Exam 2 Flashcards
(300 cards)
1
Q
Anterior internodal tract gives rise to_______.
A
Bachmann bundle
2
Q
Middle internodal tract gives rise to ___________.
A
Wenkebach tract
3
Q
Posterior
A
Thorel tract
3
Q
internodal tract gives rise to ____________.
A
Thorel tract
4
Q
_____________ is a pathological accessory pathway responsible for Wolf-Parkinson White syndrome.
A
Kent’s Bundle
5
Q
Slowest conduction
A
SA and AV nodes (0.02-0.1 m/sec)
6
Q
Intermediate conduction
A
myocardial muscle cells (0.3-1m/sec)
7
Q
fastest conduction
A
His bundle, bundle branches and Purkinje fibers (1-4m/sec)
8
Q
The conduction velocity quantifies
A
how fast an electrochemical impulse propagates along a neural pathway.
9
Q
Conduction velocity is a function of:
A
- Resting membrane potential
- Amplitude of action potential
- Rate of change in membrane potential during Phase 0
10
Q
Conduction velocity is affected by:
A
-ANS tone
-hyperkalemia induced closure of fast Na+ channels
-ischemia
-acidosis
-antiarrythmic drugs
11
Q
What is the only electrical pathway between cardiac chambers and the “gate-keeper” of electrical transmission between atria and ventricles
A
AV node
12
Q
James fiber accessory pathway connection
A
Atrium to AV node
13
Q
Atrio-hisian fiber accessory pathway and connection
A
atrium to his bundle
14
Q
Kent’s bundle accessory pathway and connection
A
atrium to ventricle
15
Q
Mahaim bundle pathway and connection
A
AV node to ventricle
16
Q
absolute refractory period
A
no stimulus (no matter how strong) can depolarize the myocyte
17
Q
Relative refractry period
A
larger than normal stimulus required to depolarize the myocyte
18
Q
Phase 0
A
-Depolarization
-Na” in
-QRS
19
Q
Phase 1
A
initial repolarization
- Cl in
-K out
-QRS
20
Q
Phase 2
A
-plateau
-Ca+ in
-K+ out
-ST segment
21
Q
Phase 3
A
-final repolarization
-K+ out
-T wave
22
Q
Phase 4
A
-resting phase
-K+ leak
-end of T wave–>QRS
23
Q
P wave duration
A
0.08-0.12 sec
24
PR interval
0.12-0.20 sec
25
Q wave duration
<0.04 sec
26
QRS complex duration
<0.10
27
Biphasic P wave (lead II) suggest what?
LA enlargement
-think about mitral stenosis
28
Tall P waves suggest what?
RA enlargement
-think about cor pulmonale
29
PR interval depression may suggest:
1. viral pericarditis
2. atrial infarction
30
Consider MI if Q wave:
-amplitude is >1/3 of R wave
-duration is greater than 0.04 sec
-depth is greater than 1mm
31
QRS complex if increased consider:
-LVH, bundle branch block, ectopic beat, WPW
32
QTc interval
men <0.45 sec
women <0.47 sec
33
ST segment consider MI if
elevation or depression greater than 1mm
34
ST segment elevation also caused by
-hyperkalemia
-endocarditis
35
U wave is usually absent. If > 1.5mm then consider______.
decreased K+
36
Osborn wave is usually absent. A small positive deflection immediately after QRS complex (at beginning of ST segment) may occur with _____.
hypothermia.
37
_______ segment is an isoelectric line. Because of this, it is used as a reference point for measuring ST elevation and depression.
PR
38
The ______ is where the QRS complex ends and the ST segment begins.
J point.
-by measuring this point relative to the PR segment, we can quantify the amount of ST elevation and depression.
-as a rule, > +1.0 or -1.0 are significant.
39
EKG changes--too high calcium
short QT
40
EKG change- calcium too low
long QT
41
EKG change-too high potassium
-narrow and peaked T
-short QT
-Wide QRS
-Low P amplitude
-nodal block
-sine wave fusion of QRS and T-->VF or asystole
order early to late
42
EKG change--too low K
-U wave
-ST depression
-Flat T wave
-long QT interval
43
What is the mean electrical vector?
The average current flow of all action potentials at any given time. The waveform on the EKG is a measure of mean electrical vector
44
A positive deflection in the EKG occurs when the vector of depolarization travels toward the positive electrode
45
A biphasic deflection on EKG occurs when vector of depolarization travels ____________.
perpendicular to positive electrode
46
Bipolar leads
I, II, III
47
Limb leads
aVR, aVL, aVFpre
48
precordial leads
V1-V6
49
Heart depolarizes (QRS) from:
base to apex
Endocardium to epicardium
50
vector of repolarization T wave
repolarizes in opposite direction
apex to base
epicardium to endocardium
51
Normal Axis
Lead 1 +
Lead aVF +
normal axis is between -30 and + 90
52
Left axis deviation
Lead 1 +
Lead aVF -
left axis deviation is more - than -30 degrees
53
Right axis deviation
Lead I -
Lead aVF +
right axis deviation is more + than 90 degrees
54
Extreme right deviation
Lead I -
Lead aVF -
55
Causes of right axis deviation
-COPD
-acute bronchospasm
-cor pulmonale
-pulmonary HTN
pulmonary embolus
56
causes of left axis deviation
-Chronic HTN
-LBBB
-aortic stenosis
-aortic insufficiency
-mitral regurgitation
57
The mean electrical vector tends to point towards______.
towards areas of hypertrophy (there is more tissue undergoing depolarization)
58
the mean electrical vector tends to point away from _______.
from the area of MI (the vector has to move around these areas)
59
Which reflex is associated with sinus arrythmia?
