Test 2 Study Guide Flashcards
1
Q
What is the best method to avoid perioperative heat loss?
A
Forced air warming
2
Q
What mechanism facilitates heat loss through air currents?
A
CONVECTION
3
Q
Evaporative heat loss results from
A
fluid loss through the skin and respiratory system
4
Q
Conductive heat loss occurs when
A
direct contact between cold and warm objects.
5
Q
Radiation involves the
A
transfer of heat from infrared rays.
6
Q
Convective heat loss requires
A
currents and is dependent on thermal gradients.
7
Q
Phase I
A
To avoid the initial drop in body temperature pre-warm the patient with aforced-air warming blanket.
8
Q
Phase II → To avoid heat loss during
A
Phase II, all other warming methods in combinationare use
9
Q
What mechanism results in the greatest amount of heat loss in the operating room?
A
RADIATION (60%),
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).
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
12
Q
Most critical factor for heat loss during anesthesia and surgery ?
A
Operating room temperature
13
Q
Most body heat is lost by 2 processes
A
RADIATION and CONVECTIOn from the skin and surgical incisions
14
Q
One of the best ways to minimize body heat loss during anesthesia and surgery ?
A
Increase OR room temperature
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
16
Q
Responsible for the metabolism of the Largest portion of drugs in the body
A
CYP450
17
Q
CYP 3A4 comprises
A
40-50% of the system’s metabolizing capabilities
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
19
Q
4 medications all metabolizes by CYP450
A
Phenytoin, ethanol, barbiturates and Ketamine,
20
Q
The hepatic microsomal enzymes of the p450 system are generally confined to the
A
Smooth Endoplasmic reticulum
21
Q
Where is the primary location of hepatic microsomal enzymes?
A
Hepatic smooth endoplasmic reticulum
22
Q
The only process that does not involve the cytochrome P450 pathway is
A
HYDROLYSIS
23
Q
Common substrate for phase II conjugation reactions:
A
Glucuronic acid
Glycine
Acetic acid
Sulfuric acid
Methyl group
24
Q
CYP2D6 substrate ->
A
Codeine ; Oxycodone ; Hydrocodone
25
Inducers of CYP2D6 →
Disulfiram
26
Inhibitors of CYP2D6 →
SSRIs, Isoniazid, Quinidine
27
Examples of Enzymes inducers (RPPCSC)
Rifampin
Phenytoin
Phenobarbital (barbiturates)
Carbamezepine
Smoking tobacco
Consuming alcohol
28
Examples of Enzyme inhibitors (CAGEKOI)
Cimetidine
Amiodarone
Grapefruit Juice
Erythromycin
Ketoconazole
Omeprazole
Isoniazid
29
CYP1A2 inhibitors →
Erythromycin; Ciprofloxacin
30
3 drugs that under perfusion dependent hepatic elimination ?
Propofol
Fentanyl
Lidocaine
31
The rule of thumb is that steady state will be achieved after
5 half lives
32
How many half lives to eliminate 97 % of the drugs?
5
33
The context sensitive half time of fentanyl ?
longs 240mns
34
Predicts the time it takes for 50% of a drug to be eliminated from the central compartment when a continuous infusion is discontinued?
Context sensitive half time
35
The plasma half-life of a drug is inversely proportional to its
RATE OF CLEARANCE
36
Hepatic enzyme induction will result in a reduction in the drugs “
HALF TIME or LIFE”
37
Elimination half-life is the
time taken for a drug to lose half of its pharmacologic or physiologic activity.
38
Formula of T ½ is :
T ½ = Vd / Cl
39
Half time of elimination is greater if Vd is ____and clearance is
volume of distribution is LARGE and Clearnce is SMALL
40
Elimination half time and volume of distribution →
Directly proportional
41
Elimination half time and clearance →
Inversely proportional
42
How does the elimination half-time of remifentanil differ from alfentanil?
Elimination half-time is shorter or remifentanil
43
Half-life (hours) =
0.693 x (Volume of distribution (L) / Clearance (L/hr))
44
What causes an increased end-tidal carbon dioxide?
