Fluids and Electrolytes Flashcards
WHat percentage is our intracellular fluid?
Intracellular fluid: 2/3 total body fluid
WHat makes up our extracellular fluid? 3
- Interstitial fluid
- Plasma
- Lymphatic fluid
Electrolytes controlled via Na-K ATPase?
6
ECF: Na+, Cl-, HCO3-
ICF: K+, Mg, Phosphates
What are the most common ions in the extracellular fluid? 2
INtracellular fluid?2
Na+ and Cl-
phosphate and K+
Water movement from ECF to ICF regulated by?
Starling forces—hydrostatic pressures and osmotic pressures
- What is osmolality?
- What is our normal plasma osmolality?
- WHat is the most important plasma osmolality factor and why?
- concentration of an osmotic solution when measured in osmols of solvent
- Plasma: 280-295 mOsm/kg
- Na+ most important plasma osmolality factor (Water essentially follows sodium)
WHat kind of electrolyte replacement is preferred when tretaing dehydration?
oral replacement
- Intravenous solutions (IV)
2 - How much can we put through a peripheral line?
- What do can we only put through a central line?
- -Saline equivalents: crystalloids
(Normal Saline or Lactated Ringers)
-Water equivalents:
(D5W) - 900 mOsm/L Max through peripheral line
- 3% Normal Saline (1028mOsm/L) centrally (hypertonic solution)
- Whats the osmolarity of D5W?
- NOrmal Saline?
- What are the lactated ringer ions (5) and what is the osmolarity?
- Parenteral colliods are which ones? 4
- D5W : 252-278 mOsm/L
- NS: 285-300 mOsm/L —also ½ NS available
- Lactated Ringer’s :
250-273 mOsm/L
Na+, Cl-, lactate, Ca+, K+ - Parenteral colloids:
- Albumin: 290-310 mOsm/L
- Blood products:
- Packed RBCs
- Fresh frozen plasma
Name the adverse affects of the following:
Normal Saline? 3
Lactated ringers? 3
Saline: 3%, 5%, D5W1/2NS? 4
Albumin? 2
Normal Saline:
- Fluid overload
- Hyperchloremic metabolic acidosis
- Hypernatremia
Lactated Ringer’s:
- Fluid overload
- Hyponatremia
- Hyperkalemia
Saline: 3%, 5%, D5W1/2NS:
- ICF depletion
- Fluid overload
- Hypernatremia
- Hyperchloremia
Albumin:
- Allergic reactions
- Possible infection transmission
How do we access the type of fluid loss?
3
- History
- Symptoms
- Vital signs and physical exam
Disorders of Water Balance:
- Hypervolemia is what?
- Etiologies? 7
- Volume contraction–What types of fluid can be missing? 5
- Hypervolemia:
- Expansion of the effective arterial blood volume - Etiologies?
- kidneys arent working,
- CHF,
- cirrohssis,
- ADH issues,
- aldosterone,
- drinking too much water.
- diabetes insipididus. - Kinds:
- hemmorhaging,
- GI losses,
- dehydrated,
- diarrhea,
- vomiting.
What is edema?
Examples of edema? 3
Too much Na+ w/ water retention in the interstitial space
- acities in ab
- extremities- peripheral edema
- CHF
- For oral fluid replacement what should we avoid?
- What are some good options?
- What should we tell the pt to do?
- AVOID fluids with a high sugar concentration
- Water and sports drinks or in children Pediolyte
- Stop activities that create ongoing losses!
- Assess degree of fluid loss:
History? 2 - Symtpoms? 3
- Clinical manifestations? 3
- History:
- GI losses??
- Excessive exercise—Loss from??
- Renal losses ??
Symptoms:
- Easy fatigability and thirst, muscle cramps
- Postural dizziness (orthostatic vitals), abdominal pain, chest pain
- Lethargy, confusion, decreased urination
Clinical manifestations:
- Decreased skin turgor (may not be seen very young or obese)
- Tachycardia
- Dry mucous membranes
- Name the hyponatremia etiologies of the following:
- Hypovolemia? 2
- Normovolemia? 3
- Hypervolemia? 5
- Hypovolemia:
- GI losses ??