Bainbridge
occurs when there is increased venous return stretches the RA and SA node causing HR to increase.
Sinus arrhythmia occurs when SA nodes pacing rate varies with respiration
-usually benign
60
What does inhalation do to HR in sinus arrhythmia?
increased HR from decreased intrathoracic pressure and increased venous return
61
What does exhalation do to HR in sinus arrhythmia?
decreases heart rate. Increased intrathoracic pressure decreases venous return.
62
What is the first line treatment of sinus bradycardia?
Atropine
63
What dose of atropine can cause parodoxical bradycardia?
<0.5mg. Probably mediated by presynaptic muscarinic receptors
64
What is useful in the setting of B blocker or CCB overdose?
glucagon
-by stimulating glucagon receptors in the myocardium, glucagon effectively increases cAMP, leading to increased HR and AV conduction
65
tx for acute onset a-fib
cardioversion (100 joules)
66
if a-fib onset >48 hours what must be performed?
TEE to r/o atrial thrombus
-new onset or undx a-fib indication to cancel sx
67
What is the most common post-op tach dysrhythmia usually occurring post-op days 2 & 4 and most common in older patients after cardiothoracic surgery?
a-fib
68
How is a-flutter different from a-fib?
it is an organized supraventricular rhythm.
Atrial rate 250-350 dpm
69
hemodynamically unstable a-flutter should be tx with?
cardioversion (start 50 joules)
70
Which rhythm occurs when the AV node functions as a dominant pacemaker?
junctional rhythm
71
In junctional rhythm, HR slow (40-60) because
rate of Phase 4 depolarization of AV node is slow
-can be caused by SA node depression (VA), SA node block or prolonged conduction at AV node
-atropine 0.5mg can be given if hemodynamics are impacted by slow rate
72
conditions associated with PVCs
-MI or infection
-valvular heart disease
-cardiomyopathy
-prolonged QT interval
-hypokalemia
-hypomagnesemia
-digitalis toxicity
-caffeine
-alcohol
-mechanical irritation
73
When should you tx PVCs?
when frequent >6/min polymorphic or when runs of 3 or more
74
Tx of PVC
-reverse underlying cause: hypoxia, hypercarbia. correction of electrolyte imbalances, D/c QT prolonging drugs. repositioning central line
-symptomatic: lidocaine 1.0-1.5mg/kg, if continue, infusion 1-4mg/min
75
Patients with Brugada syndrome have ________.
pseudo-RBBB and persistent ST elevations in V1-V2
76
Brugada syndrome is most common in___.
males from southeast asia
77
Brugada is ____ ion channelopathy in the heart.
Na++
78
Brugada syndrome may require_____
. ICD or pad placement during sx.
79
Type 1 brugada
ST elevations > or equal to 2mm
-downsloping ST segment
-inverted T wave
80
Type 2 Brugada
ST elevations > or equal to 2mm
-
saddle back ST-T wave configuration
-upright or biphasic T wave
81
1st degree heart block interval
-PR interval >0.20 sec
82
Affected region 1st degree heart block interval
AV node or HIS bundle
83
1st degree heart block poem
if r is far from P then you have a first degree
84
etiology 1st degree heart block
-age related degenerateive changes
-CAD
-digoxin
-amiodarone
85
2nd degree heart block Mobitz type 1
-longer, longer, longer drop then you have a Wenckebach
-PR interval becomes progressively longer with each cycle, but the last P wave does not conduct to the ventricles
86
affected region 2nd degree heart block type 1
Av node
87
tx asymptomatic 2nd-degree type 1 heart block
monitor
88
tx symptomatic 2nd degree type 1 heart block
atropine
89
etiology 2nd degree heart block mobitz type 1
-structural conduction defects
-MI
-B blocker
-CCB
-digoxin
-sympatholytic agent
90
2nd degree heart block 2
if some p's dont get through then you have a mobitz 2
91
affected region of 2nd degree heart block type 2
his bundle or bundle branches
92
etiology 2nd degree heart block mobitz type 2
=structural conduction defect or infarction
93
Tx 2nd degree heart block mobitz type 2
often symptomatic (palpitations and syncope)
-pacer
-atropine usually not effective
-high risk of progressing to complete heart block
94
3rd degree heart block
-if Ps and Qs dont agree then you have a 3rd degree
-atria and ventricles have their own rates (AV dissociation)
95
3rd degree heart block etiology
-fibrotic degeneration of atrial conduction system
-Lenegre's disease
96
3rd degree heart block tx
-often symptomatic(dyspnea, sncope, weakness, vertigo)
-isoproterenol (chemical pacer)
-can lead to CHF d/t decreased HR And CO
-stokes-adams attack=decreased CO -->decreased cerebral perfusion-->syncope
97
Class 1A sodium channel blockers
Quinidine, Procainamide, Disopyramide
-moderate depression Phase 0
-prolongs phase 3 repolarization (K+ channel block--> increased QT)
98
1B sodium channel blockers
Lidocaine, Phenytoin
-weakened depression phase 0
-shortened phase 3 repolarization
99
Class 1C sodium channel blockers
Flecainide, Propafenone
-strong depression phase o
-little effect phase 3
100
class 2
Beta blockers
-slow phase 4 depolarization
101
Class 3
K+ channel blockers
-Amodarone, Bretylium
-prolongs phase 3 repolarization (increased QT)
-increased effective refractory period
102
Class 4
CCB (verapamil, diltiazem)
-decreased conduction velocity through AV node
103
Adenosine is a _____________
endogenous nucleoside, slows conduction through AV node
104
By stimulating cardiac adenosine 1 receptor, this causes___________.
