Electrolytes Flashcards
1
Q
Na is principle determinant of ECF volume & ultimately shifting of what?
A
fluid b/t ECF & ICF comparments
2
Q
Major cation in ECF?
A
Na
3
Q
Major cation in ICF?
A
K
4
Q
Major anions in ECF?
A
Cl & HCO3
5
Q
Negatively charged molecules in ECF (Cl, HCO3) maintain electroneutrality with?
A
positively charged cations in ICF
6
Q
small changes in osmolality or tonicity are detected by what?
A
osmoreceptors in the hypothalamus
7
Q
Under normal circumstances, the kidney increases or decreases H2O excretion & is mediated by?
A
antidiuretic hormone (ADH)/vasopressin from pituitary
8
Q
Increased ADH secretion happens in response to what?
Decreased secretion?
A
volume contraction
Volume expansion
9
Q
Under normal circumstances, the kidney responds to altered Na level in ECF & increases or decreases Na reabsorption due to impulses from what mechanisms?
A
carotid baroreceptors
atrial stretch receptors
intrarenal mechanisms
10
Q
Normal “set point” for plasma osmolality is appox?
A
285 mOsm/kg
11
Q
Minimum urine osmolality?
Maximum urine osmolality?
A
appox 50 mOsm/kg
approx 1200mOsm/kg
12
Q
With rise in plasma osmolality >295mOsm/kg what two responses occur?
A
thirst centers of the hypothalamus are stimulated & signals individual to drink
ADH levels rise until osmolality returns to normal
13
Q
ADH is also released in response to what even if plasma osmolality is low?
A
hypotension or decreased effective arterial volume
14
Q
Maintenance IVFs needed if NPO, how much volume per day?
A
30-35 ml/kg/d
15
Q
Maintenance IVFs needed if NPO, how much UOP is necessary to excrete daily solute load consumed?
A
> 500 ml/d
16
Q
Maintenance IVFs needed if NPO, how much dextrose is necessary to minimize protein catabolism and ketoacidosis?
A
100-150 gm/d
17
Q
Volume losses to consider when prescribing IVFs
Stool?
A
typically lose 200 ml/d
18
Q
Volume losses to consider when prescribing IVFs
Insensible losses from skin, respiratory tract?
A
400-500ml/d
19
Q
Volume losses to consider when prescribing IVFs
Fever?
A
losses increase by 100-150 ml/d for each degree > 37C
20
Q
Volume losses to consider when prescribing IVFs
minimum volume/d =?
A
1400 ml or 60ml/hr
21
Q
Volume losses to consider when prescribing IVFs
What may cause patients to require more?
What may cause patients to require less?
A
burns/open wounds
CHF patients
22
Q
Reduced ECF volume in r/t capacity
May/may not have decreased ___ level.
May appear hypovolemic d/t increased capacitance of ECF or intravascular compartment (relative hypovolemia).
What can cause this appearance?
A
Na
Vasodilation: meds (vasodilators), sepsis, pregnancy
Generalized edema: CHF, cirrhosis, nephrotic syndrome
3rd spacing: sequestered compartment-SQ tissue, RP/peritoneal space, GI tract-not in equilibrium with ECF
23
Q
Absolute hypovolemia results in what effect on Na level?
A
deficit in Na level
24
Q
Absolute Hypovolemia
Renal causes?
A
inhibit or disrupt Na reabsorption
diuretics
tubule dysfunction (AKI-disrupts)
Endocrine disorders (AI, hyperaldosteronism-disrupts)
25
Absolute Hypovolemia
Extrarenal causes?
bleeding
losses from GI, skin, respiratory systems
26
Clinical presentation of hypovolemia depends on?
rate of loss
27
Clinical presentation of hypovolemia
Lab results for...
BUN (BUN:Cr ratio)
UOP
CVP/JVP
Specific gravity & urine osmolality
Urine Na
Fractional excretion of Na (FeNa)
elevated (>20:1)
decreased
low
high
< 15mEq (or may be higher in setting of diuretics)
< 1%
28
Equation for Fractional Excretion of Na?
(urine Na x serum Cr) / (urine Cr x serum Na) x 100
29
Clinical presentation of hypovolemia
Symptoms expected?
tachycardia
hypotension
lactic acidosis
hemoconcentration if not bleeding
cold extremities (unless septic)
30
Clinical presentation of hypovolemia
in what setting is hypernatremia expected?