CNS depression
45
INCREASES IN METABOLIC RATE (increased VO2)
Increases CO2 production
46
Hypotension leads to
CO2 production
47
Things that causes an increase in CO2
MASTT FPC
Malignant Hyperthermia
Anxiety
Seizures/ SEPSIS
Thyrotoxicosis
Tourniquet and vascular clamps removal
Fever/ Sodium bicarbonate administration
Pain
CO2 insufflation with laparoscopic surgeries
48
Main mechanism of Increased ETCO2?
Increase alveolar ventilation
49
Elevated ETCO2 with normal plateau?
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
50
Capnography measures
ETCO2 concentration over time.
51
Capnography measures 3 main things?
Assessment of metabolism
Circulation
Ventilation
52
CO2 diffuses airway then from the tissues on, what happen?
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
53
What point in the CO2 waverform is ETCO2 measure?
Point D
54
Normal ETCO2
35-40 mmHg
55
ETCO2 Waveform: An increase alpha angle means
EXPIRATORY AIRFLOW OBSTRUCTION such as COPD, bronchospasm or a KINKED ETT TUBE.
56
Widened beta angle on CO2 waveform means
Incompentent unidirectional valve
57
Identify caused of the abnormal waveform if there is a CARDIAC OSCILLATION?
Heart beating against the lungs
58
Leak in sample time CO2 waveform?
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.
59
2 Methods of CO2 analysis
Mainstream (in line)
Sidestream (diverting )
60
Low ETCO2 indicates
Hyperventilation
Increased alveolar dead space
Decrease CO2 production
61
Alpha angle is where?
between the first expiration upstroke and the plateau line
62
Beta angle is
REBREATHING reading
63
Baseline not returning to zero is
REBREATHING
64
What CO2 analysis method has a faster response time-
Mainstream , does not require a water trap or pumping mechanism
65
Capnogram Phases I.
Dead space gas exhaled
66
Capnogram Phases II.
Transition between airway and alveolar gas
67
Capnogram Phases III.
Alveolar plateau
68
Capnogram Phase IV
Inspiration
69
What CO2 analysis methods is the device attached to the ETT?
-Mainstream (in line)
70
Impaired RELAXATION is what phase of diastolic dysfunction
Grade I
71
Phase I of diastolic dysfunction is
Impaired relaxation
72
Phase II of diastolic dysfunction
Pseudonormal filling
73
Phase III of diastolic dysfunction
Restrictive filling
74
Phase III of diastolic dysfunction
Reversible Restrictive filling
75
Phase IV of diastolic dysfunction
Irreversible Restrictive filling
76
The early manifestation of diastolic dysfunction is characterized by an
impaired relaxation,
77
This stage of disease is known as grade I diastolic dysfunction
inability of the LV to fill adequately during the rapid filling phase. A compensatory increase in filling occurs with atrial contraction.
78
In summary, in grades II and III of diastolic dysfunction, there is a decrease in
LV compliance ensues.
79
Compliance is defined as 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.
80
Grade I : the TMF curve of an individual with abnormal relaxation is represented by a (LeHapDT)
low E, high A, and prolonged DT
81
Grade I diastolic dysfunction, as the LV is
incompletely relaxed when early ventricular filling occurs, t
The pressure gradient, and thus E wave velocity, is less than normal.
82
In Grade I, E wave velocity is
less than normal
83
In Grade I, The delayed relaxation prolongs LV filling late into diastole, and therefore the DT is
prolonged.
84
Because the DT is prolonged in grade I, A compensatory increase in
TMF during atrial contraction, due to the higher residual atrial preload, generates a high A wave velocity
85
A wave in Grade I is
High
86
Progression of diastolic disease leads to grade II diastolic dysfunction, which is marked by
decreases in LV compliance
87
For Grade II, LA pressure rises as a compensatory mechanism to normalize the pressure gradient across the MV. In this scenario, the
TMF velocities resemble the normal curve; thus, this
stage is known as pseudonorma
88
Grade III diastolic dysfunction, known as the
Restrictive phase,
89
Grade III diastolic dysfunction, known as the restrictive phase is characterized by a
significantly decreased LV compliance
90
In Grade III, The high LA–LV pressure gradient produces a
fast acceleration of blood flow in the LV.
