Exam 2 Flashcards
Anterior internodal tract gives rise to_______.
Bachmann bundle
Middle internodal tract gives rise to ___________.
Wenkebach tract
Posterior
Thorel tract
internodal tract gives rise to ____________.
Thorel tract
_____________ is a pathological accessory pathway responsible for Wolf-Parkinson White syndrome.
Kent’s Bundle
Slowest conduction
SA and AV nodes (0.02-0.1 m/sec)
Intermediate conduction
myocardial muscle cells (0.3-1m/sec)
fastest conduction
His bundle, bundle branches and Purkinje fibers (1-4m/sec)
The conduction velocity quantifies
how fast an electrochemical impulse propagates along a neural pathway.
Conduction velocity is a function of:
- Resting membrane potential
- Amplitude of action potential
- Rate of change in membrane potential during Phase 0
Conduction velocity is affected by:
-ANS tone
-hyperkalemia induced closure of fast Na+ channels
-ischemia
-acidosis
-antiarrythmic drugs
What is the only electrical pathway between cardiac chambers and the “gate-keeper” of electrical transmission between atria and ventricles
AV node
James fiber accessory pathway connection
Atrium to AV node
Atrio-hisian fiber accessory pathway and connection
atrium to his bundle
Kent’s bundle accessory pathway and connection
atrium to ventricle
Mahaim bundle pathway and connection
AV node to ventricle
absolute refractory period
no stimulus (no matter how strong) can depolarize the myocyte
Relative refractry period
larger than normal stimulus required to depolarize the myocyte
Phase 0
-Depolarization
-Na” in
-QRS
Phase 1
initial repolarization
- Cl in
-K out
-QRS
Phase 2
-plateau
-Ca+ in
-K+ out
-ST segment
Phase 3
-final repolarization
-K+ out
-T wave
Phase 4
-resting phase
-K+ leak
-end of T wave–>QRS
P wave duration
0.08-0.12 sec
PR interval
0.12-0.20 sec
Q wave duration
<0.04 sec
QRS complex duration
<0.10
Biphasic P wave (lead II) suggest what?
LA enlargement
-think about mitral stenosis
Tall P waves suggest what?
RA enlargement
-think about cor pulmonale
PR interval depression may suggest:
- viral pericarditis
- atrial infarction
Consider MI if Q wave:
-amplitude is >1/3 of R wave
-duration is greater than 0.04 sec
-depth is greater than 1mm
QRS complex if increased consider:
-LVH, bundle branch block, ectopic beat, WPW
QTc interval
men <0.45 sec
women <0.47 sec
ST segment consider MI if
elevation or depression greater than 1mm
ST segment elevation also caused by
-hyperkalemia
-endocarditis
U wave is usually absent. If > 1.5mm then consider______.
decreased K+
Osborn wave is usually absent. A small positive deflection immediately after QRS complex (at beginning of ST segment) may occur with _____.
hypothermia.
_______ segment is an isoelectric line. Because of this, it is used as a reference point for measuring ST elevation and depression.
PR
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.
EKG changes–too high calcium
short QT
EKG change- calcium too low
long QT
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
EKG change–too low K
-U wave
-ST depression
-Flat T wave
-long QT interval
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
A positive deflection in the EKG occurs when the vector of depolarization travels toward the positive electrode
A biphasic deflection on EKG occurs when vector of depolarization travels ____________.
perpendicular to positive electrode
Bipolar leads
I, II, III
Limb leads
aVR, aVL, aVFpre
precordial leads
V1-V6
Heart depolarizes (QRS) from:
base to apex
Endocardium to epicardium
vector of repolarization T wave
repolarizes in opposite direction
apex to base
epicardium to endocardium
Normal Axis
Lead 1 +
Lead aVF +
normal axis is between -30 and + 90
Left axis deviation
Lead 1 +
Lead aVF -
left axis deviation is more - than -30 degrees
Right axis deviation
Lead I -
Lead aVF +
right axis deviation is more + than 90 degrees
Extreme right deviation
Lead I -
Lead aVF -
Causes of right axis deviation
-COPD
-acute bronchospasm
-cor pulmonale
-pulmonary HTN
pulmonary embolus
causes of left axis deviation
-Chronic HTN
-LBBB
-aortic stenosis
-aortic insufficiency
-mitral regurgitation
The mean electrical vector tends to point towards______.
towards areas of hypertrophy (there is more tissue undergoing depolarization)
the mean electrical vector tends to point away from _______.
from the area of MI (the vector has to move around these areas)
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
What does inhalation do to HR in sinus arrhythmia?
increased HR from decreased intrathoracic pressure and increased venous return
What does exhalation do to HR in sinus arrhythmia?
decreases heart rate. Increased intrathoracic pressure decreases venous return.
