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SRNA4TopicsAnesthesia > Test 2 Study Guide > Flashcards

Test 2 Study Guide Flashcards

1
Q

What is the best method to avoid perioperative heat loss?

A

Forced air warming

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2
Q

What mechanism facilitates heat loss through air currents?

A

CONVECTION

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3
Q

Evaporative heat loss results from

A

fluid loss through the skin and respiratory system

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4
Q

Conductive heat loss occurs when

A

direct contact between cold and warm objects.

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5
Q

Radiation involves the

A

transfer of heat from infrared rays.

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6
Q

Convective heat loss requires

A

currents and is dependent on thermal gradients.

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7
Q

Phase I

A

To avoid the initial drop in body temperature pre-warm the patient with aforced-air warming blanket.

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8
Q

Phase II → To avoid heat loss during

A

Phase II, all other warming methods in combinationare use

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9
Q

What mechanism results in the greatest amount of heat loss in the operating room?

A

RADIATION (60%),

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10
Q

When is body temperature loss the greatest?

A

The greatest amount of heat loss occurs during the 1st hour in the operating room (0.5-1.5C).

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11
Q

Patients lose most heat through

A

radiation from their exposed skin to the surrounding cold environment.Thereafter temperature decline is gradual and then plateaus

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12
Q

Most critical factor for heat loss during anesthesia and surgery ?

A

Operating room temperature

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13
Q

Most body heat is lost by 2 processes

A

RADIATION and CONVECTIOn from the skin and surgical incisions

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14
Q

One of the best ways to minimize body heat loss during anesthesia and surgery ?

A

Increase OR room temperature

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15
Q

Padding the patient everywhere prevents heat loss by what routes?

A

Padding serves as insulation and prevents heat loss by convection and radiation

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16
Q

Responsible for the metabolism of the Largest portion of drugs in the body

A

CYP450

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17
Q

CYP 3A4 comprises

A

40-50% of the system’s metabolizing capabilities

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18
Q

The hepatic microsomal enzymes are present with the greatest degree of metabolism occuring in the

A

HEPATIC SMOOTH ER, GI, kidneys, adrenal cortex

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19
Q

4 medications all metabolizes by CYP450

A

Phenytoin, ethanol, barbiturates and Ketamine,

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20
Q

The hepatic microsomal enzymes of the p450 system are generally confined to the

A

Smooth Endoplasmic reticulum

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21
Q

Where is the primary location of hepatic microsomal enzymes?

A

Hepatic smooth endoplasmic reticulum

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22
Q

The only process that does not involve the cytochrome P450 pathway is

A

HYDROLYSIS

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23
Q

Common substrate for phase II conjugation reactions:

A 
Glucuronic acid
Glycine
Acetic acid
Sulfuric acid
Methyl group
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24
Q

CYP2D6 substrate ->

A

Codeine ; Oxycodone ; Hydrocodone

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25
Q

Inducers of CYP2D6 →

A

Disulfiram

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26
Q

Inhibitors of CYP2D6 →

A

SSRIs, Isoniazid, Quinidine

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27
Q

Examples of Enzymes inducers (RPPCSC)

A 
Rifampin
Phenytoin
Phenobarbital (barbiturates)
Carbamezepine
Smoking tobacco
Consuming alcohol
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28
Q

Examples of Enzyme inhibitors (CAGEKOI)

A 
Cimetidine
Amiodarone
Grapefruit Juice
Erythromycin
Ketoconazole
Omeprazole
Isoniazid
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29
Q

CYP1A2 inhibitors →

A

Erythromycin; Ciprofloxacin

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30
Q

3 drugs that under perfusion dependent hepatic elimination ?

A

Propofol
Fentanyl
Lidocaine

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31
Q

The rule of thumb is that steady state will be achieved after

A

5 half lives

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32
Q

How many half lives to eliminate 97 % of the drugs?

A

5

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33
Q

The context sensitive half time of fentanyl ?

A

longs 240mns

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34
Q

Predicts the time it takes for 50% of a drug to be eliminated from the central compartment when a continuous infusion is discontinued?