91
A high E velocity on the TMF curve is representative for
grade III diastolic dysfunction
92
What represent Grade III diastolic dysfunction?
A high E velocity on the TMF curve
93
In Grade III diastolic dysfunction: LV pressure and effect on DT?
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
94
Cardiac tumors either can originate
from the heart or are metastases from other sites.
95
Cardiac masses can
embolize, cause arrhythmias, or cause heart failure.
96
The most common primary tumor of cardiac is
myxoma,
97
Myxoma most common location
most frequently at the interatrial septum
98
The potential of myxomas to
obstruct the inflow or outflow region of a ventricle is
demonstrated with Doppler echocardiography.
99
The 2nd most common cardiac tumor next most frequent tumor
is . (Fig. 27-42C).
fibroma of the ventricular wall.
100
Fibromas are usually
calcified and can decrease the ventricular volume
101
Renal cell tumors often
extend into the inferior vena cava and right atrium
102
Should be differentiated from tumors.
Pacemaker wires, thrombus, and normal anatomic structures that mimic the appearance of
pathology (Eustachian valve, crista terminalis, Chiari network, or “Coumadin”ridge)
103
During exposure of the aneurysm, burst-suppression on the EEG may be desired to
decrease the impending ischemic burden on the brain from temporary occlusion of large cerebral vessels
104
Burst-suppression can be accomplished with .
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
→ Does not produce burst suppresion
Benzodiazepines
106
Electroencephalogram (EEG) burst suppression is characterized by
periods of isoelectric EEG punctuated by "bursts" of EEG activity.
107
Electroencephalogram (EEG) burst suppression is characterized by
periods of isoelectric EEG punctuated by "bursts" of EEG activity.
108
Burst suppresion is caused by
BARBITURATES and PROPOFOL
109
Burst suppression occurs at close to
to 1.5 MAC
110
Define burst suppression
The "burst" is high-frequency activity and the "suppression" is O.S· to several-second periods of isoelectric activity
111
At greater than 2 MAC, all of the potent agents can produce.
burst suppression or electrical silence
112
These are important factors to remember because EEG changes during administration of general anesthesia can also be caused by
hypoxia, hypercarbia, and hypothermia.
113
Burst suppression can be done by
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
Unlike benzodiazepines, etomidate can
achieve burst suppression with a concomitant
decrease in ICP
115
However, despite its neurodepressant properties at high
doses, etomidate is often associated with
epileptogenic activity (excitatory spikes) on EEG.
116
Thiopental induced
burst suppression and isoelectric EEG prior to potential focal ischemic insult
117
TIVA is associated with
smooth induction and rapid emergence with less postoperative nausea and vomiting.
118
is emerging as a standard method to administer safe anesthesia in neurosurgical patients.
.
Administration of TIVA using target-controlled infusion technique
119
What has become very popular due to their favorable pharmacokinetic and pharmacodynamic properties for neurosurgery case?
The propofol–remifentanil combination has
120
Attractive for ICU sedation in neurosurgery, as patients can participate in neurologic examinations while receiving this medication
Dexmedetomidine
121
The BIS uses a proprietary algorithm that processes the in near real time and computes an index between that
0 and 100
122
EEG indicates the patient’s
level of consciousness.
123
EEG; BIS A value of 100 corresponds to ____and a value of 0 is ____
being completely awake, whereas 0 corresponds to a profound state of coma or unconsciousness that is reflected by an isoelectric or flat EEG.
124
A patient is considered to be appropriately anesthetized when the BIS value is between
40 and 60
125
Since the bispectral index (BIS) is based upon the hypnotic action of agents, the BIS is not affected by
opioids or analgesics.
126
Nitrous oxide alone on BIS
will have no effect on BIS
127
At BIS values lower than 40,
cortical suppression becomes discernible in a raw electroencephalogram as a burst suppression pattern
128
BIS values o 65-85 have been recommended or sedation, whereas values o
For sedation
129
BIS valueshave been recommended for general anesthesia.
