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614 General Principles Of Anesthesia > Week 14 - Fluid & Electrolytes > Flashcards

Week 14 - Fluid & Electrolytes Flashcards

1
Q

Goals of fluid management? Maintain adequate: (5)

A
  • Intravascular fluid volume
  • Left ventricular filling pressure
  • Cardiac output
  • Systemic blood pressure
  • Oxygen delivery to tissues
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2
Q

How can you assess fluid status in a patient?

A
  • Skin turgor
  • Mucus membranes
  • Peripheral pulses
  • Resting heart rate and blood pressure
  • Orthostatic changes
  • Urine output
  • NPO Status
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3
Q

Body fluid composition percentages:

A

Extracellular: (33%)
- Interstitial (25%)
- Plasma (8%)

Intracellular: (66%)

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4
Q

Intracellular fluid (ICF) make up ___ of the body’s water and it is around _____% of your weight.

A

2/3;

40

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5
Q

The body is ___% water.

A

60

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6
Q

The intracellular fluid is primarily a solution of:

A

Potassium (K+)
Organic anions
Proteins

the cell membranes and cellular metabolism control these

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7
Q

The extracellular fluid is ____ of the body’s water and around _____% of body weight.

A

1/3

20%

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8
Q

The extracellular fluid is primarily a _____ and ____ solution.

A

NaCl and NaHCO3

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9
Q

The interstitial fluid (ISF) and Plasma are part of the _______ fluid.

A

Extracellular

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10
Q

Characteristics of the interstitial fluid (ISF):

A
  • Surrounds the cells and does not circulate
  • comprises 3/4 of the ECF
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11
Q

What are transcellular fluids? Characteristics?

A
  • fluids that are outside of the normal compartments.
  • 1-2 liters of fluid comprise the CSF, digestive (gastric) juices, mucus, etc/
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12
Q

Basic constituent of the human body

A

Water

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13
Q

Total body water (TBW) varies with age, gender and body type. What are the differences in percentages for males, females, and infants?

A

Males: 60%
Females: 50%
Infants: 80%

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14
Q

Which patients generally have less water per kg of body weight?

A
  • Obese adults
  • Patient’s with diabetes.
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15
Q

What are the characteristics of Hypovolemia? (7)

A
  • Increasing Hematocrit
  • Metabolic acidosis
  • Urine SG >1.010
  • Urine Na (less than) < 10 mEq/L
  • Urine osmolality < 450mOsm/kg
  • Hypernatremia
  • BUN: creatinine ratio > 10:1
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16
Q

Signs of Hypovolemia at 5% water loss:

Mucus
LOC
Orthostatic
HR
BP
Urine output
Pulse rate

A
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17
Q

Signs of Hypovolemia at 10% water loss:

Mucus
LOC
Orthostatic
HR
BP
Urine output
Pulse rate

A
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18
Q

Signs of Hypovolemia at 15 - 20% water loss:

Mucus
LOC
Orthostatic
HR
BP
Urine output
Pulse rate

A
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19
Q

When evaluating a hypovolemic patient, keep in mind that a drop in BP does not occur in a patient that is already in the supine position until ______% of the blood volume is lost.

A

30

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20
Q

What is the intraoperative goal for urine output in normal patients? and for burn patients?

A
  • 0.5 – 1 mL/kg/hr
  • 1.5 mL/kg/hr
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21
Q

Decrease in urine output generally does not occur until _______% of blood volume is lost

A

~20

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22
Q

Early and later signs of Hypervolemia:

A
  • Pitting edema
  • Presacral edema

later:
- Tachycardia
- Crackles
- Wheezing
- Pulmonary edema

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23
Q

The Chest X-ray is reliable to evaluate for hypervolemia. What would you see on it?

A
  • Kerly B lines: increased pulmonary and interstitial markings.
  • Diffused alveolar infiltrates
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24
Q

What labs can you check for hypervolemia?

A

Blood and urinalysis

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25
Q

Extracellular Fluid:
Major cations (+)
Major anions (-)

A

Major cations (+): Sodium, Potassium and Calcium

Major anions (-): Chloride, Bicarbonate and Proteins

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26
Q

Intracellular Fluid:

Major cations (+)
Major anions (-)

A

Major cations (+): Potassium, Magnesium and Sodium

Major anions (-): Chloride, Bicarbonate and Proteins

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27
Q

Most important electrolytes? and why?

A

Potassium and Calcium
Effect excitability of nerve & muscle

K+ effects resting membrane potential (RMP)
Ca++ determines threshold potential

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28
Q

Sodium ( ____ - _____ mEq/L)

A

135 - 145

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29
Q

Hypernatremia is secondary to: ____________.

A

Lack of water;

Not because of too much salt*.

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30
Q

Neuro symptoms of hypernatremia (Na > _____ mEq/L):

A

>145

Neuro: Symptoms reflect rate of H2O movement out of brain cells
- Altered LOC
- Weakness
- Thirst
- Restlessness
- Lethargy
- Seizures
- Death
- Intracranial bleeding: ruptured cerebral veins/ focal hemorrhage (with rapid decreases in brain volume).