potassium efflux, hyperpolarizes the membrane, slows AV conduction
105
Uses of adenosine
-SVT and WPW with narrow QRS
not useful for a-fib, a-flutter, and v-tach
106
How is adenosine metabolism?
in plasma (t1/2 5 sec)
107
Adenosine can cause______________.
bronchospasm in asthmatic patients
108
Peripheral dose of adenosine
-preferred
-1st dose=6mg
-2nd dose=12mg
109
Central line dose of adenosine
1st dose-3mg
-2nd dose=6mg
110
conduction through reentry pathway
-process where a single cardiac impulse can move backwards and exciite the same part of the myocardium over and over
-since the ratio of SA node discharge and cardiac contraction can exceed 1:1 rate, risk that impulse circles around reentry pathway and precipitate reentry tachyarrythmia
111
2 ways to distrupt the reentry circuit
1. slow conduction velocity through the circuit
2. increase refractory period of cells at the location of the unidirectional block
112
conduction occurs over long distance ex
left atrial dilation due to mitral stenosis
113
ex of conduction velocity too low
-ischemia
-hyperkalemia
114
ex of refractory period being shorter
-epinephrine
-electric shock from alternating current
115
most common preexcitation syndrome
wolf-parkinson white
116
What is the defining feature of WPW
-accessory conduction pathway (Kent's bundle) that bypasses the AV node
117
common findings on EKG in patient with WPW
-delta wave caused by ventricular preexcitation
-short PR interval (<0.12 sec)
-wide QRS complex
-possible T wave inversion
118
What is the most common tachydysrhythmia associated with WPW
AV nodal reentry tachycardia
119
What is the most common AV nodal reentry pathway associated with WPW?
orthodromic AVNRT (90%)
120
What is the more dangerous AV nodal reentry pathway associated with WPW?
antidromic
121
What is the conduction pathway in orthodromic AVNRT?
signal passes through AV node first
Atrium-->Av node-->ventricle-->accessory pathway
122
What is the conduction pathway in antidromic AVNRT?
signal passes through accessory pathway first
atrium-->accessory pathway-->ventricle-->AV node
123
Which AVNRT is associated with narrow QRS complex?
orthodromic
124
Which AVNRT is associated withe wide QRS complex?
antidromic
125
Which drugs should you avoid with antidromic AVNRT?
-adenosine
-digoxin
-CCB (diltiazem and verapamil)
-B blockers
-lidocaine
126
Tx of orthodromic AVNRT
Block conduction at AV node by increasing AV node refractory period
-cardioversion
-vagal maneuvers
-adenosine
-B blockers
-verapamil
-amiodarone
127
Tx of antidromic AVNRT
block conduction at the accessory pathway by increasing the Accessory pathways refractory period
-cardioversion
-procainamide
128
Why is antidromic AVNRT more dangerous?
Because the gatekeeper function of the AV node is bypassed and the Heart can increase well beyond the heart's pumping ability, dramatically reducing filling time
129
True or false: If you give a drug that preferentially blocks the AV node to a patient with antidromic AVNRT you'll force conduction along the accessory pathway which can induce v-fib.
true
130
How can you tx a fib in a patient with WPW?
procainamide=tx of choice because increases the refractory period in accessory pathway.
-if patient is hemodynamically unstable cardioversion is best option
131
Definitive tx for WPW
radiofrequency ablation
132
What is the risk of radiofrequency ablation?
thermal injury to LA and esophagus must closely monitor esophageal temp
133
What type of tachycardia is torsades de pointes?