- Renal losses—thiazide diuretics - Normovolemia:
- Syndrome of inappropriate ADH secretion (SIADH)
- Primary polydipsia/marathon runners
- Low dietary solute intake
Hypervolemia:
- CHF
- Cirrhosis
- hypothyroidism,
- primary adrenal insufficiency,
- drugs
- Whats the normal Na+ serum osmolality?
- What level is our “panic value”?
- At what level does treatment depend on symtpoms and situation?
- At what levels is treatment not indicated?
- lower than 135
Assess severity:
- = 120 meq/L panic value***
- 120-130—depends on symptoms and situation
- > 130 generally not directly treated
- What is the normal serum osmolality?
2. What is the main determinansts of plasma osmolality? 3
- 285-295 mOsm/kg
2. Na, glucose, urea
Hyponatremia—Clinical Manifestations:
Chronic Hyponatremia
Cerebral adaption
Cerebral adaptation as a result of Chronic Hyponatremia causes what symtpoms?
8
- Fatigue,
- nausea,
- dizziness
- Confusion,
- lethargy,
- muscle cramps
- Gait disturbances,
- forgetfulness
Hyponatremia—Clinical Manifestations:
Acute Hyponatremia
acute hyponatremic encephalopathy
- Pathophysiology of acute hyponatremic encephalopathy?
- What are usually the first symtpoms? 2
- Later symtpoms? 5
- Permanent damage? 2
- Cerebral over hydration related to degree of hyponatremia
- Fatigue and malaise usually first symptoms
- HA,
- lethargy,
- coma,
- seizures
- eventually respiratory arrest
- Acute hyponatremic encephalopathy may cause permanent neurologic damage or death
Hyponatremia Classification
3
Hypovolemic
Normovolemic
Hypervolemic
What are some examples of
- Hyponatremic-hypovolemic? 2
- Hyponatremic-normovolemic? 2
- Hyponatremic-hypervolemic? 2
- Hypovolemic:
- GI losses
- renal losses (thiazides) - Normovolemic:
- SIADH;
- low Na+ intake - Hypervolemic:
- CHF;
- cirrhosis
- Acute hypotonic, hyponatremia: can result in symtpoms of what? 2
- Can cause what symptoms? 5
- Can result in symptoms of
- neuronal cell expansion and
- cerebral edema - Nausea,
- HA,
- seizure,
- coma,
- death***
The two ADH etiologies of hyponatremia:
Inability to suppress ADH:
Causes? 3
Appropriate suppression of ADH secretion:
Causes? 3
- True volume depletion (GI or renal losses—thiazide diuretics)
- Decreased tissue perfusion (reduced cardiac output or systemic vasodilation in cirrhosis for instance)
- Syndrome of inappropriate ADH secretion (SIADH)
- Primary polydipsia*
- Low dietary solute intake
- Advanced renal failure (elevated BUN/Cr)
Hypovolemic Hyponatremia
Causes? 2
How do we treat? 4
- Such as with GI or renal losses
- If serum Na+ has not dropped critically low quickly
- Usually just volume replacement orally or IV if more severe
- Normal saline/isotonic saline
- Depending on patient status may do slow bolus
- Then maintenance depending on ongoing losses**
Hypervolemic Hyponatremia
examples? 3
Treatment? 3
- CHF
- Cirrhosis
- Renal failure
- Restrict fluids: 1000-1200 ml/day
- Restrict sodium: 1000-1200 mg/day
- Utilize loop diuretics to remove excess fluid
- What kind of hyponatremic presentation is SIADH?
- Can be induced by drugs such as? 4
- Can be induced by diseases such as? 4
- Treatment? 4
- Eu/hypervolemic hypotonic hyponatremia presentation
- Drug-induced:
- Carbamazepine,
- SSRIs,
- haloperidol,
- thorazine - Disease-induced:
- Malignancies,
- CNS disorders,
- post-surgery,
- pulmonary infections - Treatment:
- Treat underlying cause
- Fluid restriction mainstay**
- May use oral salt tablets
- Loop diuretics
Therapy for Severe Hyponatremia:
- What is the pt at risk for?
- Treatment?
- WHat is our goal?
- How often should we measure the serum Na+?
