Fluid & Electrolytes (Part 2) Flashcards
Fluid Management Goal
Euvolemia
Maintain adequate:
Intravascular fluid volume
LV filling pressure
CO
SBP
Oxygen delivery to tissues
Physical Exam
Skin turgor
Mucus membranes
Peripheral pulses
Resting heart rate and blood pressure
Orthostatic changes
Urine output
NPO Status
Body Fluid Composition
approx. 55-60% water
2/3 Intracellular
1/3 Extracellular
(Functional Compartments)
ICF
-body weight
-ions
ICF: 40% of your weight
~ 28 L (2/3 of body H20)
Primary Ions:
K+, Mg+2, PO4-2 & proteins
controls constituents of ICF
Cell membranes & cellular metabolism
Extracellular fluid
-body weight
-ions
The remaining 1/3 of body water
approx. 20% of body weight
Primarily a Na+, Cl- & NaHCO3 solution
Interstitial Fluid (ISF)
surrounds cells
does not circulate
~ 80% of the ECF
Plasma
ECF component of blood
~20% of ECF
ECF is 80% ____ & 20% ___.
80% interstit.
20% plasma
Examples of extracellular fluid
Interstitial Fluid (ISF) (80%)
Plasma (20%)
Transcellular fluid
Transcellular fluid
are fluids that are outside of the normal compartments
Transcellular fluids
examples
how many Liters?
CSF, digestive (gastric) juices, mucus, etc.
1 - 2 liters of fluid
TBW
values for M, F , infants & obese
Total body water (TBW) varies with age, gender & body type
Males: 60%
Females: 50%
Infants: 80%
Obese adults & diabetics: less water per kg
Basic constituent of the human body
water
Laboratory Evaluation
Hypovolemia
Increasing Hct
Hypernatremia
Metabolic acidosis (severe hypovolemia)
Urine SG >1.010
Urine Na < 10 mEq/L
Urine osmolality > 450 mOsm/kg
BUN: creatinine ratio > 10:1
Urine specific gravity assessment
Signs of Hypovolemia
5%
10%
15-20%
⭐️
Hypovolemia
A drop in BP does not occur in a patient that is already in the supine position until about __% of the blood volume is lost
30
Intraop Urine output goals
0.5-1 ml/kg/hr
BURN pts:
1.5 ml/kg/hr
Decrease in urine output generally does not occur until ___% of blood volume is lost
~20
Signs of Hypervolemia
Pitting edema
Presacral edema
Later signs:
Tachycardia
Crackles
Wheezing
Pulmonary edema
T/F
Chest X-ray is not a reliable assessment tool for hypervolemia.
False
Electrolytes
ECF & ICF
ECF:
Major (+): Na, K, Ca
Major (-): Cl, Bicarb, Proteins
ICF:
Major (+): Na, K, Mag
Major (-): Cl, Bicarb, Proteins
*same major anions
*difference is in major cations
“this is Ma Mag”
“Kick out Ca”
Most important electrolytes
Sodium, Potassium, and Calcium
affects resting membrane potential
K
determines threshold potential
Ca
Na fxn
resting potential
generate & propagate AP
Which ions affect excitability of nerve & muscle?
