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SEE/NCE Boards CoreConcepts > Hematology, Fluid and Electrolytes - Anesthesia Review > Flashcards

Hematology, Fluid and Electrolytes - Anesthesia Review Flashcards

1
Q

The extrinsic pathway is initiated by the release of a group of proteins known as _________when tissues are damaged?

A

Tissue Factor when tissues are damaged.

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2
Q

Tissue Factor forms a complex with and

A

Factor VII, and in an enzymatic reaction requiring calcium, catalyzes the activation of Factor X.

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3
Q

Proaccelerin is the other name for factor

A

Factor V

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4
Q

Exposure of the blood to collagen can initiate the

A

intrinsic pathway.

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5
Q

Fibrinogen is another name for

A

factor I.

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6
Q

Sickle cell and hematocrit

A

Sickle cell and hematocrit results in the destruction of red blood cells which lowers the hematocrit

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7
Q

Labs that are elevated in acute DIC

A 
PT
PTT
Thromboplastin time
D-dimer
Fibrin degradation products
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8
Q

The circulating levels of what components will be increased by DDAVP administration in a patient with von Willebrand disease? 2 answers

A

Von Willebrand disease

Factor VIII

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9
Q

Medications that are considered safe for use in patients with porphyria.

A 
morphine
Nitrous oxide, 
neostigmine
fentanyl
succinylcholine, 
pancuronium
Ppropofol
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10
Q

Medications that are NOT considered safe and should all be avoided for patients with Porphyria?

A

Ketorolac
thiopental
thiamylal
etomidate, pentazocine, methohexital, and nifedipine s

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11
Q

Factor X deficiency is _______deficiency

A

Stuart-Prower

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12
Q

Aspirin and other NSAIDs on platelet

A

acetylate and inactivate platelet cyclooxygenase.

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13
Q

Aspirin inactivates cyclooxygenase for

A

the life of the platelet

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14
Q

Unlike ASA, NSAIDs inactivate them how and how long does it last?

A

Reversibly, and the effect lasts only about 24 hours.

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15
Q

In the extrinsic coagulation pathway, disruption of the endothelium leads to exposure of tissue factor which binds to

A

factor VII

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16
Q

Tissue Factor forms a complex with Factor VII, and in an enzymatic reaction requiring

A

calcium, catalyzes the activation of Factor X.

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17
Q

Porphyria is a disorder of

A

Heme

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18
Q

Why are Heme pigments essential?

A

are essential elements in the construction of hemoglobin, myoglobin, and the cytochrome

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19
Q

Many pharmacologic agents (especially those that induce the cytochrome p450 system) can precipitate a porphyric crisis such as

A 
BarbSulfaPhenyEtha
Barbiturates
Sulfonylureas
Sulfonamides
Estrogens, phenytoin, tolbutamide, and ethanol.
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20
Q

The underlying cause of organ failure due to disseminated intravascular coagulation is

A

organ ischemia due to thrombosis

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21
Q

What is the second most common cause of hospitalization in sickle cell patients and accounts for 25% of all sickle cell related deaths.

A

Acute chest syndrome

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22
Q

How is acute chest syndrome diagnosed?

A

It is diagnosed by the development of new infiltrates on chest film and may be caused by atelectasis, pulmonary microembolic episodes, or pulmonary infection.

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23
Q

Acute chest syndrome is a potential complication of sickle cell disease. When it develops, it is typically ___days following surgery and

A

2-3

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24
Q

Treatment of acute chest syndrome

A

Aggressive hydration
Transfusions to treat anemia
Oxygenation,
Antibiotics to treat pulmonary infection, and occasionally nitric oxide may be used to treat pulmonary hypertension.

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25
Q

Which form of hemoglobin is most commonly found in the normal, adult bloodstream?

A

hemoglobin A

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26
Q

Hemoglobin C is implicated in a type of

A

hemolytic anemia,

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27
Q

2 agents would be appropriate to administer in the treatment of a patient with von Willebrand disease?

A

Cryoprecipitate AND Desmopressin

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28
Q

What is the dose of desmopressin?

A

0.3mcg/kg

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29
Q

Desmopressin given for mild to moderate hemophilia will increase what factors

A

increase plasma levels of factor VIII and vWF

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30
Q

Cryoprecipitate vs FFP which one is preferred for hemophilia A?

A

Cryoprecipitate preferred because it is hard to increase the factors level with FFP alone.

