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APEX > Fluids & Blood > Flashcards

Fluids & Blood Flashcards

1
Q

Fluid Compartments

A

60% 70 kg
TBW 42L
1. Intracellular 40% 28L
2. Extracellular 20% 14L
a. Interstitial 15% 11L
b. Plasma 5% 3L

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2
Q

↑TBW

A

Neonates

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3
Q

↓TBW

A

Females
Elderly
Obese

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4
Q

Intracellular Ions

A

K+
Mg2+
Phosphate

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5
Q

Extracellular Ions

A

Na+
Ca2+
Cl¯
HCO3¯

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6
Q

Net Filtration Pressure

A

Starling forces
(Pc - Pif) - (πc - πif)

Pc = capillary hydrostatic
Pif = interstitial hydrostatic
πc = capillary oncotic
πif = interstitial oncotic

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7
Q

OsmolaRity

A

Osmoles per LiteR solution mOsm/L

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8
Q

OsmolaLity

A

Osmoles per kg solvent mOsm/kg H2O

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9
Q

Plasma Osmolarity

A

Normal 280-290 mOsm/L

= 2[Na+] + (Glucose/18) + (BUN/2.8)

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10
Q

NaCl 0.9%

A

ISOtonic
Hyperchloremic metabolic acidosis
Na+ 154 mEq/L
Cl¯ 154 mEq/L
↑Cl¯ load → kidneys excrete HCO3¯ to maintain electroneutrality → non-gap metabolic acidosis

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11
Q

IVF Na+ Concentration

A

NaCl 154 mEq/L
Plasmalyte 140 mEq/L
LR 130 mEq/L

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12
Q

Crystalloid Replacement

A

3:1 ratio
Plasma volume ↑20-30 minutes
Dilutional effects

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13
Q

Albumin

A

Only colloid derived from human blood products
1:1 ratio
Anti-inflammatory properties
Binds Ca2+ → hypocalcemia

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14
Q

Synthetic Colloids

A

*Renal injury risk (FDA black box warning)
Dextran 40
Hetastarch
Hextend
Voluven

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15
Q

Dextran 40

A

Synthetic colloid
↓blood viscosity → improves microcirculation
1° coagulopathy
Dextran > Hetastarch > Hextend
Anaphylaxis risk

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16
Q

Hetastarch

A

Synthetic colloid
2nd highest coagulopathy risk

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17
Q

Hextend

A

Synthetic colloid
Do NOT exceed 20 mL/kg
3rd highest coagulopathy risk

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18
Q

Hyperkalemia
Definition & Causes

A

K+ > 5.5 mEq/L
↑RMP (closer to threshold potential)
Causes include PRBCs, renal failure, NSAIDs, acidosis, Succinylcholine, β blockers, cellular injury (tumor lysis, hemolysis, burns, crush injury, & rhabdomyolysis )

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19
Q

Hyperkalemia
Cardiac Dysrhythmias S/S

A

5.5-6.5 peaked T waves
6.5-7.5 P wave flattening + PR prolongation
7.0-8.0 QRS prolongation
> 8.5 QRS → sine wave → Vfib

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20
Q

What is the most common electrolyte abnormality?

A

Hypokalemia
K+ < 3.5 mEq/L
Hyperpolarizes RMP

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21
Q

Hyperkalemia
Treatment

A

Ca2+ IV
- Central 20 mEq/hr
- Peripheral 10 mEq/hr
Insulin + D50
Hyperventilation
HCO3¯
β2 agonists
Elimination - diuretics, Kayexalate, & dialysis

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22
Q

Hypokalemia
Causes

A

GI loss - vomiting/diarrhea, NG suction, Zollinger-Ellison syndrome, JG bypass
Renal loss - diuretics or metabolic alkalosis
Redistribution into cells (hyperkalemia treatment)

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23
Q

Hypokalemia
S/S

A

Skeletal muscle cramps → weakness → paralysis
Worsens dig toxicity
EKG prolonged PR & QT intervals
Flat T wave
U wave present

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24
Q

What maintains the intracellular K+ distribution?