What is the first line treatment of sinus bradycardia?
Atropine
What dose of atropine can cause parodoxical bradycardia?
<0.5mg. Probably mediated by presynaptic muscarinic receptors
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
tx for acute onset a-fib
cardioversion (100 joules)
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
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
How is a-flutter different from a-fib?
it is an organized supraventricular rhythm.
Atrial rate 250-350 dpm
hemodynamically unstable a-flutter should be tx with?
cardioversion (start 50 joules)
Which rhythm occurs when the AV node functions as a dominant pacemaker?
junctional rhythm
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
conditions associated with PVCs
-MI or infection
-valvular heart disease
-cardiomyopathy
-prolonged QT interval
-hypokalemia
-hypomagnesemia
-digitalis toxicity
-caffeine
-alcohol
-mechanical irritation
When should you tx PVCs?
when frequent >6/min polymorphic or when runs of 3 or more
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
Patients with Brugada syndrome have ________.
pseudo-RBBB and persistent ST elevations in V1-V2
Brugada syndrome is most common in___.
males from southeast asia
Brugada is ____ ion channelopathy in the heart.
Na++
Brugada syndrome may require_____
. ICD or pad placement during sx.
Type 1 brugada
ST elevations > or equal to 2mm
-downsloping ST segment
-inverted T wave
Type 2 Brugada
saddle back ST-T wave configuration
-upright or biphasic T wave
1st degree heart block interval
-PR interval >0.20 sec
Affected region 1st degree heart block interval
AV node or HIS bundle
1st degree heart block poem
if r is far from P then you have a first degree
etiology 1st degree heart block
-age related degenerateive changes
-CAD
-digoxin
-amiodarone
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
affected region 2nd degree heart block type 1
Av node
tx asymptomatic 2nd-degree type 1 heart block
monitor
tx symptomatic 2nd degree type 1 heart block
atropine
etiology 2nd degree heart block mobitz type 1
-structural conduction defects
-MI
-B blocker
-CCB
-digoxin
-sympatholytic agent
2nd degree heart block 2
if some p’s dont get through then you have a mobitz 2
affected region of 2nd degree heart block type 2
his bundle or bundle branches
etiology 2nd degree heart block mobitz type 2
=structural conduction defect or infarction
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
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)
3rd degree heart block etiology
-fibrotic degeneration of atrial conduction system
-Lenegre’s disease
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
Class 1A sodium channel blockers
Quinidine, Procainamide, Disopyramide
-moderate depression Phase 0
-prolongs phase 3 repolarization (K+ channel block–> increased QT)
1B sodium channel blockers
Lidocaine, Phenytoin
-weakened depression phase 0
-shortened phase 3 repolarization
Class 1C sodium channel blockers
Flecainide, Propafenone
-strong depression phase o
-little effect phase 3
class 2
Beta blockers
-slow phase 4 depolarization
Class 3
K+ channel blockers
-Amodarone, Bretylium
-prolongs phase 3 repolarization (increased QT)
-increased effective refractory period
Class 4
CCB (verapamil, diltiazem)
-decreased conduction velocity through AV node
Adenosine is a _____________
endogenous nucleoside, slows conduction through AV node
By stimulating cardiac adenosine 1 receptor, this causes___________.
potassium efflux, hyperpolarizes the membrane, slows AV conduction
Uses of adenosine
-SVT and WPW with narrow QRS
not useful for a-fib, a-flutter, and v-tach
How is adenosine metabolism?
in plasma (t1/2 5 sec)
Adenosine can cause______________.
