Fluid And Electrolyte Imbalance - Na, K Flashcards
With increased Na+ intake, what changes occur in sympathetic activity, ANP, plasma oncotic pressure, and RAS to maintain normal electrolyte concentration within the body?
Decreased sympathetic activity (leads to dilation of afferent arterioles and thus increased GFR —> decreased Na reabsorption in PT)
Increased ANP (leads to constriction of efferent arterioles and thus increased GFR —> decreased Na reabsorption in CDs)
Decreased plasma oncotic pressure (leads to decreased Na reabsorption in PT)
Decreased RAS (leads to decreased Na reabsorption in PT and CDs)
Overall result is increased Na+ excretion! [note that opposite would occur with decreased Na+ intake]
Hypovolemia independently stimulates secretion of what hormone?
ADH —> water retention
Signs/symptoms of hypovolemia
Decreased skin turgor
Thirst
Dry mucous membranes
Sunken eyes
Oliguria
As it worsens, may see tachycardia, hypotension, tachypnea, and confusion
Signs/symptoms of hypervolemia
Weight gain
Edema
“bounding” pulse
Causes of absolute, extrarenal hypovolemia
Bleeding GI fluid loss Skin fluid loss Resp. fluid loss Extracorporeal ultrafiltration
Causes of absolute, renal causes of hypovolemia
Diuretics
Na+ wasting tubulopathies
Genetic or acquired tubulointerstitial dz
Obstructive uropathy/postobstructive diuresis
Hormone deficiency
Hypoaldosteronism/adrenal insufficiency
What does it mean to have relative hypovolemia?
Decreased effective circulating fluid volume with increased total body sodium
Extrarenal vs. renal causes of relative hypovolemia
Extrarenal: edematous states, heart failure, cirrhosis, anaphylaxis, drugs, sepsis, pregnancy, third-spacing
Renal: severe nephrotic syndrome
Causes of hypervolemia d/t primary renal sodium retention (increased ECV)
Oliguric acute renal failure Acute glomerulonephritis Severe chronic renal failure Nephritic/nephrotic syndrome Primary hyperaldosteronism Cushing syndrome Early stage liver disease Conn syndrome Gordon syndrome Liddle syndrome
Causes of hypervolemia d/t secondary renal sodium retention (decreased ECV)
Heart failure
Late stage liver disease
Nephrotic syndrome (minimal change disease)
Pregnancy
Hyper or hyponatremia are considered WATER problems. What is considered hyper vs. hyponatremic?
Hypernatremia = plasma [Na] > 145 mEq/L
Hyponatremia = plasma [Na] < 135 mEq/L
Most common electrolyte abnormality encountered in clinical practice
Hyponatremia
Hypervolemic etiologies of hyponatremia
With decreased ECV: CHF, cirrhosis, sepsis, nephrotic syndrome, pregnancy, anaphylaxis
With increased ECV: acute renal failure, advanced chronic renal failure
Euvolemic etiologies of hyponatremia
SIADH (vascular stretch receptors cause Na dumping to keep volume relatively normal)
Drugs Glucocorticoid deficiency Hypothyroidism Primary polydipsia Poor osmolar intake Positive pressure ventilation
Hypovolemic etiologies of hyponatremia
Renal losses (indicated by U[Na]>30): diuretic excess, mineralocorticoid deficiency, salt-losing nephropathy, bicarbonaturia with RTA and metabolic alkalosis, cerebral salt wasting
Extrarenal losses (indicated by U[Na]<30): vomiting, diarrhea, third-spacing d/t burns/pancreatitis/trauma
Mnemonic for hyponatremia symptoms
SALT LOSS
Stupor/coma
Anorexia, N/V
Lethargy
Tendon reflexes decreased
Limp muscles (weakness)
Orthostatic hypotension
Seizures/HA
Stomach cramping
Treatment of patients with hyponatremia is based on presenting symptoms.
How would you treat a patient with Level 1, aka no or minimal symptoms, possibly including HA, irritability, inability to concentrate, altered mood, depression, falls, or unstable gait?
Fluid restriction
Consider a -vaptan under select circumstances like: inability to tolerate fluid restrictions, very low sodium level, need for correction to have surgery, high fracture risk with unstable gait, etc.