A

Na-K+ ATPase pump

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25
Q

K+ Supplementation

A

Do NOT administer > 0.5-1 mEq/kg/hr

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26
Q

Hypernatremia
Causes

A

↓total body Na+ content
Osmotic diuresis, N/V, adrenal insufficiency

Normal Na+
DI, renal failure, diuretics

↑total body Na+
Hyperaldosteronism ↑Na+ intake

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27
Q

Hypernatremia
S/S

A

Na+ > 145 mEq/L
Based on serum osmolality normal range 280-290 mOsm/L
350-375 HE, agitation, confusion
376-400 weakness, tremors, ataxia
401-430 hyperreflexia & muscle twitching
> 430 seizures, coma, death

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28
Q

Hyponatremia
Causes

A

↓total body Na+ content
Diuretics, salt-wasting, hypoaldosteronism

Normal Na+
SIADH, hypothyroid, H2O intoxication, periop stress

↑total body Na+
CHF or cirrhosis

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29
Q

Hyponatremia
S/S

A

Mild 125-129 N/V & malaise
115-124 HE, lethargy, & altered LOC
< 115 seizures, coma, cerebral edema, & respiratory arrest

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30
Q

Hyper/hyponatremia
Treatment

A

Dependent on cause*
Na+ restriction
IVF selection based on tonicity
Diuretics

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31
Q

What mechanisms maintain Na+ homeostasis?

A

GFR, RAAS, & ANP (BNP)

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32
Q

Na+ Supplementation

A

NaCl 3% 1-2 mL/kg/hr
↑ < 1-2 mEq/L per hour

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33
Q

What occurs when hyponatremia corrected too quickly?

A

Osmotic demyelination syndrome or central pontine myelinolysis
- Mental status changes
- Seizures
- Spastic quadriplegia
- Pseudobulbar palsy
- Encephalopathy
- Coma & death

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34
Q

Calcium
Normal Serum Levels

A

Total 8.5-10.5 mg/dL
Ionized 4.6-5.2 mg/dL

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35
Q

What is the most abundant electrolyte?

A

Calcium
2nd messenger, neurotransmitter release, & muscle contraction

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36
Q

Hypercalcemia
S/S

A

Nausea, abdominal pain, HTN, psychosis, mental status changes, seizures, & shortened QT interval

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37
Q

Hypercalcemia
Treatment

A

NS
Loop diuretic

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38
Q

Calcium Storage

A

1° bones
Albumin = intravascular Ca2+ reservoir

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39
Q

Hypocalcemia
Causes

A

Hypoparathyroidism
Vitamin D deficiency
Renal osteodystrophy
Pancreatitis
Sepsis

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40
Q

Hypocalcemia
S/S

A

Skeletal muscle cramps
Nerve irritability → paresthesia & tetany
Laryngospasm
Mental status changes → seizures
Chvostek or Trousseau signs
Prolonged QT interval

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41
Q

Hypocalcemia
Treatment

A

Calcium
Vitamin D

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42
Q

Chvostek Sign

A

Tapping on the jaw angle (facial nerve/masseter muscle) causes facial contraction on the ipsilateral side of the

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43
Q

Trousseau Sign

A

Upper extremity BP cuff inflated above SBP 3 minutes
Hand & forearm muscle spasms

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44
Q

Magnesium

A

Normal plasma Mg2+ 1.7-2.4 mg/dL or 1.5-3 mEq/L
Antagonizes Ca2+ effects

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45
Q

Parathyroid Hormone & Calcitonin

A

PTH ↑serum Ca2+
Parathyroid gland releases PTH → osteoclasts release Ca2+ from bone storage + ↑Ca2+ renal reabsorption & Ca2+ absorption in the small intestine

Calcitonin ↓serum Ca2+
↑Ca2+ → thyroid releases calcitonin → osteoclast activity inhibited + ↓Ca2+ reabsorption

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46
Q

Hypercalcemia
Causes

A

Hyperparathyroid
Cancer
Thyrotoxicosis
Thiazide diuretics
Immobilization

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47
Q

Magnesium 1° Location

A

Muscle & bone
1% ECF
0.3% plasma

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48
Q

Where is Mg2+ reabsorbed?