bronchospasm in asthmatic patients
Peripheral dose of adenosine
-preferred
-1st dose=6mg
-2nd dose=12mg
Central line dose of adenosine
1st dose-3mg
-2nd dose=6mg
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
2 ways to distrupt the reentry circuit
- slow conduction velocity through the circuit
- increase refractory period of cells at the location of the unidirectional block
conduction occurs over long distance ex
left atrial dilation due to mitral stenosis
ex of conduction velocity too low
-ischemia
-hyperkalemia
ex of refractory period being shorter
-epinephrine
-electric shock from alternating current
most common preexcitation syndrome
wolf-parkinson white
What is the defining feature of WPW
-accessory conduction pathway (Kent’s bundle) that bypasses the AV node
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
What is the most common tachydysrhythmia associated with WPW
AV nodal reentry tachycardia
What is the most common AV nodal reentry pathway associated with WPW?
orthodromic AVNRT (90%)
What is the more dangerous AV nodal reentry pathway associated with WPW?
antidromic
What is the conduction pathway in orthodromic AVNRT?
signal passes through AV node first
Atrium–>Av node–>ventricle–>accessory pathway
What is the conduction pathway in antidromic AVNRT?
signal passes through accessory pathway first
atrium–>accessory pathway–>ventricle–>AV node
Which AVNRT is associated with narrow QRS complex?
orthodromic
Which AVNRT is associated withe wide QRS complex?
antidromic
Which drugs should you avoid with antidromic AVNRT?
-adenosine
-digoxin
-CCB (diltiazem and verapamil)
-B blockers
-lidocaine
Tx of orthodromic AVNRT
Block conduction at AV node by increasing AV node refractory period
-cardioversion
-vagal maneuvers
-adenosine
-B blockers
-verapamil
-amiodarone
Tx of antidromic AVNRT
block conduction at the accessory pathway by increasing the Accessory pathways refractory period
-cardioversion
-procainamide
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
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
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
Definitive tx for WPW
radiofrequency ablation
What is the risk of radiofrequency ablation?
thermal injury to LA and esophagus must closely monitor esophageal temp
What type of tachycardia is torsades de pointes?
ventricular tachycardia
-“twisting of spikes”
-underlying cause=delay in ventricular repolarization, phase 3 of action potential
Metabolic disturbances responsible for torsades de pointes
-hypokalemia
-hypocalcemia
-hypomagnesemia
drugs responsible for torsades de pointes
-methadone
-droperidol (12 lead EKG required prior to use)
-haloperidol
-ondansetron
-halogenated agents
-amiodarone (esp with hypokalemia)
-quinidine
genetic syndrome responsible for torsades de pointes
“Think R on T phenomenon”
-Romano-ward syndrome
-Timothy syndrome
misc causes responsible for torsades de pointes
-hypertrophic cardiomyopathy
-subarachnoid hemorrhage
-bradycardia
prevention of torsades in patient with long QT
-may require B blocker prophylaxis and or ICD placement
-avoid SNS stimulation
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
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
Pacers are categorized by ____letter code. Each letter describes a function performed by a particular pacemaker
5
PaSER pneumonic
Pa=chamber paced
Se=chamber sensed
R=response
Position 1
chamber is paced
Position 2
chamber is sensed
Position 1 and 2
O=
A=
V=
D=
O=none
A=atrium
V=ventricle
D=dual (A and V)
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
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
Causes of a-fib
hyperthyroidism
hypertension
pe
extra electrical connections
valvular heart disease,
or muscular sleeves from the la to the pulmonary veins.
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
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
Which cardiac troponins are sensitive and specific for cardiac damage?
Cardiac troponins T and I are highly sensitive and specific for cardiac damage.
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.
where should arterial line be placed during EP study?
opposite side from electrophysiologists in case adjustment is needed
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
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
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
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
RFA for a-fib anesthesia
Require ~6 – 10 hours
Generally GA with ETT and anesthesia machine ventilator versus jet ventilation, radial arterial line
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
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
What is placed for symptomatic bradyarrythmias?
permanent pacer
What is placed for tachyarrythmias?
ICD
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
Transvenous pacing
pacing catheter passed into central circulation (via introducer sheath) and into appropriate cardiac chamber. Pacing lead connected to external pacemaker generator
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.
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
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)
unipolar pacer
one electrode at distal tip of negative lead; the positive pole is in the generator.
