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CDM 2 > Exam 2: Fluids > Flashcards

Exam 2: Fluids Flashcards

1
Q

Six most important electrolytes are __

A

sodium, potassium, chloride, bicarbonate, calcium and phosphate

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2
Q

Renal filtrate: sodium is ___ and potassium is ___ and is controlled via angiotensin II and aldosterone

A

Sodium is absorbed

Potassium is excreted

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3
Q

____ is released when serum potassium levels rise, serum sodium levels fall, or blood pressure drops

A

Aldosterone

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4
Q

____ produces vasoconstriction and increases filtration rates in the glomerulus, activates sodium/potassium pumps, and stimulates aldosterone synthesis

A

Angiotensin II

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5
Q

___ and ___ are directly controlled by hormones (parathyroid, calcitriol, and calcitonin, each of which is released in response to serum calcium levels

A

Calcium and Phosphate

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6
Q

____ released from the parathyroid gland in response to reduced levels of calcium. Acts to break down bone matrices, decrease renal excretion, and increase GI absorption of calcium

A

PTH

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7
Q

___ active form of vitamin D that is required for intestinal absorption. Vitamin D is converted by PTH in the GI tract

A

calcirtriol

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8
Q

____ released from the thyroid gland in the presence of elevated serum calcium. Acts to increase osteoblast activity, forming more bone matrices

A

Calcitonin

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9
Q

mEq refers to the electrolyte activity and concentrations are expressed in milliequivalents (mEq) in the US

____ is an exception as it exists in the body primarily as ____, which can have multiple valences in solution, with solubility and valence changing with pH (usually mmol)

A

Phosphorous exists as phosphate

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10
Q

mEq euation

A

mEq = [mass (mg) x valence] / MW

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11
Q

_____ (mOsm/L) the concentration of osmotically active particles per unit VOLUME of solution (i.e., the number of milliosmoles of solute per liter of solvent)

A

Osmolarity

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12
Q

_____ (mOsm/kg) the concentration of dissolved particles per unit WEIGHT of solvent (i.e., the number of milliosmoles of solute per kilogram of solvent)

A

Osmolality

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13
Q

____ osmoles: solutes that cannot freely cross membranes in the body

A

Effective

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14
Q

Examples of effective osmoles

A

Na+, requires transport by Na+/K+-ATPase

Determine tonicity or osmolality, which affects fluid movement

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15
Q

____ osmoles: solute that freely crosses membranes and reaches equilibrium

A

BUN

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16
Q

_____: effective osmotic pressure equivalent across cell membranes (effective osmoles)

A

Tonicity

Note: Not necessarily the same as osmolality
Depends on osmolality of solution and permeability of membrane

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17
Q

Tonicity depends on ____ of solution and ____ of membrane

A

Osmolality of solution

Permeability of membrane

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18
Q

Fluid distribution: ___% is stored intracellular and __% is extracellular

A

40% intracellular

60% extracellular

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19
Q

Fluid distribution: Intravascular def

A

In the cells

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20
Q

Fluid distribution: Interstitial def

A

Between blood vessels and cells (can collect and needs to be drained)

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21
Q

Fluid distribution: Transcellular def

A

Fluid that fills spaces that surround epithelial cells (CSF, peritoneal, pleural)

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22
Q

T/F: When isotonic fluids are administered, water does not move in or out of the cells

A

TRUE – because tonicity is EQUAL

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23
Q

_____ fluids create a lower concentration of water in cells than exists in blood, causing the cells to expand due to volume expansion secondary to lower tonicity in the blood.

A

Hypotonic

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24
Q

____ fluids create a higher concentration of water in the cells than exists in the blood, causing the cells to contract due to volume depletion secondary to higher tonicity in the blood

A

Hypertonic

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25
Q

Isotonic solution range

A

270-300 mOsm/L

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26
Q

Hypotonic solution range

A

<270 mOsm/L

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27
Q

Hypertonic solutions range

A

> 300mOsm/L

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28
Q

Isotonic solution examples

A 
0.9% saline (NaCl) solution (~308)
Lactated ringers (~273)
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29
Q

Hypotonic solution examples

A
  1. 45% NaCl – Half-normal saline (1/2 NS)

0. 225% NaCl – Quarter-normal saline (1/4 NS)

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30
Q

Hypertonic solution examples

A

Parenteral nutrition
10% dextrose in water (D10W)
3% NaCl - hypertonic saline

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31
Q

Significantly _____ fluids ( ____) should NOT be administered directly to patients as this can cause cellular swelling and cell death (esp. CNS)

A

hypotonic <154 mOsm/L

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32
Q

If lower sodium solutions are required, use ___- or ___-containing solutions

A

Dextrose or potassium

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33
Q

___ should NEVER be directly infused into a patient

A

Sterile Water

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34
Q

If a patient requires “free water”, administer ____

A

5% dextrose in water

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35
Q

Body water % of body weight: Infants

A

Thin: 80
Avg: 70
Obese: 65

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36
Q

Body water % of body weight: Adult Male

A

Thin: 65
Avg: 60
Obese: 55

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37
Q

Body water % of body weight: Adult Female

A

Thin 55
Avg 50
Obese 45

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38
Q

____ does not impact water distribution in humans (ineffective osmole)

A

Urea

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39
Q

_____ is the major osmotically active electrolyte in the ECF

A

Sodium

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40
Q

___ and ___ substances are osmotically active at high concentrations

A

Glucose and Mannitol

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41
Q

___, a protein, contributes to osmotic/oncotic pressure

A

Albumin

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42
Q

___ Forces regulate passive fluid movements across capillary membranes

A

Starling

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43
Q

Net filtration is the sum of all ___ and ___forces: Pc – (Pi + Πi)

A

hydrostatic and oncotic

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44
Q

Plasma osmoles are mostly sodium salts, with lesser contribution from ___ and ___

A

Glucose and Urea

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45
Q

Osmolar gap suggests presence of other osmotically-active substances such as

A 
Severe hyperglycemia
Hyperlipidemia
Azotemia/uremia
Mannitol infusion
Toxic alcohols
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46
Q

With hyperglycemia, the addition of glucose to the ECF results in water movement from the ICF which falsely ___ measured serum sodium

A

Decreases – give insulin to reduce glucose and help close the gap (less acidotic)

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47
Q

_____ is arterial blood volume that is effective in stimulating volume receptors to maintain intravascular volume and organ perfusion