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31
Q

3 treatments for hemophiliac patients : Other than desmopressin

A

Cryoprecipitate
Tranexamic acid
Epsilon aminocaproic acid.

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32
Q

Synthetic Arginine analog of Vasopressin

A

Desmopressin

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33
Q

Cryoprecipitate is made how?

A

Collected off the top of FFPs at it being thawed

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34
Q

In the intrinsic pathway, what is the component required to convert factor XII to factor XI?

A

Prekallikrein

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35
Q

Components like High Molecular Weight Kininogen required to activate

A

Factor XI.

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36
Q

A pain medication commonly given medication in the OR that you should avoid in patient with porphyria crisis is

A

Ketorolac

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37
Q

Both hemophilia A and hemophilia B exhibit a

A

prolonged PTT and a normal PT.

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38
Q

The primary function of von Willebrand factor is

A

To promote platelet aggregation and adhesion to collagen

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39
Q

Potential side effect of DDAVP administration in the treatment of von Willebrand disease?

A

Hypotension

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40
Q

What treatment regimens are effective in ameliorating the symptoms of von Willebrand disease? (select two)

A

Desmopressin and concentrated von Willebrand Factor are both effective in treating the symptoms of von Willebrand disease.

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41
Q

Factor IX-PCC is used in the treatment of

A

Hemophilia B

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42
Q

Major surgery –> how to replace vWF

A

achieve 100% vWF preoperatively and maintain trough levels of 50% until adequate wound healing

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43
Q

In treating type 1 vWD which agent is preferred?

A

Desmopressin because it produces a complete partial response in more than 90% of patients

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44
Q

In treating type 2 and type 3 vWD which agent is preferred?

A

Type 2 and type 3 require vWF concentrate administration.

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45
Q

Heparin-Induced Thrombocytopenia (HIT) Type I and Type II

A

type I non immune mediated, onset 1-4 days

type II immune mediated (immunoglobulin G) 5-14 days

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46
Q

Blood component therapy for HIT

1. Indications: active bleeding or high risk for bleeding

A
  1. Fresh frozen plasma
  2. Platelets
  3. In some cases, consider cryoprecipitate, antithrombin III
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47
Q

Most events of acute stent thrombosis occur within the

A

first 30 days after stent placement

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48
Q

Absolute contraindication to neuraxia

A

Thrombolytics

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49
Q

When is there no contraindication for heparin SC dosing for neuraxial.

A

No contraindication with twice-daily dosing and total daily dose < 10,000 units

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50
Q

Upper endoscopy and colonoscopy with or without biopsy –> Warfarin stop?

A

NO NEED for interruption in therapy

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51
Q

• Endoscopic retrograde cholangiopancreatography (ERCP) without sphincterotomy Warfarin stop ?

A

NO NEED for interruption in therapy

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52
Q

Do not need to stop warfarin for these procedures?Prosthetics
Cataracts

A

NO

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53
Q

Elective noncardiac surgery should be delayed______after bare metal stent and _______after DES

A

30 days after bare metal stent (BMS) implantation and optimally 6 months after drug eluting stent (DES) implantation

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54
Q

Discontinue ticlopidine _____days prior to neuraxial

A

14 days

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55
Q

Discontinue clopidogrel ____Days prior to neuraxial

A

7 days

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56
Q

Discontinue GP IIB/IIIa inhibitors _______prior to neuraxial.

A

8–48 hours in advance

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57
Q

A powerful vasodilator, also interferes with platelet formation and aggregation is ______

A

prostacyclin

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58
Q

Anatomy of a platelet

A

Platelets contain ALPHA (α) granules that store proteins (e.g., vWF, fibrinogen, fibronectin, platelet factor 4, and platelet growth factor) and DENSE granules that store nonproteins HE SEAT (e.g., histamine, and epinephrine) serotonin, ADP, adenosine Triphosphate [ATP],

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59
Q

Converts to plasmin

A

Plasminogen

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60
Q

3 Vasoconstrictors of vessesl

A

Thromboxane A2
ADP
Serotonin

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61
Q

Name 2 Vasodilators of vessels

A

Nitric oxide

Prostacyclin

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62
Q

Vessel Injury contracts after injury leading to

A

a tamponade, decreasing blood flow. This contraction is a result of autonomic nervous system reflexes and the expression of thromboxane- A2 and ADP. The area adjacent to the injury vasodilates and distributes blood to the surrounding organs and tissues

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63
Q

After injury to the vessel , contraction leads to what

A

Contraction is followed by three separate stages in the formation of a primary plug: adhesion, activation, and aggregation.