- What else should we measure?
- Severe hyponatremia patient at risk for brain herniation!
- Tx—3% hypertonic saline:
- Goal to increase Na+ by 4-6 meq/L in 24 hr. period
- Measure serum Na+ every hour
- Measure urine output
Risk if we correct Severe Hyponatremia too rapidly?
What are the high risk populations for this? 3
Develop osmotic demyelination
- Women and children acute postop period
- Patients w/ hyperacute hyponatremia –psychosis, marathons, ecstasy
- Those w/ intracranial pathology
Hypernatremia Etiologies?
7
Unreplaced water loss
- INsensible and sweat losses
- GI losses
- Central or nephrogenic diabetes insipidus
- Osmotic diuresis
- Hypothalamic lesions impairing thirst or osmoreceptor function
Water loss into cells
6. Severe exercise or seizures
Sodium overload
7. Intake or administration of hypertonic sodium solutions
Acute Hypernatremia Manifestations:
3
Rapid decrease in brain volume can rupture cerebral veins leading to
- focal intracerebral or
- subarachnoid hemorrhage
- Demyelinating brain lesions as seen with overly rapid correction of chronic hyopnatremia
- Chronic Hypernatremia Pathophysiology?
2. Why is assessment difficult for this?
- Brain adapts (within a day!) by pulling water from the CSF and increasing the uptake of solutes by the cells which also increases the amount of water in the cells
- Assessment is difficult because most affected adults already have neurologic disease diminishing the thirst response
- Hypernatremia is considered to be a concentraion at what?
- Etiology? 3
- Treatment?
4
more then 145
Etiology:
- **Loss of water
- Addition of hypertonic solution
- Sodium overload
Treatment:
- Replace free water with D5W
- Add normal saline solution if hypovolemic—use a second IV!!
- If replacing ongoing electrolyte losses (use 0.45% NS possibly w/ added K+)
- Calculate total body water replacement plus on going losses and needs and give fluid over extended time period-monitoring serum Na+/K+ closely
If its fast onset Hypernatremia?
If insideous?
- Fast onset ( 24 hrs): decrease serum Na+ by no more then 10 mEq/24 hrs
Why do we need fluid replacements with NS and not just water?
plasma volume is concentrated so you also have to give them Na+ and not just free water because other wise it will cause brain injury. hyponatremic too quickly
What is the pathology behind Central DI?
How should we treat? 3
- Not enough ADH production
- Tx central DI:
- Desmopressin 10 mcg/day: ADH like activity
- Titrate to 10 mcg/bid intranasally
- Also restrict fluid intake
What is the pathology behind Nephrogenic DI?
How should we treat? 2
Kidney resistant to ADH
Tx nephrogenic DI:
- Thiazide diuretic to decrease ECF and Na+
- Sodium restriction (2000 mg/day)
Hypernatremia Tx
For hypernatremia from unreplaced water loss: Steps 3
What could overly rapid correction lead to?
- Need to estimate water deficit
- Need to replace ongoing losses***:
- Determine safe rate plasma Na+ can be normalized:
Overly rapid correction can lead to cerebral edema
Hypernatremia Tx:
We Need to replace ongoing losses. What would these be from?
4
Determine safe rate plasma Na+ can be normalized:
Usually?
Any ongoing 1. GI losses and 2. urine losses Obligatory losses: 3. sweat & 4. stool
- Usually less than 0.5 mEq/L/hr or about 10 mEq/day
- Usually use 0.45% NS with K+
- Monitor lytes closely*** (every 4 hours usually)
- How much of calcium is bound to albumin?
- Each 1g/dL drop albumin below 4.5g/dL, decreases serum calcium by ___mg/dL
- Whats the calculation for corrected calcium?
- What space is calcium found mostly?
- Whats the normal serum range?
- 46% bound primarily to albumin
- 0.8
- [(4.5 - serum albumin) x 0.8] + measured Ca = Corrected Ca
- Extracellular electrolyte**
Unbound/free fraction active form - Normal serum range (free): 8.5-10.5 mg/dL
- At what level is a pt hypercalcemic? 2
- What are the primary causes of hypercalcemia?