A

Effective Arterial Blood Volume

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48
Q

If EABV decreases:
Kidneys are ____
____ Renin-Angiotensin-Aldosterone system
Sodium and water ____ to expand EABV, restore perfusion

A

Kidneys are hypoperfused
Stimulates Renin-Angiotensin-Aldosterone system
Sodium and water retention to expand EABV, restore perfusion

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49
Q

Situations where total body volume is increased but EABV is low:
“______” of fluids: ascites, peritonitis, hypoalbuminemic states such as nephrotic syndrome and cachexia
Cardiovascular conditions: shock, ____ (increased load/hydrostatic pressure)

A

“Third spacing” of fluids: ascites, peritonitis, hypoalbuminemic states such as nephrotic syndrome and cachexia
Cardiovascular conditions: shock, CHF (increased load/hydrostatic pressure)

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50
Q

Goal of water balance: maintain EABV, normal plasma osmolality/tonicity, maintain ____

A

organ perfusion

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51
Q

_____ in cardiac atria, aortic arch, carotid sinus, juxtaglomerular apparatus are stimulated by change in EABV, affect heart rate & vascular tone

A

Baroreceptors

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52
Q

Stimulate thirst, release of _____ with as little as 5 – 10% decrease in EABV

A

arginine vasopressin [also called antidiuretic hormone (ADH)]

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53
Q

_____ in hypothalamus/posterior pituitary are stimulated by as little as 1 – 2% increase in plasma osmolality, stimulate thirst and release of ADH

A

Osmoreceptors

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54
Q

_____is the primary control of water intake

A

Thirst mechanism

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55
Q

Thirst is stimulated/controlled by _____ and _____– stimulated at point of maximal endogenous water conservation

A

osmoreceptors and EABV

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56
Q

Antidiuretic Hormone or Arginine Vasopressin are hormones synthesized in the_______, released from the pituitary gland

A

hypothalamus

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57
Q

ADH or AVP Acts on the ____ of the kidneys – increases permeability to water, regulates water reabsorption and excretion

A

Collecting ducts

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58
Q

Release of ______ stimulated by plasma osmolality (responds with as little as 1 – 2% change in osmolality, maximal activity at plasma osmolality > 295 mOsm/kg), EABV, baroreceptors, and some medications

A

ADH

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59
Q

Antidiuretic hormone binds to ____receptors on the basolateral membrane of renal tubular cells.

This leads to insertion of _____ into the apical tubular lumen surface of the cell.

Water passes through the cell into the _____, then is reabsorbed into the systemic circulation.

A

vasopressin 2 (V2)

water channels (aquaporin 2)

peritubular capillary space

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60
Q

Water balance is maintained by the ____ nervous system and RAAS

A

Sympathetic

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61
Q

Sympathetic nervous system and effects on water balance

A

Sympathetic Nervous System – stretch receptors on blood vessels sense change in ECF volume, leading to increased renal sympathetic tone which enhances renal salt reabsorption

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62
Q

Daily maintenance water/fluid requirements (in 24hrs) for neonate (<10kg)

A

100mL/kg

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63
Q

Daily maintenance water/fluid requirements (in 24hrs) for Pediatric (10-30kg)

A

1000mL + 50mL/each kg 10-20kg

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64
Q

Daily maintenance water/fluid requirements (in 24hrs) for Adolescent/adult (>20kg)

A

1500mL + 20mL/each kg >20kg

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65
Q

MINIMUM daily urine production/output of ~_____ mL/day required to excrete obligatory solute load, products of metabolism/catabolism, insensible losses

A

500-800mL/day

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66
Q

Acute volume depletion is usually depletion in___ and loss of ___ fluid, so osmolality typically is normal

A

ECF and isotonic

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67
Q

Depletion of TBW and dehydration typically due to more gradual/chronic problem, often can be due to ___ fluid loss so disorders of osmolality and Na+ more common

A

hypotonic

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68
Q

Volume depletion and dehydration causes – abnormal losses examples

A

Vomiting, diarrhea, GI losses in surgical patients (e.g., ostomy, fistula, gastric suction)
Blood loss (e.g., trauma)
Diuretics/overdiuresis, osmotic diuresis (e.g., hyperglycemia)
Insensible losses (e.g., excessive sweating, fever)
Other drugs (lithium – diabetes insipidus, demeclocycline – inhibits ADH)
Sodium-wasting nephropathy, hypoaldosteronism
Iatrogenic (inappropriate maintenance and/or supplementation)

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69
Q

Most common volume depletion and dehydration causes

A

Diarrhea

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70
Q

Magnitude of dehydration: Mild

A

Mild ~ 3 – 5% weight loss or less, symptoms less likely (possibly thirst/dry mouth)

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71
Q

Magnitude of dehydration: Moderate

A

Moderate ~ 5 – 10% weight loss, symptoms may be present

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72
Q

Magnitude of dehydration: Severe

A

Severe > 10 – 15% weight loss, symptoms likely present

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73
Q

Classification of Diarrhea: Osmotic

A

Unabsorbed solute

Caused: Cathartics & laxatives (e.g. castor oil, milk of magnesia), lactase deficiency, magnesium antacids, sorbitol

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74
Q

Classification of Diarrhea: Secretory

A

Increased secretion of electrolytes

Causes: Escherichia coli infection, cholera, ileal resection, thyroid cancer

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75
Q

Classification of Diarrhea: Exudative

A

Defective colonic absorption, excretion of mucus and/or blood

Causes: Ulcerative colitis, Crohn’s disease, shigellosis, leukemia

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76
Q

Classification of Diarrhea: Motility disorder

A

Decreased contact time

Causes: Irritable bowel syndrome, prokinetic medications (e.g., metoclopramide)

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77
Q

Oral rehydration therapy (ORT) is used in _____ dehydration

A

mild

**Rapid and efficient absorption of fluid

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78
Q

Too much glucose can cause ____ diarrhea

A

osmotic

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79
Q

Sports drinks versus recommended ORS often contain significantly more___ and significantly less___

A

glucose

electrolytes

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80
Q

Crystalloid solutions (sodium-containing): ___ or ____used to expand the intravascular and interstitial spaces for Moderate/Severe Dehydration

A

Normal saline

Lactated Ringer’s

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81
Q

Gastrointestinal Fluid Losses: Replace losses at ~ 0.5 – 1 mL per ___ mL fluid lost

A

1

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82
Q

Gastrointestinal Fluid Losses: Gastric losses are assumed to have equal Na+ and Cl- concentrations if pH > __