A

Context sensitive half time

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35
Q

The plasma half-life of a drug is inversely proportional to its

A

RATE OF CLEARANCE

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36
Q

Hepatic enzyme induction will result in a reduction in the drugs “

A

HALF TIME or LIFE”

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37
Q

Elimination half-life is the

A

time taken for a drug to lose half of its pharmacologic or physiologic activity.

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38
Q

Formula of T ½ is :

A

T ½ = Vd / Cl

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39
Q

Half time of elimination is greater if Vd is ____and clearance is

A

volume of distribution is LARGE and Clearnce is SMALL

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40
Q

Elimination half time and volume of distribution →

A

Directly proportional

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41
Q

Elimination half time and clearance →

A

Inversely proportional

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42
Q

How does the elimination half-time of remifentanil differ from alfentanil?

A

Elimination half-time is shorter or remifentanil

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43
Q

Half-life (hours) =

A

0.693 x (Volume of distribution (L) / Clearance (L/hr))

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44
Q

What causes an increased end-tidal carbon dioxide?

A

CNS depression

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45
Q

INCREASES IN METABOLIC RATE (increased VO2)

A

Increases CO2 production

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46
Q

Hypotension leads to

A

CO2 production

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47
Q

Things that causes an increase in CO2

MASTT FPC

A 
Malignant Hyperthermia
Anxiety
Seizures/ SEPSIS
Thyrotoxicosis
Tourniquet and vascular clamps removal
Fever/ Sodium bicarbonate administration
Pain 
CO2 insufflation with laparoscopic surgeries
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48
Q

Main mechanism of Increased ETCO2?

A

Increase alveolar ventilation

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49
Q

Elevated ETCO2 with normal plateau?

A

Make sure you look at the baseline and that it returns to zero. Its not rebreathing. Occurs with increased production of CO2 or DECREASED ALVEOLAR VENTILATION

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50
Q

Capnography measures

A

ETCO2 concentration over time.

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51
Q

Capnography measures 3 main things?

A

Assessment of metabolism
Circulation
Ventilation

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52
Q

CO2 diffuses airway then from the tissues on, what happen?

A

from the tissue and enters the venous circulation, From here, the CO determines the rate of transfer towards the lungs. In the lungs, CO2 follows a concentration gradient as it diffuses across the alveolar capillary membrane. Once the CO2 in the alveolus, ventilation is the process by which CO2 is removed from the body

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53
Q

What point in the CO2 waverform is ETCO2 measure?

A

Point D

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54
Q

Normal ETCO2

A

35-40 mmHg

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55
Q

ETCO2 Waveform: An increase alpha angle means

A

EXPIRATORY AIRFLOW OBSTRUCTION such as COPD, bronchospasm or a KINKED ETT TUBE.

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56
Q

Widened beta angle on CO2 waveform means

A

Incompentent unidirectional valve

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57
Q

Identify caused of the abnormal waveform if there is a CARDIAC OSCILLATION?

A

Heart beating against the lungs

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58
Q

Leak in sample time CO2 waveform?

A

The beginning of the plateau is low, because dilution of alveolar gas at atmospheric air is aspirated into the sample line. NOT SEEN WITH SPONTANEOUS VENTILATION.

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59
Q

2 Methods of CO2 analysis

A

Mainstream (in line)

Sidestream (diverting )

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60
Q

Low ETCO2 indicates

A

Hyperventilation
Increased alveolar dead space
Decrease CO2 production

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61
Q

Alpha angle is where?

A

between the first expiration upstroke and the plateau line

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62
Q

Beta angle is

A

REBREATHING reading

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63
Q

Baseline not returning to zero is

A

REBREATHING

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64
Q

What CO2 analysis method has a faster response time-

A

Mainstream , does not require a water trap or pumping mechanism

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65
Q

Capnogram Phases I.

A

Dead space gas exhaled

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66
Q

Capnogram Phases II.

A

Transition between airway and alveolar gas

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67
Q

Capnogram Phases III.