BIPOLAR pacer
two electrodes located on the lead. Provides smaller, more selective sensing area, thus less “oversensing” potential. Small pacer spike.
epicardial leads
leads are placed directly on the heart during cardiac surgery or for biventricular pacing.
-direct cardiac pacing
endocardial pacer leads
leads are placed transvenously for either temporary or permanent pacing.
direct cardiac pacing
indirect cardiac pacing
Trancutaneous pacing with pacer pads.
Transesophageal pacing with electrodes positioned in the esophagus and resting behind the left atrium or ventricle.
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.
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.
Failure to output
Failure to output: no pacing spike is present
Battery failure
Lead fracture
Poor lead contact
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
crosstalk
which occurs when the atrial output is sensed by the ventricular lead
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)
undersensing
Undersensing: occurs when a pacer incorrectly misses intrinsic depolarization and paces despite intrinsic activity.
Poor lead positioning
Lead dislodgment
Magnet application
Low battery
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.
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
Which law is applied for AAA knowing that the diameter of AAA correlates with the risk of rupture?
Law of laplace
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
The classic triad of AAA rupture
-hypotension
-back back
-pulsatile abd mass
Where do most AAA rupture?
left retroperitoneum
a most common cause of postop death in AAA
MI
Independent risk factors for AAA
-cigarette smoking
-male
-gender
-advanced age
Type a Stanford
involves Ascending aorta
Type B Stanford
does not involve ascending aorta
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)
Which two Crawford types are the most difficult to repair?
Type 2 and 3
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
-
Debakey type 1
tear in ascending + dissection along entire aorta
Debakey type 2
tear in ascending and dissection only in ascending aorta
Debakey Type 3
tear in proximal descending aorta w/
3a-dissection limited to thoracic aorta
3b-dissection along thoracic and and aorta
The patient’s physiologic response to the aortic cross-clamp (AoX) is related to 3 factors:
- location of AoX placement (infrarenal most common)
- intravascular volume status
- cardiac reserve
Applying the aortic cross clamp creates central hypervolemia by:
-reducing venous capacity
-shifting greater proportion of blood volume proximal to clamp
-increasing venous return
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
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
compared to open procedures endovascular aneurysm repair has what benefits?
-shorter operative times
-lower rate of transfusion
-shorter length of stay
-reduced morbidity
Is GA or local anesthesia in EVAR associated with improved outcomes?
local/regional
Is there a need for aortic cross clamp in EVAR?
no, the patient avoids the respiratory risks associated with large midline abdominal incision
Complications associated with EVAR
-dye used-allergic rxn, renal injury
-activation of baroreceptor reflex
-massive hemorrhage
-aortic rupture
-cerebral embolism
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
How many posterior spinal arteries are there?
2
2 posterior spinal arteries perfuse how much of spinal cord?
1/3
There is ____anterior spinal artery that perfuses ____ of the SC
1; 2/3
The artery of Adamkiewicz perfuses _____________.
anterior spinal cord in the thoracolumbar region
Where does the artery of adamkiewicz originate
on the left side between T11-12
In 75% of the population the artery of adamkiewicz originates between________. another 10% arises at ____.
75% T8-12
10% L1-2
What are the s/s of spinal artery syndrome(Beck’s syndrome)?
-flaccid paralysis
-bowel and bladder dysfunction
-loss of temperature and pain sensation
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)
What is preserved because dorsal column is perfused by posterior blood supply?
touch and proprioception
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
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
Absolute contraindications to TEE Exam
-previous esophagectomy
-severe esophageal obstruction
-esophageal perforation
-ongoing esophageal hemorrhage
Relative contraindications to TEE Exam
-esophageal diverticulum
-varices
-fistula
-previous esophageal surgery
-gastric surgery
-mediastinal radiation
-unexplained swallowing difficulties
Does Cerebral oximetry detect global cerebral oxygenation?
no, only regional
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
a change of ______ from baseline suggests a reduction in cerebral oxygenation
> /= 25%
______ can contaminate the NIRS signal
scalp hypoxia
NIRS may falsely interpret scalp hypoxia as brain ischemia
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
true/false: arterial hgb, venous hgb, and tissue cytochromes absorb different frequencies of infrared light
true
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
Beta wave frequency
-highest frequency
-low voltage
-13-30 cycles/sec
What is beta wave activity associated with?