- What drugs cause hypercacemia? 3
- Symtpoms of hypercalcemia? 4
- Untreated manifestations?3
- Hypercalcemia: >10.5
- Cancer and primary hyperparathyroidism*** primary causes (benign adenoma, hypertrophy, cancer of the parathyroid gland)
- Drugs:
- thiazide diuretics,
- calcium supplements,
- lithium - EKG changes
- N/V, anorexia, constipation
- Polyuria/-dypsia
- Neuro/psych symptoms
- metastatic calcification
- nephrolithiasis,
- renal failure
Outcome of hypercalcemic crisis? 4
Treatment? 4
- Oliguric renal failure,
- coma,
- v-arrhythmias,
- death
- Saline and loop diuretics: 2-3 mg/dL drop in 24-48 hours
- Bisphosphonates:
Zoledronic acid: 4mg IV over 15 min - Osteoclast inhibitors: calcitonin
- Dialysis
Why do we give biphosphates for hypercalcemia crisis?
For malignant etiologies
- At what level is a pt hypocalcemic?
- Etiologies? 4
- What do we have to correct the levels for?
- What might be associated with refractory severe hypocalcemia?
- Symtpoms? 4
(which two are the hallmark signs?)
- Hypocalcemia: less than 8.5
- Etiologies: Hypoparathyroidism, Vitamin D deficiency, loop diuretics, phosphates
- Correct level for hypoalbuminemia!
- Hypomagnesemia associated with refractory severe hypocalcemia***
- Symptoms:
tetany, paresthesias around mouth—hallmark symptoms
ECG changes: QT prolongation
Decreased myocardial contractility
TX: Acute Symptomatic HypoCa++
5 steps
IV administration of calcium salts:
1. 100-300 mg elemental calcium IV over 5-10 minutes (chloride for peripheral administration
Less irritation
5. Magnesium if hypomagnesaemia present
Chronic Hypocalcemia
Tx?
If they arent responding what should we add?
1-3 grams oral elemental calcium/day
If not responding add Vitamin D: 1000 IU/day
What are the side effects from oral calcium? 2
What are the different kinds and what are their benefits?
- Constipation
- GI upset
- Carbonate less $$ than Gluconate/Citrate
- Citrate better absorption
- Phosphorus Homeostasis
normal serum level? - What could hyperphosphatemia be caused by? 3
- What are the symptoms of hyperphosphatemia used for?
- What imbalance results with chronic Hyperphosphatemia?
- Treatment?
- Normal serum level: 2.0-4.5 mg/dL
- Decreased excretion due to low GFR
- Chemotherapy and
- rhabdomyalysis
- Symptoms due to Ca-Phosphate interaction
- Hypocalcemia
- Treatment: GI binders…..IV calcium salts
Hyperphosphatemia Treatment:
Emergency treatment seldom necessary but if you need to what should you do? 1
Usually occurs in renal failure. How would we treat this? 4
- Can be done w/ dialysis
- Diet restriction
- Phosphate-binding gel: Selvelamer (decreases mortality)
- Calcium supplements
- Avoid alluminum-containing antacids—can cause bone disease
- Hypophosphatemia is at what level?
- Symptoms are rare until what levels?
- Long term symptoms? 2
- Severe or symptomatic hypophosphatemia treatment? 3
- Mild to moderate treatment?
- less than 2.0
- Symptoms rare until level less than 1.0 mg/dL
- Long term:
- proximal muscle weakness &
- osteomalacia - Severe or symptomatic hypophosphatemia:
- IV phosphorus: Give slowly
- Sodium PO4 (4mEq/mL Na)
- Potassium PO4 (4.4mEq/mL K) - Oral phosphate replacement for mild to moderate:
- Neutra-Phos (7meq/ml Na and K)
- Neutra-Phos K (14.25 mEq/mL K)
* 250 mg phosphate
What is the major side effect of oral phosphate replacement?
*GI upset
Causes of hypomagnesia?
3
- Reduced intake- dieting, unbalanced diet, depleted foods
- Impaired absorption- GI diseases
- Increased excretion- Alcoholism, laxative abuse, treatment with diuretics or dig
Hypomagnesemia:
- Occurs in what percent of hospitalized pts?