A

Renal tubules

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49
Q

Magnesium Clinical Uses

A

Pre-E 4G load over 10-15 min then 1G/hr infusion
Opioid-sparing techniques (ERAS)
Acute bronchospasm
Cardiac rhythm disturbances - symptomatic PVCs or Torsades de pointe

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50
Q

Hypermagnesemia
Causes

A

Excessive admin
Renal failure
Adrenal insufficiency

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51
Q

Hypermagnesemia
S/S

A

Not significant unless extremely high
Heart block
Potentiates NMBs (Succinylcholine & non-depolarizing)

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52
Q

No Hypermagnesemia S/S

A

2.5-5 mg/dL
2.1-4.2 mEq/L

53
Q

What serum magnesium level are diminished deep tendon reflexes noted?

A

5-7 mg/dL
4.2-5.8 mEq/L

Lethargy, drowsiness, flushing, N/V

54
Q

When are deep tendon reflexes lost?

A

Serum Mg2+ 7-12 mg/dL
5.8-10 mEq/L

HoTN, EKG changes, somnolence

55
Q

When does respiratory depression occur?

A

Serum Mg2+ > 12 mg/dL
> 10 mEq/L

Apnea, complete heart block, cardiac arrest, coma, paralysis

56
Q

Hypermagnesemia
Treatment

A

Calcium chloride or gluconate

57
Q

Hypomagnesemia
Causes

A

Poor intake, alcohol abuse, diuretics, critical illness, hypokalemia

58
Q

Hypomagnesemia
S/S

A

Not significant unless extremely low
Prolonged QT

59
Q

Mg2+ level when tetany & dysrhythmias present

A

< 1.2 mg/dL
< 1 mEq/L

Tetany, seizures, dysrhythmias

60
Q

Mg2+ level when neuromuscular irritability present

A

1.2-1.8 mg/dL
1-1.5 mEq/L

Neuromuscular irritability, hypokalemia, hypocalcemia

61
Q

Hypomagnesemia
Treatment

A

Magnesium sulfate supplementation

62
Q

Acid-Base
Respiratory Compensation

A

CO2 = volatile acid

63
Q

Acid-Base
Renal Compensation

A

Reabsorb filtered HCO3¯
Remove titratable acids (non-volatile)
Ammonia formation

64
Q

Acidosis
CNS/Pulmonary/Cardiac Effects

A

↑CBF/ICP
↑PVR
↑P50 (R shift)
↑SNS tone ↑dysrhythmias risk
↓contractility
Hyperkalemia H+/K+ pump

65
Q

Alkalosis
CNS/Pulmonary/Cardiac Effects

A

↓CBF/ICP
↓PVR
↓P50 (L shift)
↓Coronary blood flow
↑dysrhythmias risk
Hypokalemia
↓ionized Ca2+

66
Q

Respiratory Acidosis
Causes

A

↑CO2 production
↓CO2 elimination ↑Vd
Rebreathing

67
Q

What is the most common respiratory acidosis cause?

A

Hypoventilation

68
Q

ACUTE
Respiratory Acidosis

A

Every 10 mmHg > 40 ↓pH 0.08

69
Q

Chronic
Respiratory Acidosis

A

Every 10 mmHg > 40 ↓pH 0.03

70
Q

What causes non-anion gap acidosis?

A

Metabolic acidosis
Normal anion gap 8-12 mEq/L
HCO3¯ loss

HARDUP
- Hypoaldosteronism
- Acetazolamide
- Renal tubular acidosis
- Diarrhea
- Uretosigmoid fistula
- Pancreatic fistula

71
Q

Non-Anion Gap Acidosis
Treatment

A

Admin sodium bicarbonate

72
Q

What causes an anion gap acidosis?

