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SRNA3CoExisting > CV Conduction FINAL REVIEW > Flashcards

CV Conduction FINAL REVIEW Flashcards

1
Q

SA node is innervated by

A

SNS and PNS

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2
Q

SA node blood supply comes from

A

Right Coronary Artery (RCA)

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3
Q

% of people with SA node supplied by RCA

A

60%

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4
Q

SA node 60% provided by RCA, remaining 40% supplied by

A

Left Circumflex Coronary Artery ( LCA)

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5
Q

AV node innervated by

A

PNS and SNS

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6
Q

AV node supplied by

A

RCA

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7
Q

AV node supplied by RCA in what % of people

A

85-90%

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8
Q

AV node 85-90% provided by RCA, remaining 10-15% supplied by

A

Left Circumflex Coronary Artery ( LCA)

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9
Q

Both Right and Left Bundles receive Blood supply from branches of

A

Left Anterior Descending Coronary artery

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10
Q

LAD infarcts affect_____and _____ but rarely______, why?

A

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

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11
Q

LPF receives additional blood supply from

A

Posterior Descending coronary artery.

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12
Q

Bifascicular heart block is present when

A

RBBB is present with Left anterior or posterior fascicular block. Anterior is more common because posterior gets dual blood supply and is larger.

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13
Q

AV node allows time for

A

atrial contraction (atrial kick), which contributes an additional 20% to ventricular preload

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14
Q

Automaticity changes when

A

phase 4 of depolarization shifts, or resting membrane

changes

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15
Q

Automaticity changes: Sympathetic stimulation =

A

↑ slope of phase 4 of action potential and DECREASING resting membrane potential

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16
Q

Automaticity changes: Parasympathetic stimulation =

A

↓ phase 4 of action potential and INCREASING RESTING MEMBRANE POTENTION

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17
Q

Supraventricular (SVT) and urine

A

Polyuria can occur due to ↑ secretion of atrial natriuretic peptide

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18
Q

SVT and ANP

A

Occurs because AV desynchrony causes atrial contraction against closed AV valves, resulting in ↑ atrial pressures activating stretch receptors → ANP released

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19
Q

Triggered dysrhythmias c/ early after-depolarizations are

A

enhanced by slow heart rates and treated by

accelerating heart rate c/ drugs or pacing

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20
Q

Triggered dysrhythmias c/ delayed after-depolarizations

are

A

enhanced by fast heart rates and can be treated c/

drugs that lower heart rate

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21
Q

Sinus tachycardia and systemic diseases?

A

Most common supraventricular dysrhythmia associated c/ myocardial infarction (MI)

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22
Q

Can be a compensatory physiologic effort to ↑ cardiac output (e.g. CHF)

A

Sinus Tachycardia

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23
Q

Think twice

A

before treating tachycardia , may be a compensatory mechanism

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24
Q

Sinus tachycardia treatment

A

Treat underlying cause

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25
Q

SVT (PACs) and systemic illness

A

Chronic Lung disease
IHD (ischemic heart disease)
digitalis toxicity

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26
Q

Pathologic increase in sympathetic tone

A 
MI, CHF
PE
Hyperthyroidism
Pericarditis
MH
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27
Q

Heart beating too fast, secrete

A

ANP to decrease BV

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28
Q

MAT and systemic illness

A

Most commonly seen in ACUTE EXACERBATION of CHRONIC LUNG DISEASE

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29
Q

MAT and other related systemic illness

A

Methylxanthine toxicity (Theophyilline and caffeine)
Heart failure
Sepsis
Metabolic/ electrolyte abnormalities

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30
Q

Atrial Flutter : What is it ?

A

Atrial flutter (A-flutter) is an organized atrial rhythm c/ a rate of 250-350 bpm c/ varying degrees of AV block

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31
Q

Characteristics of Atrial flutter

A

Rapid P waves create a sawtooth appearance called flutter waves (especially noticeable in
leads II, III, aVF, and V1)

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32
Q

A flutter especially noticeable in

A

Leads II, III, aVF, and V1

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33
Q

With Aflutter: Ventricular rate may be

A

regular or irregular depending on rate of conduction

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34
Q

A-flutter Ventricular rate is normally about

A

150 bpm

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35
Q

A-flutter conduction

A

Most commonly, pts have 2:1 AV conduction (300

atrial beats per 150 ventricular beats)

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36
Q

Untreated A-flutter can

A

Deteriorate to atrial fibrillation and revert back and forth

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37
Q

A-flutter is associated c/

A

structural heart disease

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38
Q

A-flutter can have

A

more intense symptoms than atrial fibrillation due to more rapid ventricular response