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31
Q

CV and Renal symptoms of hypernatremia:

A
  • Hypovolemia
    _________
  • Polyuria, Oliguria
  • Renal insufficiency
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32
Q

Characteristics of hypernatremia in conjunction with normal total body sodium content: (4)

A
  • Most common cause is diabetes insipidus
  • Marked impairment in renal “concentreating -ability”
  • Decreased ADH secretion
    or
  • Failure of the renal tubules to respond normally to circulating ADH (polyuria).
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33
Q

Characteristics of hypernatremia in conjunction with low total body sodium content:

A
  • Patients has lost sodium and water
  • Water loss is greater than sodium loss
  • Losses can be renal (osmotic diuresis) or extrarenal (diarrhea or sweat).
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34
Q

Hypernatremia in conjuction with increased total body sodium content is most commonly caused by:

A
  • The administration of large quantities of hypertonic NA solutions (3% NaCl or 7.5% NaHCO3).
  • Cushing’s syndrome can also cause.
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35
Q

Treatment of hypernatremia:

A
  • Water (fluid) deficits corrected over ~48 hours with hypotonic solution, such as D5W.
  • Loop diuretic, then water deficit replacement
  • Decreases in sodium concentration should not be faster than 0.5 -1 mEq/L/hour
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36
Q

Elective surgery should be postponed until sodium level is < ______ mEq/L and H2O deficits corrected.

A

150

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37
Q

Hyponatremia is associated with:

A
  • Alcoholism
  • Liver failure
  • Severe burns
  • Malignant neoplasms
  • Hemodialysis
  • Sepsis
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38
Q

Hyponatremia is serum Na < ______ mEq/L and neurologic symptoms occur with a level below < ________mEq/L

A

135;

120

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39
Q

Hyponatremia clinical manifestations include:

A

Neurological:
- Seizures → Coma
- Cerebral edema
- Agitation, Confusion
- Headache
Gastrointestinal:
- N & V → anorexia
Musculoskeletal:
- Cramps and weakness

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40
Q

Diagnosis of hyponatremia is based on the assessment of

A

serum osmolality and volume status

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41
Q

________ is the most common electrolyte disorder and may be classified as:

A

Hyponatremia;

Hyponatremia - isotonic or pseudo
Hyponatremia – Hypertonic
Hyponatremia – Hypotonic

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42
Q

What is osmolality?

A

number of osmoles of solute per kilogram of water (e.g., weight)

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43
Q

what is osmolarity?

A

number of osmoles of solute per liter of water (e.g. fluid)

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44
Q

What is tonicity?

A

Effect a solution has on cell volume
- Hypertonic
- Hypotonic
- Isotonic

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45
Q

Characteristics of Isotonic or Pseudo-Hyponatremia (3)

A
  1. Normal Osmolality (280 – 295 mOsm/kg)
  2. Total normal sodium
    - Reflects fluid shifts from ICF –> ECF
    - Decreased plasma sodium levels
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46
Q

Isotonic or Pseudo-Hyponatremia may occur with what conditions or medications?

A

Hypothyroidism
Glucocorticoid insufficiency
SIADH
______

Amitriptyline
Cyclophosphamides
Tegretol
Morphine

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47
Q

Pseudohyponatremia

A
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48
Q

SIADH characteristics

A
  • clinical euvolemia
  • Inappropriately elevated urine osmolality (>300mOsm - 400)
  • in the face of low serum osmolality (<280 mOsm/kg)
  • Urine NA> 20- 30 mEq/L
  • Normal renal function
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49
Q

Causes of SIADH (5)

A
  • Pulmonary carcinoma
  • Brain metastases, other malignancies
  • CNS disorders
  • Idiopathic forms – frequent occur in older patients
  • Medications
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50
Q

Medications that cause SIADH (6):

A
  • Vasopressin
  • HCTZ
  • Antidepressants agents (SSRIs)
  • NSAIDS
  • Vincristine
  • Oxytocin
  • Neuroleptic agents
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51
Q

What is the acute treatment of SIADH for someone with severe hyponatremia ( <110 mEq/liter) ?

A
  • IV lasix
  • NS with 20 - 40 mEq/L KCL
  • Rarely will 3% saline will be utilized
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52
Q

Chronic treatment of SIADH:

A
  • Water restriction to ~1000ml per day
  • Declomycin
  • Vasopressin receptor antagonist: conivaptan, vaprisol, tolvaptan, samsca, lithium.
  • Urea
  • PO salt tablets
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53
Q

charactristics of Hyponatremia- Hypertonic:

A

High osmolality (>295 mOsm /kg)
Hypervolemia that may be caused by:
- Mannitol Excess
- Glycerol Treatment
- CHF
-Cirrhosis

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54
Q

Treatment to Hyponatremia- Hypertonic

A

Salt restriction
or
Water restriction
or
Diuretics

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55
Q

Characteristics/Causes of hyponatremia - hypotonic:

A

Low serum osmolality (<280 mOsm/kg)
Hypovolemia may be due to:
- GI losses
- Renal losses plus excess water ingestion
- Diuretics
- Ketonuria
- 3rd spacing
- Adrenal insufficiency
- N&V

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56
Q

Excessively rapid correction of hyponatremia has been associated with?

A

Demyelinating lesions in the pons ( pontine myelinolysis ) that can lead to permanent neurological damage!

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57
Q

S/S of pontine myelinolysis:

A
  • Balance problems
  • Confusion, delirium, ∆s in consciousness
  • Difficulty swallowing, dysphagia
  • Hallucinations, speech changes, poor enunciation
  • Tremors, weakness in the face, arms, or legs, usually affecting both sides of the body.
  • Acute progressive quadriplegia
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58
Q

Considerations / correction rates of hyponatremia if patient is symptomatic?

A
  • Consider treatment with 3% NaCl
  • Initial: sodium 1-2 mEq/L/hr x 2 hours then — > 0.5 mEq /L/hr
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59
Q

Correction rates of hyponatremia if patient is asymptomatic?