H2O deficit
31
Management of hypovolemia
Deficit can be difficult to estimate and requires what?
frequent assessment
32
Management of hypovolemia
Goal?
HD stability, replenish intravascular volume
33
Management of hypovolemia
Use what type of fluids for resusitation?
Isotonic IVF (NS/LR)
34
Management of hypovolemia
Isotonic IVF contain what?
small molecules that diffuse freely throughout ECF compartment
35
Management of hypovolemia
Because 2/3 of ECF is interstitial, a similar proportion is interstitial; meaning IVFs do what?
follow the same distribution with approx. 2/3 of IVF distributed to interstitial space
36
Management of hypovolemia
To acutely expand intravascular space what is often required?
1-2L bolus
37
Colloids (albumin) contain what?
large, poorly diffusible molecules that create osmotic pressure to keep H2O intravascular
38
Colloids are more effective than crystalloids at what?
Expanding intravascular volume
39
Considerations about crystalloids
cost?
availability?
side effect?
effectiveness of expanding intravascular volume?
survival compared to colloids?
mortality, ICU/hospital LOS, MV days, or days of renal-replacement tx compared to colloids?
inexpensive
readily available
edema formation
need for increased volumes to = that of colloids
have been associated with survival advantage compared to colloids
Have been associated with no difference in mortality, ICU/hospital LOS, MV days, or days of renal-replacement tx compared to colloids
40
Infusion of large volumes of NS can result in what?
metabolic acidosis (hyperchloremic acidosis)
41
NS usually has what kind of adverse consequences?
usually none
42
LR contains what? what can this affect?
Calcium
may bind to certain meds/reduce effectiveness
43
LRs effect on serum lactate levels in critically ill or those with hepatic insufficiency?
not known
44
Cost of colloids vs crystalloids
NS/LR
5% albumin
25% albumin
$1.46/L
$30.63/250ml
$30.63/50ml
45
What advantages do colloids have over crystalloids?
remain intravascular longer & provide more plasma volume expansion than crystalloids
46
Albumin is what?
Available in what % solutions?
heat-treated preparations of human serum albumin
5% (50g/L)
25% (250g/L)
47
Hypervolemia results in what kind of Na balance?
surplus of total body Na
48
Hypervolemia/Na retention is secondary to?
renal disease (AKI, glomerular disease)
Endocrine d/o (excess mineralocorticoid action)
49
Hypervolemia/Na retention d/t renal disease occurs because?
Limited ability to excrete Na & H2O
Disruption of capillary Starling forces result in shifting of fluid from intravascular space to interstitium & activation of RAAS
May be secondary to hypoalbuminemia
50
Hypervolemia/Na retention d/t endocrine d/o
usually presents as?
May have what electrolyte abnormality?
HTN
hypokalemia
51
Secondary renal response to...
Reduced effective arterial blood volume resulting in?
renal Na retention, expanded ECF
52
Secondary renal Na retention results in?
enhanced sympathetic activity, RAAS activation
CHF (from low CO)
Cirrhosis synthetic dysfunction & hypoalbuminemia
53
Hypervolemia/Na retention clinical presentation
Edema
effusions
rales
elevated JVP/CVP
hepatojugular reflux
S3
HTN
Low urine Na (<15mEq/L
54
Secondary renal Na retention results in?
enhanced sympathetic activity, RAAS activation
CHF (from low CO)
Cirrhosis synthetic dysfunction & hypoalbuminemia
55
Hypervolemia/Na retention symptoms
dypnea
abd distention
edema
56
Management of Hypervolemia/Na retention primary goals?
address underlying problem
limit Na intake (20-40mmol/d)
57
Management of Hypervolemia/Na retention
What medication should be used?
Diuretics
58
Diuretics enhance renal Na excretion by what mechanism?
blocking various sites along nephron
59
Proxmial tubule diuretic to use in management of Hypervolemia/Na retention?
Diamox
60
Loop Diuretic to use in management of Hypervolemia/Na retention?
lasix
61
Distal tubule diuretic to use in management of Hypervolemia/Na retention
HCTZ
62
Collecting duct diuretic to use in management of Hypervolemia/Na retention?