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39
Q

60% of pts get A-flutter c/ an acute exacerbation of a chronic condition such as (PIACET)

A 
Pulmonary disease
Infarction (MI)
Acute myocardial 
Cardiothoracic surgery , after surgery
Ethanol intoxication
Thyrotoxicosis
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40
Q

A-flutter that is hemodynamically significant is

A

treated c/ synchronized cardioversion

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41
Q

AFlutter that is hemodynamically stable

A

If hemodynamically stable, overdrive pacing can be used to convert to sinus rhythm

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42
Q

Pts c/ A-flutter lasting longer than

A

48 hours must be anticoagulated or should be evaluated by TEE for an atrial thrombus before cardioversion

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43
Q

When treating A-flutter pharmacologically, What is the initial goal?
 Common meds to control ventricular rate
include amiodarone, diltiazem, and
verapamil

A

ventricular control is initial goal

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44
Q

WIth AFLUTTER, what are you preventing? Prevents

A

deterioration in AV conduction to 1:1, which would cause severe hemodynamic instability (procainamide is
used in this situation)

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45
Q

AFlutter just transitioned to 1:1 what medication can be used ?

A

Procainamide

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46
Q

AFlutter: Common meds to control ventricular rate

include (VAD)

A

Verapamil
Amiodarone
Diltiazem

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47
Q

Anesthesia management for Aflutter

Preop and Intraop

A

If it occurs spontaneously before induction, cancel case

Intraoperative management depends on hemodynamic stability

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48
Q

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)

A

multiple areas of atria continuously depolarize and

contract in a disorganized manner

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49
Q

AFib and rhythm coordination

A

 No coordinated depolarization or contraction,

only quivering atrial wall

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50
Q

AFib and Pwave

A

No discernable P waves

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51
Q

AFib and electrical input?

A

Irregular electrical input to AV node results in irregularly irregular ventricular contraction

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52
Q

Atrial fibrillation, with a normal AV node,

A

ventricular rates < 180 bpm

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53
Q

Atrial fibrillation, If AV node is bypassed,

A

ventricular rates > 180 bpm (QRS complex is wide)

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54
Q

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

A 
Rheumatic heart disease (especially mitral valve disease), HTN, 
Hyperthyroidism, 
IHD,
COPD
Alcohol intake (holiday heart syndrome)
Pericarditis
Pulmonary embolus
Atrial septal defect
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55
Q

ATRIA anatomy that correlate c/ A-fib

A

 ↑ left atrial size and mass

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56
Q

AFIB Symptoms can be G- PASOH

A 
vague (generalized malaise) or prominent, including 
Palpitations
Angina pectoris
Shortness of breath, 
Orthopnea
HoTN
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57
Q

A-fib is most

A

common sustained cardiac dysrhythmia in general population

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58
Q

Incidence of AFIB

A

Increase with age

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59
Q

Most common underlying cardiovascular

diseases associated c/ A-fib are

A

systemic HTN and IHD

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60
Q

Long-term A-fib

A

↑ risk of heart failure is most common sustained cardiac

dysrhythmia in general population

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61
Q

AFib how does the conversion to thrombus occur

A

Loss of coordinated atrial contraction leads to stasis of blood and thrombus formation

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62
Q

2 most serious clinical dangers of A-fib

A

Atrial thrombi and thromboembolic stroke

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63
Q

AFIB patients require

A

Long-term prophylactic anticoagulation

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64
Q

AFIB Therapy goals include

A

ventricular rate control

electrical or pharmacologic cardioversion

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65
Q

Drugs that slow AV nodal conduction: BCD
 Side effects are dose related and most commonly
include AV block and ventricular ectopy

A

Beta Blockers
Calcium Channel Blocking drugs
Digoxin

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66
Q

AFIB, β-Blockers role -PPR

A

Prevent recurrent A-fib
Provide good heart rate control,
Reduce symptoms during subsequent episodes of A-fib

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67
Q

AFIB and Calcium channel–blocking drugs : 2 drugs use

A

(diltiazem, verapamil)

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68
Q

AFIB and Calcium channel–blocking drugs role

A

can rapidly reduce ventricular rate during A-fib

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69
Q

AFIB and CCBs, caution

A

CCBs, Have negative inotropic effects and must be used c/ caution in heart failure

70
Q

AFIB and Digoxin

A

can used to control ventricular rate but is not effective for conversion of atrial fibrillation to sinus rhythm.

