
Movement of fluid from ICF to ECF (contributes to brain cell shrinkage)
Presence and severity of symptoms depend on both the acuity and magnitude of hypernatremia
Diabetes insipidus presents with polyuria and polydipsia
What is the clinical presentation of severe or acute hypernatremia?
Severe or acute hypernatremia may present with altered LOC, weakness, focal neurological deficits, may progress to coma, seizure, death
What are some concerns with rapid treatment of hypernatremia?
May cause brain cell swelling (seizures, permanent neurological damage, or even death)
In symptomatic hypernatremia, Na+ levels should not be corrected by no more than 10-12 mEq/L
In chronic (compensated) hypernatremia, Na+ levels should be corrected even slower at 5-8mEq/L per day
What is central diabetes insipidus (associated with hypernatremia)?
Lack of ADH secretion
What is nephrogenic diabetes insipidus (associated with hypernatremia)?
Lack of renal response to ADH
How is central diabetes insipidus treated (associated with hypernatremia)?
Desmopressin is a synthetic analogue of ADH
Titrated to achieve high-normal sodium concentration, 1.5-2L of urine output/day, and minimal nocturia
Sodium levels are checked q1-3 days during initiation and titration
How is nephrogenic diabetes insipidus treated (associated with hypernatremia)?
Identify and correct concurrent hypercalcemia and hypokalemia
TZD diuretics + Na+ restriction (less than 2g/day) should decrease urine volume and normalize sodium levels
Indomethacin may also encourage ADH activity in the kidney and decrease urine volume
How is sodium overload treated (associated with hypernatremia)?
Usually iatrogenic (too much sodium containing fluid was infused)
Administer D5W and loop diuretic to facilitate Na+ excretion
Review slide 52 for a diagram of the causes of hypernatremia
What is the most abundant cation in the body?
Potassium (98% intracellular)
Normal serum concentration = 3.5 to 5 mmol/L
What is the role of potassium in the body?
- Intracellular functions, such as protein and glycogen synthesis, cell growth and metabolism
- Determines the resting membrane potential across the cell membrane
- Helps maintain BP
What factors impact potassium homeostasis?
- Dietary intake
- GI and urinary excretion
- Hormones (Insulin, epinephrine, aldosterone)
- Acid-base balance (excessive H+ ions and metabolic ketoacidosis)
What is the influence of hormones on potassium homeostasis?
Insulin - drives K+ into liver, muscle, and fat cells (decrease serum K+)
Epinephrine/norepi - stimulate K+ uptake by cells
Aldosterone - promote urinary K+ excretion
What is the influence of acid-base balance on homeostasis?
Excessive H+ ions = increased serum acidity, encourages H+ to enter cells in exchange for K+ release into blood (higher serum K+)
Metabolic alkalosis (less H+ ions in serum = fewer K+ ions)
What K+ values are considered to be hypokalemia?
Under 3.5mmol/L
Mild: 3.1-3.5 mmol/L
Moderate: 2.5-3.0 mmol/L
Severe: Under 2.5 mmol/L
What are some causes of hypokalemia?
Total-body K+ deficit (inadequate dietary intake, excessive GI or renal K+ loss)
Intracellular shift of K+
How does hypomagnesemia affect potassium levels?
Hypomagnesemia contributes to hypokalemia by promoting renal K+ loss
Therefore may need to treat low Mg2+ before low K+
What are some symptoms of hypokalemia?
Mild: Generally asymptomatic
Moderate hypokalemia: Muscle cramping, myalgias, weakness, malaise
Severe hypokalemia:
- Impaired muscle contraction
- ECG changes (ST depression, T-wave inversion)
- Heart block
- Atrial flutter
- Paroxysmal atrial tachycardia
- Ventricular tachycardia
How is mild hypokalemia treated?
Mild and asymptomatic hypokalemia may respond to increased dietary K+ intake
How is moderate or refractory hypokalemia treated (still asymptomatic and no ECG changes)?
Oral replacement preferred
ex. 10mmol K+ should increase serum K+ by 0.1mmol/L
How does chronic loop diuretic or TZD therapy affect how we treat hypokalemia?
