CV Conduction FINAL REVIEW Flashcards
SA node is innervated by
SNS and PNS
SA node blood supply comes from
Right Coronary Artery (RCA)
% of people with SA node supplied by RCA
60%
SA node 60% provided by RCA, remaining 40% supplied by
Left Circumflex Coronary Artery ( LCA)
AV node innervated by
PNS and SNS
AV node supplied by
RCA
AV node supplied by RCA in what % of people
85-90%
AV node 85-90% provided by RCA, remaining 10-15% supplied by
Left Circumflex Coronary Artery ( LCA)
Both Right and Left Bundles receive Blood supply from branches of
Left Anterior Descending Coronary artery
LAD infarcts affect_____and _____ but rarely______, why?
LAF and RBB ; LPF, it receives additional blood supply from posterior descending coronary artery
This is why LBB blocks (LBBB) indicate more extensive cardiac disease/damage
LPF receives additional blood supply from
Posterior Descending coronary artery.
Bifascicular heart block is present when
RBBB is present with Left anterior or posterior fascicular block. Anterior is more common because posterior gets dual blood supply and is larger.
AV node allows time for
atrial contraction (atrial kick), which contributes an additional 20% to ventricular preload
Automaticity changes when
phase 4 of depolarization shifts, or resting membrane
changes
Automaticity changes: Sympathetic stimulation =
↑ slope of phase 4 of action potential and DECREASING resting membrane potential
Automaticity changes: Parasympathetic stimulation =
↓ phase 4 of action potential and INCREASING RESTING MEMBRANE POTENTION
Supraventricular (SVT) and urine
Polyuria can occur due to ↑ secretion of atrial natriuretic peptide
SVT and ANP
Occurs because AV desynchrony causes atrial contraction against closed AV valves, resulting in ↑ atrial pressures activating stretch receptors → ANP released
Triggered dysrhythmias c/ early after-depolarizations are
enhanced by slow heart rates and treated by
accelerating heart rate c/ drugs or pacing
Triggered dysrhythmias c/ delayed after-depolarizations
are
enhanced by fast heart rates and can be treated c/
drugs that lower heart rate
Sinus tachycardia and systemic diseases?
Most common supraventricular dysrhythmia associated c/ myocardial infarction (MI)
Can be a compensatory physiologic effort to ↑ cardiac output (e.g. CHF)
Sinus Tachycardia
Think twice
before treating tachycardia , may be a compensatory mechanism
Sinus tachycardia treatment
Treat underlying cause
SVT (PACs) and systemic illness
Chronic Lung disease
IHD (ischemic heart disease)
digitalis toxicity
Pathologic increase in sympathetic tone
MI, CHF PE Hyperthyroidism Pericarditis MH
Heart beating too fast, secrete
ANP to decrease BV
MAT and systemic illness
Most commonly seen in ACUTE EXACERBATION of CHRONIC LUNG DISEASE
MAT and other related systemic illness
Methylxanthine toxicity (Theophyilline and caffeine)
Heart failure
Sepsis
Metabolic/ electrolyte abnormalities
Atrial Flutter : What is it ?
Atrial flutter (A-flutter) is an organized atrial rhythm c/ a rate of 250-350 bpm c/ varying degrees of AV block
Characteristics of Atrial flutter
Rapid P waves create a sawtooth appearance called flutter waves (especially noticeable in
leads II, III, aVF, and V1)
A flutter especially noticeable in
Leads II, III, aVF, and V1
With Aflutter: Ventricular rate may be
regular or irregular depending on rate of conduction
A-flutter Ventricular rate is normally about
150 bpm
A-flutter conduction
Most commonly, pts have 2:1 AV conduction (300
atrial beats per 150 ventricular beats)
Untreated A-flutter can
Deteriorate to atrial fibrillation and revert back and forth
A-flutter is associated c/
structural heart disease
A-flutter can have
more intense symptoms than atrial fibrillation due to more rapid ventricular response
60% of pts get A-flutter c/ an acute exacerbation of a chronic condition such as (PIACET)
Pulmonary disease Infarction (MI) Acute myocardial Cardiothoracic surgery , after surgery Ethanol intoxication Thyrotoxicosis
A-flutter that is hemodynamically significant is
treated c/ synchronized cardioversion
AFlutter that is hemodynamically stable
If hemodynamically stable, overdrive pacing can be used to convert to sinus rhythm
Pts c/ A-flutter lasting longer than
48 hours must be anticoagulated or should be evaluated by TEE for an atrial thrombus before cardioversion
When treating A-flutter pharmacologically, What is the initial goal?