A
  • Consider sodium 0.5mEq/L/hr
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60
Q

Max sodium correction rate in 24 hr:

A

10 mEq TOTAL rise

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61
Q

Max sodium correction rate in 48 hr:

A

18 mEq TOTAL rise

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62
Q

Potassium lab range:

A

(3.0 – 5.5 mEq)

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63
Q

What is hyperkalemia?

A
  • Increase in total K content
  • Altered distribution of K between intra- & extracellular sites
  • Adverse effects are secondary to acute ↑ in serum concentration.
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64
Q

Most detrimental effects of hyperkalemia occur in cardiac conduction system. What are they?

A
  • Prolonged PR interval
  • Widening QRS complex
  • Peaked T wave
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65
Q

Causes of hyperkalemia K+> 5.5: (9)

A
  • Acidosis
  • Hemolysis
  • Tissue necrosis
  • Renal insufficiency and failure
  • K+ sparing diuretics
  • Hypoaldosteronism
  • Suppliementation
  • Salt substitutes
  • Rapid infusion - banked blood
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66
Q

Clinical manifestation of hyperkalemia? (7)

A
  • Tall, peaked T waves
  • Wide QRS
  • Ventricular arrhythmias
  • Muscle weakness
  • Confusion
  • Paresthesia
  • Cardiac arrest
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67
Q

Treatment of Hyperkalemia (6)

A
  • NaHCO3 (~50 mEq) promotes cellular uptake of K+ within 15 minutes (Note: cannot be used alone)
  • Beta agonists
  • Glucose 30-50 g + Insulin 10 units (can take up to 1 hour)
  • Hyperventilation
  • Hemodialysis
  • Calcium
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68
Q

Why is calcium given for hyperkalemia? and how much?

A
  • Administration of Ca++ will protect ♥ from hyperkalemia (1 amp = 1 gm Calcium Chloride)
  • Ca++ will decrease excitability and depress the membrane threshold potential.
  • Ca++ 500-1000 mg IV partially antagonizes cardiac effects; effects rapid but short-lived

Careful: Ca++ potentiates digoxin toxicity

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69
Q

What is hypokalemia?

A

Decreased total body potassium
Altered distribution

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70
Q

Changes in EKG with hypokalemia:

A

Flattened T waves and presence of U wave

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71
Q

__________ change in arterial ph can change plasma K+ concentration by ___________ meq ( _________ proportional relationship)

A

0.1;
0.6
indirectly

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72
Q

Causes of hypokalemia:

A
  • Thiazide, loop diuretics
  • Aminoglycosides
  • Adrenal steroids
  • Chronic laxative abuse
  • Vomiting
  • Gastric outlet obstruction
  • Gastric suction
  • Severe diarrhea
  • Poor dietary intake
  • Therapeutic alkalinization of the urine
  • Hyperaldosteronism
  • Cushing syndrome
  • Magnesium deficiency associated with alcoholism
  • Renal tubular acidosis
  • Salt-losing nephropathies
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73
Q

Treatment of Hypokalemia:

A
  • Oral replacement with potassium chloride : 60-80 mEq/day is safest .
  • Peripheral IV potassium should not exceed >8 mEq/hr so as not to irritate veins.
  • Central IV K + can be infused at 10-20 mEq/hr
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74
Q

Remember that NMBD dose should be decreased by _____ - ___% since hypokalemia causes increased sensitivity to NMBDs.

A

25-50

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75
Q

Normal calcium range:

A

8.5 - 10.5 mg/dl

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76
Q

Hypocalcemia causes: (6)

A
  • Hypoparathyroid
  • Pancreatitis
  • Renal failure
  • Decreased serum albumin levels
  • Bone cancer
  • Insufficient vitamin D
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77
Q

Why should you avoid hyperventilation with hypocalcemia?

A

Alkalosis should be avoided to prevent further decreases in Ca2+.

0.1 < in arterial ph can decrease ionized Ca concentration by 0.16 mg/dL

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78
Q

Heart effects with mild and severe hypocalcemia:

A

Mild: broad based tall peaking T waves

Severe:
- extremely wide QRS,
- low R wave,
- disappearance of p waves,
- tall peaking T waves

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79
Q

Signs of hypocalcemia: (7)

A
  • Skeletal muscle spasm including laryngospasm/bronchospasm
  • Decreased myocardial contractility
  • Hypotension
  • HF
  • Tetany
  • Trousseau’s sign
  • Chvostek’s sign
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80
Q

Trousseau’s Sign is seen with:

A

Hypocalcemia

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81
Q

Chvostek’s Sign is seen with:

A

Hypocalcemia

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82
Q

Symptomatic hypocalcemia is a true medical emergency! What is the treatment ?