They both lower K+, so a higher dose of K+ needs to be administered to correct mild-moderate hypokalemia
Divide doses to help with GI tolerability
How is severe hypokalemia treated?
Avoid overly rapid correction of K+ due to concerns about potential cardiac conduction abnormalities
Need continuous ECG if high doses of K+ need to be given quickly
Usually infused at 20mmol/hour IV
What is the role of potassium-sparing diuretics in management of hypokalemia?
May help prevent loop diuretic or TZD-associated hypokalemia
What values are considered to be hyperkalemia?
Over 5mmol/L
Mild: 5.1-5.9 mmol/L
Moderate: 6-7 mmol/L
Severe: over 7 mmol/L
Much less common compared to hypokalemia
What are some causes of hyperkalemia?
Decreased K+ excretion
- AKI or CKD
- Adrenal insufficiency (reduced aldosterone release = hyperkalemia)
- Drugs (ACEI/ARBs, K+ sparing diuretics, NSAIDs, TMP/SMX, cyclosporine, tacrolimus)
What are some treatment options for hyperkalemia?
If asymptomatic and mild: decrease dietary K+
If moderate, symptomatic, ECG changes, or severe hyperkalemia = immediate treatment:
- Calcium gluconate IV
- Promote intracellular K+ shift: insulin+dextrose, beta-2 agonists, sodium bicarbonate
- Eliminate excess K+ from body: loop. diuretics, oral cation exchange resins, if severe/refractory then hemodialysis
What is the role of magnesium in the body?
Important for cellular function, and as a cofactor for numerous biochemical processes
Where is magnesium found in the body?
Primarily intracellular
Found in bone (67%) and muscle (20%)
Normal serum magnesium (0.7-0.95 mmol/L)
What are some symptoms associated with hypomagnesemia?
Neuromuscular: Tetany, muscle twitches
Cardiac: Heart palpitations, ECG changes, cardiac arrhythmias
What are some causes of hypomagnesemia?
Decreased intestinal Mg absorption (ex. ulcerative colitis, chronic diarrhea, pancreatic insufficiency, chronic PPI use)
Renal Mg2+ loss due to TZDs or loop diuretics
When a patient has hypomagnesemia, is that the only electrolyte issue?
No, hypomagnesemia may cause hypokalemia
Therefore, we need to resolve hypomagnesia before hypokalemia can be adressed properly
How is hypomagnesemia treated?
Oral supplementation is preferred, except in severe deficiency
Caution: High doses may induce diarrhea
What are some conditions associated with hypermagnesemia?
Generally seen in CKD with excess Mg2+ consumption (ex. vitamins and antacids)
What are some symptoms associated with hypermagnesemia?
Muscle weakness, lethargy, confusion, dysrhythmias
What are some treatment options for hypermagnesemia?
In mild cases: identify and correct the cause
In severe cases:
- IV calcium to antagonize cardiac effects of hypermagnesemia
- Loop diuretics to increase magnesium elimination
What is the normal physiological pH range?
Normal pH = 7.4 (7.35-7.45)
pH under 6.7 and over 7.7 are incompatible with life
What organs are responsible for maintaining acid-base balance?
The lungs and kidneys are primarily responsible for maintaining acid-base homeostasis
Lungs regulate pH via CO2, which is acidic
Kidneys regulate pH via bicarbonate, which is basic
How are acid-base disorders categorized?
Categorized by the primary abnormality (respiratory vs. metabolic (kidney))
Review slides 78 and 79
What are the two respiratory acid-base disorders?
Respiratory:
- When increased CO2 is primary abnormality: respiratory acidosis
- When low CO2 is primary abnormality: respiratory alkalosis
What are the two metabolic (kidney) acid-base disorders?
Metabolic (kidneys):
- When low bicarbonate is primary abnormality: metabolic acidosis
- When high bicarbonate is primary abnormality: metabolic alkalosis
What are the compensatory mechanisms for respiratory acid-base disorders?
For any respiratory abnormality, the kidneys compensate by adjusting bicarbonate concentrations
What are the compensatory mechanisms for metabolic acid-base disorders?