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64
Q

Factor not produced by the liver

A

III

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65
Q

What is the substance synthesized vascular wall and extravascular cell membranes and is released from traumatized cells?

A

vonWillebrand

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66
Q

Bleeding time Normal

A

3-7 minutes

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67
Q

Normal ACT

A

80-150

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68
Q

Normal PT

A

12-14 sec

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69
Q

Normal PTT`

A

25-33

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70
Q

Extrinsic (Warfarin vs Heparin)

A

Warfarin

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71
Q

Intrinsic (Warfarin vs Heparin)

A

Heparin

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72
Q

A normal platelet count is

A

150,000 to 300,000/mm3.2

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73
Q

Adhesion is associated with which platelet releasing substance?

A

Vonwillebrand

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74
Q

Platelet Activation and aggregation are associated with which 2 substances?

A

ADP and thromboxane A2

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75
Q

When are PRBCs transfused? are

A

transfused to improve tissue oxygenation

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76
Q

The major reasons for transfusion therapy in the operating room are to

A

replace volume and coagulation factors and improve oxygen-carrying capacity.

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77
Q

The recommended dose for platelet replacement is

A

one plateletpheresis pack per each 10 kg of patient weight

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78
Q

Protamine sulfate dosing

A

1 mg neutralizes 100 units of heparin

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79
Q

1 unit of platelet is ______ml

A

250 mL

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80
Q

1 unit of platelet increases the platelet count by how much?

A

30,000–60,000/mm3

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81
Q

FFP unit = _____ml

A

200-250 ml

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82
Q

Hypofibrinogenemia, massive hemorrhage –> what is used

A

Cryoprecipitate.

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83
Q

With the patient with Hemophilia OR massive hemorrhage

A

Factor VII

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84
Q

1 unit single- donor apheresis platelets comes from how many platelet concentrates?

A

Four to five platelet concentrates,

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85
Q

Laboratory analysis will reveal the need for FFP by a

A

PT and aPTT prolonged more than 1.5 times normal.

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86
Q

Cryoprecipitate is then refrozen and thawed on use. It is rich in which 4 factors?

A

fibrinogen
Factors VIII
Factor XIII
Fibronectin

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87
Q

The recommended dose of factor VII for hemophilia is

A

90 to 120 mcg/kg

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88
Q

Cryoprecipitate Infusion Guidelines

A

1) When a test of fibrinogen activity indicates a fibrinolysis
(2) When the fibrinogen concentration is less than 80 to 100 mg/dL IN THE PRESENCE OF EXTENSIVE BLEEDING
(3) As an adjunct in massively transfused patients when fibrinogen concentrations cannot be measure in a timely fashion;
(4) For patients with congenital fibrinogen deficiencies.

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89
Q

Transfusion of cryoprecipitate is rarely indi- cated if fibrinogen concentration is

A

greater than 150 mg/dL in non- pregnant patients.

90
Q

A sickle cell crisis may be triggered by which factors?

A

hypoxemia, hypothermia, infection, dehydration, venous stasis, and acidosis.

91
Q

P2Y12 ADP Receptor Inhibitors: name 3

A

ticlopidine, clopidogrel, prasugrel

92
Q

Platelet Glycoprotein IIb/IIIa Receptor Blockers: Name 3

A

abciximab, tirofiban, eptifibatide

93
Q

Heparin half life

A

1.5 hours

94
Q

Warfarin half life

A

2-4 days

95
Q

Abciximab half life

A

30 minutes

96
Q

ASA half life

A

20 minutes

97
Q

NSAIDs half life

A

2-10 hours

98
Q

It is the COX-1 receptor inhibition that is responsible for the gastric irritation caused by

A

NSAIDs

99
Q

COX-1 receptor inhibition by NSAIDS is responsible for the

A

Gastric irritation

Decrease in renal blood flow, and platelet inhibition associated with nonselective NSAIDs.