Common meds to control ventricular rate
include amiodarone, diltiazem, and
verapamil
ventricular control is initial goal
WIth AFLUTTER, what are you preventing? Prevents
deterioration in AV conduction to 1:1, which would cause severe hemodynamic instability (procainamide is
used in this situation)
AFlutter just transitioned to 1:1 what medication can be used ?
Procainamide
AFlutter: Common meds to control ventricular rate
include (VAD)
Verapamil
Amiodarone
Diltiazem
Anesthesia management for Aflutter
Preop and Intraop
If it occurs spontaneously before induction, cancel case
Intraoperative management depends on hemodynamic stability
Atrial fibrillation (A-Fib)occurs when
c/ a normal AV node, ventricular rates < 180
bpm
If AV node is bypassed, ventricular rates > 180
bpm (QRS complex is wide)
multiple areas of atria continuously depolarize and
contract in a disorganized manner
AFib and rhythm coordination
No coordinated depolarization or contraction,
only quivering atrial wall
AFib and Pwave
No discernable P waves
AFib and electrical input?
Irregular electrical input to AV node results in irregularly irregular ventricular contraction
Atrial fibrillation, with a normal AV node,
ventricular rates < 180 bpm
Atrial fibrillation, If AV node is bypassed,
ventricular rates > 180 bpm (QRS complex is wide)
Conditions that can lead to A-fib include: RHHICAPPA
Symptoms can be vague (generalized malaise)
or prominent, including palpitations, angina
pectoris, shortness of breath, orthopnea, and
HoTN
Rheumatic heart disease (especially mitral valve disease), HTN, Hyperthyroidism, IHD, COPD Alcohol intake (holiday heart syndrome) Pericarditis Pulmonary embolus Atrial septal defect
ATRIA anatomy that correlate c/ A-fib
↑ left atrial size and mass
AFIB Symptoms can be G- PASOH
vague (generalized malaise) or prominent, including Palpitations Angina pectoris Shortness of breath, Orthopnea HoTN
A-fib is most
common sustained cardiac dysrhythmia in general population
Incidence of AFIB
Increase with age
Most common underlying cardiovascular
diseases associated c/ A-fib are
systemic HTN and IHD
Long-term A-fib
↑ risk of heart failure is most common sustained cardiac
dysrhythmia in general population
AFib how does the conversion to thrombus occur
Loss of coordinated atrial contraction leads to stasis of blood and thrombus formation
2 most serious clinical dangers of A-fib
Atrial thrombi and thromboembolic stroke
AFIB patients require
Long-term prophylactic anticoagulation
AFIB Therapy goals include
ventricular rate control
electrical or pharmacologic cardioversion
Drugs that slow AV nodal conduction: BCD
Side effects are dose related and most commonly
include AV block and ventricular ectopy
Beta Blockers
Calcium Channel Blocking drugs
Digoxin
AFIB, β-Blockers role -PPR
Prevent recurrent A-fib
Provide good heart rate control,
Reduce symptoms during subsequent episodes of A-fib
AFIB and Calcium channel–blocking drugs : 2 drugs use
(diltiazem, verapamil)
AFIB and Calcium channel–blocking drugs role
can rapidly reduce ventricular rate during A-fib
AFIB and CCBs, caution
CCBs, Have negative inotropic effects and must be used c/ caution in heart failure
AFIB and Digoxin
can used to control ventricular rate but is not effective for conversion of atrial fibrillation to sinus rhythm.
AFIB and digoxin and acute setting use
In acute settings, usefulness is limited due peak therapeutic effects being delayed by several hours
AFIB and digoxin Side effects are
Dose related and most commonly include AV block and ventricular ectopy
AFIB and Pharmacological cardioversion
is most efficacious if initiated within 7 days of onset
AFIB: What are Drugs capable of converting A-fib? include: APIS
Amiodarone
Propafenone
Ibutilide
Sotalol
For Treatment of AFIB, when is Amiodarone preferred?