Spironolactone
63
Which is the most potent diuretic to use in management of Hypervolemia/Na retention?
lasix
64
How does spironolactone work?
competes with aldosterone
65
How does spironolactone improve survival of those with Left Ventricular Dysfunction?
competitive blockade of nonepithelial mineralocorticoid receptors in heart and other vascular structures reducing fluid/Na retention
66
Hyponatremia results from?
processes that limit elimination of H2O or expands volume around fixed Na content
67
Antidiuretic hormone secretion leads to hyponatremia how?
either appropriate secretion in response to low circulating volume or inappropriate d/t neuro d/o, pulmonary disease, malignancy
68
Hyperosmolar Hyponatremia occurs when plasma osmolality is what?
> 295 mOsm/kg
69
Hyperosmolar hyponatremia is d/t?
hyperglycemia
70
Hyperosmolar hyponatremia causes increased ECF resulting in?
dilution of Na content
71
Hyperosmolar hyponatremia
For every 100 mg/dL rise in plasma glucose Na falls by?
1.6-2.4 mEq/L
72
Pseudohyponatremia Osmolality is?
Cause?
280-295 mOsm/kg
Lab phenomenon in which high concentrations of plasma proteins, lipids expand non-aqueous portion of plasma sample
73
Diagnostic approach to hyponatremia
Isotonic Hyponatremia 280-295 mOsm/kg?
Pseudohyponatremia
74
Diagnostic approach to hyponatremia
Hypertonic Hyponatremia >295 mOsm/kg
Hyperglycemia
Hypertonic fluid admin
75
Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg first step?
Second step?
Assessment of volume status
hypovolemic
euvolemic
hypervolemic
Check urine sodium
76
Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypovolemic: urine sodium > 20 mEq/L
Renal solute loss
77
Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypovolemic: urine sodium
Extrarenal solute loss
78
Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Euvolemic: urine sodium always >20 mEq/L
SIADH
Endocrinopathies (Glucocorticoid deficiency)
Potassium depletion (diuretic use)
79
Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypervolemic: urine sodium > 20 mEq/L
Renal failure
80
Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypervolemic: urine sodium
Edematous d/o's
Heart failure
Cirrhosis
Nephrotic Syndrome
81
Hyponatremic Clinical presentation
Neurologic abnormalities d/t cerebral edema from shifting of H2O from ECF to ICF
82
Hyponatremic Clinical Presentation
neurologic abnormalities severity depends on?
magnitude & rapidity of fall
83
Hyponatremic Clinical Presentation
Acute: timeframe?
symptoms?
<2 days
nausea
malaise
H/A
lethargy
confusion
obtundation
84
Hyponatremic Clinical Presentation
Na 115 mEq/L results in?
stupor
seizures
coma
85
Hyponatremic Clinical Presentation
Chronic: timeframe?
symptoms?
>3 days
minimization of increased ICF/symptoms
86
Management of Hyponatremia is determined by?
ECV (extracellular volume): low, normal, high
Presence of neuro symptoms
87
Symptomatic hyponatremia requires more rapid correction, however no greater increase in plasma Na than what rate?
not to exceed what level?
or how much Na mEq/L/d?
why?
0.5mEq/L/hr
130 mEq/L
>12 mEq/L/d
possible occurrence of central pontine myelinolysis (CPM) from neuronal damage from rapid osmotic shifts
88
Management of Hyponatremia for low ECV?
hypertonic saline 3% if symptomatic
NS if asymptomatic
89
Management of Hyponatremia for normal ECV?
lasix
hypertonic saline if symptomatic
NS if asymptomatic
90
Management of Hyponatremia for high ECV?
lasix
hypertonic saline if symptomatic
lasix if asymptomatic
water restriction
91
Formula for expected change in Na?
[(Na conc in IVF + K conc in IVF) - serum Na] / (kg x 0.6 +1)
92
ADH is secreted by and transmitted to?
hypothalamus
posterior pituitary
93
ADH is released in response to?
decreased effective circulating volume as sensed by baroreceptors
94
ADH MOA?