A

4

With lower pH, Na+ is assume to be ~ half the Cl- loss\

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83
Q

Dehydration Monitoring Parameters

A

Physical signs and symptoms: thirst, sweat, saliva, skin texture (dry, edematous, elasticity), orthostatic changes (blood pressure, syncope, dizziness), pulse (intensity, tachycardia)

Weight changes, urine output

Measurements of “in’s and out’s: (fluid intake and output)

Serum and/or urine electrolyte profile, plasma and urine osmolality

Lost body fluids, volume lost, and their electrolyte composition

Changes/resolution of mental status or any other symptoms

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84
Q

___is expanded extracellular fluid volume, increased volume/accumulation of plasma ultrafiltrate in the interstitial space

A

Edema

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85
Q

___ is pronounced generalized edema

A

Anasarca

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86
Q

___ edema is severe edema or anasarca that can be felt or observed when pressing the fingers on the skin of the edematous area(s)

A

Pitting

Arbitrarily classified as 1+, 2+, 3+, or 4+ when the dent is said number of centimeters in depth

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87
Q

Examples of common edematous disorders

A

Heart failure leading to ”congestion”
Liver cirrhosis
Nephrotic syndrome

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88
Q

Treatment of Edema

A

Fluid and Na+ restriction
Diuretic therapy
Treat underlying cause

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89
Q

Osmotic diuretics like Mannitol, urea, glycerol act within the ___ and ____ of the kidney and create osmotic gradient and increase water excretion

Extract___ water via expansion of ECF and renin release inhibition
Results in___ renal blood flow, removes NaCl and urea from the renal medulla
Decreases water extraction from the___ thin limb, diminishes passive reabsorption of NaCl in____ thin limb

A

proximal tubule and loop of Henle

intracellular

increased

descending

ascending

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90
Q

Carbonic Anhydrase Inhibitors like ______ acts mainly in the proximal tubule

A

Acetazolamide

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91
Q

Loop diuretics act in the ____ limb of the loop of Henle and causes a profound increase in urinary excretion of ____ via inhibition of ____ co-transporter

A

thick ascending

Na+ and Cl- (water and K+)

the Na+-K+-2Cl-

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92
Q

Loop diuretic examples

A

bumetanide; furosemide; torsemide

Furosemide 20 mg IV = Furosemide 40 mg PO = Torsemide 20 mg PO = Bumetanide 1 mg PO/IV

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93
Q

Furosemide (Lasix®) has ___ hour duration of action

A

6

Lasix = “Lasts Six”

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94
Q

___ diuretics all contain “sulfa” group

A

Loop

**Ethacrynic acid does not, can be used for patients with sulfa allergy

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95
Q

Thiazide diuretics act in the ______ of the kidney and causes inhibition of NaCl (and water) reabsorption
by inhibiting the ___ transporter

A

DCT

Na+/Cl-

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96
Q

Thiazide diuretics volume loss is not isotonic –> risk of ___

A

hyponatremia

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97
Q

Thiazide diuretic examples

A

Hydrochlorothiazide (HCTZ); Chlorothiazide; Chlorthalidone; Metolazone; Indapamide

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98
Q

Potassium-Sparing Diuretics act in the ___ and ___

A

DCT and Collecting duct

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99
Q

Potassium-Sparing Diuretics: Amiloride and triamterene MOA

A

Renal Na+ channel inhibitors – Block Na+ channels causing inhibition of Na+ reabsorption

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100
Q

Potassium-Sparing Diuretics: Spironolactone and eplerenone MOA

A

aldosterone antagonists – Competitively inhibit the binding of aldosterone to the mineralocorticoid receptor, inhibiting Na+ reabsorption

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101
Q

Potassium-Sparing Diuretics decrease the excretion of __ and ___

A

K+ and H+

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102
Q

___ activity is weak, generally used in combination with loop or thiazide diuretics to restrict K+ losses

A

Potassium-Sparing diuretics

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103
Q

Vasopressin (ADH) Antagonists examples

A

Conivaptan and tolvaptan

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104
Q

Vasopressin (ADH) Antagonists: Conivaptan MOA

A

V1A and V2 receptor antagonist

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105
Q

Vasopressin (ADH) Antagonists: Tolvaptan MOA

A

Selective V2 receptor antagonist

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106
Q

Vasopressin (ADH) Antagonists

Antagonists of vasopressin receptors, primarily___ receptors in kidney and block reabsorption of water via aquaporin channels
Antagonism of ___&raquo_space;> , can also antagonize ___ receptors on vascular smooth muscle and cause vasodilation

A

V2
V2&raquo_space;»> V1
V1

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107
Q

Vasopressin (ADH) Antagonists
___ excretion of free water, ____ urine osmolality, ____ urine output, increase net fluid loss
Increases serum osmolality and serum Na+ but does not alter ____
Gets rid of water but retains ____!

A

Increase, decrease, increase

Na+ excretion

electrolytes

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108
Q

Complications of Diuretic Tx – Non-electrolyte mediated:
____: primarily peak effect with loops due to damage to tight cell junctions within cochlea
Hypertriglyceridemia and increased LDL cholesterol concentrations with thiazides possibly due to liver output
Possibly hyperglycemia (primarily loop and thiazide) due to impaired insulin sensitivity
____ with spironolactone due to progesterone-like effects
Hypersensitivity reactions – caution in patients with sulfonamide allergy (loops and thiazides)

A

Ototoxicity

Gynceomastia

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109
Q

A pH of 7.4 is seen with a ratio of ___:__

A

A pH of 7.4 is seen with a ratio of 20:1

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110
Q

Acid/base balance

Pulmonary system adjusts pH via ___ (retainment or removal)
___ system adjusts pH via HCO3- and H+

A

CO2

Renal

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111
Q

Acidemia: pH <____ – higher bicarb (renal system?)