40-65
130
BIS and Ketamine
has minimal effect on BIS, and may slightly increase BIS transiently
131
Common second-messenger molecules include
Identify the cyclic nucleotide second messenger that mediates the cellular actions of natriuretic peptide?
cyclic adenosine 3′-5′-monophosphate (cAMP), inositol 1,4,5-trisphosphate (IP 3), 1,2-diacylglycerol (DAG), and calcium ions (Ca 2+).
132
lpratropium (Atrovent) works by blocking the production of what second messenger?
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
By what receptor and second messenger system does glucagon exert its positive inotropic and chronotropic effects?
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
Cyclic GMP, a second messenger, action?
relaxes vascular smooth muscle, thereby promoting vasodilation and a decrease in blood pressure.
135
Certain G-protein subunits
can stimulate or inhibit membrane-bound adenylate cyclase, which catalyzes cAMP formation.
136
Cyclic guanosine monophosphate (cGMP) mediates the
cellular actions of natriuretic peptides.
137
Nitroprusside and nitroglycerin donate nitric oxide (NO).
Nitric oxide (NO) activates the enzyme soluble
guanylate cyclase, which increases the production of cyclic guanosine monophosphate (cGMP).
138
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
cyclic guanosine monophosphate [cGMP])
139
cGMP associated with this medication
Sodium Nitroprusside
140
The b1-adrenergic receptor located on the cardiac sarcolemma is coupled to
adenyl cyclase via a G protein.
141
When activated, adenyl cyclase converts
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
For CCB , The Ca21 functions as a s
econdary messenger—its divalent charge is sufficient to produce conformational change in a number
of cytoplasmic proteins, such as actin-myosin.
143
Name four second messengers for mediating intracellular hormonal functions besides cAMP.
Calcium ions, calmodulin, cyclic guanosine monophosphate (cGMP), and inositol triphosphate ([P3).
144
opioids action can be reversed by direct antagonism with
naloxone,inhibitors of cyclooxygenase, histamine antagonist
145
A direct acting antagonist has
affinity for a receptor but lacks efficacy
146
Silent antagonists are competitive receptor antagonists that have
zero intrinsic activity for activating a receptor.
147
What local anesthetics, those with high pKas or those with low pKas, are most ionized at physiological pH (pH=7.4)? ,
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
The speed of onset of a local anesthetic is determined by its
degree of ionization which, in turn, is determined by its pKa.
149
The greater the degree of ionization of a local anesthetic {the higher the pKa),
the slower the speed of onset.
150
Bupivacaine has a slower onset than
lidocaine because it is more ionized (has a higher pKa of 8.1) than lidocaine (pKa - 7.9) at physiological pH
151
Approximately what % of CO delivered to the vessel-rich organs, although they constitute ______-%only body mass.
75% of resting cardiac output; 10% of total
152
Muscle group % of CO
16% CO
153
Adipose tissue Bone , ligament % CO
6% of CO
154
Phase II of drug metabolism is CONJUGATION
Compound can be readily eliminated from the body
155
What is the significance of phase II reactions?
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
Phase I metabolites may be excreted without
undergoing phase II, and a phase II reaction can precede or occur without a phase I reaction
157
CYP2D6 is functionally absent in 7 percent of , while deficiency is rare among
Caucasians and African Americans; Asians
158
At conventional doses, subjects who are poor metabolizers based upon CYP2D6 genotype will
derive no therapeutic benefit from codeine
159
Cytochrome P450 2C19 enzymes are involved in the metabolism of
proton pump inhibitors and antidepressants.
160
An example is the enzyme CYP2D6, which catalyzes the
conversion of codeine into morphine.
161
Patients with multiple copies of the CYP2D6 gene and who receive codeine will have
large plasma morphine concentrations with all related
beneficial and adverse side effects
162
This is important for drugs that rely on CYP2D6 to convert an
inactive precursor (prodrug), such as codeine, into the active component of pain therapy (for codeine this is
morphine)
163
Poor metabolizers display incomplete analgesia. The
frequency of poor metabolizers varies by ethnicity and is reported to be
8% in whites, 2% to 7% in African Americans and 0% to 0.5% in Asian populations.