ventricular tachycardia
-"twisting of spikes"
-underlying cause=delay in ventricular repolarization, phase 3 of action potential
134
Metabolic disturbances responsible for torsades de pointes
-hypokalemia
-hypocalcemia
-hypomagnesemia
135
drugs responsible for torsades de pointes
-methadone
-droperidol (12 lead EKG required prior to use)
-haloperidol
-ondansetron
-halogenated agents
-amiodarone (esp with hypokalemia)
-quinidine
136
genetic syndrome responsible for torsades de pointes
"Think R on T phenomenon"
-Romano-ward syndrome
-Timothy syndrome
137
misc causes responsible for torsades de pointes
-hypertrophic cardiomyopathy
-subarachnoid hemorrhage
-bradycardia
138
prevention of torsades in patient with long QT
-may require B blocker prophylaxis and or ICD placement
-avoid SNS stimulation
139
acute tx of torsades
-reverse underlying cause and/or shorten QT interval
-mag sulfate
-cardiac pacing to increase HR with decrease AP duration and QT interval
140
indications for cardiac pacemaker
-symptomatic disease of impulse formation(Sa node disease)
-symptomatic disease of impulse conduction (AV node disease)
-long QT syndrome
-dilated cardiomyopathy
-hypertrophic obstructive cardiomyopathy
141
Pacers are categorized by ____letter code. Each letter describes a function performed by a particular pacemaker
5
142
PaSER pneumonic
Pa=chamber paced
Se=chamber sensed
R=response
143
Position 1
chamber is paced
144
Position 2
chamber is sensed
145
Position 1 and 2
O=
A=
V=
D=
O=none
A=atrium
V=ventricle
D=dual (A and V)
146
Position 3
-response sensed by native cardiac activity
O=none
T=triggered
I=inhibited
D=dual (T & I)
T=sensed activity tells pacer to fire
I=sensed activity tells pacer not to fire
D= if native activity sensed then pace inhibited
if native activity not sensed pacer fires
147
Position 4
indicated programmaility of pacemaker
-describes ability to adjust HR in response to physiologic need
sensors can measure respiration, acid-base states, vibration etc
O=none
R=rate modulation
148
Causes of a-fib
hyperthyroidism
hypertension
pe
extra electrical connections
valvular heart disease,
or muscular sleeves from the la to the pulmonary veins.
149
Brugada syndrome tx if patient were to develop VT/torsades
If patient were to develop VT/torsade “[electrical] storm,” you would treat with isoproterenol (isuprel) and not beta blockers
150
Troponin levels increased in the presence of:
Ischemia or infarction
CHF or fluid overload, pneumonias
Pulmonary embolism, pulmonary HTN
Pericarditis or myocarditis
Cardioversion or s/p ablation
Cardiac surgery
151
Which cardiac troponins are sensitive and specific for cardiac damage?
Cardiac troponins T and I are highly sensitive and specific for cardiac damage.
152
Troponin levels increase in timing
Serum levels increase within 3 - 12 hours from the onset of chest pain, peak at 24 - 48 hours, and return to baseline over 5 - 14 days.
If the troponin value remains level over 3 days, it is not cardiac ischemia. Ischemia should cause a rise and decrease in the troponin level.
153
where should arterial line be placed during EP study?
opposite side from electrophysiologists in case adjustment is needed
154
IF cardioversion or defibrillation needed:
-ensure soft bite block so patient does not bite on tongue
-restrain and pad wrists and extremities-can cause significant muscle contracture
155
3 procedural categories for radiofrequency ablation
Supraventricular tachycardia (SVT), atrial flutter, WPW
Atrial fibrillation
Ventricular tachycardia (vtach), premature ventricular contraction (PVC), ventricular nodal re-entrant tachycardia
Note: cases may have epicardial approach
156
Acute increase in _____ during RFA with esophageal temp, requires a warning.
Esophageal temperature monitoring: an acute increase of 1° C requires a WARNING!
Cool the catheter tip
constant vigilance for pericardial tamponade
157
RFA for SVT, WPW, atrial flutter
anesthesia management
Require ~2 – 4 hours
MAC or mild- moderate sedation, need sedation bolus for local femoral access and if foley catheter placed
-remifentanil
158
RFA for a-fib anesthesia
Require ~6 – 10 hours
Generally GA with ETT and anesthesia machine ventilator versus jet ventilation, radial arterial line
159
Anesthesia management for Vtach or PVC mapping
Vtach or PVC mapping (~ 6 – 10 hours)
Most complex – start with MAC during the mapping phase. Assess mental status during Vtach to determine need to cardiovert
Patient factors may preclude MAC (anxiety, obesity).
Use cerebral oximetry to determine need to treat hypotension
Femoral arterial access (may not need radial aline), if patient unstable at end of case, may need radail A-line for post-op care
GA with ETT during RFA ablation or epicardial approach
160
RFA complications
-Vascular (hematoma, bleeding, vascular injury)
-Cardiac tamponade, perforation
-Complete heart block
-Line insertion related (air embolism or pneumothorax)
-Airway trauma/hematoma due to traumatic intubation followed by heparinization
-Nerve palsy as a result of improper positioning
-Esophageal stricture/perforation
-Risk reduction: esophageal temperature probe is positioned directly behind the atrium with fluoroscopic guidance and temperature closely monitored particularly during ablation
-Phrenic nerve injury
-The electrophysiologist can avoid harming the phrenic nerve by identifying its location with pacing and observing where the pacing causes the diaphragm to move avoid muscle relaxants
161
What is placed for symptomatic bradyarrythmias?
permanent pacer
162
What is placed for tachyarrythmias?
ICD
163
External pacing
transcutaneous pacing pads applied to a. anteriorly to right upper chest and anteriorly to left lower chest or b. anteriorly to midchest posteriorly btwn scapulae. Pads plugged into defibrillator/pacing machine
164
Transvenous pacing
pacing catheter passed into central circulation (via introducer sheath) and into appropriate cardiac chamber. Pacing lead connected to external pacemaker generator
165
Bi-ventricular and CRT device lead placement
Bi-ventricular and cardiac resynchronization therapy (CRT) devices have a 3rd lead placed across the coronary sinus on the left ventricle.
