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.
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.
3
Q
Proaccelerin is the other name for factor
A
Factor V
4
Q
Exposure of the blood to collagen can initiate the
A
intrinsic pathway.
5
Q
Fibrinogen is another name for
A
factor I.
6
Q
Sickle cell and hematocrit
A
Sickle cell and hematocrit results in the destruction of red blood cells which lowers the hematocrit
7
Q
Labs that are elevated in acute DIC
A
PT PTT Thromboplastin time D-dimer Fibrin degradation products
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
9
Q
Medications that are considered safe for use in patients with porphyria.
A
morphine Nitrous oxide, neostigmine fentanyl succinylcholine, pancuronium Ppropofol
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
11
Q
Factor X deficiency is _______deficiency
A
Stuart-Prower
12
Q
Aspirin and other NSAIDs on platelet
A
acetylate and inactivate platelet cyclooxygenase.
13
Q
Aspirin inactivates cyclooxygenase for
A
the life of the platelet
14
Q
Unlike ASA, NSAIDs inactivate them how and how long does it last?
A
Reversibly, and the effect lasts only about 24 hours.
15
Q
In the extrinsic coagulation pathway, disruption of the endothelium leads to exposure of tissue factor which binds to
A
factor VII
16
Q
Tissue Factor forms a complex with Factor VII, and in an enzymatic reaction requiring
A
calcium, catalyzes the activation of Factor X.
17
Q
Porphyria is a disorder of
A
Heme
18
Q
Why are Heme pigments essential?
A
are essential elements in the construction of hemoglobin, myoglobin, and the cytochrome
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.
20
Q
The underlying cause of organ failure due to disseminated intravascular coagulation is
A
organ ischemia due to thrombosis
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
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.
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
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.
25
Which form of hemoglobin is most commonly found in the normal, adult bloodstream?
hemoglobin A
26
Hemoglobin C is implicated in a type of
hemolytic anemia,
27
2 agents would be appropriate to administer in the treatment of a patient with von Willebrand disease?
Cryoprecipitate AND Desmopressin
28
What is the dose of desmopressin?
0.3mcg/kg
29
Desmopressin given for mild to moderate hemophilia will increase what factors
increase plasma levels of factor VIII and vWF
30
Cryoprecipitate vs FFP which one is preferred for hemophilia A?
Cryoprecipitate preferred because it is hard to increase the factors level with FFP alone.
31
3 treatments for hemophiliac patients : Other than desmopressin
Cryoprecipitate
Tranexamic acid
Epsilon aminocaproic acid.
32
Synthetic Arginine analog of Vasopressin
Desmopressin
33
Cryoprecipitate is made how?
Collected off the top of FFPs at it being thawed
34
In the intrinsic pathway, what is the component required to convert factor XII to factor XI?
Prekallikrein
35
Components like High Molecular Weight Kininogen required to activate
Factor XI.
36
A pain medication commonly given medication in the OR that you should avoid in patient with porphyria crisis is
Ketorolac
37
Both hemophilia A and hemophilia B exhibit a
prolonged PTT and a normal PT.
38
The primary function of von Willebrand factor is
To promote platelet aggregation and adhesion to collagen
39
Potential side effect of DDAVP administration in the treatment of von Willebrand disease?
Hypotension
40
What treatment regimens are effective in ameliorating the symptoms of von Willebrand disease? (select two)
Desmopressin and concentrated von Willebrand Factor are both effective in treating the symptoms of von Willebrand disease.
41
Factor IX-PCC is used in the treatment of
Hemophilia B
42
Major surgery --> how to replace vWF
achieve 100% vWF preoperatively and maintain trough levels of 50% until adequate wound healing
43
In treating type 1 vWD which agent is preferred?
Desmopressin because it produces a complete partial response in more than 90% of patients
44
In treating type 2 and type 3 vWD which agent is preferred?
Type 2 and type 3 require vWF concentrate administration.
45
Heparin-Induced Thrombocytopenia (HIT) Type I and Type II
type I non immune mediated, onset 1-4 days
| type II immune mediated (immunoglobulin G) 5-14 days
46
Blood component therapy for HIT
| 1. Indications: active bleeding or high risk for bleeding
1. Fresh frozen plasma
2. Platelets
3. In some cases, consider cryoprecipitate, antithrombin III
47
Most events of acute stent thrombosis occur within the
first 30 days after stent placement
48
Absolute contraindication to neuraxia
Thrombolytics
49
When is there no contraindication for heparin SC dosing for neuraxial.