164
With CYP 2D6 Patients without an active gene will have no
benefit from treatment with codeine.
165
With CYP2D6 Dangerous circumstances may occur when a
patient is an extensive metabolizer and produces large amounts of the active component.
166
Loading dose is =
Vd x target concentration
167
The loading dose is contingent on the
volume of distribution
168
Maintenance doses are dependent on
plasma clearance.
169
The loading dose is only required for a
few drugs in certain situations while maintenance doses are required for most drugs to maintain the steady-state plasma concentration
170
However, from the clinical perspective, the single most important utility of Vd is calculating the
loading dose of a drug.
171
The most significant aspect of the metabolism of barbiturates (e.g., phenobarbital, thiopental, methohexital) is their effect on the Chronic use of
hepatic microsomal enzyme system (cytochrome P450 (CYP) enzymes).
172
These effects are dependent on the duration of exposure to the barbiturate. Acutely, barbiturates interact with various
CYPs and inhibit the biotransformation of other CYP substrates;
173
Other substrates (e.g., other drugs or endogenous substrates) can inhibit the barbiturate
metabolism.
174
Barbiturates will cause upregulation, or induction, of the microsomal enzymes (CYPs 1A2, 2C9, 2C19, and 3A4), increasing the
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
Acute barbiturates abuse
decrease anesthetic requirements.
176
A phenol group substitution at position 5 of barbiturates forms phenobarbital. What clinically useful feature does the phenol substitution create
Phenobarbital has a phenol group substitution at position 5-the phenol substitution confers an anticonvulsant property to the barbiturate.
177
On the ECG, ST segment depression of greater
than 1 mm provides evidence of myocardial ischemia
178
ST segment monitoring To interpret ST segment changes properly, the
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
ST-segment elevation
(J point
180
The “a” wave on the central venous pressure tracing corresponds to which on the EKG tracing?
P wave
181
The y-descent of the CVP waveform corresponds to the
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
The a wave follows the
P wave on the ECG.
183
The c wave immediately follows the
start of the QRS complex on ECG.
184
The v wave appears
shortly after the start of the wave on the ECG.
185
Y descent Mechanical event vs electrical events →
RA empties through open tricuspid valve (mechanical) After T wave ends
186
V wave Mechanical event vs electrical events -->
Passive filling of RA (mechanical) Just after T wave begins (ventricular repolarization)
187
X Descent Mechanical event vs electrical events→
RA relaxation (mechanical) ST segment (Electrical event)
188
C wave Mechanical event vs electrical events -->
Right ventricular contraction (building of Tricuspid in RA)'->mechanical Just after the QRS complex (ventricular depolarization)
189
A wave Mechanical event vs electrical events →
Right atrial contraction (mechanical)
Just after the P wave (Atrial depolarization)
190
T wave corresponds with _____wave →
v wave
191
ST segment corresponds with _______→
x descent
192
QRS complex corresponds with --->
C wave
193
V wave is the →
passive filling
194
X descent is →
Right atrial relaxation
195
What three measures are taken to increase the accuracy and precision of the cardiac outputs measured by thermodilution?
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
Factors that influence themodilution CO measurement: Underestimate CO
Injectate volume too high
Injectate solution too cold
197
Which situation underestimates CO obtained by the thermodilution method?
High Injectate volume
198
False high thermodilution cardiac output determinations occur when the injectate volume is
TOO SMALL
199
False low determinations occur when injectate volume is
TOO LARGE
200
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?
Calculated cardiac output will be lower than the true cardiac output
201
The area under the curve will be larger if a greater volume is injected; so cardiac output will be
falsely low
202
Avoid measurements of cardiac output using the thermodilution method during
electrocautery.