Sodium, Potassium, and Calcium
He didn’t emphasize this chart much
Hypernatremia
cause
at risk population
Secondary to lack of water
At risk:
Debilitated and dehydrated
Extremes of age
Altered LOC
T/F
Hypernatremia is often d/t excessive sodium intake
False
Secondary to lack of water – not because of too much salt
HyperNa
S/S
S/S:
Restlessness, lethargy, seizures and death
-reflect rate of H20 movement from brain
-Ruptured cerebral veins, focal hemorrhage
(Coma = HypoNa)
Na NR
135 - 145 mEq/L
Most common cause of diabetes insipidus
Hypernatremia w/ normal total body sodium
results from medical intervention
diabetes insipidus
w/ normal total body sodium
↓↓↓ renal “concentrating-ability”
↓ ADH secretion
renal tubules don’t respond normally to circulating ADH (polyuria)
polyuria
excessive pale urine
⭐️
HyperNa w/ low total body Na
Lost sodium & water
Water loss > sodium loss
Losses:
renal (osmotic diuresis)
or
extrarenal (diarrhea or sweat)
⭐️
HyperNa w/ increased total body sodium
Most commonly caused by the administration of large quantities of hypertonic Na+ solutions (3% NaCl or 7.5% NaHCO3)
Cushing’s syndrome – too much ACTH
hypertonic Na+ solutions
3% NaCl or 7.5% NaHCO3
⭐️
Most commonly caused by the administration of large quantities of hypertonic Na+ solutions
HyperNa w/ increased total body Na
Cushing’s syndrome = too much ___
ACTH
Hypernatremia > 145 mEq/L
S/S
Neuro:
Extreme Thirst
Progressive Weakness & Fatigue
Intracranial bleeding (brain shrinks→vessels pull/shear)
Disorientation, Hallucination, Irritability
CV:
Hypovolemia
Renal:
Oliguria
Renal Insufficiency
⭐️
Treatment of Hypernatremia
how fast can we correct it?
fluid deficits corrected over 48 - 72 hours:
hypotonic solution (D5W)
MAX Na decrease: 0.5 - mEq/L/hour
Rapid fluid deficit correction can result in
seizure, cerebral edema and coma
Elective surgery should be postponed until sodium level is ___ mEq/L and H2O deficits corrected
< 150
Hyponatremia
Associated conditions/diagnosis
alcoholism
liver failure
severe burns
malignant neoplasms
hemodialysis and sepsis
⭐️
Na
Neurologic symptoms occur below…
120 mEq/L
Hyponatremia is serum Na less than ___
< 135 mEq/L
Hyponatremia
S/S
Neurological:
Seizures → Coma
Cerebral edema
Agitation, Confusion, h/a
GI:
N/V → anorexia
Musculoskeletal: cramps and weakness
May not see when under GA!
Hyponatremia
Diagnosis is based on the assessment of:
serum osmolality
volume status
Osmolality & Osmolarity
Osmolality: osmoles of solute per kilogram of water (e.g., weight)
Osmolarity: osmoles of solute per liter of water (e.g. fluid)
Tonicity
Effect a solution has on cell volume
Hypertonic
Hypotonic
Isotonic
Osmosis is movement of ___
H20
Plasma Osmolarity
NR and equation
Plasma Osmolarity
Most important determinant
Na+
What increases plasma osmolarity?
Hyperglycemia or high BUN
⭐️
Normal Osmolality
280 – 295 mOsm/kg
H20 flows from compartment of low to high (osmolarity/osmolality) if the membrane between the compartments is permeable to H2O
osmolality
(a cell in relatively hyperosmolar solution: fluid moves out of cell → highly [ ] compartment to reach homeostasis →→ cell shrinks)
Osmolality
Reflects fluid shifts from ….
what happens to Na?
ICF → ECF
Decreased plasma sodium levels
Meds that can change normal plasma osmolality
amitriptyline
cyclophosphamides
Tegretol
morphine
Disease processes that can shift fluid from ICF → ECF
hypothyroidism,
glucocorticoid insufficiency
SIADH
SIADH
(inappropriate antidiuretic secretion)
clinical presentation
Clinically euvolemic & good renal fxn!
but
↑ urine osmolality (>200mOsm) WITH ↓ serum osmolality
Urine Na >20 mEq/L
Causes of SIADH
Dz & Rx
Pulmonary carcinoma
Brain metastases, other malignancies
CNS disorders
Idiopathic forms – esp old ppl
Meds:
antidepressants agents (SSRIs)
HCTZ
NSAIDs
Vincristine (chemo for leukemia & others)
Neuroleptic agents
Haldol (PONV; D2 receptor antag in CTZ)
Zyprexa (ADHD)
Vasopressin
Oxytocin
⭐️
SIADH Acute treatment starts @ Na levels of ____.
<110 (SEVERE hypoNa)
SIADH Acute treatment
interventions
(Na <110)
IV Lasix – diuresis
NS with 20–40 mEq/L KCL
⭐️
Can we use 3% NS for Acute SIADH? Why or why not?