71
Q

AFIB and digoxin and acute setting use

A

In acute settings, usefulness is limited due peak therapeutic effects being delayed by several hours

72
Q

AFIB and digoxin Side effects are

A

Dose related and most commonly include AV block and ventricular ectopy

73
Q

AFIB and Pharmacological cardioversion

A

is most efficacious if initiated within 7 days of onset

74
Q

AFIB: What are Drugs capable of converting A-fib? include: APIS

A

Amiodarone
Propafenone
Ibutilide
Sotalol

75
Q

For Treatment of AFIB, when is Amiodarone preferred?

A

Is preferred in pts c/ significant heart disease (IHD, LVF, left ventricular dysfunction, and heart failure)

76
Q

AFIB: Amiodarone Action

A

suppresses atrial ectopy and recurrence of atrial fibrillation and improves success rate of electrical cardioversion

77
Q

AFIB and Cardioversion

A

Electrical cardioversion is most effective method for converting A-fib to normal sinus rhythm and is indicated in

78
Q

AFIB, when is cardioversion indicated? (HAH)

A

pts c/ coexisting symptoms of heart failure, angina

pectoris, or hemodynamic instability

79
Q

Intraoperative management of A-fib depends

A

on hemodynamic stability

80
Q

Intra-operative AFIB Instability is treated c/

A

synchronized cardioversion 100-200J biphasic

81
Q

Intra-operative AFIB if vitals are stable, rate control can be achieved with

A

c/ β-Blockers and calcium channel blockers

82
Q

Intraoperative management of A-fib: DRUGS

A

Procainamide or amiodarone are drugs of choice to control rate in a pt c/ known or suspected electrical accessory pathway and pre-excitation

83
Q

AFIB: INTRAOP may be attempted if vital signs allow:

A

Pharmacologic conversion to sinus rhythm c/ IV

amiodarone –> Can result in bradycardia, HoTN

84
Q

A-fib is most common

A

postoperative tachydysrhythmia, occurring early (first 2-4 days)

85
Q

CHRONIC AFIB and medication

A

Pts c/ chronic A-fib should continue antidysrhythmic drugs perioperatively

86
Q

AFIB and electrolytes monitoring

A

Check magnesium and potassium levels (especially if

on digoxin)

87
Q

AFIB and team

A

Coordination c/primary care team is needed to manage anticoagulation

88
Q

Ventricular Pre-excitation Syndromes

A

Alternate (accessory) conduction pathways can function as electrically active muscle bridges bypassing normal
conduction pathways and providing a pathway for re-entrant tachycardias

89
Q

Example of Ventricular Pre-Excitation syndromes

A

Wolff-Parkison-White (WPW)

90
Q

What is Wolff-Parkinson-White (WPW) syndrome cause?

A

caused by an accessory pathway between atria and ventricles, called bundle of Kent

91
Q

In WPW Impulses in

A

bundle of Kent can cause PVCs that can result in a unique type of SVT (Atrioventricular nodal re-entrant Tachycardia)

92
Q

WPW Common in pts

A

Transposition of great vessels
Hypertrophic cardiomyopathy, and
Ebstein’s malformation

93
Q

WPW Symptoms include: PADS DP

A 
Paroxysmal palpitations
Angina
Dizziness, 
Syncope, 
Dyspnea
Pectoris
94
Q

Evident on ECG for WPW

A

Delta wave

95
Q

WPW is diagnosed when

A

both pre-excitation and

tachydysrhythmias are present

96
Q

WPW is diagnosed when both pre-excitation and

tachydysrhythmias are present: Pre-excitation causes an

A

earlier deflection of QRS called a delta wave

97
Q

WPW _______is commonly triggered by a PAC

A

Atrioventricular nodal re-entrant tachycardia (AVNRT)

98
Q

WPW antidromic,

A

cardiac impulses are conducted from atrium to ventricle via accessory pathway and return from ventricles to atria via normal AV node

99
Q

WPW Drugs Contraindicated:

A 
SLOW AV nodal conduction ↑ conduction along
accessory pathway (and are contraindicated
100
Q

Drugs contraindicated with WPW that slow AV node conduction and increase accessory pathway? ABCDL

A 
Adenosine
β-blockers,
Calcium channel blockers
Digoxin
Lidocaine
101
Q

Orthodromic AVRT

A

Antegrade conduction through AV node

102
Q

Antidromic AVRT

A

Retrograde conduction through AV node.

103
Q

WPW ↑

A

conduction along accessory pathway

produces a rapid ventricular rate (V-Tach/Fib)

104
Q

WPW treatment drug and its mechanism of aciton

A

Treatment: procainamide 10mg/kg IV

Slows conduction along accessory pathway and slows ventricular response

105
Q

WPW if drug therapy fails?