A

Alveolar plateau

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68
Q

Capnogram Phase IV

A

Inspiration

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69
Q

What CO2 analysis methods is the device attached to the ETT?

A

-Mainstream (in line)

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70
Q

Impaired RELAXATION is what phase of diastolic dysfunction

A

Grade I

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71
Q

Phase I of diastolic dysfunction is

A

Impaired relaxation

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72
Q

Phase II of diastolic dysfunction

A

Pseudonormal filling

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73
Q

Phase III of diastolic dysfunction

A

Restrictive filling

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74
Q

Phase III of diastolic dysfunction

A

Reversible Restrictive filling

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75
Q

Phase IV of diastolic dysfunction

A

Irreversible Restrictive filling

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76
Q

The early manifestation of diastolic dysfunction is characterized by an

A

impaired relaxation,

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77
Q

This stage of disease is known as grade I diastolic dysfunction

A

inability of the LV to fill adequately during the rapid filling phase. A compensatory increase in filling occurs with atrial contraction.

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78
Q

In summary, in grades II and III of diastolic dysfunction, there is a decrease in

A

LV compliance ensues.

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79
Q

Compliance is defined as a

A

change of volume with respect to a change in pressure. decrease in LV compliance will lead to a disproportionate increase in LV pressures and, ultimately, LA pressures.

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80
Q

Grade I : the TMF curve of an individual with abnormal relaxation is represented by a (LeHapDT)

A

low E, high A, and prolonged DT

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81
Q

Grade I diastolic dysfunction, as the LV is

incompletely relaxed when early ventricular filling occurs, t

A

The pressure gradient, and thus E wave velocity, is less than normal.

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82
Q

In Grade I, E wave velocity is

A

less than normal

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83
Q

In Grade I, The delayed relaxation prolongs LV filling late into diastole, and therefore the DT is

A

prolonged.

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84
Q

Because the DT is prolonged in grade I, A compensatory increase in

A

TMF during atrial contraction, due to the higher residual atrial preload, generates a high A wave velocity

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85
Q

A wave in Grade I is

A

High

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86
Q

Progression of diastolic disease leads to grade II diastolic dysfunction, which is marked by

A

decreases in LV compliance

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87
Q

For Grade II, LA pressure rises as a compensatory mechanism to normalize the pressure gradient across the MV. In this scenario, the

A

TMF velocities resemble the normal curve; thus, this

stage is known as pseudonorma

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88
Q

Grade III diastolic dysfunction, known as the

A

Restrictive phase,

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89
Q

Grade III diastolic dysfunction, known as the restrictive phase is characterized by a

A

significantly decreased LV compliance

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90
Q

In Grade III, The high LA–LV pressure gradient produces a

A

fast acceleration of blood flow in the LV.

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91
Q

A high E velocity on the TMF curve is representative for

A

grade III diastolic dysfunction

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92
Q

What represent Grade III diastolic dysfunction?

A

A high E velocity on the TMF curve

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93
Q

In Grade III diastolic dysfunction: LV pressure and effect on DT?

A

LV pressure increases rapidly during filling because of the increased LV stiffness resulting in a short DT. The forward filling velocity at atrial contraction is low (small A wave) because of the decreased compliance

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94
Q

Cardiac tumors either can originate

A

from the heart or are metastases from other sites.

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95
Q

Cardiac masses can

A

embolize, cause arrhythmias, or cause heart failure.

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96
Q

The most common primary tumor of cardiac is

A

myxoma,

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97
Q

Myxoma most common location

A

most frequently at the interatrial septum

98
Q

The potential of myxomas to

A

obstruct the inflow or outflow region of a ventricle is

demonstrated with Doppler echocardiography.

99
Q

The 2nd most common cardiac tumor next most frequent tumor

is . (Fig. 27-42C).

A

fibroma of the ventricular wall.

100
Q

Fibromas are usually

A

calcified and can decrease the ventricular volume

101
Q

Renal cell tumors often

A

extend into the inferior vena cava and right atrium

102
Q

Should be differentiated from tumors.