203
Right atrium:
15-22 cm (15-20)
204
Right ventricle:
25- 35 cm (30)
205
Pulmonary artery
40- 50 cm (40)
206
The distance from SKIN to the junction of the VC and RA is
15 cm
207
Insertion site to VC and RA junction: Left IJ insertion site.
20 cm
208
Pulmonary wedge distance
45- 50 cm (45)
209
Vena Cava and R atrial Junction --> catheter tip:
PA 40cm
210
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
The subclavian vein
211
Distance to the junction of the vena cava and the
internal jugular veins ; femoral vein and right basilica vein
(15–20 cm); 40 ; 40
212
O2-Hb Curve Shifts Right Shift means
lower affinity for O2 = increased unloading at tissues)
213
O2 dissociation curve shifts to the RIGHT with
Acidosis • Hyperthermia • Hypercarbia • Increased 2,3-DPG • Sickle Cell Hb • Pregnancy • Volatile anesthetics • Chronic anemia
214
O2 dissociation curve: Left Shift means
(higher affinity for O2 = decreased unloading at tissues)
215
O2 dissociation curve shifts to the LEFT with
• Alkalosis • Hypothermia • Hypocarbia • Decreased 2,3-DPG • CO-Hb • Met-Hb • Sulf-Hb • Fetal Hb • Myoglobin
216
The P50 is the oxygen tension at which
hemoglobin is 50% saturated.
217
The normal P50 is
26.7 mm Hg. or 27 mmHg
218
The gold standard of verification is sustained detection of D tube positively identified in it,
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
Therefore, absence of Petco2 indicates
esophageal intubation, circuit disconnection, cardiac arrest, or airway obstruction.
220
A false-positive result may be obtained after
gastric inflation with CO2 containing gas or digestion of carbohydrate-enriched beverages. E
221
ETT-misplacement can be excluded by observing a
normal Petco2 waveform for three to six consecutive breaths.
222
An end-tidal C02 (ETC02) partial pressure of< 5 mm-Hg is diagnostic of what
Esophageal intubation.
223
Reliable signs to avoid esophageal intubation
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
Esophageal probe contraindicated in
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
may also cause an increase in CO2 concentration.
A leak or obstruction in the anesthesia machine circuit, common gas outlet, or fresh gas supply line
226
“Curare” cleft—seen normally in the last part of phase III caused by 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
Drugs with significant renal excretion with anesthesia \
AACDENN
Aminoglycosides
Atenolol
Cephalosporins
Digoxin
Edrophonium
Nadolol
Neogstimine
228
Drugs with significant renal excretion with anesthesia
4Ps and QRS
Pancuronium
PCN
Procainamide
Pyridostigmine
Quinolones
Rocuroncium
Sugammadex
229
CYP2C19 Substrate
POWD
Propranolol
Omeprazole
Warfarin
Diazepam
230
Cyclic Guanosine Monophosphate (cGMP) target responses
Activate protein kinase
231
Cyclic Guanosine Monophosphate (cGMP) common drugs effectors are
Nitroglycerin
Sodium Nitroprusside
232
Phosphoinositides and calcium : Target responses
Activate Calmodulin
233
Phosphoinositides and calcium : common drug effector
Lithium
234
Cyclic Adenosine monophosphate cAMP (CMC)
Caffeine
Milrinone
Catecholamines
235
Cyclic AMP responses
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
Distance to the Junction of the Venae Cavae and Right Atrium from Various Distal Anatomic Sites Subclavian
10cm
237
Distance to the Junction of the Venae Cavae and Right Atrium from Various Distal Anatomic Sites Right Internal J vein
15 cm
238
For example, at a PO2 of 40 mm Hg, Hgb is approximately
75% saturated
239
Phenytoin on NDNMB
shortens the duration of action of the nondepolarizing neuromuscular junction blocking agents by inducing CYP3A4 and therefore increasing elimination
clearance of the drug.
240
The patient undergoing surgery has a decline in core
body temperature that occurs via five mechanisms:
(1) redistribution,
(2) radiation
(3) conduction
(4) convection
(5) evaporation.
241
Redistribution is the transfer of heat from
the peripheral compartments of the body to the central core