Rare
replacement MUST be done slowly, over days
risk: central pontine myelinolysis (demyelinate brain’s white matter)
↓
quadraplegia
SIADH (Chronic treatment)
-Water restriction ~1000 ml QD
-Declomycin – mechanism unknown
-Urea
-PO Salt tablets
-Vasopressin receptor antagonists:
Conivaptan, Vaprisol, Tolvaptan, Samsca
-Lithuim
HypoNa in HYPERtonic state
pt has high osmolality (>295 mOsm /kg)
Hypervolemia caused by:
Mannitol excess
Glycerol Treatment
Nephrotic Syndrome
CHF
Cirrhosis
Treatment:
Salt/water restriction or diuretics
HypoNa in a Hypotonic state
-osmolality
-causes
Low serum osmolality (<280 mOsm/kg)
assess volume status
hypovolemia may be due to:
-GI losses
-Renal losses + excess water ingestion
-Diuretics
-ketonuria
-3rd Spacing
-adrenal insufficiency
-N & V
⭐️
Hyponatremia
How fast do we correct it?
Not too fast!
Pontine myelinolysis risk permanent damage!
Pontine myelinolysis
S/S
Balance problems
Confusion/delirium/∆s in consciousness
dysphagia
Hallucinations
speech changes/poor enunciation
Tremors
weakness face, arms, or legs; usually B/L
Acute progressive quadriplegia
HypoNa Tx
symptomatic: consider 3% NaCl
sodium 1-2 mEq/L/hr x 2H →0.5 mEq /L/hr
asymptomatic: sodium 0.5 mEq/L/hr
Max in 24 hr: 10 mEq TOTAL rise
Max in 48 hr: 18 mEq TOTAL rise
HypoNa Tx
MAX rise in Na over 24 & 48 H
Max in 24 hr: 10 mEq TOTAL rise
Max in 48 hr: 18 mEq TOTAL rise
Potassium
NR
3.0 – 5.5 mEq
Hyperkalemia results in altered distribution of ___ between…
K
intra- & extracellular sites
HyperK
Adverse effects are d/t…
to acute ↑ in serum concentration
HyperK
Most detrimental effect occurs in….
What do we see?
cardiac conduction system
Prolonged PR interval
Widening QRS complex
Peaked T wave
Hyperkalemia is serum K greater than….
5.5
HyperK
causes & S/S
Treatment of Hyperkalemia
-NaHCO3 (~50 mEq) ↑cell uptake of K+ w/in 15 minutes (Note: cannot be used alone)
-Beta agonists
-Glucose 30-50 gm + Insulin 10 units (can take up to 1 hour)
-Hyperventilation
-dialysis
-Ca (cont on another card)
Treatment of Hyperkalemia
Ca
protect 🩷 from hyperK (1 amp = 1 gm CaCl)
↓ excitability & threshold potential
500-1000 mg IV: antag 🩷 effects; rapid but short-lived
⚠️Ca potentiates digoxin toxicity
Ca potentiates ____ toxicity
Digoxin
Hyperkalemia
Tx algorithm
HyperK vs HypoK
ECG changes
HYPER:
Prolonged PR interval
Widening QRS complex
Peaked T wave
HYPO:
Flattened T waves and presence of U wave
How does pH affect K?
(indirectly proportional relationship)
0.1 change in arterial pH = 0.6 meq change plasma K+
Acidosis:
-high Plasma K in relation to total body stores
-K depletion d/t urinary or GI losses: plasma concentration may be normal or reduced
The bajillion causes of hypoK
Treatment of Hypokalemia
PO KCL 60-80 mEq/day (sour tummy common)
IV:
Peripheral: MAX 8 mEq/hr (vein irritation)
Central: 10-20 mEq/hr
What K values do we need to proceed with surgery?
greater than 3-3.5mEq/L
(hypo/hyper)kalemia causes increased sensitivity to NMBs. So we should decrease the dose by ___%
hypoK
25-50%
Ca NR
8.5-10.5 mg/dl
Hypocalcemia
is a/w…
hypoparathyroid
pancreatitis
renal failure
decreased albumin
HypoCa
affects on muscle
Skeletal muscle spasm including laryngospasm
↓ 🩷 contractility
⚠️ Avoid Hyperventilation
pH 0.1 increase (alkalosis) = 0.16 mg/dL decrease ionized Ca
What should we avoid with hypoCa?