A

Cardioversion is indicated if drug therapy fails

106
Q

WPW , other arrythmias that can lethal –>

A

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

107
Q

A-Fib/Flutter c/ WPW should be treated c/

A

procainamide

108
Q

A-Fib/Flutter c/ WPW drugs contraindicated and why?

A

Verapamil and digoxin are contraindicated because

they accelerate conduction through accessory pathway

109
Q

WPW If hemodynamically unstable_________, what may be necessary?

A

cardioversion ; Radiofrequency catheter

ablation may be necessary

110
Q

Pts c/ WPW should continue their

A

antidysrhythmic medications intraoperatively

111
Q

WPW Anesthesia management involves

A

minimizing any event (e.g. ↑ sympathetic nervous system activity) or drug (digoxin, verapamil) that enhances conduction of impulses via accessory pathway

112
Q

What is a BBB?

A

Conduction disturbances at various levels of His-Purkinje system

113
Q

BBB is usually associated with

A

significant structural heart disease, especially dilated

cardiomyopathies

114
Q

Clinical significance of Right bundle branch block (RBBB)

A

Does not always imply cardiac disease and often of

no clinical significance

115
Q

RBBB can be related to (VIA)

A

Valvular heart disease
IHD
Atrial septal defect

116
Q

RBBB is recognized on ECG by a WR1,2

DS 1 V6

A

widened QRS complex and

rSR’ configuration in leads V1 and V2, deep S wave in leads I and V6

117
Q

Bifascicular heart block is present when

A

RBBB is present c/ left anterior or posterior fascicular block (anterior is more common because posterior gets dual blood supply and is larger)

118
Q

Complete RBBB, Lead I

A

Wide Slurred S wave in Lead I

119
Q

Complete RBBB, Lead V1

A

Terminal R wave in V1 (R, rR’, rsR’,

120
Q

Normal in RBBB

A

T wave inversion

and ST depression in V1-V3

121
Q

Complete RBBB, Lead V6

A

Slurred S wave

S wave should be > duraton then the R wave or greater than 40ms in V1 and V6 in adults.

122
Q

Left bundle branch block (LBBB) is recognized on ECG as

A

a QRS complex of longer than 0.12 seconds in duration and absence of Q waves in leads I and V6

123
Q

LBBB waves

A

Broad notched or slurred R wave in leads I, aVL, V5, and V6 and an occasional RS pattern in V5 and V6

124
Q

LBBB classification

A

Can be classified as unifascicular (hemiblock) or

complete

125
Q

LBBB is often associated c IHV

A

/ IHD, HTN, and valvular heart disease

126
Q

Complete LBBB ECG Lead I: LIMB LEADS

A

T wave discordance

Monophasic QRS in left sided leads

127
Q

Complete LBBB ECG lead V1:

A

Right sided leads
NEGATIVE QRS Right sided leads
QRS > 0.12

128
Q

Complete LBBB ECG lead V6

A

Left sided chest leads
Monophasic QRS
Left sided Leads

129
Q

Appearance of LBBB during anesthesia,

A

particularly during hypertensive or tachycardic

episodes, may be a sign of myocardial ischemia

130
Q

LBBB is a

A

marker of serious heart disease (CAD, aortic valve disease, cardiomyopathy)

131
Q

Third-degree heart block can occur

A

if a central line catheter induces RBBB in a pt c/ preexisting LBBB

132
Q

RBBB (usually transient) occurs during

A

insertion of a pulmonary artery catheter in approximately 2% to 5% of pts

133
Q

Surgery c/ Cardiac Implantable Devices
Complications that can occur related to
automatic implantable cardioverterdefibrillator (AICD) include: TBHMM DDR

A

Tachydysrhythmias or
Bradydysrythmias,
HoTN,
myocardial damage,
myocardial ischemia or infarction,
device malfunction, delay or cancellation of
surgery, readmission to a health care facility

134
Q

Surgery c/ Cardiac Implantable Devices: If pt has a device, they have one of following: THOROUGH ASSESSMENT

A

bradydysrhythmia,

tachydysrhythmia, or heart failure

135
Q

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)

A 
Type of device present
Identification of
Clinical indication for device
Appraisal of patient’s degree of dependence on
device, and 
Assessment of device function
136
Q

Surgery c/ Cardiac Implantable Devices

Syncope

A

in a pt c/ a pacemaker could reflect device dysfunction

137
Q

Surgery c/ Cardiac Implantable Devices What Indicates pulse generator function?