A

Pacemaker wires, thrombus, and normal anatomic structures that mimic the appearance of
pathology (Eustachian valve, crista terminalis, Chiari network, or “Coumadin”ridge)

103
Q

During exposure of the aneurysm, burst-suppression on the EEG may be desired to

A

decrease the impending ischemic burden on the brain from temporary occlusion of large cerebral vessels

104
Q

Burst-suppression can be accomplished with .

A

propofol administered as a 1- to 2-mg/kg bolus followed

by infusion of 100 to 150 μg/kg/min. Additional vasopressor may be required during this time to maintain CPP.

105
Q

→ Does not produce burst suppresion

A

Benzodiazepines

106
Q

Electroencephalogram (EEG) burst suppression is characterized by

A

periods of isoelectric EEG punctuated by “bursts” of EEG activity.

107
Q

Electroencephalogram (EEG) burst suppression is characterized by

A

periods of isoelectric EEG punctuated by “bursts” of EEG activity.

108
Q

Burst suppresion is caused by

A

BARBITURATES and PROPOFOL

109
Q

Burst suppression occurs at close to

A

to 1.5 MAC

110
Q

Define burst suppression

A

The “burst” is high-frequency activity and the “suppression” is O.S· to several-second periods of isoelectric activity

111
Q

At greater than 2 MAC, all of the potent agents can produce.

A

burst suppression or electrical silence

112
Q

These are important factors to remember because EEG changes during administration of general anesthesia can also be caused by

A

hypoxia, hypercarbia, and hypothermia.

113
Q

Burst suppression can be done by

A

It can be attained at concentrations of propofol (8 μg/mL) that are significantly higher than the blood concentrations needed to reach the initial stages of general anesthesia (3 μg/mL). A further increase in propofol concentration will lead to an isoelectric EEG pattern.

114
Q

Unlike benzodiazepines, etomidate can

A

achieve burst suppression with a concomitant

decrease in ICP

115
Q

However, despite its neurodepressant properties at high

doses, etomidate is often associated with

A

epileptogenic activity (excitatory spikes) on EEG.

116
Q

Thiopental induced

A

burst suppression and isoelectric EEG prior to potential focal ischemic insult

117
Q

TIVA is associated with

A

smooth induction and rapid emergence with less postoperative nausea and vomiting.

118
Q

is emerging as a standard method to administer safe anesthesia in neurosurgical patients.
.

A

Administration of TIVA using target-controlled infusion technique

119
Q

What has become very popular due to their favorable pharmacokinetic and pharmacodynamic properties for neurosurgery case?

A

The propofol–remifentanil combination has

120
Q

Attractive for ICU sedation in neurosurgery, as patients can participate in neurologic examinations while receiving this medication

A

Dexmedetomidine

121
Q

The BIS uses a proprietary algorithm that processes the in near real time and computes an index between that

A

0 and 100

122
Q

EEG indicates the patient’s

A

level of consciousness.

123
Q

EEG; BIS A value of 100 corresponds to ____and a value of 0 is ____

A

being completely awake, whereas 0 corresponds to a profound state of coma or unconsciousness that is reflected by an isoelectric or flat EEG.

124
Q

A patient is considered to be appropriately anesthetized when the BIS value is between

A

40 and 60

125
Q

Since the bispectral index (BIS) is based upon the hypnotic action of agents, the BIS is not affected by

A

opioids or analgesics.

126
Q

Nitrous oxide alone on BIS

A

will have no effect on BIS

127
Q

At BIS values lower than 40,

A

cortical suppression becomes discernible in a raw electroencephalogram as a burst suppression pattern

128
Q

BIS values o 65-85 have been recommended or sedation, whereas values o

A

For sedation

129
Q

BIS valueshave been recommended for general anesthesia.

A

40-65

130
Q

BIS and Ketamine

A

has minimal effect on BIS, and may slightly increase BIS transiently

131
Q

Common second-messenger molecules include

Identify the cyclic nucleotide second messenger that mediates the cellular actions of natriuretic peptide?