For any metabolic abnormality, the lungs compensate by adjusting CO2 concentration
What is the role of the lungs in acid-base balance?
Sense alterations in blood pH
Adjust breathing rate to increase or decrease PaCO2 (to resolve metabolic alkalosis or metabolic acidosis respectively)
The lungs are able to make adjustments to resp rate (and PaCO2) relatively quickly (within minutes-hours)
What is the role of the kidneys in acid-base balance?
Sense alterations in blood pH
Adjust rate of bicarbonate excretion to increase of decrease serum bicarb (to resolve respiratory acidosis or respiratory alkalosis respectively)
The kidneys response to acid-base balance changes is slower (2-3 days)
Review slide 74 for example of compensatory mechanisms in response to acid-base balance changes
What are some normal ABG lab values?
pH: 7.4
PaO2: 80-100 mmHg
PaCO2: 40 mmHg
Bicarbonate (HCO3-): 24-30 mmol/L
Review slide 76
What are the steps to assess acid-base balance?
Step 1: Evaluate the “emia” (is it an acidic or basic disturbance)
Step 2: Evaluate the “osis” (is the problem metabolic or respiratory)
- Metabolic: primary problem is increased or decreased serum bicarb
- Respiratory: primary problme is increased or decreased PaCO2
Step 3: Evaluate whether appropriate compensation has occured to correct disturbance
Review slide 77
What is metabolic acidosis?
pH is under 7.4 and low serum bicarb (acidic blood)
Respiratory compensation will reduce PaCO2
What are some causes of metabolic acidosis?
Accumulation of acidic anions
- Lactic acidosis (rare side effect of metformin)
- Ketoacidosis
- Intoxications (methanol, ethylene glycol, salicylates)
Disturbance of endogenous H+/HCO3-
- Renal tubule acidosis
- Diarrhea (leads to bicarb loss)
- Drugs (lithium, carbonic anhydrase inhibitors, AmpB, topirimate)
How is metabolic acidosis treated?
Identify and correct cause of metabolic acidosis (lactic acidosis, ketoacidosis, drugs)
Bicarbonate administration
What is metabolic alkalosis?
pH over 7.4 and elevated serum bicarbonate
Respiratory compensation will increase PaCO2 by decreasing resp rate
What are some causes of metabolic alkalosis?
Loss of gastric acid due to vomiting
Loss of intravascular volume and chloride due to diuretics
Iatrogenic (improper ion balance in parenteral nutrition or overcorrection of metabolic acidosis with bicarbonate)
How is metabolic alkalosis treated?
- Correct underlying factors (start anti-emetics, stop or reduce diuretics)
- Volume repletion with normal saline
- Carbonic anhydrase inhibitors (increase carbonic acid levels which is acidic)
What is respiratory alkalosis?
pH over 7.4 and low PaCO2
Metabolic compensation occurs slowly (if disturbance is acute (less than 24h), then bicarb levels will be normal. if disturbance is chronic (over 24h), then bicarb levels will be low to compensate for resp. alkalosis)
What are some causes of respiratory alkalosis?
Occurs physiologically in pregnancy and individuals living in high altitudes. Also seen in hospitalized patients
Excretion of CO2 by lungs exceeds metabolic production
See slide 83
How is respiratory alkalosis treated?
Identify and correct underlying cause (manage pain, decrease anxiety, correct hypoxemia, oxygen if necessary)
What is respiratory acidosis?
pH is under 7.4 and PaCO2 is high
Metabolic compensation occurs slowly (if less than 24h, then bicarb will be normal. if more than 24h, then bicarb will be higher to compensate for respiratoty acidosis)
What causes respiratory acidosis?
Central (drugs, stroke, head injury, infection)
Perfusion abnormalities
Airway and pulmonary abnormalities
See slide 86
How is respiratory acidosis treated?
Assess whether disturbance is acute (compensatory mechanisms have not fully kicked in) or chronic (compensatory mechanisms have kicked in)
Chronic, compensated respiratory acidosis may not require treatment
Acute respiratory acidosis and severe hypoxia present (increase tissue oxygenation stat and treat underlying cause and the acidosis will correct rapidly)