100
Q

The removal of multiple units of blood from the patient right before surgery and replacement of the removed blood volume with crystalloid is referred to as

A

Acute normovolemic hemodilution

101
Q

Preoperative autologous donation is most effective when it is

A

combined with erythropoietin therapy

102
Q

Which of the following are disadvantages to storing blood? (select two)

A

Adenosine triphosphate levels decrease in stored blood

. 2, 3 DPG levels decrease in stored blood

103
Q

Which of the following are disadvantages to storing blood? (select two)

A

Adenosine triphosphate levels decrease in stored blood

2, 3 DPG and ATP levels decrease in stored blood

104
Q

The potassium present in the plasma of PRBCs stored for __days can reach as high as ____-mEq/L

A

packed red blood cells stored for 21 days can reach levels as high as 35 mEq/L.

105
Q

COX-1 receptors where in the body?

A

distributed throughout the body

106
Q

Which COX inhibition results in inhibition of thromboxane A2?

A

COX-1 receptor. By doing so, it disrupts thromboxane A2’s ability to promote platelet aggregation.

107
Q

COX-2 receptors are present in the

A

kidneys and central nervous system and can be synthesized in response to inflammatory processes.

108
Q

What are the effects of COX-2 receptor inhibition?

A

reduce prostacyclin release from the vascular epithelium and can result in increased platelet aggregation.

109
Q

How does The ability of coagulation factors to function correctly change with temperature? What Rapid transfusions of cold blood products can increase the likelihood of

A

decreases 10% with every 1 degree Celsius drop in body temperature; further bleeding

110
Q

Which infectious disease has the highest risk of transmission via blood transfusion?

A

CMV

111
Q

Acute hemolytic transfusion reaction is an _____ mediated reaction.

A

IgM

112
Q

Phosphodiesterase inhibitors increase the level of cyclic AMP which is an

A

inhibitor of platelet aggregation.

113
Q

What sign is consistent with an acute hemolytic transfusion reaction?

A

Hematuria

114
Q

Transfusion-Associated Cardiovascular Overload (TACO) refers to the development of______due to __________. Is it immune related? is due to permeability of pulmonary capillary membrane? What is it responsive to?

A

pulmonary edema due to blood product administration. It is not immune-related or due to an alteration in the permeability of pulmonary capillary membranes and is responsive to diuretics and reduction of afterload.

115
Q

During preoperative assessment, a patient reveals a prolonged PT due to vitamin K deficiency. How long does it take for intravenous vitamin K to improve the PT?

A

6-8 hours

116
Q

Vitamin K oral administration exhibits the highest bioavailability, it can take up to ___hours to see effects.

A

24 hours to exhibit significant clinical effects.

117
Q

What is the most bioavailable parenteral preparation of calcium ?

A

Calcium chloride

118
Q

Why is calcium chloride not used to treat hypocalcemia routinely?

A

It can cause significant venous irritation and tissue necrosis as compared to calcium gluconate. If a central line is present, then administration via the central route can decrease the incidence of complications

119
Q

How do you treat hypocalcemia?

A

One regimen is administration of 10 mL of 10% calcium GLUCONATE (93 mg of elemental calcium) over 10 minutes, followed by an infusion of 0.3 to 2 mg/kg per hr of elemental calcium.

120
Q

In the intraoperative period, what are the most likely causes of hypocalcemia?

A

Hyperventilation

Massive rapid transfusion.

121
Q

How does hyperventilation lead to hypocalcemia?

A

Hyperventilation leads to an increased pH, which facilitates increased protein-binding of calcium, thus decreasing serum ionized calcium (remember, free ions only can have an effect)

122
Q

For patients who rapidly develop hypercalcemia, which results in life threatening dysrhythmias, What is the treatment that can rapidly lower serum calcium?

A

hemodialysis is an acute treatment to rapidly lower serum calcium.

123
Q

1st, 2nd and 3rd way to treat hypercalcemia?

A
  1. Volume expansion with NS which increases renal excretion of calcium
  2. Addition of LOOP diuretics to further enhances renal excretion
  3. Biphosphonates, CALCITONIN and phosphate salts
124
Q

Normal magnesium plasma concentrations range from

A

1.5 to 3.0 mEq/L.

125
Q

Severe hypomagnesemia can be treated with

A

IV administration of 1 to 2 g of magnesium sulfate over 5 minutes while the ECG is monitored, followed by administration of 1 to 2 g/hr.

126
Q

ECG changes seen with hypomagnesemia include:

QT

A

flat T-waves, presence of U-waves, prolonged QT interval, widened QRS complexes, and atrial and ventricular arrhythmias

127
Q

Low magnesium and BP

A

Hypotension

128
Q

Magnesium and effects on NMBAs.