A

Metabolic acidosis
Add +acid
Anion gap > 12 mEq/L

MUDPILES
- Methanol
- Uremia
- DKA
- Paraldehyde
- Isoniazid
- Lactate ↓DO2, sepsis, cyanide poison
- Ethanol or ethylene glycol
- Salicylates → inhibit Krebs cycle

73
Q

Anion Gap Acidosis
Treatment

A

Lactic acidosis = IVF, O2, cardiopulmonary support
DKA = IVF + insulin
Uremia or drug-induced = dialysis

74
Q

Metabolic Acidosis
Respiratory Compensation

A

↑minute ventilation ↓PaCO2
PaCO2 ↓1-1.5 mmHg ↓HCO3¯ 1 mEq/L

75
Q

What causes metabolic alkalosis?

A

HCO3¯ addition = massive transfusion
Loss non-volatile acid = NG suction, vomiting, loop diuretics, acid loss via urine, ECF depletion ↑Na+ reabsorption H+/K+ excretion to maintain electroneutrality
Antacids
↑mineralocorticoid activity = Cushing or hyperaldosteronism

76
Q

Metabolic Alkalosis
Respiratory Compensation

A

↓minute ventilation ↑PaCO2
PaCO2 ↑0.5-1 mmHg ↑HCO3¯ 1 mEq/L

77
Q

Shock Stage
I

A

Blood loss < 15% or < 750 mL
Pulse < 100
BP normal
Pulse pressure normal
RR 14-20
UOP > 30 mL/hr
Fluid management = crystalloid

78
Q

Shock Stage
II

A

Blood loss 15-30% or 750-1,500 mL
Pulse 100-120
BP normal
↓pulse pressure
RR 20-30
UOP 20-30 mL/hr
Fluid management = crystalloid

79
Q

Shock Stage
III

A

Blood loss 30-40% or 1,500-2,000 mL
Pulse 120-140
↓BP ↓pulse pressure
RR 30-40
UOP 5-15 mL/hr
Fluid management = crystalloid + blood

80
Q

Shock Stage
IV

A

Blood loss > 40% or > 2L
Pulse > 140
↓BP ↓pulse pressure
RR > 40
Minimal/absent UOP
Fluid management = crystalloid + blood

81
Q

Universal Donor

A

RBCs O ¯
Plasma AB +

82
Q

Universal Recipient

A

RBCs AB +
Plasma O ¯

83
Q

O ¯

A

Contains NO RBC antigens
Anti-A & anti-B plasma antibodies

84
Q

O +

A

85% population Rh-D positive (+)
O + an acceptable emergency transfusion RBC type when patient NOT childbearing age & has not received a previous transfusion

85
Q

Rh

A

Rh+ RBC antigen D present
No plasma antibodies
Rh+ able to receive (+) OR (-)

Patient w/ Rh¯ + exposure to Rh+ blood → develops antibodies to Rh antigen (anti-D)

86
Q

Rh & Pregnancy

A

Fetus receives Rh+ antigen from father
Maternal Rh¯& fetal blood Rh+ do not mix during pregnancy
Rh+ antigen able to cross the placenta during delivery
Mother sensitized when Rh+ antigen crosses the placenta during delivery
Develops antibodies to Rh+ antigen (anti-D)
Subsequent pregnancy w/ Rh+ fetus → erythroblastosis fetalis

87
Q

Erythroblastosis Fetalis

A

Hemolytic disease that affects the newborn d/t Rh incompatibility

88
Q

Who & when to administer Rhogam?