⚠️ Avoid Hyperventilation
pH 0.1 increase (alkalosis) = 0.16 mg/dL decrease ionized Ca
Hypocalcemia
EKG changes
Mild: broad-based tall peaking T waves
Severe: extremely wide QRS, low R wave, no p waves, tall peaking T waves
Hypocalcemia
S/S
HTN before hypovolemia (usually)
Anorexia, N/V
Weakness, muscle aches, tingling lips
Muscle spasms of the throat (laryngospasm)
Polyuria
Ataxia
Irritability, lethargy, or confusion
Seizures, Coma → Death
*Trousseau’s Sign: BP cuff = carpopedal spasm
*Chvosteks’s Sign: tap facial CN; edge of mouth spasms
Trousseau’s & Chvostek’s sign are a/w
HypoCa
Treatment of Hypocalcemia
Symptomatic = true medical emergency
Rule of 10’s:
10mL 10% calcium gluconate/Cl over 10 mins
↓
drip: elemental calcium 0.3-2 mg/kg/hr
serial ionized Ca
Check magnesium and consider giving magnesium 1 gm
Which is a/w necrosis?
Ca gluconate
CaCl
CaCl
(Ca gluconate is better for periph IV)
When correcting hypoCa, what other electrolyte should we gve?
Check magnesium
consider magnesium 1 gm
Hypercalcemia
ranges
Serum Ca+ > 10.5
ionized >5.6 mg/dL
HyperCa
causes
Hyperparathyroidism
Malignancy - bone
Renal Failure
Thiazide Diuretics
Excess Ca+ supplements
HyperCa
S/S
HTN
Dysrhythmias →CHB
Shortened QT
Sedation
Polyuria
Anorexia
Pancreatitis
Treatment of Hypercalcemia
1) Rehydrate w/ NS
2) brisk diuresis (200-300 ml/hr)
*loop diuretic to ↑Ca excretion
3) serial ionized calcium
Avoid acidosis may further elevate calcium levels
How does pH affect Ca?
Acidosis can further elevate Ca
Magnesium
NR
1.7 – 2.2
Low Magnesium
causes
Alcoholism
Chronic diarrhea
polyuria
sweating
Hyperaldosteronism
Malnutrition
Malabsorption syndromes (celiac, IBS)
meds:
diuretics
aminoglycoside antibiotics
chemotherapy
Symptoms: Hypomagnesemia
Abnormal eye movements (nystagmus)
Seizure
Fatigue
Muscle spasms or cramps
Muscle weakness
Numbness
Dysrhythmias
Treatment of Hypomagnesemia
IV mag sulfate 1-2 G slowly over 60 minutes
-Assess for concomitant hypoK or hypoCa
-Monitor EKG for arrhythmias
(Identical to hypokalemia: Flattened T waves and presence of U wave)
HypoMg shows the same EKG abnormalities as ….
hypoK
Flattened T waves and presence of U wave
Hypomag is often accompanied by which other ‘lyte imbalances?
hypoK or hypoCa
Hypermagnesemia
S/S
Flushing
Nausea & vomiting
Drowsiness
Weakness
Loss of patellar reflex, decreased DTRs
Respiratory depression
Cardiac arrest
Coma
Treatment of Hypermagnesemia
Stop all sources of magnesium
-IV Ca 1G (temporarily antagonize most effects)
-Loop diuretic + rehydration D1/2 NS (enhances excretion)
-Monitor for vasodilation and negative inotropic effects
-Decrease dosages of NDMB by 25-50%
Hypermag
anesthesia considerations
Decrease dosages of NDMB by 25-50%
(hypoK: decrease NMB dose 25-50%)
Hypervolemia
What would we see in a CXR?
What labs should we draw?
Kerly B lines: Increased pulmonary & interstitial markings
Diffuse alveolar infiltrates
Labs: blood & UA