Treatment of patients with hyponatremia is based on presenting symptoms.
How would you treat a patient with Level 2, aka moderate symptoms, possibly including nausea, confusion, disorientation, or altered mental status?
-vaptan or hypertonic NaCl infusion, followed by fluid restriction
Treatment of patients with hyponatremia is based on presenting symptoms.
How would you treat a patient with Level 3, or severe symptoms, possibly including vomiting, seizures, obtundation, respiratory distress, or coma?
Hypertonic NaCl, followed by fluid restriction or vaptan
Why must correction of hyponatremia be done slowly?
Overly rapid correction can cause Osmotic Demyelination Syndrome
- In acute symptomatic hyponatremia you can use a faster rate of infusion (2.5 mEq/L/h) to get to a safer zone, but do not increase more than 20 mEq/L/day
- If chronic, rate of increase should be ~0.5 mEq/L/h until 120 mEq/Na/L with total increase not to exceed 8-12 mEq/L/day and no more than 18 in the first 48 hrs
Hypervolemic causes of hypernatremia
Administration of hypertonic saline, hypertonic sodium bicarb
Hypertonic dialysis
Hypertonic feedings
Primary hyperaldosteronism
Cushing syndrome
Euvolemic causes of hypernatremia
Diabetes insipidus (central or nephrogenic) — again counterintuitive but note that vascular stretch receptors are keeping volume ~normal
Hypodipsia
Insensible dermal and skin losses (only if hypodipsic)
Hypovolemic causes of hypernatremia
Lack of access to water
“Broken” thirst mechanisms
Mnemonic for hypernatremia symptoms
TRIP
T - twitching, tremors, hyperreflexia
R - restlessness, irritable, confusion, etc. (d/t brain cell shrinkage)
I - intense thirst, dry mouth, decreased urine output
P - pulmonary and peripheral edema
Treatment for hypernatremia
If hypovolemic, they have a sodium deficit as well as a water deficit, so use isotonic saline
In other patients, use hypotonic IV solutions (e.g., D5W, half-normal saline, quarter-normal saline)
Calculation of water deficit = 0.6% body weight (kg) x (1-[140/Na])
Why must hypernatremia be corrected slowly?
If corrected too quickly can cause brain edema; so correct over 48 hours at < 0.5 mEq/L/h (i.e., <12 mEq/L/day)
Lab values representing hyper- vs. hypokalemia
Hyperkalemia = plasma [K] > 5.5 mEq/L
Hypokalemia = plasma [K] < 3.5 mEq/L
How does hyper vs. hypokalemia relate to heart rate?
Hyperkalemia —> bradycardia
Hypokalemia —> tachycardia
Effects of hyperkalemia seen on ECG
[in order of increasing severity of hyperkalemia]
HIGH T WAVE ([K] ~ 7)
Prolonged PR interval, depressed ST segment, high T wave
Auricular standstill, intraventricular block
Ventricular fibrillation ([K] ~ 10)
Effects of hypokalemia seen on ECG
[in order of increasing severity of hypokalemia]
Low T wave ([K] ~ 3.5)
Low T wave + high U wave
Low T wave + high U wave + low ST segment ([K] ~ 2.5)
Rapid absorption of K+ in the diet (e.g., 25-50 mEq/meal) into the ECF could lead to fatal hyperkalemia if not for its rapid redistribution into the ICF; what hormone is the most important for this to occur?
Insulin
If the body is in a state of acidemia, this can be buffered by ______ the ECF [K]
Increasing
[note that in state of alkalemia, low [H+] is buffered by lowering ECF [K]]
Acute factors leading to enhanced cell uptake of K+
Insulin
Beta-catecholamines
Alkalosis
[alpha catecholamines and acidosis cause impaired cell uptake]
What effect does hyperosmolarity have on potassium efflux?
Enhanced cell efflux
What effect do chronic conditions involving thyroid, adrenal steroids, exercise, and growth have on ATP pump density?
Enhanced
What effect do chronic conditions involving diabetes, potassium deficiency, or chronic renal failure have on ATP pump density?
Impaired
Hyperkalemia causes what change in aldosterone levels?