No contraindication with twice-daily dosing and total daily dose < 10,000 units
50
Upper endoscopy and colonoscopy with or without biopsy --> Warfarin stop?
NO NEED for interruption in therapy
51
• Endoscopic retrograde cholangiopancreatography (ERCP) without sphincterotomy Warfarin stop ?
NO NEED for interruption in therapy
52
Do not need to stop warfarin for these procedures?Prosthetics
Cataracts
NO
53
Elective noncardiac surgery should be delayed______after bare metal stent and _______after DES
30 days after bare metal stent (BMS) implantation and optimally 6 months after drug eluting stent (DES) implantation
54
Discontinue ticlopidine _____days prior to neuraxial
14 days
55
Discontinue clopidogrel ____Days prior to neuraxial
7 days
56
Discontinue GP IIB/IIIa inhibitors _______prior to neuraxial.
8–48 hours in advance
57
A powerful vasodilator, also interferes with platelet formation and aggregation is ______
prostacyclin
58
Anatomy of a platelet
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],
59
Converts to plasmin
Plasminogen
60
3 Vasoconstrictors of vessesl
Thromboxane A2
ADP
Serotonin
61
Name 2 Vasodilators of vessels
Nitric oxide
| Prostacyclin
62
Vessel Injury contracts after injury leading to
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
63
After injury to the vessel , contraction leads to what
Contraction is followed by three separate stages in the formation of a primary plug: adhesion, activation, and aggregation.
64
Factor not produced by the liver
III
65
What is the substance synthesized vascular wall and extravascular cell membranes and is released from traumatized cells?
vonWillebrand
66
Bleeding time Normal
3-7 minutes
67
Normal ACT
80-150
68
Normal PT
12-14 sec
69
Normal PTT`
25-33
70
Extrinsic (Warfarin vs Heparin)
Warfarin
71
Intrinsic (Warfarin vs Heparin)
Heparin
72
A normal platelet count is
150,000 to 300,000/mm3.2
73
Adhesion is associated with which platelet releasing substance?
Vonwillebrand
74
Platelet Activation and aggregation are associated with which 2 substances?
ADP and thromboxane A2
75
When are PRBCs transfused? are
transfused to improve tissue oxygenation
76
The major reasons for transfusion therapy in the operating room are to
replace volume and coagulation factors and improve oxygen-carrying capacity.
77
The recommended dose for platelet replacement is
one plateletpheresis pack per each 10 kg of patient weight
78
Protamine sulfate dosing
1 mg neutralizes 100 units of heparin
79
1 unit of platelet is ______ml
250 mL
80
1 unit of platelet increases the platelet count by how much?
30,000–60,000/mm3
81
FFP unit = _____ml
200-250 ml
82
Hypofibrinogenemia, massive hemorrhage --> what is used
Cryoprecipitate.
83
With the patient with Hemophilia OR massive hemorrhage
Factor VII
84
1 unit single- donor apheresis platelets comes from how many platelet concentrates?
Four to five platelet concentrates,
85
Laboratory analysis will reveal the need for FFP by a
PT and aPTT prolonged more than 1.5 times normal.
86
Cryoprecipitate is then refrozen and thawed on use. It is rich in which 4 factors?
fibrinogen
Factors VIII
Factor XIII
Fibronectin
87
The recommended dose of factor VII for hemophilia is
90 to 120 mcg/kg
88
Cryoprecipitate Infusion Guidelines
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.
89
Transfusion of cryoprecipitate is rarely indi- cated if fibrinogen concentration is
greater than 150 mg/dL in non- pregnant patients.
90
A sickle cell crisis may be triggered by which factors?
hypoxemia, hypothermia, infection, dehydration, venous stasis, and acidosis.
91
P2Y12 ADP Receptor Inhibitors: name 3
ticlopidine, clopidogrel, prasugrel
92
Platelet Glycoprotein IIb/IIIa Receptor Blockers: Name 3
abciximab, tirofiban, eptifibatide
93
Heparin half life
1.5 hours
94
Warfarin half life
2-4 days
95
Abciximab half life
30 minutes
96
ASA half life
20 minutes
97
NSAIDs half life
2-10 hours
98
It is the COX-1 receptor inhibition that is responsible for the gastric irritation caused by
NSAIDs
99
COX-1 receptor inhibition by NSAIDS is responsible for the
Gastric irritation
| Decrease in renal blood flow, and platelet inhibition associated with nonselective NSAIDs.