166
Epicardial pacing placement
inserted at completion of cardiac sx. Pacing wires directly sewn by cardiac surgeon into epicardium,, passed through skin, attached to external pacing device
167
indications for cardiac pacing
-AV heart block: second degree type II and third degree heart block.
-Symptomatic bradycardia
-AV heart block, post myocardial infarction
-Heart block, post MAZE procedure
-Chronic bifascicular or trifascicular block
-Sinus node dysfunction (sick sinus syndrome)
168
unipolar pacer
one electrode at distal tip of negative lead; the positive pole is in the generator.
169
BIPOLAR pacer
two electrodes located on the lead. Provides smaller, more selective sensing area, thus less “oversensing” potential. Small pacer spike.
170
epicardial leads
leads are placed directly on the heart during cardiac surgery or for biventricular pacing.
-direct cardiac pacing
171
endocardial pacer leads
leads are placed transvenously for either temporary or permanent pacing.
direct cardiac pacing
172
indirect cardiac pacing
Trancutaneous pacing with pacer pads.
Transesophageal pacing with electrodes positioned in the esophagus and resting behind the left atrium or ventricle.
173
dual chamber pacing mode benefits
Intended to preserve a more normal relationship between atrial and ventricular contractions by providing AV synchrony.
Lowers incidence of af (risk of systemic embolism and stroke)
Decreases incidence of CHF; increases LV filling and increases CO by 30-40%
Decreases incidence of mitral and tricuspid regurgitation.
174
biventricular pacing
Biventricular pacers involve 3 leads pacing the RA and the RV and LV
LV lead is passed from the RA into the coronary sinus vein and is placed in a vein on the lateral wall of the LV
Inhibition of BiV pacing with cautery or DOO pacing by using a magnet can result in significant decrease cardiac output and blood pressure.
175
Failure to output
Failure to output: no pacing spike is present
Battery failure
Lead fracture
Poor lead contact
176
oversensing
Oversensing: occurs when a pacer incorrectly senses electrical activity and is inhibited from correctly pacing:
Muscular activity (shivering, contractions, fasciculations)
Electromagnetic interference from cautery
Use bipolar as opposed to monopolar
177
crosstalk
which occurs when the atrial output is sensed by the ventricular lead
178
failure to capture
Failure to capture: occurs when a pacing spike is not followed by either an atrial or a ventricular complex
Lead fracture
Lead dislodgement
Elevated pacing threshold
MI
VF
Metabolic abnormalities (hyperkalemia, acidosis)
179
undersensing
Undersensing: occurs when a pacer incorrectly misses intrinsic depolarization and paces despite intrinsic activity.
Poor lead positioning
Lead dislodgment
Magnet application
Low battery
180
pacer emergencies
Perforation – danger lies in the placement of the right ventricular lead when the patient has a thin ventricular wall.
Rupture or tear – although rare, may occur as a result of the stylet used to “stiffen” the lead during placement, which results in the left ventricular lead lying inside the coronary sinus on the outside of the left ventricle.
“Ventricular standstill” – 2° pre–existing right or left bundle branch block. As the ventricular lead is passing the bundle of his, it can brush against the bundle of his and stun it.
Recognition is key! The physician can quickly advance the lead into the ventricle while the rep turns on the pacing output on the programmer. Once the lead is in the ventricle, the physician can hook up the (hot) pacing cables from the programmer, which creates a sustainable rhythm while the “stunned” bundle of his recovers.
181
What is the mechanism for development of AAA?
destruction of elastin and collagen that form matrix of vessel wall (primary)
-inflammation
-endothelial dysfunction
-platelet activation
-atherosclerosis
182
Which law is applied for AAA knowing that the diameter of AAA correlates with the risk of rupture?
Law of laplace
183
When is surgical correction warranted for AAA?
when anuerysm exceeds 5.5 cm or if it grows more than 0.6-0.8cm per year
184
The classic triad of AAA rupture
-hypotension
-back back
-pulsatile abd mass
185
Where do most AAA rupture?
left retroperitoneum
186
a most common cause of postop death in AAA
MI
187
Independent risk factors for AAA
-cigarette smoking
-male
-gender
-advanced age
188
Type a Stanford
involves Ascending aorta
189
Type B Stanford
does not involve ascending aorta
190
Which crawford type has the most significant periop risks?
Type 2
-paraplegia
and/or
-renal failure because there is a mandatory period of stopping blood flow to renal arteries and some of radicular arteries that perfuse anterior SC (artery of adamkewicz)
191
Which two Crawford types are the most difficult to repair?
Type 2 and 3
192
Which aneurysm is a sx emergency?