Increased
Effect of high Na+ intake on K+ excretion
K+ excretion should be unchanged, because effects of increased Na intake are balanced out
Hypokalemia causes mnemonic
GRAPHIC IDEA
GI losses (vomiting/diarrhea) Renal tubular acidosis Aldosterone Paralysis (periodic) Hypothermia Insulin excess Cushing’s syndrome
Insufficient intake
Diuretics
Elevated beta adrenergic activity
Alkalosis
Signs and symptoms of hypokalemia
CNS: drowsiness, lethargy
Neuromuscular (most prominent manifestations): skeletal muscle weakness, smooth muscle weakness —- may lead to ileus and constipation
CV: ventricular arrhythmias, hypotension, cardiac arrest
Renal: polyuria, nocturia
Metabolic: hyperglycemia
Causes of hypokalemia in normal acid-base state
Redistribution: catecholamine excess, alkalosis, hypokalemic periodic paralysis, insulin administration, barium poisoning
Extrarenal losses: decreased intake (e.g., anorexia nervosa), laxative abuse
Causes of hypokalemia in a state of metabolic acidosis
Extrarenal losses: diarrhea, laxative abuse
Renal losses: renal tubular acidosis, organic acidosis (lactic and ketoacidosis), carbonic anhydrase inhibitors
Causes of hypokalemia in state of metabolic alkalosis
With urine K <20 mEq/L: vomiting, diuretics
With urine Cl > 20 mEq/L and normal BP: bartter syndrome, diuretics
With urine Cl > 20 mEq/L and HTN: hyperaldosteronism, essential HTN with diuretic use, hypercortisolism, apparent mineralocorticoid excess (licorice ingestion, liddle syndrome)
Tx of hypokalemia
Goal is to prevent life-threatening conditions like diaphragmatic weakness, rhabdomyolysis, and cardiac arrhythmias; especially urgent if rapid K+ falls to <2.5 mEq/L
K+ replacement is mainstay of tx
Then dx/correct underlying cause: stop K+ losing diuretics, give beta blocker if evidence of increased SNS tone
Mnemonic for causes of hyperkalemia
RED FETS
Renal disease: ARF, CKD, type IV RTA
Excessive intake: food, K+ IV fluids, blood transfusion
Drugs: K+ sparing diuretics, K+ salts of penicillin
Factitious: prolonged use of tourniquet, hemolysis
Endocrine: Addison’s disease
Tissue release: rhabdomyolysis, burns, hemolysis, cytotoxic therapy
Shift out of cell: acidosis, beta-antagonists, insulin deficiency, tissue damage
Signs and symptoms of hyperkalemia
Cardiac (most important and most frequent): abnormal heart rhythm — BRADYCARDIA, peaked T wave, Vfib, cardiac arrest, flattened P wave, prolonged PQ interval, widened QRS, sine wave
Neuromuscular: numbness, weakness, flaccid paralysis
Causes of pseudohyperkalemia
Hemolysis
Thrombocytosis
Leukocytosis
Causes of redistribution hyperkalemia
Acidosis Decreased insulin Beta-blockers Arginine infusion Succinylcholine Digitalis overdose Periodic paralysis
Causes of hyperkalemia with GFR > 20 mL/min (impaired K+ secretion) and LOW aldosterone
Addison disease
Hyporeninemic hypoaldosteronism
Drugs: PG synthetase inhibition, Captopril
Causes of hyperkalemia with GFR > 20 mL/min (impaired K+ secretion) and normal or HIGH aldosterone
Primary tubular disorders: acquired, renal transplant, lupus erythematosus, amyloid, sickle cell, obstructive uropathy
Drugs: spironolactone, triamterene, amiloride
Emergency management of hyperkalemia (3 categories)
- Give IV calcium to antagonize cardiac effects
- Give insulin and glucose to redistribute K+ into cells (can also use beta agonist like albuterol)
- Administer K-losing diuretic to facilitate K elimination (can also consider mineralocorticoid in pts with hypoaldosteronism, cation exchange resin, or dialysis)
Then it is important to monitor intake (e.g., < 60 mEq/day), paying attention to hidden sources like abx