100
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
Acute normovolemic hemodilution
101
Preoperative autologous donation is most effective when it is
combined with erythropoietin therapy
102
Which of the following are disadvantages to storing blood? (select two)
Adenosine triphosphate levels decrease in stored blood
| . 2, 3 DPG levels decrease in stored blood
103
Which of the following are disadvantages to storing blood? (select two)
Adenosine triphosphate levels decrease in stored blood
| 2, 3 DPG and ATP levels decrease in stored blood
104
The potassium present in the plasma of PRBCs stored for __days can reach as high as ____-mEq/L
packed red blood cells stored for 21 days can reach levels as high as 35 mEq/L.
105
COX-1 receptors where in the body?
distributed throughout the body
106
Which COX inhibition results in inhibition of thromboxane A2?
COX-1 receptor. By doing so, it disrupts thromboxane A2's ability to promote platelet aggregation.
107
COX-2 receptors are present in the
kidneys and central nervous system and can be synthesized in response to inflammatory processes.
108
What are the effects of COX-2 receptor inhibition?
reduce prostacyclin release from the vascular epithelium and can result in increased platelet aggregation.
109
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
decreases 10% with every 1 degree Celsius drop in body temperature; further bleeding
110
Which infectious disease has the highest risk of transmission via blood transfusion?
CMV
111
Acute hemolytic transfusion reaction is an _____ mediated reaction.
IgM
112
Phosphodiesterase inhibitors increase the level of cyclic AMP which is an
inhibitor of platelet aggregation.
113
What sign is consistent with an acute hemolytic transfusion reaction?
Hematuria
114
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?
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
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?
6-8 hours
116
Vitamin K oral administration exhibits the highest bioavailability, it can take up to ___hours to see effects.
24 hours to exhibit significant clinical effects.
117
What is the most bioavailable parenteral preparation of calcium ?
Calcium chloride
118
Why is calcium chloride not used to treat hypocalcemia routinely?
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
How do you treat hypocalcemia?
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
In the intraoperative period, what are the most likely causes of hypocalcemia?
Hyperventilation
| Massive rapid transfusion.
121
How does hyperventilation lead to hypocalcemia?
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
For patients who rapidly develop hypercalcemia, which results in life threatening dysrhythmias, What is the treatment that can rapidly lower serum calcium?
hemodialysis is an acute treatment to rapidly lower serum calcium.
123
1st, 2nd and 3rd way to treat hypercalcemia?
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
Normal magnesium plasma concentrations range from
1.5 to 3.0 mEq/L.
125
Severe hypomagnesemia can be treated with
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
ECG changes seen with hypomagnesemia include:
| QT
flat T-waves, presence of U-waves, prolonged QT interval, widened QRS complexes, and atrial and ventricular arrhythmias
127
Low magnesium and BP
Hypotension
128
Magnesium and effects on NMBAs.
potentiates the action of nondepolarizing neuromuscular relaxants and their use should be carefully monitored in patients with hypermagnesemia
129
The majority of phosphate is located where in the body ?
in bone (85%)
130
When magnesium levels are 10–15 (mg/dL) what symptoms will you see?
Heart block
131
When magnesium levels are 10 what symptoms will you see ?
Respiratory paralysis, coma
132
At what magnesium levels would you see Hypotension? what about loss of Deep Tendon reflexes?
```
4–5 = Decreased deep tendon reflexes
5–7 = Hypotension
```
133
The concentration of phosphate in plasma is inversely proportional that of which electrolyte?
Calcium
134
Hyperphosphatemia is defined as a serum phosphate level greater than
4.7 mg/dL.
135
The majority of phosphate exists within the ICV or ECV?
ECV.
136
Leading cause of Hyperphosphatemia?
Cellular destruction (e.g., metastatic disease) is a leading cause
137
Hypophosphatemia is defined as a serum phosphate concentration of less than.
2.0 mg/dL
138
The most likely causes of hypophosphatemia are
increased renal excretion and intestinal malabsorption.
139
The consequence of decreased ATP includes
hypoxia, heart block, bradycardia, and asystole.