H2O reabsorption
urine concentration
95
SIADH is what?
inappropriate levels of ADH are secreted despite absence of osmotic or volume related stimuli
96
SIADH is a dysregulation of what?
cells secreting ADH or in feedback mechanisms responsible for release
97
SIADH causes CNS disease
tumor
trauma
infection
CVA
SAH
GBS
DTs
MS
98
SIADH causes pulmonary disease
tumor
pneumonia
COPD
PPV
99
SIADH causes malignancies
lung
pancreas
ovarian
lymphoma
100
SIADH causes meds
NSAIDs
narcotics
diuretics
antidepressants
haldol
!
101
SIADH other causes?
surgery
idopathic
102
SIADH labratory
euvolemia
hyponatremia secondary to H2O excess
Elevated urine osmolality (>200 mOsm/kg)
elevated urine Na (> 20mEq/L)
decreased serum osmolality (<280 mOsm/kg)
103
Hypernatremia results from?
Na gain or H2O deficit
104
Hypernatremia Na gain comes from?
NS/hypertonic saline admin
chronic mineralocorticoid excess
105
Hypernatremia H2O deficit comes from?
diaphoresis
diarrhea
osmotic diuresis (hyperglycemia)
diabetes insipidus
106
Hypernatremia Clinical Presentation is r/t?
magnitude & rapidity of rise in Na
107
Hypernatremia Clinical Presentation results form?
shifting of ICF to ECF & resultant contraction of brain cells
108
Hypernatremia Clinical Presentation symptoms
altered MS
weakness
neuromuscular irritability
focal deficits
coma
seizures occasionally
thirst
polyuria if DI
109
Diabetes Insipidus results from impaired what?
renal H2O conservation
110
Diabetes Insipidus causes an excessive loss of what?
urine that is near pure H2O
111
Diabetes insipidus r/t ADH
Central DI is d/t?
impaired ADH secretion from posterior pituitary
112
Diabetes insipidus r/t ADH
Central DI causes?
trauma
anoxic encephalopathy
surgery
meningitis
brain death
ethanol
neoplastic
idiopathic
113
Diabetes insipidus r/t ADH
Nephrogenic DI is d/t?
defective end-organ responsiveness to ADH
114
Diabetes insipidus r/t ADH
Nephrogenic DI causes?
ampho
lithium
dye
hypokalemia
115
Diabetes insipidus hallmark is what?
urine osmolarity in central is?
urine osmolarity in nephrogenic is?
dilute urine
<200 mOsm/L
200-500 mOsm/L
116
Diabetes insipidus causes what Na balance?
hypernatremia
117
Diabetes insipidus serum osmolality is?
> 290 mOsm/kg
118
Diabetes insipidus dx is confirmed by?
response to fluid restriction
failure of urine osmolarity to increase by >30 mOsm/L in initial hours is diagnositc
119
How to distinguish central DI from nephrogenic DI?Q
Response to vasopressin/dDAVP (1mcg SQ or IV)
120
Expected response to dDAVP if its Central DI?
Expected response to dDAVP if its Nephrogenic DI?
Urine osmolarity will increase by >50% & UOP will decrease after admin
unchanged
121
Diagnostic Approach to Hypernatremia
Urine Output is low?
Urine Osmolality will be high
Was there hypotonic fluid loss?
insensible losses
GI losses
Prior Renal Losses from Diuretics
122
Diagnostic Approach to Hypernatremia
Urine Output is High; Urine Osmolality is Low
Diabetes Insipidus
Response to DDAVP indicates Central
No Response to DDAVP indicates Neprhogenic
123
Diagnostic Approach to Hypernatremia
Urine Output is High; Urine Osmolality is High
Osmotic Diuresis?
124
Management of Diabetes Insipidus depends on?
Acuity of development & symptoms
125
Management of Diabetes Insipidus avoid rapid correction nto prevent what?
seizures & permanent neuro damage
126
DI H2O deficit should not be corrected more rapid than?
10-12 mEq/L/d
less if chronic state
127
Management of Diabetes Insipidus free H2O admin should be done how?
calculate free H2O deficit
Correct H2O deficit over 2-3 days to reduce risk of cerebral edema
128
Formula for FW deficit = ?
0.6 x weight(kg) x [(current Na/140) - 1]
129
Management of Diabetes Insipidus if central?