A

cyclic adenosine 3′-5′-monophosphate (cAMP), inositol 1,4,5-trisphosphate (IP 3), 1,2-diacylglycerol (DAG), and calcium ions (Ca 2+).

132
Q

lpratropium (Atrovent) works by blocking the production of what second messenger?

A

Blockade of the muscarinic receptor by ipratropium will lead to a decrease in inositol triphosphate (IPJ). Notes: In the absence of IP3, what happens to calcium? less calcium is released from intracellular vesicles, so smooth muscle tone is decreased.

133
Q

By what receptor and second messenger system does glucagon exert its positive inotropic and chronotropic effects?

A

Glucagon acts through its own G-protein coupled receptor (GPCR) and generation of cyclic adenosine monophosphate (cAMP). In other words, glucagon binds to glucagon receptors to promote the formation of cAMP.

134
Q

Cyclic GMP, a second messenger, action?

A

relaxes vascular smooth muscle, thereby promoting vasodilation and a decrease in blood pressure.

135
Q

Certain G-protein subunits

A

can stimulate or inhibit membrane-bound adenylate cyclase, which catalyzes cAMP formation.

136
Q

Cyclic guanosine monophosphate (cGMP) mediates the

A

cellular actions of natriuretic peptides.

137
Q 
Nitroprusside and nitroglycerin donate nitric oxide (NO). 
Nitric oxide (NO) activates the enzyme soluble
A

guanylate cyclase, which increases the production of cyclic guanosine monophosphate (cGMP).

138
Q

Within the VSMCs, NO reacts with the heme moiety in soluble guanylate cyclase, leading to a greater than
100-fold increase in the conversion of guanosine triphosphate to the secondary messenger

A

cyclic guanosine monophosphate [cGMP])

139
Q

cGMP associated with this medication

A

Sodium Nitroprusside

140
Q

The b1-adrenergic receptor located on the cardiac sarcolemma is coupled to

A

adenyl cyclase via a G protein.

141
Q

When activated, adenyl cyclase converts

A 
adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP), a secondary intracellular messenger, that stimulates protein kinase A to phosphorylate membrane calcium channels,
leading to an increase in cytoplasmic Calcium
142
Q

For CCB , The Ca21 functions as a s

A

econdary messenger—its divalent charge is sufficient to produce conformational change in a number
of cytoplasmic proteins, such as actin-myosin.

143
Q

Name four second messengers for mediating intracellular hormonal functions besides cAMP.

A

Calcium ions, calmodulin, cyclic guanosine monophosphate (cGMP), and inositol triphosphate ([P3).

144
Q

opioids action can be reversed by direct antagonism with

A

naloxone,inhibitors of cyclooxygenase, histamine antagonist

145
Q

A direct acting antagonist has

A

affinity for a receptor but lacks efficacy

146
Q

Silent antagonists are competitive receptor antagonists that have

A

zero intrinsic activity for activating a receptor.

147
Q

What local anesthetics, those with high pKas or those with low pKas, are most ionized at physiological pH (pH=7.4)? ,

A

Those local anesthetics with the highest pKas are most ionized at pHz:7.4. Procaine (pKa = 8.9, 97% ionized), chloroprocaine (pKa = 8.7, 95% ionized), and tetracaine (pKa = 8.5, 93% ionized) are most ionized at pH =7.4.

148
Q

The speed of onset of a local anesthetic is determined by its

A

degree of ionization which, in turn, is determined by its pKa.

149
Q

The greater the degree of ionization of a local anesthetic {the higher the pKa),

A

the slower the speed of onset.

150
Q

Bupivacaine has a slower onset than

A

lidocaine because it is more ionized (has a higher pKa of 8.1) than lidocaine (pKa - 7.9) at physiological pH

151
Q

Approximately what % of CO delivered to the vessel-rich organs, although they constitute ______-%only body mass.

A

75% of resting cardiac output; 10% of total

152
Q

Muscle group % of CO

A

16% CO

153
Q

Adipose tissue Bone , ligament % CO

A

6% of CO

154
Q

Phase II of drug metabolism is CONJUGATION

A

Compound can be readily eliminated from the body

155
Q

What is the significance of phase II reactions?