A

7.35

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112
Q

Alkalosis: pH >____

A

7.45

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113
Q

Arterial:___ blood in the circulatory system

A

oxygenated

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114
Q

Venous:____ blood from the peripheral vessels

A

deoxygenated

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115
Q

___fluids: exert high oncotic pressures e.g. provide volume expansion

Examples: albumin, blood (both natural), hydroxyethyl hetastarch (synthetic)

A

Colloid

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116
Q

___fluids: as discussed, offer balanced electrolytes and are generally isotonic
Examples: D5W, 0.9% NS, LR

A

Crystalloid

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117
Q

While reference range of Na is ____ mEq/L, symptoms tend not to develop until levels are above/below by 10 mEq/L

A

135 to 146

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118
Q

ADH___ to respond to LOW osmolality

ADH____ to respond to HIGH osmolality

A

formed

blocked

119
Q

If serum osmolality decreases, so is___ secretion, reducing free water clearance via kidneys (concentrating the urine)

A

ADH

120
Q

SIADH (syndrome of inappropriate anti-diuretic hormone): Body produces excessive ADH, causing ___ of free water

A

retention

121
Q

_____ is a disorder where the kidneys do not respond to ADH, causing excessive free water clearance

A

Diabetes insipidus

122
Q

Glucocorticoids can____ ADH release and can stimulate production of aquaporin channels (allowing for water flow between cells)

A

suppress

123
Q

Serum sodium level: < ___ mEq/L is hyponatremia

A

135

124
Q

Causes of hyponatremia

A

Loss of sodium, gain of water, or both, can induce hyponatremia

**Can be both– drink too much water (diluting) after a hot yoga class (sweating)

125
Q

Hyponatremia sodium loss examples

A

Excess sweating, nausea/vomiting, medication (diuretics), or shifting from extra to intracellular spaces.

126
Q

Hyponatremia: Water gain exampels

A

Increased intake

SIADH (syndrome of inappropriate anti-diuretic hormone) which incr. water retention

127
Q

Symptoms of hypnatremia

A

Fatigue, confusion, muscle weakness/spasms, and coma in serious cases
Migraines might be a first symptom (pressure in the brain), brain edema too
Most complain about fatigue, confusion, and headaches

128
Q

Mild hyponatremia is typically is asymptomatic/non-specific – range is ___

A

126 –135 mEq/L

129
Q

Moderate hyponatremia (____ mEq/L): depending on onset, may range from mild to profound confusion but NO concern/presentation of seizures

A

120 – 125

130
Q

Severe hyponatremia (___ mEq/L): depending on onset may include stupor/coma, or any presentation including seizures or severe neurologic changes e.g. musculoskeletal changes

A

<120

Even if its above 120 but they have neurologic changes – consider as severe

131
Q

Total body water may be normal (___), increased (____), or decreased (___)

A

euvolemic

hypervolemic

hypovolemic

132
Q

(Urine Na + Urine K) / Serum Na

Ratio of 1: urine output does not impact serum sodium
Ratio ____: urine does contribute to serum sodium LOWERING
Ratio ___: urine does contribute to serum sodium ELEVATION

A

> 1

<1

133
Q

Hypovolemic hyponatremia – Low urine sodium: often due to ___

A

volume loss

134
Q

Hypovolemic hyponatremia – High urine sodium: often due to ___

A

diuretics, cerebral salt-wasting/Addison disease

135
Q

Hypovolemic hyponatremia def

A

Excessive electrolyte-rich solute loss relative to TBW loss

Renal and extra (non) renal causes
Renal loses account for a larger proportion of Na loss

136
Q

Euvolemic hyponatremia def

A

Slightly decreased/normal total body Na and normal/slightly elevated TBW (no fluid overload)
Most commonly seen due to SIADH (may be drug-induced), alcohol-induced, or primary polydipsia

137
Q

Euvolemic hyponatremia def

A

Slightly decreased/normal total body Na and normal/slightly elevated TBW (no fluid overload)
Most commonly seen due to SIADH (may be drug-induced), alcohol-induced, or primary polydipsia

Hypothyroidism, corticosteroids, or other ADH-stimulating conditions may exacerbate this (volume depletion, anxiety, hypoxia, pregnancy)
Increased aquaporin in the collecting ducts lead to water retention and down regulation of RAAS

138
Q

Euvolemic hyponatremia: Low urine sodium: often due to ___

A

polydipsia, beer potomania

139
Q

Euvolemic hyponatremia: High urine sodium: often due to ___

A

physiologic abnormalities (cortisol, thyroid)

140
Q

Hypervolemic hyponatremia def

A

Excessive volume overload leads to a dilutional effect in the serum
Typically patients present w/peripheral or pulmonary edema, ascites or anasarca
Progressive/rapid weight gain and shortness of breath

141
Q

Hypervolemic hyponatremia may be exacerbated by underlying conditions:

A

Heart failure, renal failure, cirrhosis

**“wee for a wii – person drank gals of water and then didn’t pee it out (body couldn’t regulate changes to concentrations) and died”

142
Q

Hyponatremia treatment:

Correction may be as low as 1-2 mEq/L per hour
Typical rate maximum: __ mEq/L in 6 hours; ___mEq/L per 24 hours; ___ mEq/L in 48 hours
Chronic, w/risk factors for ODS: _____

A

6
12
18

4 – 6 mEq/L per 24 hours

NOTE: Too fast of correction can cause CNS toxicities – be careful !!

143
Q

Hyponatremia:
___ is the destruction of the myelin sheath which covers nerve cells of the brainstem (pons)
Rapid changes in sodium levels can cause swelling/rupture – It’s like putting too much water in a balloon too quickly – it’ll pop

A

osmotic demyelinating syndrome

144
Q

Risk factors for ODS include:

A

Alcoholism; malnutrition; hypokalemia; cirrhosis; malignancy

Severe hyponatremia <105 mEq/L

145
Q

Treatment of hypovolemic hyponatremia

A

Given intravascular depletion, first goal is fluid resuscitation

Need to identify total body sodium deficit and calculate total amount of sodium required to “correct” deficiency
Identify estimated change in serum sodium caused by infusion of 1 liter of infusate
Calculate rate of repletion of chosen infusate and compare to previously discussed rates of repletion
Verify your selection will not cause too “rapid” correction, or cause overcorrection

Mild/moderate 0.9% NS or LR

Severe (or seizure) initial 3% NS 100mL up to 3 doses , maintenance with 0.9% NS or LR

146
Q

Max dosing for hypertonic saline in hyponatremia treatment

A

Up to 100mL / dose

3 doses / day

147
Q

Treatment of hypovolemic hyponatremia: Target increase in serum Na by ___ mEq/hour with a 6-hour limit of ___ mEq/L

A

1-2

6

148
Q

Euvolemic or hypervolemic hyponatremia management principles

A

Volume status/symptoms differentiates from hypovolemic
Patients may present as hypervolemic, and then become euvolemic after diuresis
Similar treatment targets as hypovolemic with respect to rate change per hour/day of serum sodium
Mild/moderate:
- Initial treatment is volume restriction, 1000 to 1500 mL/day, to allow internal AVP regulation to “normalize”
- Need to evaluate potassium and magnesium, if deficient, replete accordingly
- If this fails, may consider pharmacologic agents
Severe:
- Use of bolus hypertonic saline (similar dosing as hypovolemic) should be prioritized over volume restriction in the first 12-24 hours