DDAVP 2-5 u SQ q 4-6hrs
130
Management of Diabetes Insipidus if neprhogenic?
low Na diet
thiazide diuretic
131
K content in ECF (mEq/L, %)?
K content in ICF (mEq/L, %)?
3.5 - 5 mEq/L, 2%
150 mEq/L 98%
132
How is the K gradient maintained b/t ICF and ECF?
Na-KATPase pumps
133
Small changes in ECF K alters the ratio significantly & may result in?
serious or lethal consequences from tissue dysfunction
134
If just 2% of ICF K leaked into ECF, plama K (Pk) would increase by how much?
immediately doubles
135
Kidneys are almost entirely responsible for maintaining balance of output to intake, dependent on?
Increased (Pk) increased what?
flow/Na delivery & aldosterone
aldosterone production & renal K excretion
136
Factors causing cellular K influx?
insulin
beta agonists
137
Factors causing cellular K efflux?
cell ischemia
exercise
plasma hypertonicity (drag)
acidosis (hyperchloremic)
138
What is the distribution of K with acute loading
excretion?
transport into cells?
approx. 50% in urine
approx. 90% of remainder into cells over 4-6 hrs
139
Acute hyperkalemia causes (<48hrs)?
excessive intake
ARF (30-50% of time)
rhabdo
tumor lysis syndrome
ischemia/infarction
burns
hyperglycemia
meds - digoxin OD, succinylcholine
140
Chronic Hyperkalemia causes
CRF
mineralocorticoid deficiency
ACEIs, ARBs
Heparin
RTA
K sparing diuretics
141
What should be on your radar if hyperkalemia & hypotension occur together?
how can meds cause this?
mineralocorticoid deficiency
COX1 & 2 inhibitors d/t decreased renin release
142
How does ACEIs and ARBs cause chronic hyperkalemia?
decrease aldosterone synthesis
143
How does heparin cause chronic hyperkalemia?
inhibits aldosterone synthesis
144
How does RTA cause chronic hyperkalemia?
defect in renal K secretion association with SS disease/trait, SLE
145
How does K sparing diuretics cause chronic hyperkalemia?
blocks Na reabsorption in distal nephron
146
Clinical Manifestations of hyperkalemia
Cardiac
depolarizes cell membrane, slows ventricular conduction, decreases action potential duration which leads to
peaked T waves
prolonged PR interval
widened QRS
loss of P wave
Vfib or
asystole
147
Clinical Manifestations of hyperkalemia
Neuromuscular
paresthesias
weakness progressing to paralysis
decreased/absent reflexes
148
Clinical Manifestations of hyperkalemia
Metabolic
mild hyperchloremic acidosis
149
Evaluation of Acute Hyperkalemia includes?
ECG
re-send unclotted blood sample for electrolytes, glucose, BUN, Cr, CBC
assess urine for heme to exclude rhabdo/hemolysis
review med list and diet
150
Management of acute hyperkalemia
Effects are proportional to?
level & rate of rise
151
Management of acute hyperkalemia
1st disturbance seen may be?
vfib
152
Management of acute hyperkalemia
most exhibit ECG changes with what K level?
>6.7 mEq/L
153
Management of acute hyperkalemia
tx should be immediate for what K level?
> 6.5 mEq/L
154
Management of acute hyperkalemia
tx should be immediate regardless of levels when?
ECG changes
155
Management of acute hyperkalemia
tx should focus on?
membrane stabilization
redistribution of K into cells
K elimination
156
Management of acute hyperkalemia
Membrane stabilization includes?
CaGluconate (1g IV over 10 min) onset is immediate
157
Management of acute hyperkalemia
Redistribution of K into cells includes?
insulin (10u IVP + 1 amp D50 IV)
albuterol (20mg/4mL)
Bicarb 150 mEq/L
158
Management of acute hyperkalemia
insulin admin lowers K by how much?