A
  1. Rule of 10’s:
    - Infusion of 10ml of 10% calcium gluconate over 10 minutes (or calcium chloride).
  2. Followed by a continuous infusion of elemental calcium 0.3 - 2mg/kg/hr
  3. Follow serial ionized Ca+ levels
  4. check magnesium: consider giving magnesium 1G
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83
Q

Hypercalcemia Values:

A

Serum Ca+ > 10.5;

Ionized >5.6 mg/dL

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84
Q

Hypercalcemia causes:

A
  • Hyperparathyroidism
  • Malignancy - bone
  • Renal Failure
  • Thiazide Diuretics
  • Excess Ca+ supplements
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85
Q

Hypercalcemia clinical signs: 7

A

HTN
Dysrhythmias → Congenital Heart Block (CHB)
Shortened QT
Sedation
Polyuria
Anorexia
Pancreatitis

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86
Q

Treatment of Hypercalcemia

A
  • Rehydration with NS followed by brisk diuresis (200 - 300 ml/hr) with loop diuretic to accelerate calcium excretion.
  • Follow serial ionized calcium levels
  • Avoid acidosis, since it may further elevate calcium levels
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87
Q

Normal magnesium range

A

1.7 – 2.2

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88
Q

What causes hypomagnesemia < 1.7

A
  • Alcoholism
  • Chronic diarrhea, polyuria, sweating
  • Hyperaldosteronism
  • Malnutrition
  • Malabsorption syndromes, such as celiac disease and IBS.
  • Medications:
    • Diuretics
    • Aminoglycoside
    • Antibiotics
    • Chemotherapy
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89
Q

Symptoms of hypomagnesemia: 7

A
  • Abnormal eye movements ( nystagmus )
  • Seizure
  • Fatigue
  • Muscle spasms or cramps
  • Muscle weakness
  • Numbness
  • Dysrhythmias
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90
Q

Treatment of hypomagnesemia:

A
  • IV magnesium sulfate 1- 2 grams given slowly over 60 minutes.
  • Monitor labs for concomitant hypokalemia or hypocalcemia.
  • Monitor EKG for arrhythmias ( similar to hypokalemia).
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91
Q

S/S of hypermagnesemia >2.2: (8)

A
  • Flushing
  • N/V
  • Drowsiness
  • Weakness
  • Loss of patellar reflex, decreased DTRs
  • Respiratory depression
  • Cardiac arrest
  • Coma
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92
Q

Treatment of Hypermagnesemia

A
  • Stop all sources of Mg.
  • IV calcium 1 gram - can temporarily antagonize most effects.
  • Loop diuretic with rehydration of D1/2 NS enhances magnesium excretion.
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93
Q

What should you monitor with hypermagnesemia?

A

Monitor for vasodilation and negative inotropic effects

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94
Q

With hypermagnesemia you should decrease the dosages of NDMB by:

A

25- 50%

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95
Q

PeriOperative Fluid Therapy goals:

A
  • Replacement of pre-existing fluid deficits
  • Replace normal losses (maintenance requirements)
  • Replacement NPO deficit
  • Replacement of surgical wound losses (e.g., “third space losses” and blood loss)
96
Q

acute chemical pneumonitis caused by the aspiration of stomach contents in patients under general anesthesia.

A

Mendelson syndrome

97
Q

Why are NPO guidelines enforced?

A

due to risk of pulmonary aspiration

98
Q

Prolonged fasting can contribute to:

A
  • Hypovolemia
  • Hypoglycemia
  • Anxiety
99
Q

Traditional NPO Guidelines for adults:

A

No solid food for 8 hours pre-op;

most medications can be continued with a small sip of water (excluding some cardiac and diabetic meds)

100
Q

Longer fasting times should be enforced in those patients at an increased risk for aspiration:

A
  • Renal failure
  • Increased ICP
  • Decreased LOC
  • Cerebral palsy
  • Anorexia
  • Esophageal disorders
  • Diabetes
  • Delayed gastric emptying
  • Difficulty swallowing
101
Q

Traditional NPO Guidelines for pediatrics:

A

Up to 2 hours pre-op: clear liquids.
Up to 4 hours pre-op: Human breast milk.
At least 6 hours pre-op: Infant formula, nonhuman milk, light meal:
Up to 8 hours pre-op: “full” meal, carbonated drinks

No chewing gum or mints after midnight

102
Q

refers to patient-centered, evidence-based, multidisciplinary team developed pathways for a surgical specialty and facility culture to reduce the patient’s surgical stress response, optimize their physiologic function, and facilitate recovery.

A

Enhanced Recovery after Surgery (ERAS®)

103
Q

What is the 4-2-1 Rule?

A

It calculates the hourly maintenance:

4 cc/kg/hr first 10 kg of body weight

2 cc/kg/hr second 10 kg

1 cc/kg/hr for the remaining weight kg

104
Q

NPO Deficit

A

equals the number of hours the patient is NPO x the hourly maintenance rate

105
Q

After calculating NPO deficit, how are fluids administered?

A

Administer:

  • 50% during the 1st hour.
  • 25% in the 2nd hour.

-25% in the 3rd hour.

106
Q

Typical fluid output sources:

A
  • Urine (may be measured by Foley and a urometer).
  • Respiratory tract
  • Evaporative losses
  • Losses due to surgical wound and/or bleeding
  • Insensible or “third spacing” losses
107
Q

Tissue manipulation & surgical trauma supports movement of fluid from the ECF compartment into non-functional compartments, and are called:

A

3rd space fluid losses.

108
Q

Intra-operative Fluid loss

Small Incision/minimal trauma:

Moderate Incision/moderate trauma:

Large/Incision/severe trauma:

Major vascular case/extreme trauma:

A
  • 4-6 ml/kg/hr
  • 6-8 ml/kg/hr
  • 8-10 ml/kg/hr
  • 10-12 ml/kg/hr
109
Q

Crystalloids: contain electrolytes dissolved in water or dextrose and water.
What are some examples

A
  • 0.9% Normal saline: “isotonic”; 9 gm of NaCl per 1 liter of fluid.
  • Lactated Ringer’s.
110
Q

Colloids are ______ or _______ molecules, somewhat impermeable to vascular membrane.