140
2 main causes of Hyperphosphatemia you need to know
Intestinal malabsorption related to vitamin D deficiency Magnesium/aluminum containing antacids
141
Mechanism Action of calcium chloride in the treatment of hyperkalemia? What is the dose? (think rule of 10)
Membrane Stabilization
| Dose is 10 mL of 10% calcium chloride of 10 minutes
142
Mechanism Action of calcium GLUCONATE in the treatment of hyperkalemia? What is the dose? (think rule of 10 -5)
Membrane Stabilization
| Dose is 10 mL of 10% calcium chloride of 3-5 minutes
143
Mechanism Action of SODIUM BICARBONATE in the treatment of hyperkalemia? What is the dose?
Shifts potassium intracellularly
| 50-100 mEq over 10-20 minutes
144
Medications indicated for a HYPERKALEMIC patient showing LOSS of "p waves" and widening of the QRS?
IMMEDIATE effective therapy indicated
Calcium Chloride/Calcium gluconate
Sodium bicarbonate
145
Medications indicated with a HYPERKALEMIC patient showing Peaked "T waves" ?
Glucose infusion of 50ml D50 and 10 units of REGULAR insulin
| Immediate hemodialysis
146
Action of Glucose and insulin?
Shifts potassium intracellularly
147
BIOCHEMICAL evidence of hyperkalemia with NO ECG changes , what is indicated? Effective therapy needed within hours
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
ONSET of Glucose and insulin in the treatment of hyperkalemia?
30 min
149
Onset of Potassium binding resins such as kayexalate
1-2 hour
150
ONSET of calcium chloride and calcium gluconate in treatment of hyperkalemia?
1-3 min
151
Hypercalcemia and ________PTH
Decrease
152
Hypocalcemia and ________PTH
Increase
153
With hypercalcemia, There is a decrease in PTH leading to ________Renal activation of vitamin D
Decrease
154
With HYPOcalcemia, There is a decrease in PTH leading to ________Renal activation of vitamin D
Increase
155
```
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
```
↓ Intestinal absorption of calcium
↓ Renal reabsorption of calcium
↓ excretion of phosphate
↓ Calcium resorption from bone
156
By decreasing angiotensin, ACE inhibitors/ARBs can cause what electrolyte abnormality?
hyponatremia and hyperkalemia.
157
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 _________.
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
ECG signs of P wave flattening or disappearance, PR prolongation is associated with what levels of Hyperkalemia?
6.5 - 7.5 mEq/L
159
ECG changes: PEAKED T waves are associated with what potassium level?
5.5 - 6.5 mEq/L
160
At what potassium levels would you see "QRS complex degrades to sine wave pattern, ventricular fibrillation and cardiac arrest"
> 8.5 mEq/L
161
For HYPERKALEMIA treatment: The treatment strategy accomplishes three physiologic events:
(1) stabilization of cardiac membrane
(2) driving K from ECV to ICV
(3) removal of K from the body
162
What ECG changes occur when the potassium level is > 7.0 - 8.0?
QRS prolongation
163
Hypocalcemia and QTc
QT prolongation primarily by prolonging ST segment
164
Intracellular K LEVEL range
150–160 mEq/L)
165
Extracellular K range
3.5–5.0 mEq/L
166
Sodium level : 135-130 mEq/L signs and symptoms
No signs/symptoms, mild neurologic signs/symptoms possible
167
Sodium level : 129-125 mEq/L signs and symptoms
Nausea and malaise
168
Sodium level at which you'll see Headache Lethargy
| Altered LOC
124-115 mEq/L
169
Sodium level at which you would see Seizures, coma, respiratory arrest, cerebral herniation
<115 mEq/L
170
It has been suggested that serum NA concentrations should be increased by no more than _______Why?
1 to 2 mEq/L per hr ; reduce risk of myelinolysis
171
To treat hyponatremia you can give?
3% saline at a rate of 1-2 mg/kg/hr
172
Confusion, restlessness, agitation, headache seen with which levels of serum osmolality? > 430
Hyperreflexia, muscle twitching/spasm
Coma, seizures, death
350–375 mOsm/kg
173
Ataxia, tremors, weakness seen with which levels of serum osmolality?
376–400 mOsm/kg
174
Hyperreflexia, muscle twitching/spasm
| seen with which levels of serum osmolality?
401–430 mOsm/kg
175
Coma, seizures, death seen with which levels of serum osmolality?
> 430 mOsm/kg
176
What is the most common electrolyte abnormality in hospitalized patients?
Hyponatremia
177
Strove Volume Variation (SVV) what % predicts preload responsiveness?
> 13%
178
Normal SvO2
60-80%
179
What is the normal serum osmolality?
280 - 285 mOsm
180
If your serum osmolality is low, you should evaluate which volume?