Is preferred in pts c/ significant heart disease (IHD, LVF, left ventricular dysfunction, and heart failure)
AFIB: Amiodarone Action
suppresses atrial ectopy and recurrence of atrial fibrillation and improves success rate of electrical cardioversion
AFIB and Cardioversion
Electrical cardioversion is most effective method for converting A-fib to normal sinus rhythm and is indicated in
AFIB, when is cardioversion indicated? (HAH)
pts c/ coexisting symptoms of heart failure, angina
pectoris, or hemodynamic instability
Intraoperative management of A-fib depends
on hemodynamic stability
Intra-operative AFIB Instability is treated c/
synchronized cardioversion 100-200J biphasic
Intra-operative AFIB if vitals are stable, rate control can be achieved with
c/ β-Blockers and calcium channel blockers
Intraoperative management of A-fib: DRUGS
Procainamide or amiodarone are drugs of choice to control rate in a pt c/ known or suspected electrical accessory pathway and pre-excitation
AFIB: INTRAOP may be attempted if vital signs allow:
Pharmacologic conversion to sinus rhythm c/ IV
amiodarone –> Can result in bradycardia, HoTN
A-fib is most common
postoperative tachydysrhythmia, occurring early (first 2-4 days)
CHRONIC AFIB and medication
Pts c/ chronic A-fib should continue antidysrhythmic drugs perioperatively
AFIB and electrolytes monitoring
Check magnesium and potassium levels (especially if
on digoxin)
AFIB and team
Coordination c/primary care team is needed to manage anticoagulation
Ventricular Pre-excitation Syndromes
Alternate (accessory) conduction pathways can function as electrically active muscle bridges bypassing normal
conduction pathways and providing a pathway for re-entrant tachycardias
Example of Ventricular Pre-Excitation syndromes
Wolff-Parkison-White (WPW)
What is Wolff-Parkinson-White (WPW) syndrome cause?
caused by an accessory pathway between atria and ventricles, called bundle of Kent
In WPW Impulses in
bundle of Kent can cause PVCs that can result in a unique type of SVT (Atrioventricular nodal re-entrant Tachycardia)
WPW Common in pts
Transposition of great vessels
Hypertrophic cardiomyopathy, and
Ebstein’s malformation
WPW Symptoms include: PADS DP
Paroxysmal palpitations Angina Dizziness, Syncope, Dyspnea Pectoris
Evident on ECG for WPW
Delta wave
WPW is diagnosed when
both pre-excitation and
tachydysrhythmias are present
WPW is diagnosed when both pre-excitation and
tachydysrhythmias are present: Pre-excitation causes an
earlier deflection of QRS called a delta wave
WPW _______is commonly triggered by a PAC
Atrioventricular nodal re-entrant tachycardia (AVNRT)
WPW antidromic,
cardiac impulses are conducted from atrium to ventricle via accessory pathway and return from ventricles to atria via normal AV node
WPW Drugs Contraindicated:
SLOW AV nodal conduction ↑ conduction along accessory pathway (and are contraindicated
Drugs contraindicated with WPW that slow AV node conduction and increase accessory pathway? ABCDL
Adenosine β-blockers, Calcium channel blockers Digoxin Lidocaine
Orthodromic AVRT
Antegrade conduction through AV node
Antidromic AVRT
Retrograde conduction through AV node.
WPW ↑
conduction along accessory pathway
produces a rapid ventricular rate (V-Tach/Fib)
WPW treatment drug and its mechanism of aciton
Treatment: procainamide 10mg/kg IV
Slows conduction along accessory pathway and slows ventricular response
WPW if drug therapy fails?
Cardioversion is indicated if drug therapy fails
WPW , other arrythmias that can lethal –>
A-fib/flutter c/ WPW can be lethal because impulses will conduct via accessory pathway and cause very rapid ventricular rates that can deteriorate to V-Fib
A-Fib/Flutter c/ WPW should be treated c/
procainamide
A-Fib/Flutter c/ WPW drugs contraindicated and why?