A

natural or synthetic.

111
Q

What do colloids do?

A

They determine the colloid osmotic pressure that balances distribution of water between intravascular and interstitial spaces

112
Q

Examples of colloids

A
  • 5% albumin
  • 6% hydroxyethyl starch (Hespan, Hextend)
113
Q

used for most neurological or renal patients; or with blood administration.

What fluid?

A

NaCl 0.9%

114
Q

Plasmalyte contains:

A

Magnesium
Acetate
Gluconate

115
Q

Lactated ringers contains:

A

Sodium
Potassium
Chloride
Calcium
Dextrose
Lactate

116
Q

D5W – contains _____ gm dextrose per liter

A

5

117
Q

used for volume expansion; each has limitations.

What fluids?

A

Dexran/Hespan/Hetastarch

118
Q

what are Balance Salt Solutions (BSS) ?

A

They are fluids that have an electrolyte concentration similar to ECF.

119
Q

Characteristics of Normal Saline Solution?

what happens if you give too much?

A
  • Contains more chloride than ECF.
  • Too much can cause hyperchloremic-induced metabolic acidosis
120
Q

Normal Saline Solution is good choice for which patients?

A

Good choice for renal (diabetic) and neurosurgical patients.

121
Q

When are Dextrose Containing Solutions used?

A
  • In prevention of hypoglycemia in neonates and pediatric patients.
  • In conjunction with insulin infusions.
122
Q

Hyperglycemia is associated with increased risk for:

A

ischemic neurologic injury.

123
Q

Advantages of Crystalloids (5):

A
  • Inexpensive
  • Promotes urinary flow
  • Restores third - space loss.
  • Used for extracellular fluid repletion
  • Used for initial resuscitation.
124
Q

Disadvantages of crystalloids (5):

A
  • Dilutes plasma proteins
  • Causes reduction in capillary osmotic pressure.
  • Causes peripheral edema
  • Has transient effect
  • Potential for pulmonary edema.
125
Q

Colloid advantages (6):

A
  • Causes sustained increase in plasma volume
  • Requires smaller volumes for resuscitation.
  • Causes less peripheral edema.
  • Tends to remain intravascular.
  • causes more rapid resuscitation
  • Useful in conditions of altered vascular permeability.
126
Q

Colloid disadvantages (7):

A
  • Expensive
  • Can cause coagulopathy: (Dextran > hetastarch > Hextend).
  • Can cause anaphylactic reaction (dextran)
  • Decreases Ca2+ (albumin).
  • Can cause renal failure (dextran).
  • Can cause osmotic diuresis
  • Can cause impaired immune response (albumin).
127
Q

When is hypertonic saline beneficial?

A

in fluid resuscitation from shock/trauma and major surgical losses.

128
Q

Hypertonic Saline is commercially available in:

A

2% or 3 %.

129
Q

Hypertonic Saline indicated for? (6)

A
  • Major surgical procedures: aortic, radical cancer surgeries
  • Shock
  • Slow correction of hyponatremia.
  • TURP syndrome
  • Reduce perioperative edema.
  • Reduce ICP
130
Q

Hypertonic Saline effects:

A
  • Hypernatremia
  • Hyperosmolality
  • Hyperchloremia
  • Increased cardiac output
  • Increased solute to kidneys
  • Improved microcirculatory blood flow
  • Decreased potassium: Hypokalemia
  • Decreased SVR/PVR;
  • Decreased ICP
131
Q

What is albumin?

A

Pooled plasma in saline

132
Q

Albumin is:

  1. ________ soluble
    .
  2. _________ protein.
  3. Accounts for ____- ___% of the colloid osmotic pressure of plasma.

– _____ % - rapid intravascular volume expansion.

— ______% hypoalbuminemia

A
  1. Highly
  2. Globular
  3. 70 - 80%
    – 5%
    – 25%
133
Q

Albumin has an intravascular half-life of ________ hours.

A

> 24 hours

134
Q

Crystalloids or Colloids?

Most perioperative volume deficits are _______.

_________ solutions eventually equilibrate between plasma & interstitial space therefore more is needed to maintain intravascular volume

A

ECF

Crystalloid

135
Q

T/F albumin and plasma derivatives:

  1. you need ABO compatibility
  2. They have no coagulation factors
  3. safe for critically ill patients
A
  1. False… not needed.
  2. True.
  3. False: associated with increased mortality in critically ill patients
136
Q

How is the possibility of transmission of blood- borne disease eliminated for albumin?

A

it is heat treated at 60 degrees C for 10 hours

137
Q

Dextran is composed of ________ ________ molecules.

Intravascular half-life _____ hours.

A

polymerized glucose;;

6

138
Q

Dextran’s potential complications include: (7)

A
  • Anaphylaxis,
  • Volume overload
  • Pulmonary edema,
  • Cerebral edema
  • Platelet dysfunction
  • Acute renal failure
  • PT. w/ hx of diabetes mellitus = renal insufficiency at ↑ risk.
139
Q

non-ionic starch derivatives (2)

A

Hetastarch, Voluven

140
Q

Hextend (6% in HES in ____)

A

LR

141
Q

Hespan (6% HES in _____)

A

NS

142
Q

Hextend & Hespan are
________ polymer and contain:

A

Synthetic
___________

Sodium
Potassium
Calcium
Magnesium

143
Q

Hextend & Hespan intravascular half-life :

A

> 24 hours

144
Q

Synthetic plasma expanders

Anaphylactoid reactions have been reported with both ______ and ________, but much rarer with _________.