Onset is how long?
when to not give D50?
approx. 1 mEq/L
20 min
if patient is already hyperglycemic
159
Management of acute hyperkalemia
albuterol lowers K by how much?
drawback of albuterol?
approx 1 mEq/L
some may be resistant to albuterol; use as adjunct
160
Management of acute hyperkalemia
Elimination of K includes?
diuretics (lasix 40-80 mg IV)
kayexalate - 15-30 g/ 15-30ml or lokelma
hemodialysis
161
Management of acute hyperkalemia
onset for...
diuretics
sodium bicarb
sodium polystyrene sulfonate (kayexalate)
15 min
1 hr
> 2 hr
162
Management of acute hyperkalemia
How does sodium polystyrene sulfonate work?
what are the effects?
what adverse reaction is potential?
exchanges Na for K in colon
variable
intestinal necrosis
163
Acute hypokalemia is almost always a result of what?
shift from ECF to ICF
164
Causes of acute hypokalemia?
tx for DKA (secondary to insulin tx)
refeeding (secondary to glucose stimulated hyperinsulinemia)
meds (beta agonists, epinephrine)
165
Chronic Hypokalemia causes
decreased intake
excessive losses (mostly renal)
meds
mineralocorticoids
Mg deficiency
hypercalcemia
166
Chronic Hypokalemia causes:
excessive losses from?
diuretics inhibit Na & Cl reabsorption causing secondary hypoaldosteronism
167
Chronic Hypokalemia causes:
what meds?
ampho B
PCNs d/t renal K wasting
168
Chronic Hypokalemia causes:
from Mineralocorticoids
diuretics in secondary aldosteronism (CHF, cirrhosis) are to blame d/t increased nephron flow rate
169
Chronic Hypokalemia causes:
Hypercalcemia causes what?
Na & H2O diuresis
170
Clinical Manifestations hypokalemia
Cardiac
hyperpolarizes cell membrane, prolongs action potential which leads to
ST depression
decreased T wave amplitude
increased U wave amplitude
ECG can be nonspecific and less reliable than w/ hyperkalemia
may be assoc. w/ arrhythmias, conduction defects
171
Clinical Manifestations hypokalemia
Neuromuscular
weakness
myalgias
fatigue
restless legs
paralysis w/ more severe hypokalemia
ileus
gastroparesis
rhabdo w/ profound hypokalemia
172
Management of Acute Hypokalemia includes?
KCL @ infusion rate of 0.6 mEq/kg/hr (normal renal function)
KCL@ infusion rate of 0.1 mEq/kg/hr (renal failure)
maximum increases seen in @ end of infusion w/ approx. 50% lost over next 2-3 hrs
Check levels @ end of infusion & in 2-3 hrs
173
Serum Postassium (mEq/L) = Potassium deficit (mEq)/ % total body K
3.0
2.5
2.0
1.5
1.0
175 / 5
350 / 10
470 / 15
700 / 20
875 / 25
174
What is the second most abundant ICF cation?
Mg
175
Hypermagnesia causes
meds
tx for preeclampsia/eclampsia
hypothyroidism
hyperparathyroidism
addison's disease
lithium tx
176
What meds can cause Hypermagnesia?
mg containing antacids (mg aluminum hydroxide)
laxatives (mg citrate) in setting of renal insufficiency
177
Clinical manifestations of Hypermagnesia
Cardiac
hypotension
bradycardia
SA/AV block
asystole
178
Clinical manifestations of Hypermagnesia
GI
N/V
ileus
179
Clinical manifestations of Hypermagnesia
Neuromuscular
hyporeflexia
paralysis
respiratory muscle weakness
lethargy
coma
180
Hypomagnesia causes
insufficient intake (ETOHism)
renal losses
GI losses
Redistribution
181
Hypomagnesia from renal losses are caused by?
diuretics
abx
chemo (cisplatin)
volume expansion
osmotic diuresis
ETOH
182
Hypomagnesia from GI losses are caused by?
diarrhea
SB disorders/resection d/t disrupted absorption
183
Hypomagnesia from redistribution is caused by?
acute pancreatitis d/t saponification
hungry bone syndrome following parathyroidectomy d/t rapid bone uptake during remineralization
184
Management of Hypermagnesia includes?
no tx if normal renal fxn & mild symptoms
remove exogenous sources
saline administration
diuretics
CaGluconate 1g if symptoms are severe
HD
185
Management of Hypomagnesia includes?
MgSO4 2g IV if vfib or torsades
MgSO4 IVPB or po
186
Management of Hypomagnesia
Mg level 0.9 - 1.8 requires how much IVPB?
Mg level 1.9-2.0 requires how much IVPB?