A

Rate of discharge of an atrial/ventricular

asynchronous (fixed-rate) cardiac pacemaker (usually 70 bpm)

138
Q

Surgery c/ Cardiac Implantable Devices may reflect battery depletion

A

10% ↓ from baseline

139
Q

Surgery c/ Cardiac Implantable Devices :An irregular rate could indicate

A

Competition of pulse generator c/ patient’s intrinsic heart rate, or failure of pulse generator to sense R waves

140
Q

Best way to determine AICD function preoperatively is

A

AICD interrogation by a qualified consultant

141
Q

Surgery c/ Cardiac Implantable Devices Due to comorbidities of pts c/ AICD (CAD, HTN, DM), good clinical outcomes depend on

A

Evaluation and optimal treatment of co-existing diseases in addition to management of issues directly
involving AICD

142
Q

Most common CIED-related problem

encountered in perioperative period

A 
is interference c/ device function resulting from
electromagnetic interference (EMI)
143
Q

EMI Most common effects are

A

inhibition of pacing and resetting of device to asynchronous pacing

144
Q

EMI can cause

A

inappropriate defibrillation or complete device failure

145
Q

Procedures that have reported EMI-induced

dysfunction are

A

MR
Electrocautery,
Radiofrequency ablation,

146
Q

Anesthesia usually will not directly effect aes

A

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

147
Q

Most literature suggests Doing this before surgery?

A

reprogramming AICD to an asynchronous mode before surgery if pt is pacemaker dependent (magnet)

148
Q

Use of monopolar electrocautery remains

A

principal concern intraoperatively in pts c/ AICD

149
Q

This causes more EMI problems?

A

Use of “coagulation” settings in monopolar
electrocautery causes more EMI problems
than use of “cutting” settings

150
Q

Keep electrocautery current

A

as low as possible and applied in short bursts, especially if near pulse generator

151
Q

SCAPEL and EMI

A

bipolar electrocautery or ultrasonic Harmonic scalpel is associated c/ lower rates of EMI effects on pulse generator and leads

152
Q

EMI and Grounding pad

A

should be placed so that current path does not cross chest or AICD system

153
Q

Pacemaker rate and function

A

Application of a magnet to a pacemaker often
results in asynchronous pacemaker function at a
fixed rate

154
Q

Magnet must

A

MUST remain in place to maintain asynchronous
mode of pacing, and removal of magnet results in
reversion to baseline program

155
Q

Application of a magnet to a cardioverter defibrillator

A

rarely alters pacing capabilities, but most often suspends antitachycardia therapy (defibrillation)

156
Q

Some ICDs have

A

no magnet response; others can

be permanently disabled by magnet exposure

157
Q

Recommendations for pts c/ ICDs who undergo a

procedure c/ a high risk of EMI include

A

turning off defibrillator and electronically adjusting pacing
modes as appropriate in pacemaker-dependent
individuals.

158
Q

Temporary transvenous cardiac pacemakers

create a situation in which there is a

A

direct connection between an external electrical source

and endocardium.

159
Q

Risk of Vfib resulting from

A

microshock

160
Q

Risk of lead dislodgment is

A

minimal a month or longer after lead implantation

161
Q

Recommendations for pts undergoing lithotripsy include

A

keeping focus of lithotripsy beam away from pulse

generator

162
Q

Potential AICD problems from radiation therapy include

A

pacemaker failure and “runaway” pacemaker

163
Q

Sudden rapid and erratic pacing

A

multiple internal component malfunctions

164
Q

Before electroconvulsion therapy, device

should be

A

interrogated and antitachycardia

functions suspended

165
Q

In pacemaker-dependent pts, programming to

A

asynchronous mode is recommended

166
Q

Other potential sources of EMI during anesthetic care include CELSM

A 
Current from peripheral nerve stimulators 
Evoked potential monitors
Large tidal volumes
Shivering, and 
Medication-induced muscle fasciculations
167
Q

If emergency defibrillation is necessary in

a pt c/ a AICD, what to do? Where to place electrodes?

A

defibrillation current should be kept away from pulse

generator and lead system. Place electrode pads in an anterior– posterior position

168
Q

What may follow external defibrillation?

A

An acute ↑ in pacing threshold and loss of capture –> Transcutaneous cardiac pacing or temporary transvenous pacing may be required

169
Q

Postop management of pt c/ a AICD consists of

postoperative period, including during transport

A

interrogating device and restoring appropriate baseline

settings

170
Q

POSTOP interrogation of the device should be done when?

A

Should be done as soon as possible after procedure

171
Q

Implantaable devices, should be monitored throughout?

A

Cardiac rate and rhythm should be monitored throughout

immediate

172
Q

Postoperative interrogation may NOT BE NEEDED if:

No EBIS

A

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

SRNA3CoExisting (16 decks)

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