A

Phase II reactions couples (conjugate a parent drug) or a phase I metabolite with an endogenous substrate such as GLUCURONIC acid to form water soluble metabolites that are eliminated in urine or stoool

156
Q

Phase I metabolites may be excreted without

A

undergoing phase II, and a phase II reaction can precede or occur without a phase I reaction

157
Q

CYP2D6 is functionally absent in 7 percent of , while deficiency is rare among

A

Caucasians and African Americans; Asians

158
Q

At conventional doses, subjects who are poor metabolizers based upon CYP2D6 genotype will

A

derive no therapeutic benefit from codeine

159
Q

Cytochrome P450 2C19 enzymes are involved in the metabolism of

A

proton pump inhibitors and antidepressants.

160
Q

An example is the enzyme CYP2D6, which catalyzes the

A

conversion of codeine into morphine.

161
Q

Patients with multiple copies of the CYP2D6 gene and who receive codeine will have

A

large plasma morphine concentrations with all related

beneficial and adverse side effects

162
Q

This is important for drugs that rely on CYP2D6 to convert an

A 
inactive precursor (prodrug), such as codeine, into the active component of pain therapy (for codeine this is
morphine)
163
Q

Poor metabolizers display incomplete analgesia. The

frequency of poor metabolizers varies by ethnicity and is reported to be

A

8% in whites, 2% to 7% in African Americans and 0% to 0.5% in Asian populations.

164
Q

With CYP 2D6 Patients without an active gene will have no

A

benefit from treatment with codeine.

165
Q

With CYP2D6 Dangerous circumstances may occur when a

A

patient is an extensive metabolizer and produces large amounts of the active component.

166
Q

Loading dose is =

A

Vd x target concentration

167
Q

The loading dose is contingent on the

A

volume of distribution

168
Q

Maintenance doses are dependent on

A

plasma clearance.

169
Q

The loading dose is only required for a

A

few drugs in certain situations while maintenance doses are required for most drugs to maintain the steady-state plasma concentration

170
Q

However, from the clinical perspective, the single most important utility of Vd is calculating the

A

loading dose of a drug.

171
Q

The most significant aspect of the metabolism of barbiturates (e.g., phenobarbital, thiopental, methohexital) is their effect on the Chronic use of

A

hepatic microsomal enzyme system (cytochrome P450 (CYP) enzymes).

172
Q

These effects are dependent on the duration of exposure to the barbiturate. Acutely, barbiturates interact with various

A

CYPs and inhibit the biotransformation of other CYP substrates;

173
Q

Other substrates (e.g., other drugs or endogenous substrates) can inhibit the barbiturate

A

metabolism.

174
Q

Barbiturates will cause upregulation, or induction, of the microsomal enzymes (CYPs 1A2, 2C9, 2C19, and 3A4), increasing the

A

metabolism of drugs metabolized by these enzymes. This can lead to patients requiring larger dosages of medication to achieve therapeutic effect and/or increased clearance. This enzyme induction also causes barbiturate tolerance due increased barbiturate metabolism

175
Q

Acute barbiturates abuse

A

decrease anesthetic requirements.

176
Q

A phenol group substitution at position 5 of barbiturates forms phenobarbital. What clinically useful feature does the phenol substitution create

A

Phenobarbital has a phenol group substitution at position 5-the phenol substitution confers an anticonvulsant property to the barbiturate.

177
Q

On the ECG, ST segment depression of greater

A

than 1 mm provides evidence of myocardial ischemia

178
Q

ST segment monitoring To interpret ST segment changes properly, the

A

ECG must be standardized so that a 1-mV signal results in a deflection of 10mm on a standard strip monitor. Newer units continuously analyze ST segments for early detection of myocardial infarction.

179
Q

ST-segment elevation

A

(J point

180
Q

The “a” wave on the central venous pressure tracing corresponds to which on the EKG tracing?

A

P wave

181
Q

The y-descent of the CVP waveform corresponds to the

A

opening of the tricuspid valve during diastole and therefore is observed immediately following the v wave on CVP and shortly after the wave on the ECG.