4g MgSO4
2g MgSO4
187
Calcium balance is regulated by what?
parathyroid hormone and calcitriol
188
PTH has what effect on serum Ca?
how?
increases
thru bone resorption & promoting renal conversion of vit D to calcitriol
189
Serum Ca regulates PTH secretion how?
through a negative feedback system
low serum Ca stimulates PTH release
high serum Ca suppresses PTH release
190
What is the active form of vit D?
how does it affect serum Ca?
calcitriol (1,25-dihyrdoxycholecalciferol, 1.25 -dihyrdoxyvitamin D3)
stimulates intestinal absorption of Ca & provides feedback to parathyroid
191
What is the best measurement for assessing calcium concentrations?
ionized Ca or iCa
192
Ionized Ca
Acid-base status & protein concentrations affect total Ca concentrations.
Acidemia has what effect on Ca?
Alkalosis has what effect on Ca?
acidemia displaces Ca from ablumin & results in increased iCa
alkalosis causes Ca to bind to albumin & results in decreased iCa
193
Ionized Ca
Changes in plasma proteins (albumin) affect total Ca concentration.
Hypoalbuminemia results in what effect on total Ca concentration?
Hyperalbuminemia?
hypoalbuminemia results in reduced total Ca concentration
hyperalbuminemia results in increased total Ca concentration
194
Corrected Ca formula is?
4.2 - albumin level + total Ca level
195
Hypercalcemia causes
primary hyperparathyroidism
malignancy
rhabdo
immobility
meds
196
Most common cause of Hypercalcemia?
most common cause of this problem?
primary hyperparathyroidism
benign adenoma (80-90% of cases)
197
Hypercalcemia causes
malignancy causes?
secondary to PTH r/t peptide secretion by malignant cells
increased 1,25-dihyroxycholecalciferol production by malignant cells in lymphoma
osteolytic bone lesions
198
Hypercalcemia causes
from meds?
lithium (induces hyperparathyroidsim)
thiazides (increased reabsorption)
vit D supplementation
199
Clinical Manifestations of Hypercalcemia depend on?
rate of increase & level
200
Clinical Manifestations of Hypercalcemia
Neuro?
weakness
fatigue
depression
altered MS
201
Clinical Manifestations of Hypercalcemia
Cardiovascular
increased rate of repolarization
shortened QT interval
arrhythmias
202
Clinical Manifestations of Hypercalcemia
GI
anorexia
N/V
Constipation
203
Management of Hypercalcemia
assess what?
is PTH intact
vit D metabolites
204
Management of Hypercalcemia
mild hypercalcemia (total Ca < 12 mg/dL) is usually d/t?
primary hyperparathyroidism
thiazides
supplementation
lithium
immobility
205
Management of Hypercalcemia
mild hypercalcemia (total Ca < 12 mg/dL) txs?
remove offending agent
mobilize
hydrate
206
Management of Hypercalcemia
moderate hypercalcemia (total Ca 12-14 mg/dL) usually d/t?
primary hyperparathyroidism
thiazides
supplementation
lithium
immobility
207
Management of Hypercalcemia
moderate hypercalcemia (total Ca 12-14 mg/dL) txs?
remove offending agent
hydrate
diuresis to increase excretion, but avoid volume depletion
208
Management of Hypercalcemia
severe hypercalcemia (total Ca > 14mg/dL) txs
volume expansion with NS
loop diuretics after resuscitation for increased renal excretion
HD
bisphosphonates (pamidronate, zoledronic acid-inhibit osteoclast function & number & inhibit bone turnover
209
Hypocalcemia causes
Hypoparathyroidsm
Vit D deficiency
210
Vit D deficiency causes?