149
Q

Hyponatremia tx: If fluid restriction fails, add on ____

A

loop diuretics

IV Furosemide 20-40 mg (or equivalent) every 6 to 12 hours
“Adequate” trial may be 48-72 hours, or until patient cannot tolerate use e.g. develops hypovolemia or symptoms, due to diuresis

150
Q

Vasopressin receptor antagonist use for hyponatremia tx

A

inhibit receptors in pituitary gland that regulate release of adrenocorticotropin hormone and vasopressin receptors within collecting duct
Thus ADH cannot bind, water is eliminated without removal of solutes (aquaresis – just water)

*Not indicated for hypovolemic hyponatremia or urgent management, reserved for non-responders to fluid restriction/IV diuretics

151
Q

Vasopressin Receptor Antagonists: which is preferred due to specificity?

A

Tolvapatan

152
Q

For hypovolemia hyponatremia; start with an isotonic solution
- NS or LR at a rate of 0.5 to 1 mL/kg/hr
For euvolemic or hypervolemic hyponatremia: start with fluid restriction
- Typically no more than ___liters of fluid/day or ___ mL less than urine output/day
- IV diuresis for up to ___hours, consideration of VRA

A

1.5, 500

72

153
Q

Hypernatremia Serum sodium level:___ mEq/L

A

145 or greater

154
Q

Hypernatremia is usually due to ___ loss, but also ___ gain

A

water
sodium

**TBW is typically decreased secondary to reduced intake and/or GI / GU losses

155
Q

Hypernatremia: Hypovolemic due to

A

excessive urine output

156
Q

Hypernatremia: Hypervolemic due to __

A

mineralocorticoid or hypertonic solution administration

157
Q

Hypernatremia: Euvolemic due to___

A

diabetes insipidus (insufficient ADH secretion, decreased ADH responsiveness in kidney) leads to dilute urine

158
Q

Hypernatremia pt presentation

A

Intense thirst may seen, along with varying levels of lethargy, weakness, and consciousness
If hyperreflexia, myoclonus, tremor, or asterixis is present, constitutes “severe” symptoms as these may progress to seizure, coma, mortality

Urine sodium, osmolality, and overall volume are key monitoring parameters, in addition to serum electrolytes
Osmotic shifting from intra to extracellular space may lead to brain shrinkage, which can induce rupture and hemorrhage

159
Q

Hypernatremia treatment: Calculate total free water deficit with a plan to replace ___ within 12 – 24 hours, and remaining ___24 hours after

Avoid reducing serum Na by no more than ___mEq/L in 24 hours (0.5 mEq/L per hour)

A

50%

10

160
Q

Hypernatremia tx: Use of ____ sodium content solutions are preferred
If unable to take PO, use of______ should be used unless severe hypovolemia exists (isotonic)

A

oral, low/no

D5W IV (or other hypotonic fluids)

161
Q

Chronic hypernatremia is not as severe as acute hypernatremia due to ___

A

brain adaptations (less CNS toxicity)

162
Q

Hypernatremia: Hypovolemia: isotonic solution over ___ at a low rate

A

2-4 days

163
Q

Hypernatremia: Hypervolemia: ___ eliminates excess fluid and sodium

A

loop diuresis

164
Q

Hypernatremia: Nephrogenic diabetes insipidus:___ intranasal

A

desmopressin

*Acts as a vasopressin analog, enhancing antidiuresis

165
Q

Chloride General reference range: __

A

96 – 106 mEq/L

166
Q

Chloride is primarily absorbed via ___, secreted to aid in protein digestion, and regulated via ___

A

intestine (GI tract)

renal tubules

167
Q

Chlroide has an inverse relationship with _____

A

Bicarbonate HCO3-

168
Q

Dysfunction in chloride channels can also produce myriad disease states:

A

cystic fibrosis, bronchiectasis, and epilepsy among others

169
Q

Hypochloremia Serum chloride level: ___

A

97 mEq/L or less

170
Q

Hypochloremia: Given primary absorption points, most common cause is ____ secondary to vomiting or prolonged/excessive diuresis and/or renal failure

In response, bicarbonate reabsorption is stimulated, producing in a metabolic___

A

GI loss

alkalosis

171
Q

Hypochloremia: Urine chloride concentration aids in evaluation: <___mEq/L is considered responsive

A

10

172
Q

Chloride responsive metabolic___: commonly seen in diuresis or vomiting outpatient, excessive bicarbonate administration inpatient

Kidneys attempt to resorb chloride, sodium, and potassium resulting in low urine concentration (dilute)

A

alkalosis

173
Q

Chloride responsive hypochloremia tx:

A

Discontinue or reduce causative agent (diuretic, acid suppression) and replete chloride

Typically replacement with oral agents (sodium chloride tablets) or IV rehydration with NS
600 mg oral tablet = 10 mEq of sodium/chloride
1 Liter of NS = 154 mEq of sodium/chloride

174
Q

Hypochloremia non-reponsive hpyochloremia tx

A

Typically seen as excessive aldosteronism (e.g use ACEI, ARB, or AA diuretic) or mineralocorticoid state (hyperaldosteronism, tumors)
Manage underlying condition(s),

AVOID use of chloride-containing products as these will increase extracellular volume, treat with potassium supplementation (see next section)

175
Q

Hyperchloremia serum chloride level: ____

A

108 mEq/L or greater

176
Q

Hyperchloremia: Common causes are agents that induce a non-anion gap metabolic acidosis (opposite of hypochloremia)

A

Use/ingestion of corticosteroids, diuretics that promote chloride resorption (acetazolamide/triamterene) or strong acids (outpatient), rapid administration of sodium chloride (inpatient)
May also be seen with bowel, pancreatic, or biliary fistulas

177
Q

Hyperchloremia: Given development of metabolic acidosis, common symptoms include ___

A

arrhythmia, hypotension, and immunosuppression

178
Q

Hyperchloremia Assessed via monitoring of ___ and ___

A

serum and urinary electrolytes

179
Q

Hyperchloremia: Treatment principles

A

Discontinue or reduce causative agent (diuretic, acid suppression) and replete bicarbonate, if deficit