A

Rh immune globulin
Pregnant Rh¯ mothers
Starting at 28 weeks gestation to prevent sensitization
Protects the fetus during delivery

89
Q

Type

A

Determines ABO & Rh-D antigens in the recipients blood
5 minutes
0.2% probability incompatibility reaction

90
Q

Screen

A

Determines most clinically significant antibodies present
45 minutes
0.06% probability incompatibility reaction

91
Q

Crossmatch

A

Provides the most accurate compatibility
Mixes the recipient plasma w/ blood in the actual unit to be transfused
45 minutes
0.05% probability incompatibility reaction

92
Q

Emergency PRBCs Transfusion

A
  1. Type-specific partially crossmatched blood
  2. Type-specific uncrossmatched blood
  3. Type O ¯ uncrossmatched blood

*After 2 units type O blood transfused must continue to use type O despite patient’s blood type!

93
Q

PRBCs

A

Hgb 6-10 g/dL ?
Hgb < 6 g/dL TRANSFUSE
↑CaO2
1 unit 300 mL Hct 70%
↑Hgb 1 g/dL or Hct 2-3%

94
Q

Platelets

A

1 pack per 10 kg
Do NOT use filter or warm
Stored at room temp 5 days
↑bacterial contamination risk → sepsis

95
Q

FFP

A

All coagulation factors, fibrinogen, & plasma proteins
↑factor concentration 20-30%
Factor VII 1/2 life 3-6 hours
Complete infusion w/in 24 hours thawing

96
Q

FFP Indications

A

Coagulopathy 10-20 mL/kg
Warfarin reversal 5-8 mL/kg
Antithrombin deficiency
Massive transfusion
DIC
C1 esterase deficiency
Hereditary angioedema

97
Q

Cryo

A

Contains fibrinogen, factor VIII & XIII, vWF
Dose 5 bag pool
↑fibrinogen 50 mg/dL
Complete infusion w/in 6 hours thawing

98
Q

EBVs

A

Adult 70 mL/kg
Child 70 mL/kg
Infant 75-80 mL/kg
Full term 80-90 mL/kg
Premature 90-100 mL/kg

99
Q

Stored Blood Additives

A

Citrate (anticoagulant) inhibits Ca2+ → hypocalcemia
Phosphate (buffer combats acidosis) → alkalosis
Dextrose (1° glycolysis substrate) → hyperglycemia
Adenine (substrate helps RBCs re-synthesize ATP) extends storage 21 → 35 days

100
Q

What temperature is blood stored at?

A

1-6° C
Extents lifespan via slowing glycolysis

101
Q

RBC Storage Lesion

A

↓2,3 DPG → shifts oxyhemoglobin curve L
↓ATP
↓pH ↑lactic acid
↑K+
Impaired ability to change shape → impacts capillary flow
Hemolysis
↑proinflammatory mediators production

102
Q

Leukoreduction

A

Removes WBCs
Leukocytes (WBCs) responsible HLA alloimmunization, febrile non-hemolytic transfusion reactions, & CMV transmission

103
Q

HLA Alloimmunization

A

Body develops antibodies against non-self antigens (human leukocyte antigens)
The body attacks HLA proteins present on the platelet surface
Most common cause platelet refractoriness

104
Q

Washing

A

Washing blood products w/ saline removes any plasma & antigens in the donor RBCs
RBC antigens are not removed
Prevents anaphylaxis in IgA deficient patients

105
Q

Irradiation

A

Exposes blood to gamma radiation
Disrupts WBC DNA in the donor cells & destroys donor leukocytes
Prevents graft-vs-host disease in immunocompromised patients
GVHD → donor leukocytes attach recipient bone marrow → pancytopenia, fever, hepatitis, & diarrhea

106
Q

When to administer irradiated blood?