A

dextran;

hetastarch

hetastarch

145
Q

Ultimately indication for blood transfusion:

A

to maintain oxygen-carrying capacity to the tissues.

146
Q

When blood loss occurs replace with _____ or _______ to maintain intravascular volume until risk of anemia outweighs the risk of the blood transfusion.

A

crystalloids or colloids

147
Q

Healthy patient without cardiac disease: can usually tolerate decrease in Hgb to __________ or a Hct ___________.

A

7 - 8 g/dL

21-24%

148
Q

what happens when hemoglobin is <7 g/dL?

A
  • the resting cardiac output increases to maintain normal O2 delivery —–> myocardial strain
  • Morbidity & mortality rates start to be affected.
149
Q

Generally, a hemoglobin of __________ is limit for elderly and those with existing cardiac/pulmonary disease.

A

9 - 10 g/dL

150
Q

Evaluating Blood Loss:

Soaked 4 x 4 contains:

Soaked “lap sponge” contains:

A

~10 ml of blood

~100 ml of blood

151
Q

Fluid replacement
to blood loss ratios:

Crystalloids:

Colloid:

A

3:1

1:1

152
Q

To Transfuse or Not to Transfuse:

what should you keep in mind?

A
  • You must anticipate on a patient to patient basis.
  • The minimum Hgb level that will avoid organ damage due to O2 deprivation.
  • Balance between O2 delivery (DO2) and O2 consumption (VO2)
153
Q

Factors that increase O2 demand and effect O2 delivery:

A
  • Inability to increase CO
  • Shifts to the oxyhemoglobin curve
  • Inadequate oxygenation
  • Abnormal Hgb
154
Q

Assessment of Fluid Resuscitation includes:

A
  • HR,
  • BP,
  • U/O,
  • Arterial oxygenation,
  • pH
155
Q

In adults, _________ is an insensitive, nonspecific indicator of hypovolemia.

A

tachycardia

156
Q

What strongly suggest adequate fluid replacement?

A

eservation of BP and a CVP of 6 - 12 mmHg

157
Q

In procedures with large fluid losses, an arterial line is more accurate at estimating BP than indirect measures. Variations in the a-line waveform during positive pressure ventilation may indicate :

A

hypovolemia

158
Q

EBV

A

Estimated blood volume

159
Q

ABL

A

Allowable blood loss

160
Q

Estimated Blood Volume (EBV)

Premature Neonates:
Term Neonates:
Infants & Children:
Adult Males:
Adult Females:

A
  • 95 ml/kg
  • 85 ml/kg
  • 80 ml/kg
  • 75 ml/kg
  • 65 ml/kg
161
Q

Allowable Blood Loss equations:

A
162
Q

Routine typing of blood is performed to

A

identify antigens on the erythrocyte membranes (A, B, Rh)

163
Q

Antibodies (anti-A, anti-B) are formed whenever membranes lack what?

and

what are these antibodies capable of causing?

A

lack A and/or B antigens

They are capable of causing rapid intravascular destruction of erythrocytes that contain the corresponding antigens.

164
Q

Red cell membranes contain at least ______ different antigenic systems

A

300

165
Q

Chromosomal locus produces 3 alleles: _ _ _.

and each represents an enzyme that modifies a cell surface _______ , producing a different antigen.

A

A, B, and O

glycoprotein

166
Q

The Rh system is based on:

A

only the presence or absence of the most common, immunogenic allele, the D antigen.

167
Q

________ of caucasians have the D antigen.

Individuals lacking this are called _______.

A

80-85%

Rh -

168
Q

How can someone develop antibodies against the D antigen?

A

After exposure to a previous Rh-positive transfusion
or
Pregnancy (Rh-negative mother delivering an Rh-positive baby).

169
Q

ABO blood grouping …exposure.

A
170
Q

Compatibility Testing

Type Specific:
what does it do?

A
  • ABO-Rh typing only 99.8% compatible.
  • Requires 5-15 minutes
171
Q

Compatibility Testing

**Type and Screen: **

and

what is the screen portion detecting?

A
  • ABO-Rh and screen; 99.94% compatible
  • Requires 15-45 minutes

-Screen (indirect Coombs test) detects presence of antibodies in serum that are most commonly associated with non-ABO hemolytic reactions.

172
Q

Compatibility Testing

Type and cross match:
What does it do?

A
  • ABO-Rh, screen, and crossmatch;
    99.95% compatible
  • Mimics transfusion; donor cells are mixed with recipient serum
  • Confirms ABO-Rh typing (in < 5 min)
  • Detects antibodies to other blood group systems.
  • Detects antibodies in low titers or those that do not agglutinate easily
  • Takes at least 45 mins or more if patient has received prior transfusions!
173
Q

For a transfusion what compatibility test:

  1. Always want to use:
  2. In an emergency – can use:
  3. Last resort will be:
A
  1. typed & cross-matched blood.
  2. type-specific, uncross-matched blood
  3. O negative blood.
174
Q

Packed Red Blood Cells (PRBCs)contain:

A
  • RBC’s,
  • WBC’s,
  • Platelets,
  • Reduced plasma
175
Q

Packed Red Blood Cells (PRBCs)are use for:

A

Used to restore oxygen-carrying capacity and for controlled surgical blood Loss.

176
Q

Packed Red Blood Cells (PRBCs)usually contain a volume between:
and a hematocrit of :

A

250- 350 ml

70%

177
Q

What is “washed PRBCs”? And who is it generally used for?