182
Q

The a wave follows the

A

P wave on the ECG.

183
Q

The c wave immediately follows the

A

start of the QRS complex on ECG.

184
Q

The v wave appears

A

shortly after the start of the wave on the ECG.

185
Q

Y descent Mechanical event vs electrical events →

A

RA empties through open tricuspid valve (mechanical) After T wave ends

186
Q

V wave Mechanical event vs electrical events –>

A

Passive filling of RA (mechanical) Just after T wave begins (ventricular repolarization)

187
Q

X Descent Mechanical event vs electrical events→

A

RA relaxation (mechanical) ST segment (Electrical event)

188
Q

C wave Mechanical event vs electrical events –>

A

Right ventricular contraction (building of Tricuspid in RA)’->mechanical Just after the QRS complex (ventricular depolarization)

189
Q

A wave Mechanical event vs electrical events →

A

Right atrial contraction (mechanical)

Just after the P wave (Atrial depolarization)

190
Q

T wave corresponds with _____wave →

A

v wave

191
Q

ST segment corresponds with _______→

A

x descent

192
Q

QRS complex corresponds with —>

A

C wave

193
Q

V wave is the →

A

passive filling

194
Q

X descent is →

A

Right atrial relaxation

195
Q

What three measures are taken to increase the accuracy and precision of the cardiac outputs measured by thermodilution?

A

Triplicate determinations are averaged to increase precision the variability of cardiac output measurements can be reduced by performing the measurement at end-inspiration or at end-expiration;
(3) ensuring that the rate of injection and volume of injectate are constant.

196
Q

Factors that influence themodilution CO measurement: Underestimate CO

A

Injectate volume too high

Injectate solution too cold

197
Q

Which situation underestimates CO obtained by the thermodilution method?

A

High Injectate volume

198
Q

False high thermodilution cardiac output determinations occur when the injectate volume is

A

TOO SMALL

199
Q

False low determinations occur when injectate volume is

A

TOO LARGE

200
Q

If you inject 10 ml of cold normal saline when the cardiac output computer is set for 5 ml, will calculated cardiac output be higher or lower than actual cardiac output?

A

Calculated cardiac output will be lower than the true cardiac output

201
Q

The area under the curve will be larger if a greater volume is injected; so cardiac output will be

A

falsely low

202
Q

Avoid measurements of cardiac output using the thermodilution method during

A

electrocautery.

203
Q

Right atrium:

A

15-22 cm (15-20)

204
Q

Right ventricle:

A

25- 35 cm (30)

205
Q

Pulmonary artery

A

40- 50 cm (40)

206
Q

The distance from SKIN to the junction of the VC and RA is

A

15 cm

207
Q

Insertion site to VC and RA junction: Left IJ insertion site.

A

20 cm

208
Q

Pulmonary wedge distance

A

45- 50 cm (45)

209
Q

Vena Cava and R atrial Junction –> catheter tip:

A

PA 40cm

210
Q

Provides the shortest distance to the junction of the vena cava and the right atrium (approximately 10 cm) compared to other anatomic sites such as the he

A

The subclavian vein

211
Q

Distance to the junction of the vena cava and the

internal jugular veins ; femoral vein and right basilica vein

A

(15–20 cm); 40 ; 40

212
Q

O2-Hb Curve Shifts Right Shift means

A

lower affinity for O2 = increased unloading at tissues)

213
Q

O2 dissociation curve shifts to the RIGHT with

A

Acidosis • Hyperthermia • Hypercarbia • Increased 2,3-DPG • Sickle Cell Hb • Pregnancy • Volatile anesthetics • Chronic anemia

214
Q

O2 dissociation curve: Left Shift means

A

(higher affinity for O2 = decreased unloading at tissues)

215
Q

O2 dissociation curve shifts to the LEFT with

A

• Alkalosis • Hypothermia • Hypocarbia • Decreased 2,3-DPG • CO-Hb • Met-Hb • Sulf-Hb • Fetal Hb • Myoglobin

216
Q

The P50 is the oxygen tension at which

A

hemoglobin is 50% saturated.