Verapamil and digoxin are contraindicated because
they accelerate conduction through accessory pathway
WPW If hemodynamically unstable_________, what may be necessary?
cardioversion ; Radiofrequency catheter
ablation may be necessary
Pts c/ WPW should continue their
antidysrhythmic medications intraoperatively
WPW Anesthesia management involves
minimizing any event (e.g. ↑ sympathetic nervous system activity) or drug (digoxin, verapamil) that enhances conduction of impulses via accessory pathway
What is a BBB?
Conduction disturbances at various levels of His-Purkinje system
BBB is usually associated with
significant structural heart disease, especially dilated
cardiomyopathies
Clinical significance of Right bundle branch block (RBBB)
Does not always imply cardiac disease and often of
no clinical significance
RBBB can be related to (VIA)
Valvular heart disease
IHD
Atrial septal defect
RBBB is recognized on ECG by a WR1,2
DS 1 V6
widened QRS complex and
rSR’ configuration in leads V1 and V2, deep S wave in leads I and V6
Bifascicular heart block is present when
RBBB is present c/ left anterior or posterior fascicular block (anterior is more common because posterior gets dual blood supply and is larger)
Complete RBBB, Lead I
Wide Slurred S wave in Lead I
Complete RBBB, Lead V1
Terminal R wave in V1 (R, rR’, rsR’,
Normal in RBBB
T wave inversion
and ST depression in V1-V3
Complete RBBB, Lead V6
Slurred S wave
S wave should be > duraton then the R wave or greater than 40ms in V1 and V6 in adults.
Left bundle branch block (LBBB) is recognized on ECG as
a QRS complex of longer than 0.12 seconds in duration and absence of Q waves in leads I and V6
LBBB waves
Broad notched or slurred R wave in leads I, aVL, V5, and V6 and an occasional RS pattern in V5 and V6
LBBB classification
Can be classified as unifascicular (hemiblock) or
complete
LBBB is often associated c IHV
/ IHD, HTN, and valvular heart disease
Complete LBBB ECG Lead I: LIMB LEADS
T wave discordance
Monophasic QRS in left sided leads
Complete LBBB ECG lead V1:
Right sided leads
NEGATIVE QRS Right sided leads
QRS > 0.12
Complete LBBB ECG lead V6
Left sided chest leads
Monophasic QRS
Left sided Leads
Appearance of LBBB during anesthesia,
particularly during hypertensive or tachycardic
episodes, may be a sign of myocardial ischemia
LBBB is a
marker of serious heart disease (CAD, aortic valve disease, cardiomyopathy)
Third-degree heart block can occur
if a central line catheter induces RBBB in a pt c/ preexisting LBBB
RBBB (usually transient) occurs during
insertion of a pulmonary artery catheter in approximately 2% to 5% of pts
Surgery c/ Cardiac Implantable Devices
Complications that can occur related to
automatic implantable cardioverterdefibrillator (AICD) include: TBHMM DDR
Tachydysrhythmias or
Bradydysrythmias,
HoTN,
myocardial damage,
myocardial ischemia or infarction,
device malfunction, delay or cancellation of
surgery, readmission to a health care facility
Surgery c/ Cardiac Implantable Devices: If pt has a device, they have one of following: THOROUGH ASSESSMENT
bradydysrhythmia,
tachydysrhythmia, or heart failure
Surgery c/ Cardiac Implantable Devices: If pt has a device, they have one of following: bradydysrhythmia,
tachydysrhythmia, or heart failure
Preoperative assessment should include (TICAA)
Type of device present Identification of Clinical indication for device Appraisal of patient’s degree of dependence on device, and Assessment of device function
Surgery c/ Cardiac Implantable Devices
Syncope
in a pt c/ a pacemaker could reflect device dysfunction
Surgery c/ Cardiac Implantable Devices What Indicates pulse generator function?