A

complete removal of plasma.

For neonatal transfusions
or
patients with a history of severe transfusion reaction, immunocompromised patients

178
Q

1 unit PRBC increase Hgb by _____ gm/dl or Hct by ________.

A
  • 1 g/dl
  • 2- 3%
179
Q

PRBCs administration steps:

A
  • NS to decrease viscosity, increase speed of administration.
  • Utilize fluid warmer to avoid hypothermia.
  • Use 170 micronfilter to trap clots & debris.
180
Q

PRBCs tubing should contain _____ - ______ mm filter to trap clots and debris (degenerated platelets, leukocytes, fibrin).

A

170 - 230 mm

181
Q

PRBCS should be warmed to?
and why?

A
  • Warm to 37*C
  • Hypothermic effects and low levels of 2,3 DPG in stored blood cause leftward shift of oxygen Hgb dissociation curve –> tissue Hypoxia.
182
Q

Why should PRBCs be infused with NS and not glucose or LR?

A
  • Glucose solutions may cause RBC hemolysis
  • LR contains calcium and may induce clot formation.
  • NS, albumin, and FFP are all compatible with PRBC.
183
Q

Whole blood volume and Hct:

A

Volume 450 - 500 mL
40% Hct

184
Q

Whole blood is used primarily in :

A
  • hemorrhagic shock (massive blood Loss; >25% of EBV).
185
Q

Whole blood contains:

A

all factors:
RBC’s,
WBC’s,
Platelets,
Plasma - including factors V and VIII

185
Q

Whole blood contains:

A

all factors:
RBC’s,
WBC’s,
Platelets,
Plasma - including factors V and VIII

186
Q

Unit of whole blood will raise Hct ________ and Hgb ________ gm/dL

A

3-4%

1

187
Q

With whole blood:
*Platelet activity decreases to < ______% after 24° storage;

If given within ______° after collection, it delivers functional platelets*.

A

5;

6

188
Q

Cons of Whole blood:

A
  • Not economical for routine use d/t blood shortages.
  • Increased risk of allergic transfusion reaction
189
Q

In Emergency Transfusions: if the type is known, what can confirm ABO compatibility?

A

an abbreviated cross-match can be done in 5 min. (type- specific).

190
Q

universal donor

A

O Rh-negative

191
Q

In emergency transfusions:

If > _______ or more units of O Rh-negative given, screen recipient’s blood for antibodies before own type given.

A

2

Old school: must continue to use O - even after type known ( True only for Whole blood, not PRBC.)

192
Q

O+ can also be given in emergency transfusions, just not to:

A

women of childbearing age.

193
Q

If > ______ units of O- given, continue with it.
Can go back to type specific blood in ___ - ____ months (RBC last ~ 120 days)

A

10;

3-4

194
Q

Fresh Frozen Plasma contains:

A

plasma proteins & clotting factors.

No platelets

195
Q

Fresh Frozen Plasma Utilized in:

A
  • coagulation deficiencies.
  • reversal of warfarin therapy.
  • microvascular bleeding.
196
Q

1 unit of FFP will increase clotting factors by _______%

A

3%

197
Q

What could result from massive transfusion of FFP?

A

Hypernatremia

198
Q

Thrombocytopenia (Platelet count less than <___________)

A

50,000

199
Q

1 unit of Platelet concentrate increase platelet count by _______ to _________.

A

5,000 to 10,000

200
Q

Each unit of platelet contains about ______ ml of ________.

A

50ml of plasma.

presence of plasma poses a risk of transfusion reaction

201
Q

what is Cryoprecipitate?

A

Fraction of plasma that precipitates once FFP is thawed

202
Q

Cryoprecipitate has high concentrations of what two things and help to treat what?

A
  • High concentrations of Factor VIII to treat Hemophilia A.
  • High concentrations of fibrinogen to treat Hypofibrinogenemia
202
Q

Cryoprecipitate has high concentrations of what two things and help to treat what?

A
  • High concentrations of Factor VIII to treat Hemophilia A.
  • High concentrations of fibrinogen to treat Hypofibrinogenemia.
203
Q

Transfusion Reactions

Febrile Reaction facts:

A
  • Most common with a 1% incidence
  • Increase in temperature by 1 degree C
204
Q

Transfusion Reactions

Allergic Reaction facts:

A
  • 2nd most common
  • Pruritus, hives increase in temperature
205
Q

Transfusion Reactions

What is a Hemolytic Reaction? and number of occurrences? and fatal in how many?

A
  • ABO incompatibility
  • 1 in 6000 transfusions
  • Fatal in 1 in 100,000
206
Q

Common cause of hemolytic reaction in a transfusion?

A

Patient mis-identification is the common cause

207
Q

Presumptive diagnosis of hemolytic reaction is based on:

A

Free Hgb in urine & plasma

208
Q

Steps to take if a transfusion reaction is suspected: (5)

A
  1. stop transfusion
  2. treat hypotension.
  3. consider steroids.
  4. send donor blood and patient blood sample for crossmatch.
  5. Preserve renal function by maintaining brisk urine output (IVF, Lasix, Mannitol).
209
Q

After a blood transfusion reaction pt’s blood sample is sent for a crossmatch and what other tests?

A
  • Free Hgb.
  • Haptoglobin
  • Coomb’s test
  • DIC screening
210
Q

Infection complications/occurrences with a blood transfusion:

A
  • Hepatitis B (1: 220,00)
  • Hepatitis C (1:1.6 M)
  • HIV (1:1.8 M)
  • rare bacterial infections
211
Q

Besides infection, what other complications can occur from blood transfusions?