217
Q

The normal P50 is

A

26.7 mm Hg. or 27 mmHg

218
Q

The gold standard of verification is sustained detection of D tube positively identified in it,

A

expired carbon the endotracheal tube is placed in the dioxide.irect visualization of the laryngeal inlet with the endotracheal trachea and not the esophagus

219
Q

Therefore, absence of Petco2 indicates

A

esophageal intubation, circuit disconnection, cardiac arrest, or airway obstruction.

220
Q

A false-positive result may be obtained after

A

gastric inflation with CO2 containing gas or digestion of carbohydrate-enriched beverages. E

221
Q

ETT-misplacement can be excluded by observing a

A

normal Petco2 waveform for three to six consecutive breaths.

222
Q

An end-tidal C02 (ETC02) partial pressure of< 5 mm-Hg is diagnostic of what

A

Esophageal intubation.

223
Q

Reliable signs to avoid esophageal intubation

A

auscultation of the chest and abdomen
full chest excursion
humidity in the ETT
detection of expired carbon dioxide with a capnograph or disposable colorimeter (Easy Cap) also provide
reliable evidence of tracheal rather than esophageal intubation.

224
Q

Esophageal probe contraindicated in

A

The patient who has an esophageal perforation and the patient with liver disease who has or could have esophageal varices. Do not instrument the esophagus of these patients.

225
Q

may also cause an increase in CO2 concentration.

A

A leak or obstruction in the anesthesia machine circuit, common gas outlet, or fresh gas supply line

226
Q

“Curare” cleft—seen normally in the last part of phase III caused by a

A

lack of synchrony between diaphragm and intercostal muscles in a patient who has received neuromuscular-blocking agents and in whom muscle strength is returning.

227
Q

Drugs with significant renal excretion with anesthesia \

AACDENN

A 
Aminoglycosides
Atenolol
Cephalosporins
Digoxin
Edrophonium
Nadolol 
Neogstimine
228
Q

Drugs with significant renal excretion with anesthesia

4Ps and QRS

A 
Pancuronium
PCN
Procainamide
Pyridostigmine
Quinolones
Rocuroncium 
Sugammadex
229
Q

CYP2C19 Substrate

A 
POWD
Propranolol
Omeprazole
Warfarin
Diazepam
230
Q

Cyclic Guanosine Monophosphate (cGMP) target responses

A

Activate protein kinase

231
Q

Cyclic Guanosine Monophosphate (cGMP) common drugs effectors are

A

Nitroglycerin

Sodium Nitroprusside

232
Q

Phosphoinositides and calcium : Target responses

A

Activate Calmodulin

233
Q

Phosphoinositides and calcium : common drug effector

A

Lithium

234
Q

Cyclic Adenosine monophosphate cAMP (CMC)

A

Caffeine
Milrinone
Catecholamines

235
Q

Cyclic AMP responses

A

Release protein kinases
Beta receptor stimulation of energy release
Inotropic and chronotropic cardiac effects
Production of adrenal and sex steroids
Many endocrine and neural processes

236
Q

Distance to the Junction of the Venae Cavae and Right Atrium from Various Distal Anatomic Sites Subclavian

A

10cm

237
Q

Distance to the Junction of the Venae Cavae and Right Atrium from Various Distal Anatomic Sites Right Internal J vein

A

15 cm

238
Q

For example, at a PO2 of 40 mm Hg, Hgb is approximately

A

75% saturated

239
Q

Phenytoin on NDNMB

A

shortens the duration of action of the nondepolarizing neuromuscular junction blocking agents by inducing CYP3A4 and therefore increasing elimination
clearance of the drug.

240
Q

The patient undergoing surgery has a decline in core

body temperature that occurs via five mechanisms:

A

(1) redistribution,
(2) radiation
(3) conduction
(4) convection
(5) evaporation.

241
Q

Redistribution is the transfer of heat from

A

the peripheral compartments of the body to the central core

SRNA4TopicsAnesthesia (47 decks)

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