A

potentiates the action of nondepolarizing neuromuscular relaxants and their use should be carefully monitored in patients with hypermagnesemia

129
Q

The majority of phosphate is located where in the body ?

A

in bone (85%)

130
Q

When magnesium levels are 10–15 (mg/dL) what symptoms will you see?

A

Heart block

131
Q

When magnesium levels are 10 what symptoms will you see ?

A

Respiratory paralysis, coma

132
Q

At what magnesium levels would you see Hypotension? what about loss of Deep Tendon reflexes?

A 
4–5 = Decreased deep tendon reflexes
5–7 = Hypotension
133
Q

The concentration of phosphate in plasma is inversely proportional that of which electrolyte?

A

Calcium

134
Q

Hyperphosphatemia is defined as a serum phosphate level greater than

A

4.7 mg/dL.

135
Q

The majority of phosphate exists within the ICV or ECV?

A

ECV.

136
Q

Leading cause of Hyperphosphatemia?

A

Cellular destruction (e.g., metastatic disease) is a leading cause

137
Q

Hypophosphatemia is defined as a serum phosphate concentration of less than.

A

2.0 mg/dL

138
Q

The most likely causes of hypophosphatemia are

A

increased renal excretion and intestinal malabsorption.

139
Q

The consequence of decreased ATP includes

A

hypoxia, heart block, bradycardia, and asystole.

140
Q

2 main causes of Hyperphosphatemia you need to know

A

Intestinal malabsorption related to vitamin D deficiency Magnesium/aluminum containing antacids

141
Q

Mechanism Action of calcium chloride in the treatment of hyperkalemia? What is the dose? (think rule of 10)

A

Membrane Stabilization

Dose is 10 mL of 10% calcium chloride of 10 minutes

142
Q

Mechanism Action of calcium GLUCONATE in the treatment of hyperkalemia? What is the dose? (think rule of 10 -5)

A

Membrane Stabilization

Dose is 10 mL of 10% calcium chloride of 3-5 minutes

143
Q

Mechanism Action of SODIUM BICARBONATE in the treatment of hyperkalemia? What is the dose?

A

Shifts potassium intracellularly

50-100 mEq over 10-20 minutes

144
Q

Medications indicated for a HYPERKALEMIC patient showing LOSS of “p waves” and widening of the QRS?

A

IMMEDIATE effective therapy indicated
Calcium Chloride/Calcium gluconate
Sodium bicarbonate

145
Q

Medications indicated with a HYPERKALEMIC patient showing Peaked “T waves” ?

A

Glucose infusion of 50ml D50 and 10 units of REGULAR insulin

Immediate hemodialysis

146
Q

Action of Glucose and insulin?

A

Shifts potassium intracellularly

147
Q

BIOCHEMICAL evidence of hyperkalemia with NO ECG changes , what is indicated? Effective therapy needed within hours

A
  1. Potassium-binding resins in the gastrointestinal (GI) tract (GI excretion)
  2. Promotion of renal potassium excretion: diuretic—Furosemide 40 mg IV (Renal excretion)
148
Q

ONSET of Glucose and insulin in the treatment of hyperkalemia?

A

30 min

149
Q

Onset of Potassium binding resins such as kayexalate

A

1-2 hour

150
Q

ONSET of calcium chloride and calcium gluconate in treatment of hyperkalemia?

A

1-3 min

151
Q

Hypercalcemia and ________PTH

A

Decrease

152
Q

Hypocalcemia and ________PTH

A

Increase

153
Q

With hypercalcemia, There is a decrease in PTH leading to ________Renal activation of vitamin D

A

Decrease

154
Q

With HYPOcalcemia, There is a decrease in PTH leading to ________Renal activation of vitamin D

A

Increase

155
Q 
Hypercalcemia --> ↓ PTH --> ↓ Renal activation of vitamin D which in turns lead to what effects on 
intestinal absorption of calcium
renal absorption of calcium
excretion of phosphate
Calcium resorption from bone
A

↓ Intestinal absorption of calcium
↓ Renal reabsorption of calcium
↓ excretion of phosphate
↓ Calcium resorption from bone

156
Q

By decreasing angiotensin, ACE inhibitors/ARBs can cause what electrolyte abnormality?