Acute dissection of ascending aorta (Debakey 2 or 3)
-the aortic valve often affected so consider aortic insufficiency in plan
-
193
Debakey type 1
tear in ascending + dissection along entire aorta
194
Debakey type 2
tear in ascending and dissection only in ascending aorta
195
Debakey Type 3
tear in proximal descending aorta w/
3a-dissection limited to thoracic aorta
3b-dissection along thoracic and and aorta
196
The patient's physiologic response to the aortic cross-clamp (AoX) is related to 3 factors:
1. location of AoX placement (infrarenal most common)
2. intravascular volume status
3. cardiac reserve
197
Applying the aortic cross clamp creates central hypervolemia by:
-reducing venous capacity
-shifting greater proportion of blood volume proximal to clamp
-increasing venous return
198
removing the aortic cross clamp creates hypovolemia by:
-restoring venous capacity
-shifting a greater proportion of blood to lower body
-decreasing venous return
-creating a capillary leak that contributes to loss of intravascular volume
199
Application of the cross-clamp starves distal tissues of oxygen. These cells convert to anaerobic metabolism which leads to:
-increased lactic acid production-->metabolic acidosis
-increased prostaglandins
-increased activated complement
-increased myocardial depressant factors
-decreased temperature
200
compared to open procedures endovascular aneurysm repair has what benefits?
-shorter operative times
-lower rate of transfusion
-shorter length of stay
-reduced morbidity
201
Is GA or local anesthesia in EVAR associated with improved outcomes?
local/regional
202
Is there a need for aortic cross clamp in EVAR?
no, the patient avoids the respiratory risks associated with large midline abdominal incision
203
Complications associated with EVAR
-dye used-allergic rxn, renal injury
-activation of baroreceptor reflex
-massive hemorrhage
-aortic rupture
-cerebral embolism
204
What is an endoleak?
-occurs when original graft fails to prevent blood from entering aortic sac. Some resolve spontaneously while others require placement of a second graft or open repair
205
How many posterior spinal arteries are there?
2
206
2 posterior spinal arteries perfuse how much of spinal cord?
1/3
207
There is ____anterior spinal artery that perfuses ____ of the SC
1; 2/3
208
The artery of Adamkiewicz perfuses _____________.
anterior spinal cord in the thoracolumbar region
209
Where does the artery of adamkiewicz originate
on the left side between T11-12
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In 75% of the population the artery of adamkiewicz originates between________. another 10% arises at ____.
75% T8-12
10% L1-2
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What are the s/s of spinal artery syndrome(Beck's syndrome)?
-flaccid paralysis
-bowel and bladder dysfunction
-loss of temperature and pain sensation
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Aortic cross clamp placed above artery of adamkiewicz can cause:
ischemia to lower portion of anterior spinal cord causing spinal artery syndrome (beck's syndrome)
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What is preserved because dorsal column is perfused by posterior blood supply?
touch and proprioception
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thoracic cross clamp times >30 min pose significant risk of cord ischemia. Spinal cord strategies include:
-moderate hypothermia (30-32 C) to reduce cord oxygen consumption
-CSF drainage-spinal cord perfusion dependent on pressure gradient between anterior spinal artery and CSF pressure, so a CSF drain will reduce CSF pressure and increase pressure gradient
-proximal HTN during cross clamping (MAP ~100mmHg)
-avoid hyperglycemia
-SSEP and MEP monitoring
-partical CPB (left atrium to femoral artery)
drugs: corticosteroids, CCB and/or mannitol
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What is Amaurosis Fugax?
temporary blindness in one eye
-sign of impending stroke
-occurs in 25% of patients with high-grade stenosis
-emboli travel from internal carotid artery to ophthalmic artery which impairs perfusion to optic nerve causing retinal dysfuction
215
Absolute contraindications to TEE Exam
-previous esophagectomy
-severe esophageal obstruction
-esophageal perforation
-ongoing esophageal hemorrhage
216
Relative contraindications to TEE Exam
-esophageal diverticulum
-varices
-fistula
-previous esophageal surgery
-gastric surgery
-mediastinal radiation
-unexplained swallowing difficulties
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Does Cerebral oximetry detect global cerebral oxygenation?
no, only regional
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How does the cerebral oximetry work?
-contains light emitting diode and 2 light sensors
-a surface photodetector and deep photodetector
-an infrared light follows an elliptical pathway
from emitting diode-->scalp-->skull-->brain-->skull-->scalp-->photodetector
221
a change of ______ from baseline suggests a reduction in cerebral oxygenation
>/= 25%
222
______ can contaminate the NIRS signal
scalp hypoxia
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NIRS may falsely interpret scalp hypoxia as brain ischemia
224
What does cerebral oximetry rely on?
the fact that cerebral blood volume is 1 part arterial to 3 parts venous
75% of blood in the brain is on the venous side of the circulation
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true/false: arterial hgb, venous hgb, and tissue cytochromes absorb different frequencies of infrared light
true
226
The EEG provides information about the electrical activity in the cerebral cortex but offers little information about:
-subcortical structures
-spinal cord
-cranial and peripheral nerves
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Beta wave frequency
-highest frequency
-low voltage
-13-30 cycles/sec
228
What is beta wave activity associated with?
awake and mental stimulation and "light anesthesia"
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Alpha wave frequency
2nd highest frequency
-frequency 8-12 cycles/sec
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What is alpha wave frequency associated with?
awake but restful state with eyes closed
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Theta wave frequency
3rd highest frequency
-4-7 cycles/sec
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what is theta waves associated with?
general anesthesia
children during normal sleep
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Delta wave frequency
<4 cycles/sec
234
what are delta waves associated with?
general anesthesia
deep sleep
brain ischemia or injury
235
Burst suppression
associated with general anesthesia, hypothermia, CPB (cerebral ischemia (especially if its unilateral burst suppression)
236
isoelectricity
-absence of electrical activity
-associated with very deep anesthesia or death
237
induction of anesthesia is associated with:
increased beta wave activity
238
light anesthesia is also associated with
increased beta wave activity
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______ & _______ waves predominate during general anesthesia.
theta and delta
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deep anesthesia
burst suppression
241
at ____ MAC general anesthetics cause complete suppression or isoelectricity.