Clinical controversy remains over appropriate “balanced” crystalloid for hospitalized patients
Recent literature supports use of LR over NS to prevent development of hyperchloremia, among other outcomes during hospitalization
Rates of renal replacement therapy, 30-day mortality and length of hospital stay favored LR

180
Q

Potassium General reference range: ___

A

3.5 – 5 mEq/L

181
Q

Potassium is orimarily regulated by___ and regulated via ___ with up to 90% being reabsorbed via ___

A

kidneys
excretion
tubules

182
Q

Potassium most concerning adverse effects include

A

arrhythmias and/or seizure development

183
Q

Hypokalemia: Serum potassium level:

A

3.4 mEq/L or lower

184
Q

Hypokalemia often arises due to

A

intracellular shifting, urinary loss (drug-induced diuretics), or volume loss (GI loss)

185
Q

Hypokalemia: Intracellular shifting exmaples

A

β2 agonists/catecholamines, insulin, hypomagnesemia

186
Q

Hypokalemia: Urinary alteration/excretion examples

A

diuretics, aminoglycosides, amphotericin

187
Q

Hypokalemia: Removal examples

A

sodium polystyrene sulfonate, patiromer

188
Q

Hypokalemia can present as generalized weakness due to ___

A

respiratory muscle paralysis or breakdown, and arrhythmia

189
Q

Hypokalemia treatment principles

A

If possible, discontinuation/reduction of offending agent
Check potassium deficiency (recheck 2-4 hours after repletion)

Mild (3.0 – 3.4): 20 mEq orally x 1
Moderate (2.5 – 2.9): 40 mEq orally x 1
Severe (2.4 or lower) asymptomatic: 80 mEq orally (40 mEq x 2)
Severe and symptomatic (ECG changes): 80 mEq orally (40 mEq x 2) plus 20 to 40 mEq IV

190
Q

Hypokalemia Mild range and treatment

A

Mild (3.0 – 3.4): 20 mEq orally x 1

191
Q

Hypokalemia Moderate range and treatment

A

Moderate (2.5 – 2.9): 40 mEq orally x 1

192
Q

Hypokalemia Severe range and treatment

A

Severe (2.4 or lower) asymptomatic: 80 mEq orally (40 mEq x 2)

193
Q

Hypokalemia Severe and symptomatic (ECG changes) range and treatment

A

Severe and symptomatic (ECG changes): 80 mEq orally (40 mEq x 2) plus 20 to 40 mEq IV
(ORAL and then IV)

194
Q

Hypokalemia goal

A

Goal: somewhere 3.5 - 5

195
Q

Hypokalemia

IV administration can either be added into fluids if indicated, or slow IV and preferably via central line due to phlebitis/vesicant
Rate typically capped at ___mEq/hour without cardiac monitoring
Generally no more than ___mEq administered via peripheral line; ___ mEq via central line

A

10
80
120

196
Q

Hypokalemia If patient has impaired renal function (Crcl <30 mL/min) reduce dose by___

A

50%

197
Q

Hypokalemia: Oral replacement is preferred but may induce gastritis in doses >___

A

40 mEq

198
Q

Hyperkalemia Serum potassium level: ___

A

5 mEq/L or lower

199
Q

Hyperkalemia Often arises due to ___

A

extracellular shifting, urinary impairment (drug-induced), or increased ingestion/administration

Extracellular shifting: metabolic acidosis
Urinary alteration/retention: acute kidney injury, rhabdomyolysis, adrenal insufficiency

200
Q

Hyperkalemia: Arrhythmia, including ventricular fibrillation and asystole are of greatest concern (more common w/ potassium levels of ___mEq)

A

6 or greater

201
Q

Hyperkalemia treatment principles

A

If possible, discontinuation/reduction of offending agent
If symptomatic/ECG changes:
- Calcium gluconate (over chloride) administration: 1-2 grams IV push
- Stabilizes cardiac cell membranes and prevents arrhythmia
- (Provides calcium that will help kick out potassium in the heart to stabilize – THEN figure out potassium)
Monitor serum potassium levels every 2-4 hours after treatment approach

202
Q

Hyperkalemia if symptomatic/ECG changes: Treatment

A 
Calcium gluconate (over chloride) administration: 1-2 grams IV push
Stabilizes cardiac cell membranes and prevents arrhythmia
203
Q

Hyperkalemia tx: Calcium gluconate admin dosgin

A

1-2g IV push

204
Q

Hyperkalemia calcium gluconate rationale

A

Stabilizes cardiac cell membranes and prevents arrhythmia

Provides calcium that will help kick out potassium in the heart to stabilize – THEN figure out potassium

205
Q

Hyperkalemia: Monitor serum potassium levels every ___ hours after treatment approach

A

2-4 h

206
Q

Hyperkalemia acute treatmnet: intracellular SHIFTING of potassium

A

Regular insulin: 10 units plus dextrose 50 mL x 1 (avoid hypoglycemia)
Sodium bicarbonate: 50 mEq x 1
Albuterol: 20 mg (16 puffs) x 1, responsiveness is less predictable than above

207
Q

Hyperkalemia acute treatment: Removal (fecally)

A

Sodium polystyrene sulfonate (Kayexalate): cation exchange resin
- 15 to 30 grams PO or PR x 1 or 2 doses as needed
Hemodialysis: if patient remains hyperkalemic/non-responsive to other modalities and life-threatening symptoms develop, acute dialysis can be considered

208
Q

Hyperkalemia simplified treatment (my words)

A

First give calcium gluconate
Then given then either of these (insulin)
ECG changes still occur, then consider removal (Kayexalate)
Hemodialysis (last line therapy)

209
Q

Hyperkalemia chronic treatment

A

Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) – have delayed onset

210
Q

Hyperkalemia acute vs chronic treatment

A

Know kayexalate is for ACUTE vs Veltassa and Lokelma is for CHRONIC

211
Q

Phosphorus General reference range: ___

A

2.7 – 4.5 mg/dL

212
Q

Phosphorus is predominately found within ___ and___; main component of lipid membranes

A

bones

soft tissue

213
Q

Phosphorous facilitates ___ and ___

Also a co-factor for ____ by providing ___

A

Nerve conduction and muscle function

Cellular activity by providing ATP

214
Q

Significant proportion of phosphorus is reabsorbed via ____

A

proximal/distal tubules

Diuresis enhances loss
Regulated via calcitonin, parathyroid hormone

215
Q

Hypophosphatemia Serum phosphate level: ___

A

2.6 mg/dL or lower

216
Q

Hypophosphatemia – Increased excretion can commonly be seen with:

A

Vitamin D deficiency, hyperparathyroidism, use of loop diuretics or corticosteroids

217
Q

Hypophosphatemia: Loss from the system can be seen with:___

A

vomiting/diarrhea

218
Q

Hypophosphatemia Redistribution can be commonly seen with:

A

DKA, malnutrition, alkalosis, hormonal alterations (cortisol, glucagon, insulin)

219
Q

Hypophosphatemia: Most severe presentations can include: ___

A

respiratory failure, decreased cardiac contractility, paralysis, seizure, death

220
Q

Hypophosphatemia Identified via ___

A

serum and urinary electrolytes, parathyroid and vitamin D concentrations

221
Q

Hypophsophatemia: Mild to moderate - range and treatment

A

Mild (2 – 2.5) to moderate (1 – 1.9):

If functioning GI tract and asymptomatic, oral supplementation

222
Q

Hypophosphatemia severe or symptomatic: range and treatment

A

Severe (<1) or symptomatic:

IV phosphate replacement is required, avoid potassium-based products if serum K >4

223
Q

Hypophosphatemia safety

Reminder: must check ___ levels

A

potassium levels
Avoid / minimize potassium-based products replacement if >4
Both PO and IV forms exist

224
Q

Hypophosphatemia: IV doses
IV doses typically infused over 4-6 hours due to risk of ____
IV doses >30 mmol are administered via central line, capped at __mmol/day
Diluted into 250 mL of NS or D5W; avoid concomitant ___ (precipitation)

A

phlebitis

45

calcium

225
Q

Hyperphosphatemia: Serum phosphate level: ___

A

4.5 mg/dL or greater

226
Q

Hyperphosphatemia is most commonly seen with ___

A

CKD

Can also be seen w/parenteral/enteral feeding, vitamin D toxicity, hypoparathyroidism

227
Q

Hyperphosphatemia Most severe presentations can include:____

A

respiratory failure, decreased cardiac contractility, paralysis, seizure, death

228
Q

Hyperphosphatemia is identified via____

A

serum and urinary electrolytes, parathyroid and vitamin D concentrations

229
Q

Hyperphosphatemia may present with ___

A

osteopenia/osteomalacia/fracture, heart failure/arrhythmia

230
Q

Hyperphosphatemia Treatment Principles

A

Treat any underlying conditions e.g. vitamin D, PTH disorders
Avoidance of high-phosphorus-containing foods: dairy, meat, nuts

231
Q

Hyperphosphatemis: Treatment:

Most patients with CKD, or chronic elevations, require oral ___
Depending on calcium levels, may use calcium or non-calcium containing agents

Older guidelines recommended monitoring of Calcium x Phosphorus levels with a target of <55;
KDIGO currently recommends monitoring trends (no threshold but see trends instead)
Dosing is guided by phosphate levels, and not a specific ratio

A

phosphate binders

232
Q

Phosphate Binder examples

A 
Calcium carbonate
Lanthanum carbonate
Calcium acetate 
Sevelamer HCl
Sevelamer carbonate
233
Q

Phosphate binder most effective

A

Most effective is calcium acetate for binding capacity but we might have to watch out for levels of calcium [consider hypercalcemia for calcium carbonate and calcium acetate]

234
Q

Non-calcium phosphate binders

A

Sevelamer HCl

Sevelamer carbonate

235
Q

Phosphate binders all work via ___ and calcium containing products should be administered with ___

A

reducing absorption of dietary phosphorus within GI tract

Food (so it works on phosphate binding, not acid suppression – empty stomach will cause acid binding, less phosphate binding)

236
Q

Calcium containing phosphate binders may exceed ___ tabs/day

A

16

237
Q

Non-calcium containing phosphate binders may alter _____ and may still require ___ doses per day

A

fat soluble vitamin absorption

6-8

238
Q

Calcium Serum reference range:

A

8.5 – 10.2 mg/dL

239
Q

Ionized calcium range

A

1.1 – 1.35 mg/dL

240
Q

Ionized calcium is ___

A

the “free” calcium and most active form

241
Q

Serum calcium is regulated by ___

A

PTH
Vitamin
Calcitonin

242
Q

Calcium is predominately stored within ____ and almost 50% is bound to ____

A

bones

Serum proteins (albumin)

243
Q

serum calcium may need to be corrected for ____

A

hypoalbuminemia (<4)

244
Q

If calcium levels in the blood INCREASES, ____ is released

A

Calcitonin

245
Q

If calcium levels FALL, ___ is released

A

PTH

246
Q

Hypocalcemia: Serum calcium range

A

8.5 mg/dL or lower

247
Q

Hypocalcemia: ionized calcium range

A

<1.1 mmol/L

248
Q

Hypocalcemia: Increased excretion of calcium can be commonly be seen with

A

Vitamin D deficiency, hyperparathyroidism, use of loop diuretics or corticosteroids
Drug-induced: corticosteroids, alcohol, phenytoin/phenobarbital/carbamazepine

249
Q

Hypocalcemia: Acute presentation can include

A

neuromuscular excitability (twitching/spasm), QT prolongation leading to seizure/arrhythmia

250
Q

Hypocalcemia: Acute treatmnet

A

Serum calcium <7.5 ; ionized calcium <0.9:
3 grams of IV calcium gluconate (or 1 gram of calcium chloride)
Calcium gluconate usually preferred over calcium chloride due to toxicities

Serum calcium 7.6– 8.4; ionized calcium 1.1:
1-2 grams of calcium gluconate plus initiation of oral maintenance calcium therapy after normalization

251
Q

Hypocalcemia: Chronic treatment principles

A

Oral maintenance calcium therapy to prevent hypocalcemia, and management of hypoparathyroidism if present
Oral calcium: dosed at 1-2 grams of elemental calcium in divided doses
Hypoparathyroidism: 0.5 to 2 mcg of calcitriol/day

252
Q

Hypocalcemia caution when selecting IV calcium replacement products: ____ is more potent but produces higher rates of____

A

Calcium chloride
Tissue nescrosis

**why calcium gluconate is preferred

253
Q

Hypocalcemia: Caution of precipitation with ____products

A

Phosphorus

254
Q

Hypocalcemia: Serum levels should be re-checked after___ hours for acute and over the course of days/weeks in chronic

A

4-6

255
Q

Hypercalcemia Serum calcium range

A

10.2 mg/dL or higher

256
Q

Hypercalcemia: ionized calcium:

A

> 1.35 mmol/L

257
Q

Mild to moderate hyper calcemia

A
  1. 2 mg/dL – 12.9 mg/dl

2. 61 – 3

258
Q

Severe hypercalcemia

A

13 mg/dL
>3

Symptomatic

259
Q

Hypercalcemia: common causes include

A

hyperactive parathyroid gland; malignancy/tumor of the bone, toxic calcium/vitamin D ingestion

260
Q

Hypercalcemia: Acute presentation can include:

A

mental status changes (fatigue to encephalopathy), neuromuscular changes (hyperreflexia,), cardiac (bradycardia, arrhythmias)

261
Q

Hypercalcemia: Chronic presentation can include:

A

nephrolithiasis, renal failure, calcifications

262
Q

Hypercalcemia: Acute treatment 1st step

A

HYDRATION THERAPY – 1st step regardless of severity

Mild/moderate: 100 – 150 mL/hour of NS for 1 – 2 liters

Severe: 200 – 300 mL/hour of NS for 2 – 6 liters
Not a couple sips, it’s cups until you reach 2-6L
Hydration to have you pee it all out

263
Q

Hypercalcemia acute treatment: bisphosphonate thearpy rationale

A

inhibits bone resorption, stimulates calcium excretion

264
Q

Hypercalcemia: Bisphosphonate therapy examples

A

Zoledronic acid

Pamidronate

265
Q

Bisphosphonate thearpy renal adj

A

Zoledronic acid: AVOID w CrCl <30

Pamidronate use 60mg w CrCl <30

266
Q

Hypercalcemia: RANK ligand inhibitor rationale

A

Blocks osteoclast maturation and function, reducing bone resorption

267
Q

RANK ligand inhibitor example

A

Denosumab 120mg x1

Reserved for bisphosphonate-refractory

268
Q

Hypercalcemia: Acute Treatment options

A

1st step: Hydration

Bisphosphonate therapy (zoledronic acid, pamidronate)

RANK ligand inhibitor (denosumab)

Calcitonin

Dialysis

269
Q

Hypercalcemia chronic treatment principles

A

Management of underlying disease is required e.g. malignancy

Primary hyperparathyroidism:
Cincalcet: calicimimetic that downregulates PTH via calcium sensing receptors
30 mg/day twice daily to start, up to 90 mg four times/daily
Bisphosphonates: (a little slower acting, useful for longer half-ilfe longer therapy)
Zoledronic acid: 4 mg 7 days apart, may repeat every 1 – 3 months
Pamidronate: 60 – 90 mg every 2 weeks
Denosumab: 120 mg on days 0, 8, 15 and then monthly thereafter

270
Q

Hypercalcemia: Hyperparathyroidism treatment options

A

Cincalcet (calcimimetic that downregulates PTH via calcium sensing receptors)

Bisphosphonates

Denosumab

271
Q

Hypercalcemia: hyperparathyroidism: Cincalcet MOA

A

calicimimetic that downregulates PTH via calcium sensing receptors

272
Q

Hypercalcemia safety notes:

Caution with IV bisphosphonates: Increased risk of___ of the jaw, especially with creatinine clearance <30 mL/min
Repeat dosing in chronic hypercalcemia is not clearly outlined, follows oncology literature
No role for___ calcitonin (indicated for osteoporosis)
Serum levels should be re-checked after ___hours for acute and over the course of days/weeks in chronic

A

osteonecrosis

intranasal

4-6

273
Q

Magnesium Serum reference range:

A

1.5 – 2.5 mg/dL

274
Q

Magnesium predominately stored within ___

A

bones, soft tissue and muscles

275
Q

___ maintains sodium, potassium, and calcium homeostasis

A

Magnesium

276
Q

Magnesium is reabsorbed primarily through___ and regulated by ___

A

small intestines

kidneys

277
Q

Hypomagnesemia Serum magnesium:

A

1.5 mg/dL or lower

278
Q

Hypomagnesemia primary cause

A

Excessive gastric or renal loss
- Celiac, Crohn’s IBS, diuretics
Also noted with sepsis/infections, burns, malnutrition and/or alcoholism

279
Q

Hypomagnesemia may exacerbate concomitant ___ and __

A

Hypokalemia and hypocalcemia

280
Q

Hypomagnesemia presentation is similar to ___

A

hypocalcemia

281
Q

Severe <1 hypomagnesemia make produce ___ and ___

A

ECG changes and arrhythmia

282
Q

Mild/moderate hypomagnesemia range

A

1-1.5

283
Q

Mild/moderate treatment principles

A

8-32 mEq

Can be achieved with oral agents

284
Q

Severe hypomagnesemia range

A

<1

285
Q

Severe hypomagnesemia treatment principles

A

requires IV agents (reduce dose by 20-50% if CrCl <30)

286
Q

1 gram of magnesium sulfate contains ___ mEq = __mg of elemental mg

A

8mEq = 98.6mg of elemental mg

287
Q

Hypomagnesemia safety notes

Caution with oral magnesium:
Often included as part of laxation for its ability to exert osmotic effects in ____
Doses often capped at ___ per day

A 
GI tract (GI Distress) 
800 mg
288
Q

Hypomagnesemia safety notes

IV magnesium: required to be diluted to 20% or less, and administered at a maximum rate of ___
Thus, for patients requiring 2-4 grams (16 – 32 mEq) dose is administered over several hours
If symptomatic, doses up to ___ grams can be administered rapidly via IV push

A

8 mEq/hour

4

289
Q

Hypomagnesemia Safety notes

Monitoring

A

Cardiac monitoring is required, due to risk of arrhythmia

290
Q

Hypermagnesemia: Serum magnesium range

A

2.4 mg/dL or greater

291
Q

Hypermagnesemia is extremely rare, often seen with ___ but may be seen with DKA, adrenal insufficiency, or hyperparathyroidism

A

acute kidney injury

292
Q

Hypermagnesemia presentation may include

A

nausea/vomiting, parasthesias, dysarthria, seizure, and/or respiratory paralysis

293
Q

Hypermagnesemia treatment principles

A

If patient is on hemodialysis, repeat dialysis sessions may be indicated

IV calcium: reverse cardio or neuromuscular defects
Calcium chloride: 500 – 1000 mg IV over 10 minutes
If no central line, calcium gluconate 1 – 2 grams can be substituted

As previously discussed, caution should be used with calcium products due to vesicant status

294
Q

___ is usually reserved for hypermagnesemia NOT hypocalcemia

A

Calcium chloride

CDM 2 (8 decks)

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