Extracellular fluid volume
181
When would you see isotonic hyponatremia (aka pseudhyponatremia ) when consider low sodium due to lab artifact and hence not treat?
When hyponatremia occurs with a NORMAL serum osmolarity (280-285 mOsm).
182
If your sodium osmolality is LOW it means that the level is less than
280 mOsm
183
If you have HYPONATREMIA and SODIUM OSMOLALITY is LOW What are the 3 possibilities
Hypovolemic HYPOTONIC HYPONATREMIA
ISOVOLEMIC HYPOTONIC HYPONATREMIA
HYPERVOLEMC HYPOTNOIC HYPONATREMIA
184
In HYPOVOLEMIC HYPOTONIC HYPONATREMIA, whether your Urine Na is> 20 or low than 10 what is the treatment for both?
0.9% NS
185
In ISOVOLEMIC HYPOTONIC HYPONATREMIA, when your URINE NA is >20 what is the treatment?
WATER RESTRICTION
186
In ISOVOLEMIC HYPOTONIC HYPONATREMIA, when your URINE NA is <10 what is the treatment?
Hypertonic saline,
fluid restriction,
loop diuretic
187
In HYPERVOLEMIC HYPOTONIC HYPONATREMIA, when your URINE NA is >20 or LESS than Urine NA < 10 what is the treatment for both?
Sodium and water restriction
| +/- diuretics
188
Serum Osmolality (Calculated) Formula
(2 × [Na]) + (BUN/2.8) + (glucose/18)
189
TBW = total body water =. ____ (formula)
body weight × 60%
190
FENA Less than 1% =
prerenal (hypovolemia)
191
FENA Greater than 2% =
intrinsic renal disorder
192
What is the first step in assessing hypernatremia?
Assess extracellular volume status.
193
CPB : roller pump vs Centrifugal pump
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
Roller pump vs Centrifugal pump: Which one is more economical and simple to use?
The roller pump is economical and simple to use.
195
Disadvantage of roller pump?
increased destruction of blood elements.
196
Which one is more common: centrifugal vs roller pump?
As a result, centrifugal pumps are replacing roller head pumps in contemporary practice.
197
In the even of a power failure, what can be done to the Both roller pump and centrifugal pump?
a hand crank can be used to manually operate either pump.
198
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.
199
Traditionally, the priming volume for the CPB is
1 to 2 L.
200
Upon instituting CPB, the prime added to the circulating blood volume causes
dilutional anemia, which will often result in a decrease in hematocrit (22% to 25%).
201
What offsets the dilution caused by the CPB?
The dilution offsets some of the increase in blood viscosity that occurs when the blood cools during CPB.
202
Hypocalcemia : ________QT while hypercalcemia________QT
Prolonged
| Shortened
203
Potentiation of digoxin toxicity occurs with electrolyte imbalance?
Hypercalcemia
204
Insensitivity to digoxin occurs with electrolyte imbalance?
HYPOCALCEMIA
205
Correction of calcium should be guided by
IONIZED CALCIUM levels
206
What is the most common laboratory finding, and serves as an important predictor of pulmonary complications.
Hypoalbuminemia
207
It is important to note that calcium levels must be corrected for _________concentration so that overcorrection does not occur.
serum albumin
208
What is the major intracellular ANION? pay close attention
Phosphate
209
The primary extracellular anion is
chloride.
210
The primary intracellular cation is
potassium.
211
The primary extracellular cation is
sodium.
212
The majority of total body magnesium is found in
bone
213
Coronary artery dominance is determined by which artery supplies the
posterior descending artery
214
Total blood calcium levels parallel the serum
albumin.
215
If the serum albumin decreases, the total blood calcium level will.
decrease as well
216
What is the most common cause of hypocalemia?
Hypoalbuminemia
217
Hormones that use the phospholipase C system include:
| PAVO
Parathyroid hormone
Alpha receptor catecholamines
Vasopressin V1
Oxytocin
218
Hormones that use the adenylyl cyclase system include
```
Calcitonin
ACTH
Glucagon,
Secretin
Somatostatin
vasopressin V2, parathyroid hormone, luteinizing hormone, and beta-receptor catecholamines.
```
219
SIRS results in
It results in a stress response that includes increases in circulating angiotensin, cortisol, catecholamines, and vasopressin.
220
Tetanic fade is a response to blocking which type of receptor?
Presynaptic nicotinic acetylcholine receptors
221
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
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.