Rate of discharge of an atrial/ventricular
asynchronous (fixed-rate) cardiac pacemaker (usually 70 bpm)
Surgery c/ Cardiac Implantable Devices may reflect battery depletion
10% ↓ from baseline
Surgery c/ Cardiac Implantable Devices :An irregular rate could indicate
Competition of pulse generator c/ patient’s intrinsic heart rate, or failure of pulse generator to sense R waves
Best way to determine AICD function preoperatively is
AICD interrogation by a qualified consultant
Surgery c/ Cardiac Implantable Devices Due to comorbidities of pts c/ AICD (CAD, HTN, DM), good clinical outcomes depend on
Evaluation and optimal treatment of co-existing diseases in addition to management of issues directly
involving AICD
Most common CIED-related problem
encountered in perioperative period
is interference c/ device function resulting from electromagnetic interference (EMI)
EMI Most common effects are
inhibition of pacing and resetting of device to asynchronous pacing
EMI can cause
inappropriate defibrillation or complete device failure
Procedures that have reported EMI-induced
dysfunction are
MR
Electrocautery,
Radiofrequency ablation,
Anesthesia usually will not directly effect aes
AICD, but physiologic changes (acid-base,
electrolytes) and hemodynamic shifts (heart rate, heart rhythm, HTN, coronary ischemia) can induce changes in AICD function and adversely affect pt outcomes
Most literature suggests Doing this before surgery?
reprogramming AICD to an asynchronous mode before surgery if pt is pacemaker dependent (magnet)
Use of monopolar electrocautery remains
principal concern intraoperatively in pts c/ AICD
This causes more EMI problems?
Use of “coagulation” settings in monopolar
electrocautery causes more EMI problems
than use of “cutting” settings
Keep electrocautery current
as low as possible and applied in short bursts, especially if near pulse generator
SCAPEL and EMI
bipolar electrocautery or ultrasonic Harmonic scalpel is associated c/ lower rates of EMI effects on pulse generator and leads
EMI and Grounding pad
should be placed so that current path does not cross chest or AICD system
Pacemaker rate and function
Application of a magnet to a pacemaker often
results in asynchronous pacemaker function at a
fixed rate
Magnet must
MUST remain in place to maintain asynchronous
mode of pacing, and removal of magnet results in
reversion to baseline program
Application of a magnet to a cardioverter defibrillator
rarely alters pacing capabilities, but most often suspends antitachycardia therapy (defibrillation)
Some ICDs have
no magnet response; others can
be permanently disabled by magnet exposure
Recommendations for pts c/ ICDs who undergo a
procedure c/ a high risk of EMI include
turning off defibrillator and electronically adjusting pacing
modes as appropriate in pacemaker-dependent
individuals.
Temporary transvenous cardiac pacemakers
create a situation in which there is a
direct connection between an external electrical source
and endocardium.
Risk of Vfib resulting from
microshock
Risk of lead dislodgment is
minimal a month or longer after lead implantation
Recommendations for pts undergoing lithotripsy include
keeping focus of lithotripsy beam away from pulse
generator
Potential AICD problems from radiation therapy include
pacemaker failure and “runaway” pacemaker
Sudden rapid and erratic pacing
multiple internal component malfunctions
Before electroconvulsion therapy, device
should be
interrogated and antitachycardia
functions suspended
In pacemaker-dependent pts, programming to
asynchronous mode is recommended
Other potential sources of EMI during anesthetic care include CELSM
Current from peripheral nerve stimulators Evoked potential monitors Large tidal volumes Shivering, and Medication-induced muscle fasciculations
If emergency defibrillation is necessary in
a pt c/ a AICD, what to do? Where to place electrodes?
defibrillation current should be kept away from pulse
generator and lead system. Place electrode pads in an anterior– posterior position
What may follow external defibrillation?
An acute ↑ in pacing threshold and loss of capture –> Transcutaneous cardiac pacing or temporary transvenous pacing may be required
Postop management of pt c/ a AICD consists of
postoperative period, including during transport
interrogating device and restoring appropriate baseline
settings
POSTOP interrogation of the device should be done when?
Should be done as soon as possible after procedure
Implantaable devices, should be monitored throughout?
Cardiac rate and rhythm should be monitored throughout
immediate
Postoperative interrogation may NOT BE NEEDED if:
No EBIS
surgery did not use EMI-generating devices
no electronic preoperative device reprogramming was
done,
no blood transfusions were administered, and
no intraoperative problems were identified that related to
AICD function