A

hyponatremia and hyperkalemia.

157
Q

Ionized calcium accounts for _____% of the calcium in the ECV and is the ___________. The remainder of circulating calcium is bound to either ______, or plasma proteins, primarily _________.

A

50% of the calcium in the ECV and is the physiologically active portion of circulating calcium. The remainder of the circulating calcium is bound either to anions (10%) or plasma proteins, primarily albumin (40%).

158
Q

ECG signs of P wave flattening or disappearance, PR prolongation is associated with what levels of Hyperkalemia?

A

6.5 - 7.5 mEq/L

159
Q

ECG changes: PEAKED T waves are associated with what potassium level?

A

5.5 - 6.5 mEq/L

160
Q

At what potassium levels would you see “QRS complex degrades to sine wave pattern, ventricular fibrillation and cardiac arrest”

A

> 8.5 mEq/L

161
Q

For HYPERKALEMIA treatment: The treatment strategy accomplishes three physiologic events:

A

(1) stabilization of cardiac membrane
(2) driving K from ECV to ICV
(3) removal of K from the body

162
Q

What ECG changes occur when the potassium level is > 7.0 - 8.0?

A

QRS prolongation

163
Q

Hypocalcemia and QTc

A

QT prolongation primarily by prolonging ST segment

164
Q

Intracellular K LEVEL range

A

150–160 mEq/L)

165
Q

Extracellular K range

A

3.5–5.0 mEq/L

166
Q

Sodium level : 135-130 mEq/L signs and symptoms

A

No signs/symptoms, mild neurologic signs/symptoms possible

167
Q

Sodium level : 129-125 mEq/L signs and symptoms

A

Nausea and malaise

168
Q

Sodium level at which you’ll see Headache Lethargy

Altered LOC

A

124-115 mEq/L

169
Q

Sodium level at which you would see Seizures, coma, respiratory arrest, cerebral herniation

A

<115 mEq/L

170
Q

It has been suggested that serum NA concentrations should be increased by no more than _______Why?

A

1 to 2 mEq/L per hr ; reduce risk of myelinolysis

171
Q

To treat hyponatremia you can give?

A

3% saline at a rate of 1-2 mg/kg/hr

172
Q

Confusion, restlessness, agitation, headache seen with which levels of serum osmolality? > 430
Hyperreflexia, muscle twitching/spasm
Coma, seizures, death

A

350–375 mOsm/kg

173
Q

Ataxia, tremors, weakness seen with which levels of serum osmolality?

A

376–400 mOsm/kg

174
Q

Hyperreflexia, muscle twitching/spasm

seen with which levels of serum osmolality?

A

401–430 mOsm/kg

175
Q

Coma, seizures, death seen with which levels of serum osmolality?

A

> 430 mOsm/kg

176
Q

What is the most common electrolyte abnormality in hospitalized patients?

A

Hyponatremia

177
Q

Strove Volume Variation (SVV) what % predicts preload responsiveness?

A

> 13%

178
Q

Normal SvO2

A

60-80%

179
Q

What is the normal serum osmolality?

A

280 - 285 mOsm

180
Q

If your serum osmolality is low, you should evaluate which volume?

A

Extracellular fluid volume

181
Q

When would you see isotonic hyponatremia (aka pseudhyponatremia ) when consider low sodium due to lab artifact and hence not treat?

A

When hyponatremia occurs with a NORMAL serum osmolarity (280-285 mOsm).

182
Q

If your sodium osmolality is LOW it means that the level is less than

A

280 mOsm

183
Q

If you have HYPONATREMIA and SODIUM OSMOLALITY is LOW What are the 3 possibilities

A

Hypovolemic HYPOTONIC HYPONATREMIA
ISOVOLEMIC HYPOTONIC HYPONATREMIA
HYPERVOLEMC HYPOTNOIC HYPONATREMIA

184
Q

In HYPOVOLEMIC HYPOTONIC HYPONATREMIA, whether your Urine Na is> 20 or low than 10 what is the treatment for both?

A

0.9% NS

185
Q

In ISOVOLEMIC HYPOTONIC HYPONATREMIA, when your URINE NA is >20 what is the treatment?

A

WATER RESTRICTION

186
Q

In ISOVOLEMIC HYPOTONIC HYPONATREMIA, when your URINE NA is <10 what is the treatment?