A

1st/2nd degree relative blood donors
Leukemia
Lymphoma
Hematopoietic stem cell transplants
DiGeorge syndrome

107
Q

Blood Transfusion Infectious Complications

A

CMV
Hepatitis B
Hepatitis C
HIV

108
Q

Acute Hemolytic Reaction
S/S

A

Occurs when patient receives incompatible blood product

Hemoglobinuria, HoTN, & bleeding
- Fever/chills
- Chest pain
- Dyspnea
- Nausea
- Flushing

109
Q

Acute Hemolytic Reaction
Treatment

A
  1. Stop the transfusion
  2. Maintain UOP > 75-100 mL/hr (IVF, Mannitol 12.5-25 g, Furosemide 20-40 mg)
  3. Alkalinize the urine HCO3¯
  4. Send urine & plasma Hgb samples to blood bank
  5. Check platelets, PT, & fibrinogen
  6. Send unused blood to the blood bank to double-check cross-match
  7. Support hemodynamics
110
Q

Non-Hemolytic Transfusion Reaction

A

Fever most common
Presentation includes fever, chills, HE, nausea, & malaise

111
Q

Non-Hemolytic Transfusion Reaction
Treatment

A

Supportive
Acetaminophen

112
Q

Allergic Transfusion Reaction

A

Rarely severe
Present w/ urticaria & facial swelling

113
Q

Allergic Transfusion Reaction
Treatment

A

Antihistamines

114
Q

TRALI

A

Transfusion-related ALI non-cardiogenic pulmonary edema
Most common cause transfusion related mortality
Cause: HLA human leukocyte antigens & neutrophil antibodies present in the donor plasma
Donor antibodies cause neutrophil activation → endothelial injury → capillary leak → pulmonary edema → impaired gas exchange → hypoxemia → acidosis & death

115
Q

Donor populations /w high antibodies concentration

A

Multiparous women
Blood transfusion history
Organ transplant

116
Q

Blood products w/ highest TRALI incidence

A

Blood products containing plasma
Platelets or FFP

HLA & neutrophil antibodies present in donor plasma

117
Q

Recipients at increased risk to develop TRALI

A

Critical illness
Sepsis
Burns
Post- CPB

118
Q

TRALI S/S

A

Onset < 6 hours after transfusion
Bilateral infiltrates on CXR
PaO2/FiO2 < 300 mmHg
SpO2 < 90% on RA
Normal PAOP

119
Q

TRALI Management

A

1° supportive
Maximize PEEP
LPV low VT
Avoid overhydration

120
Q

TACO

A

Transfusion-associated circulatory overload
Volume overload cause by expanding the patient plasma volume beyond compensatory ability

121
Q

TACO S/S

A

Pulmonary edema
Hypervolemia
LV dysfunction
Mitral regurgitation
↑PAOP
↑BNP

122
Q

TACO Management

A

Supportive

123
Q

Massive Transfusion

A

Alkalosis - citrate metabolizes HCO3¯
Hypocalcemia
Hypothermia
Hyperglycemia (dextrose)
Hyperkalemia - stored RBCs the cell membrane become dysfunctional & allows K+ to leak; reduce risk by admin washed or fresh cells < 7 days old

124
Q

Trauma Lethal Triad

A

Acidosis (hypoperfusion)
Hypothermia
Coagulopathy
- Acidosis impairs hemostasis
- PT & PTT prolonged < 34°C
- Massive volume resuscitation causes dilutional coagulopathy

125
Q

Intraop Blood Salvage
Indications

A

EBL expected > 1L or 20% EBV
Pre-existing anemia
Patient refuses allogenic blood products

126
Q

How much volume required to admin 250 mL (1 unit) saline diluted RBCs?

A

500-750 mL 2-3x
Hct 50-60%

127
Q

What blood products are not returned to the patient w/ intraop blood salvage?

A

Platelets & coagulation factors
Dilutional coagulopathy

128
Q

How does salvaged blood compared to blood bank?

A

↑O2 carrying capacity
Better maintain concave shape

129
Q

Intraop Blood Salvage
CONTRAINDICATIONS

A

Sickle cell anemia
Thalassemia
Oncologic procedures
Topical drugs (antibiotics) in the sterile field
Infected surgical site
C-section controversial d/t theoretical amniotic fluid embolism risk

APEX (18 decks)

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