- Clinical manifestations? 3
- Drugs that cause it? 5
- Occurs in nearly 12% of hospitalized patients
- Clinical manifestations:
- Neuromuscular: muscle cramps, tetany, seizures, coma
- Abnormalities of calcium metabolism–hypocalcemia
- Cardiovascular: widened QRS, a fib, ventricular arrhythmias - Drugs that cause it:
- diuretics,
- aminoglycosides,
- cisplatin,
- cyclosporine and
- alcohol
- Hypomagnesemia occurs at what level?
- When should we treat?
- Severe/symptomatic treatment?
- Mild to moderate treatment?
- less than 1.4 mEq/L
- Treat if less than 1.0 mEq/mL or symptomatic
- IV MgSO4 if symptomatic/severe:
- Bolus: can cause flushing, sweating - Oral replacement if mild-moderate:
- Sustained release preparations preferred
- Otherwise usual dosing 800-1600mg a day in divided dosing
IV MgSO4: A large amount is secreted in the urine so what is needed after the bolus to raise the magnesium level?
What does oral mag often cause?
a continuous infusion is needed after the bolus to raise the magnesium level
Often causes diarrhea
Hypermag symptoms:
- Mg 3-5 meq/L? 2
- Mg 4-7? 3
- Mg 5-10? 3
- Mg 10-15? 3
- Nausea, vomiting
- sedation, weakness, decreased reflexes
- hypotension, bradycardia, quadriplegia
- no reflexes, resp. paralysis, cardiac arrest
- Hypermagnesemia occurs at what levels?
- Treatment? (why do we do this?)
- What do we need to add if they have renal failure?
- What do we add if they have normal kidney function?
- How would a pregnant woman become hypermag?
- > 2mEq/L
- IV calcium (100-200 mg elemental Ca++) to antagonize neuromuscular and cardiovascular effects of magnesium
Treatment:
- Renal failure: hemodialysis
- Normal renal function: forced diuresis w/ fluid and loop diuretics
- preg woman can get hypermag because of their treatment for preeclampsia (which is mag sulfate)
- Hypokalemia occurs at what level?
- Drugs that could cause this? 4
- Medical causes of hypokalemia? 3
- Cardiac symtpoms? 3
- less than 3.5mEq/L
- Beta2-agonists
- Loop diuretics, ACE inhibitors, thiazides
- High-dose penicillin’s, amphotericin B
- Insulin
- metabolic acidosis,
- vomiting,
- diarrhea
- EKG changes: “u” wave
- Cardiac arrhythmias
- Danger in persons on digoxin!!!
Hypokalemia Treatment
Loop or thiazide induced deficit: 3
Severe or symptomatic:
3
- 40-100 mEq potassium supplementation (BID or TID)
- Oral therapy is preferred: KCL (given in mEq NOT mg!)
- With food to avoid GI upset
- IV potassium in saline bag
dextrose stimulates insulin to further shift K (dont give dextrose) - 10-20 mEq KCl in 100 mL 0.9% saline over one hour
- > 10 meq/hour monitor ECG
Why do we have to limit 40-60 mEq/L to the peripheral line?
phlebitis
- Hyperkalemia occurs at what level?
- Etiologies? 4
- Clincial manifestations? 2
- Cardiac effects? 2
- > 5.5mEq/L
2.
- Increased K+ intake
- Decreased excretion
- Aldosterone resistance
- Shift to ECF
- Ascending muscle weakness
- Usually does NOT affect respiratory muscles
- EKG changes: initially peaked T waves and shortened QT interval
- Progresses to prolonged QRS and QT interval and P waves may disappear, can then lead to dysrhythmias
Hyperkalemia
treatment?
3
- Abnormal ECG: calcium gluconate IV
- Give D5W to create a hyperglycemic state then insulin
- Consider bicarbonate if acidotic:
- -H+ exchanged for K+ in ICF to compensate for acidosis: bicarbonate reverses this
Hyperkalemia: If the pt is in renal failure?
2
- Dialysis
2. Potassium binders: Sodium polystyrene sulfonate (Kayexelate): exchanges Na for K in gut: constipation
When can we give loop diuretics in hyperkalemia?
if they arent volume depleated then you can give it.