A

Hypertonic saline,
fluid restriction,
loop diuretic

187
Q

In HYPERVOLEMIC HYPOTONIC HYPONATREMIA, when your URINE NA is >20 or LESS than Urine NA < 10 what is the treatment for both?

A

Sodium and water restriction

+/- diuretics

188
Q

Serum Osmolality (Calculated) Formula

A

(2 × [Na]) + (BUN/2.8) + (glucose/18)

189
Q

TBW = total body water =. ____ (formula)

A

body weight × 60%

190
Q

FENA Less than 1% =

A

prerenal (hypovolemia)

191
Q

FENA Greater than 2% =

A

intrinsic renal disorder

192
Q

What is the first step in assessing hypernatremia?

A

Assess extracellular volume status.

193
Q

CPB : roller pump vs Centrifugal pump

A

A major difference between the two pumps is that the flow from the CENTRIFUGAL pump will vary with changes in preload and afterload. For this reason, a flowmeter must be attached to the arterial side of the pump.

194
Q

Roller pump vs Centrifugal pump: Which one is more economical and simple to use?

A

The roller pump is economical and simple to use.

195
Q

Disadvantage of roller pump?

A

increased destruction of blood elements.

196
Q

Which one is more common: centrifugal vs roller pump?

A

As a result, centrifugal pumps are replacing roller head pumps in contemporary practice.

197
Q

In the even of a power failure, what can be done to the Both roller pump and centrifugal pump?

A

a hand crank can be used to manually operate either pump.

198
Q

Flow from the CENTRIFUGAL pump will vary with changes in

A

preload and afterload.For this reason, a flowmeter must be attached to the arterial side of the pump.

199
Q

Traditionally, the priming volume for the CPB is

A

1 to 2 L.

200
Q

Upon instituting CPB, the prime added to the circulating blood volume causes

A

dilutional anemia, which will often result in a decrease in hematocrit (22% to 25%).

201
Q

What offsets the dilution caused by the CPB?

A

The dilution offsets some of the increase in blood viscosity that occurs when the blood cools during CPB.

202
Q

Hypocalcemia : ________QT while hypercalcemia________QT

A

Prolonged

Shortened

203
Q

Potentiation of digoxin toxicity occurs with electrolyte imbalance?

A

Hypercalcemia

204
Q

Insensitivity to digoxin occurs with electrolyte imbalance?

A

HYPOCALCEMIA

205
Q

Correction of calcium should be guided by

A

IONIZED CALCIUM levels

206
Q

What is the most common laboratory finding, and serves as an important predictor of pulmonary complications.

A

Hypoalbuminemia

207
Q

It is important to note that calcium levels must be corrected for _________concentration so that overcorrection does not occur.

A

serum albumin

208
Q

What is the major intracellular ANION? pay close attention

A

Phosphate

209
Q

The primary extracellular anion is

A

chloride.

210
Q

The primary intracellular cation is

A

potassium.

211
Q

The primary extracellular cation is

A

sodium.

212
Q

The majority of total body magnesium is found in

A

bone

213
Q

Coronary artery dominance is determined by which artery supplies the

A

posterior descending artery

214
Q

Total blood calcium levels parallel the serum

A

albumin.

215
Q

If the serum albumin decreases, the total blood calcium level will.

A

decrease as well

216
Q

What is the most common cause of hypocalemia?

A

Hypoalbuminemia

217
Q

Hormones that use the phospholipase C system include:

PAVO

A

Parathyroid hormone
Alpha receptor catecholamines
Vasopressin V1
Oxytocin

218
Q

Hormones that use the adenylyl cyclase system include

A 
Calcitonin
ACTH
Glucagon, 
Secretin
Somatostatin
vasopressin V2, parathyroid hormone, luteinizing hormone, and beta-receptor catecholamines.
219
Q

SIRS results in

A

It results in a stress response that includes increases in circulating angiotensin, cortisol, catecholamines, and vasopressin.

220
Q

Tetanic fade is a response to blocking which type of receptor?

A

Presynaptic nicotinic acetylcholine receptors

221
Q

There are three potential reasons that the CO2-ventilatory response curve would shift to the left and/or develop a steeper slope. These are the only causes of

A

true hyperventilation (where the patient’s minute ventilation increases to the point that respiratory alkalosis results). They are: arterial hypoxemia, metabolic acidosis, and central nervous system alteration.

SEE/NCE Boards CoreConcepts (49 decks)

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