1.5-2.0
242
nitrous oxide alone
increases beta wave activity
243
Sevoflurane can increase ______
epileptiform EEG activity
244
Etomidate can cause
myoclonus but is not associated with epileptiform EEG activity
245
Ketamine can increased ______ and may confuse EEG interpretation
increase high frequency cortical activity
the patient may be deeper than the EEG suggests
246
burst suppression may occur with :
-hypothermia especially during CPB
247
The development of new ____waves during anesthetic maintenance may signify that the brain is at risk for ischemia.
delta
248
procedures where EEG monitoring is useful
-carotid endarterectomy (cross clamping impairs cerebral perfusion)
-cerebral aneurysm
-arteriovenous malformation
-cardiopulmonary bypass
-deliberate hypotension
-assessment of barbiturate coma
-epilepsy dx and tx
-coma and death
249
Most common complaint with ascenting aorta
chest pain
250
most common complaint with descending aorta
back or abdominal pain
251
syncope is ominous sign
cardiac tamponda
cerebral hypoperfusion
252
acute ascending aortic dissection motality ____% after symptom onset
1-2%
without surgery mortality exceeds 50% in 1 month
253
aortic aneurysm that is large enough can cause local mass effect due to compression
-trachea-cough
-esophagus-dysphagia
-recurrent larygneal nerve-hoarseness
254
patients should continue taking aspirin until day of surgery for :
carotid and lower extremity surgery
255
surgery indicated for ascending aneurysm
>5.5cm
256
What does aortic arch anuerysm require?
total circulatory arrest
-risk of neurologic damage (global ischemia injury)
-embolization of atherosclerotic debris)
cerebral protection
-cerebral perfusion
-retrograde (via superior venacava cannula)
antegrade (direct cannulation of cerebral vessels)
257
surgery indicated for descending aneuryms
>6cm (notes from PPT)
258
descending aortic aneurysm can be repaired by
-endovascular stent/ graft placed via transluminal approach
-
259
surgical repair associated with postop paraplegia associated with spinal cord blood supply ____%
13-17%
260
spinal cord protection for surgical repair for descending surgical repair
cerebrospinal fluid drainage (lumbar drain)
reimplantation of critical spinal arteries
distal aortic perfusion LA-left femoral artery bypass circuit
intraoperative epidural cooling
somatosensory evoked potentials (SSEPs)
261
The CSF pressure (CSFP) increases during clamping, further decreasing the perfusion pressure of the spinal cord. As more of the blood supply to the spinal cord is interrupted, the likelihood of paraplegia is increased. Various treatments are used to reduce the ischemic insult to the spinal cord, including CSF drainage.
Draining CSF from lumbar region may lessen CSF pressure, thereby improving blood flow to the spinal cord & reducing the risk of ischemic spinal cord injury.
262
The National Veterans Affairs Surgical Risk Study found the highest predictors of morbidity and mortality after vascular surgery include:
Low serum albumin
High ASA physical classification
263
prevention of kidney injury during aneurysm repair
Perioperative kidney injury (AKI) is a common complication of vascular surgery and is associated with high morbidity & mortality
Incidence 16-22% with aortic surgeries
Mortality is 4-5 fold higher with kidney injury
Pathophysiology is multifactorial and includes ischemia/reperfusion injury (IRI); the use of nephrotoxic drugs (ACE inhibitors, NSAIDs, aminoglycosides, diuretics); atheroembolization to renal arteries; and, rhabdomyolosis secondary to injury or immobilization
264
what is the most powerful predictor of postop renal dysfunction in anuerysm repair
preop renal dysfunction
if patient receives chronic dialysis tx they should receive dialysis the day before or same day as sx
-some patients will be hypovolemic as a result hypotension on induction
-women > men increased incidence of perioperative AKI
265
suprarenal versus infrarenal decrease in blood flow
suprarenal decreases renal blood flow by 80%
infrarenal 45%
reduced flow can persist for 30 minutes after release of cross-clamp
266
mannitol effects in renal protection
induces osmotic diuresis, decreases epithelial and endothelial cell swelling, acts as a hydroxyl free-radical scavenger and increases synthesis of prostagladin resulting in renal vasodilation
267
dopamine effects on renal protection
0.5- 2mcg/kg/min renal blood flow, Na+ excretion, and glomerular filtration rate (GFR)
268
non-pharmalogical approaches to prevention of renal injury during aneurysm repair
Goal is to minimize renal ischemia
Cold renal artery perfusion to produce local hypothermia
Remote ischemic preconditioning is thought to prevent IRI in multiple organ systems by inducing ischemic protection pathways
Intermittent cross clamping of the internal iliacs reduce the incidence of renal insufficiency by 23%
However, repeated clamping of non-operative arteries in patients with severe atherosclerosis increases the risk adverse events
269
most effective prevention measure in preventing pulmonary complications following aneurysm repair
postoperative lung expansion, either CPAP or incentive spirometry
270
Spinal cord ischemia occurs up to ____% in operations involving a distal aortic repair
11%
271
Surgeons may place a “________ (a heparinized tube that can decompress the heart and also provide distal perfusion); however, even with a _____ shunt or partial bypass, there may be a period of visceral ischemia
Gott shunt
272
CSF drain protection
A markedly decreased incidence of neurologic deficits were reported with distal aortic perfusion combined with drainage of CSF
CSF drainage improves the pressure gradient, allowing spinal cord blood flow as aortic occlusion lowers distal arterial pressures and increases the CVP
CSF drainage is employed in both endovascular/open techniques
273
risk factors for AAA
Advanced age
Smoking > 40 years
Hypertension
Low serum high density lipoprotein cholesterol
High level of plasma fibrinogen
Low blood platelet count
AAA screening should be done in men age 65 to 75 years of age who smoke.