A
  • Transfusion Related Acute Lung Injury (TRALI)
  • Hyperkalemia
  • Acidosis
  • Hypothermia
212
Q

Storage temp for banked blood:

A

1 – 6 degrees C to slow glycolysis

213
Q

Biochemical changes in stored blood: (8)

A
  1. Progressive acidosis due to RBC metabolism (pyruvic and lactic acid).
  2. Increased K: 21 mEq
  3. Increased pCO2: 140 mmHg
  4. Increased lactate
  5. Decreased glucose
  6. Decreased 2,3 DPG
  7. Decreased platelets
  8. Decreased Factor V (15%) and Factor VIII (50%)
214
Q

pH of blood at collection and 21 days later:

A

pH at collection 7.1; pH at 21 days 6.9

215
Q

what is CPD (citrate-phosphate-dextrose)?

and what does each of its ingredients do?

and shelf life?

A

A banked blood preservative.

Citrate: anticoagulant that binds with ionic calcium; prevents clotting

Phosphate: acts as buffer

Dextrose: substrate used for glycolysis of RBC for energy

Shelf life: 21 days

216
Q

What is CPDA (citrate-phosphate-dextrose-adenine)?

what does it do?

and shelf life?

A

A banked blood preservative.

Includes adenine (adenosine) for incorporation into ATP and extra glucose to prolong storage;

most common

Shelf life: 35 days

Hct 70-80%

217
Q

whats a complication of MASSIVE blood transfusion? and why does it occur?

A

Citrate intoxication: from the addition of CPD as preservative for stored blood; can occur with rapid transfusion (>150ml/min).

218
Q

Citrate is mainly metabolized by ?

what happens if rate of transfusion is too fast?

A

liver;

If rate of transfusion exceeds 1 unit of blood per minute in an adult, decreased calcium may result (binds calcium and magnesium)

Due to accumulation of citrate-chelating serum calcium

Pediatric patients and those with liver disease are more likely to become intoxicated

219
Q

Symptoms of Citrate Intoxication

A
  • Hypocalcemia
  • Hypotension
  • Increased LVEDP
  • Increased CVP
  • Prolonged QT interval
  • Hypomagnesemia manifesting as tachyarrhythmias, TdP, or refractory V Fib
220
Q

Treatment of Citrate Intoxication

A
  • Calcium or magnesium
  • Citrate will be metabolized quickly in Kreb’s cycle so symptoms may abate before treatment needed
  • Supportive treatment
221
Q

Transfusion blood is routinely screened for:

A

HIV 1/2
Hepatitis B and C
- Hepatitis C (nonA/nonB): most symptomatic (90%)
HTLV1/2 (human T-cell lymphocytic virus)
Syphilis

222
Q

Request “______ Negative” blood;

it is used for immunocompromised like BMT or organ transplants, and infants.

______ is the MOST COMMONLY TRANSMITTED VIRUS in blood transfusions.

A

CMV;

CMV

223
Q

Others Diseases That Can Be Transmitted in Blood

A

exposure.

224
Q

What is TRALI?

A

Transfusion-Related Acute Lung Injury (TRALI)

is a non-cardiogenic form of pulmonary edema associated with blood product administration.

225
Q

TRALI occurs more frequently with what blood products?

A

RBCs
FFP
Platelets

226
Q

TRALI occurence and mortality rate:

A
  • 1 in 5000 units transfused
  • TRALI-mortality rate of 5 to 8%
227
Q

The clinical appearance of TRALI is similar to:

A

adult respiratory distress syndrome (ARDS)

228
Q

TRALI S/S:

A
  • Symptoms usually begin within 6 hours after the transfusion.

Often more rapidly, the patient develops:
- Dyspnea
- Cyanosis
- Chills
- Fever
- Hypotension
- Noncardiogenic pulmonary edema.

229
Q

On CXR TRALI reveals

A

bilateral infiltrates

Severe pulmonary insufficiency can develop

230
Q

TRALI treatment:

A
  • Supportive tx.
  • Transfusion stopped.
  • Oxygen and ventilatory support - with a low tidal volume strategy to prevent barotrauma.
231
Q

Dilutional Coagulopathy is seen with:

A

Massive transfusions > 1 EBV (or >10 units)

**I don’t know what they mean by 1 EBV?

232
Q

Signs of Dilutional Coagulopathy

A

Microvascular bleeding
Hematuria
Bleeding at IV sites
Clinically oozing
Increased PT/PTT
Decreased platelets

233
Q

Treatment for Dilutional Coagulopathy

A
  • Surgically control the bleeding.
  • Keep patient warm
  • Maintain perfusion and euvolemia.
  • Don’t overhydrate and further dilute patient
  • Consider FFP, platelets
  • Consider Vitamin K, DDAVP (enhances platelet adhesiveness).
234
Q

Alternatives to Traditional Blood Transfusion Therapy

A
  • Normovolemic hemodilution
  • Cell saver: 50 - 60% Hct (intraop salvage).
  • Autologous donation (pre-op).
  • Postop salvage (chest tube drainage system).
  • Oxygen-carrying substitutes (Bovine blood/ Petroleum- based therapies).
235
Q

Complication with postop salvage.

A
  • reinfused anticoagulants,
  • dilutional coagulopathy,
  • air embolism

Can’t reinfuse blood if it contains pus, malignancy, or spilled GI contents

614 General Principles Of Anesthesia (14 decks)

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