awake and mental stimulation and “light anesthesia”
Alpha wave frequency
2nd highest frequency
-frequency 8-12 cycles/sec
What is alpha wave frequency associated with?
awake but restful state with eyes closed
Theta wave frequency
3rd highest frequency
-4-7 cycles/sec
what is theta waves associated with?
general anesthesia
children during normal sleep
Delta wave frequency
<4 cycles/sec
what are delta waves associated with?
general anesthesia
deep sleep
brain ischemia or injury
Burst suppression
associated with general anesthesia, hypothermia, CPB (cerebral ischemia (especially if its unilateral burst suppression)
isoelectricity
-absence of electrical activity
-associated with very deep anesthesia or death
induction of anesthesia is associated with:
increased beta wave activity
light anesthesia is also associated with
increased beta wave activity
______ & _______ waves predominate during general anesthesia.
theta and delta
deep anesthesia
burst suppression
at ____ MAC general anesthetics cause complete suppression or isoelectricity.
1.5-2.0
nitrous oxide alone
increases beta wave activity
Sevoflurane can increase ______
epileptiform EEG activity
Etomidate can cause
myoclonus but is not associated with epileptiform EEG activity
Ketamine can increased ______ and may confuse EEG interpretation
increase high frequency cortical activity
the patient may be deeper than the EEG suggests
burst suppression may occur with :
-hypothermia especially during CPB
The development of new ____waves during anesthetic maintenance may signify that the brain is at risk for ischemia.
delta
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
Most common complaint with ascenting aorta
chest pain
most common complaint with descending aorta
back or abdominal pain
syncope is ominous sign
cardiac tamponda
cerebral hypoperfusion
acute ascending aortic dissection motality ____% after symptom onset
1-2%
without surgery mortality exceeds 50% in 1 month
aortic aneurysm that is large enough can cause local mass effect due to compression
-trachea-cough
-esophagus-dysphagia
-recurrent larygneal nerve-hoarseness
patients should continue taking aspirin until day of surgery for :
carotid and lower extremity surgery
surgery indicated for ascending aneurysm
> 5.5cm
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)
surgery indicated for descending aneuryms
> 6cm (notes from PPT)
descending aortic aneurysm can be repaired by
surgical repair associated with postop paraplegia associated with spinal cord blood supply ____%
13-17%
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)
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.
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
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
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
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
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
dopamine effects on renal protection
0.5- 2mcg/kg/min renal blood flow, Na+ excretion, and glomerular filtration rate (GFR)
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
most effective prevention measure in preventing pulmonary complications following aneurysm repair
postoperative lung expansion, either CPAP or incentive spirometry
Spinal cord ischemia occurs up to ____% in operations involving a distal aortic repair
11%
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
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
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.
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.”
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
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”
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
secondary conversion from EVAR to OAR
Secondary conversion is aneurysm rupture despite successful sac exclusion
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.
Which clamping carries the highest risk?
supraceliac
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.
Carotid disease is usually a problem with _____.
embolization and less often occlusion or insufficiency
most common noninvasive test for carotid stenosis
carotid duplex u/s
amaurosis fugas
-temporary blindness in 1 eye
-sign of impending stroke
25% of pt with high-grade stenosis
during cross clamping BP management
maintain a normal to slightly elevated BP
after cross-clamp removed, keep SBP ____
under 145mmHg to decrease bleeding
is patients have suffered a stroke are they candidates for CEA?
no, consideration to chronic issues related to the stroke must be evaluated
normal cerebral blood flow
40-60ml/100G/min
15% CO
normal CMRO2
3-4ml/100G/min
20% o2 consumption
What IV solution should not be given to a patient undergoing CEA?
D5W
Gray matter blood flow
80ml/100g/min
white matter blood flow
20ml/100g/min
flow rates <______are associated with impairment
20-25ml/100g/min
flow rates between ______show a flattened EEG
15-20ml/100g/min
flow rates <______are associated with irreversible brain damage
10ml/100g/min
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.
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
maintain ACT> _____seconds for Carotid artery angioplasty stenting
250 sec
most common complication CEA is _____
thromboembolic stroke due to atherosclerotic debris that lodges in cerebral vasculature