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how to minimize hypotension after unclamping?
Minimize hypotension after unclamping by:
Volume loading (most important)
Decrease anesthetic depth
Discontinue vasodilators
Slow cross clamp release
A temporary increase in minute ventilation maybe useful to:
Control acidosis
Hypocarbia constricts blood vessels and decreases perfusion to tissues proximal to the clamp thus diverting blood flow to the ischemic tissues (distal to the clamp) creating a “Reverse/Inverse steal or Robin Hood effect.”
275
Beck's snydrome
Flaccid paralysis of the lower extremities = corticospinal tract
Bowel and bladder dysfunction = autonomic motor fibers
Loss of temperature & pain sensation = spinothalamic tract
Touch and proprioception are preserved = dorsal column
276
primary conversion from EVAR to OAR
Primary conversion is classified as an open reoperation within 30 days following EVAR and is most commonly associated with type I “endoleak”
277
most complication of EVAR
Endoleaks – most common complication (30%) defined as persistent blood flow outside the wall of the stent graft into the aneurysm sac
278
secondary conversion from EVAR to OAR
Secondary conversion is aneurysm rupture despite successful sac exclusion
279
Which endoleak types require urgent management due to high-risk sac rupture?
Types I and III are high pressure leaks and generally require urgent management due to high risk of sac rupture.
280
Which clamping carries the highest risk?
supraceliac
281
PAD affecting the lower extremities can bePAD diagnostics
PAD affecting the lower extremities can be detected by the ankle-brachial index, the ratio of the highest systolic ankle pressure to the highest systolic arm blood pressure.
The ankle-brachial index is the single best initial screening test to perform in a patient suspected of having PAD.
The index is obtained with a blood pressure cuff and a hand held continuous wave doppler. It is calculated by dividing the systolic blood pressure at the ankle by the systolic blood pressure in the arm.
A ratio < 0.9 is considered abnormal and a ratio of < 0.4 is often associated with limb threatening ischemia.
282
Carotid disease is usually a problem with _____.
embolization and less often occlusion or insufficiency
283
most common noninvasive test for carotid stenosis
carotid duplex u/s
284
amaurosis fugas
-temporary blindness in 1 eye
-sign of impending stroke
25% of pt with high-grade stenosis
285
during cross clamping BP management
maintain a normal to slightly elevated BP
286
after cross-clamp removed, keep SBP ____
under 145mmHg to decrease bleeding
287
is patients have suffered a stroke are they candidates for CEA?
no, consideration to chronic issues related to the stroke must be evaluated
288
normal cerebral blood flow
40-60ml/100G/min
15% CO
289
normal CMRO2
3-4ml/100G/min
20% o2 consumption
290
What IV solution should not be given to a patient undergoing CEA?
D5W
291
Gray matter blood flow
80ml/100g/min
292
white matter blood flow
20ml/100g/min
293
flow rates <______are associated with impairment
20-25ml/100g/min
294
flow rates between ______show a flattened EEG
15-20ml/100g/min
295
flow rates <______are associated with irreversible brain damage
10ml/100g/min
296
hyperglycemia and CEA
Avoid D5W
Moderate hyperglycemia worsens ischemic brain injury.
Elevated blood glucose levels contribute to the development of severe lactic acidosis during brain ischemia in carotid occlusion resulting in unfavorable neurological outcomes.
297
What corrective measures should the nurse anesthetist implement if intraoperative bradycardia & hypotension occurs?
Surgical manipulation of the carotid sinus & baroreceptors cause symptomatic bradycardia & hypotension.
Request the surgeon locally infiltrate the carotid bifurcation with 1% Lidocaine to control the symptoms.
Treat hypotension with phenylephrine
298
maintain ACT> _____seconds for Carotid artery angioplasty stenting
250 sec
299
most common complication CEA is _____
thromboembolic stroke due to atherosclerotic debris that lodges in cerebral vasculature
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