decreased intake
inadequate sunlight
impaired synthesis (requires hydroxylation in liver & kidneys to be converted to active form; if dysfunction, impaired vit D synthesis)
211
Hypocalcemia causes
Redistribution
chelation of Ca by citrate from massive blood transfusions
elevated phospohorus levels - binds to Ca
rhabdo (d/t Ca deposition in injured muscle, ARF/decreased synthesis of vit D)
acute pancreatitis (unclear; may be secondary to accumulation in pancreas, liver, skeletal muscle, high levels of endotoxin)
212
Hypocalcemia causes
meds
cisplatin
biphosphonates
213
Hypocalcemia causes
sepsis
sequestration
PTH resistance
vit D deficiency
214
Clinical manifestations of hypocalcemia
neuro
paresthesias (perioral)
hyperactive reflexes
tetany (Chvostek sign - ipsilateral muscle twitching w/ facial nerve tapping, Trousseau sign - carpal smasm w/ occlusion of brachial artery)
seizures
215
Clinical manifestations of hypocalcemia
Cardiovascular
prolonged QT interval
bradycardia
hypotension
heart block/cardiac arrest
216
Management of hypocalcemia
iCa < 3.2 mg/dL w/ serious CV or neuo signs requires?
urgent tx
CaGluc 10%/10 ml (90mg) IV over 5-10 min followed by 500-1000mg/500 ml over 6 hrs
CaCl 10/10 ml (272mg)
freq iCa levels
217
Management of hypocalcemia
iCa > 3.2 mg/dL manifestations?
may have few or none
218
Management of hypocalcemia
PO supplementation for chronic conditions which are?
dose?
vit D deficiency, hypoparathyroidism
1-4gm/d + vit D in divided doses
219
Management of hypocalcemia
correct hyperphosphatemia (in renal failure) with?
binders & hypocalcemia will often correct
220
Management of hypocalcemia
correct what other electrolyte abnormality?
Mg deficits
221
Phosphorus balance is determined by?
PTH regulates bone stores, decreases reabsorption & increases excretion
phosphate conc regulates reabsorption
insulin shifts into cells
calcitriol increases intestinal absorption
222
Phos normal level?
2.5-4.5 mg/dL
223
Hyperphosphatemia (plasma level > 5 mg/dL) causes?
redistribution
increased intake
decreased renal excretion
224
Hyperphosphatemia (plasma level > 5 mg/dL) causes
redistribution from?
tumor lysis syndrome
rhabdo
pancreatitis
resp acidosis
225
Hyperphosphatemia (plasma level > 5 mg/dL) causes
decreased renal excretion from?
hypoparathyroidism
226
Clinical manifestations of hyperphosphatemia?
Similar to hypocalcemia d/t binding
227
Management of hyperphosphatemia?
reduce intake
phosphate binders
volume expansion to increase excretion
228
Hypophosphatemia (plasma level < 2.5 mg/dL) causes?
redistribution
increased renal excretion
decreased intestinal absorption
229
Hypophosphatemia (plasma level < 2.5 mg/dL) causes
redistribution from?
acute resp alkalosis
refeeding syndrome
DKA
230
Hypophosphatemia (plasma level < 2.5 mg/dL) causes
increased renal excretion from?
primary hyperparathyroidism causing phosphaturia
vit D deficiency causes decreased absorption
volume expansion
post-obstructive diuresis
diuretics
231
Hypophosphatemia (plasma level < 2.5 mg/dL) causes
decreased intestinal absorption
malnutrition
phosphate binders
chronic diarrhea
chronic ETOH
232
Clinical manifestations of hypophosphatemia
patients are usually asymptomatic until?
level < 1.5 mg/dL
233
Clinical manifestations of hypophosphatemia
skeletal
weakness
rhabdo
234
Clinical manifestations of hypophosphatemia
cardiac
decreased CO
235
Clinical manifestations of hypophosphatemia
hematologic
decreased 2,3-DPG (decreased O2 delivery)
impaired leukocyte & platelet fxn
236
Clinical manifestations of hypophosphatemia
neuro
irritability
confusion
paresthesias
237
Clinical manifestations of hypophosphatemia
endocrine
insulin resistance
238
Management of Hypophosphatemia includes?
anticipate hypophosphatemia
Supplementation is weight based
239
Phos supplementation for patients weighing 40-60kg
phos level <1mg?
phos level 1-1.7mg?
phos level 1.8-2.2mg?
30mmol
20mmol
10mmol
240
Phos supplementation for patients weighing 61-80kg
phos level <1mg?
phos level 1-1.7mg?
phos level 1.8-2.2mg?
40mmol
30mmol
15mmol
241
Phos supplementation for patients weighing 81-120kg
phos level <1mg?
phos level 1-1.7mg?
phos level 1.8-2.2mg?
50mmol
40mmol
20mmol
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