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Clinical Medicine 3 > Lecture 6 (Dysarrhythmias)-Exam 2 > Flashcards

Lecture 6 (Dysarrhythmias)-Exam 2 Flashcards

1
Q

SA node:
* Where is it?
* What is it?
* What does it control?

A
  • Tiny 1 mm collection of cells in upper R corner of RA
  • Primary pacemaker site of heart
  • Controls rhythm of heart by having fastest intrinsic rate of depolarization(60-100 beats/min)
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2
Q

SA node:
* Starts what?
* SA node discharges too small to generate what?
* What is inscribed by depolarization of atria?

A
  • Starts cardiac cycle by initiating atrial systole
  • SA node discharges too small to generate any deflection on ECG
  • P wave inscribed by depolarization of atria
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3
Q

AV node:
* Located where?
* What does it provide?
* What does it protect?

A
  • Located near inferior portion of interatrial septum
  • Provides a physiologic conduction delay to allow atria to fill ventricles prior to ventricular systole
  • Protects ventricle form excessive stimulation from atria such as in atrial flutter or AF
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4
Q

His-purkinje system
* What does the his bundle divde into?
* Where does the left bundle go into?
* What does the systm provide?

A
  • His Bundle divides into R & L bundles
  • Left bundle further divides into L anterior & posterior fascicles
  • His-Purkinje system provides for orderly depolarization of ventricles
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5
Q

What are the rates of SA, AV, purkinje fibers?

A

Farther from SA node, slower intrinsic rate of pacemaker site.

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6
Q

Review of Pertinent Anatomy

  • Where is the SA node located? What is the blood supply?
  • What is the SA and AV nodal rate?
  • What is the blood supply of the AV node?
A
  • SA node is at the junction of the RA and SVC. Its blood supply is from RCA in 55% and LCA in 45% of individuals
  • SA nodal rate is 60-90, AV nodal rate is 45-60
  • AV node is supplied by RCA in 90%, LCA in 10% (ST elevations in inferior leads, might have bradycardia)
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7
Q

Review of Pertinent Anatomy

  • Where are rates slowed? How?
  • What does the PR interval indicate?
  • What does the QRS and QT intercal represent?
A
  • Rates are slowed though the AV node due to slow ion channels but may be bypassed by accessory pathways, allowing for rapid ventricular rates
  • PR interval indicates time it takes to conduct from node to ventricle
  • QRS represents ventricular depolarization and QT interval is total ventricular depolarization and repolarization
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8
Q

What contributes the most to the membrane potential in stage 3?
A. Calcium channels close, potassium channels open
B. Calcium channels open, potassium channels close
C. Sodium channels close
D. Sodium channels open
E. Magnesium channels close

A

A. Calcium channels close, potassium channels open

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9
Q

Sodium channel blockade results in what? What are the examples that can cause this (4)

A

Sodium channel blockade results in widening of the QRS
* TCAs
* Antidysrhythmics
* Local anesthesics
* Benadryl

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10
Q

Potassium channel blockade causes what? What are the examples (4)

A

Potassium channel blockade prolongs the QT
* Antipsychotics
* Antidysrhythmics
* Antimalarials
* Macrolide abx

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11
Q

What are the dysrhythmias dx options?

A
  • Monitor
  • 12-lead EKG
  • Holter Monitor
  • Patient-activated Event Monitor
  • Implantable event monitor
  • Stress testing
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12
Q

What is this?

A

Holter and event monitors
* Patient has to record it when they are feeling it

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13
Q

What is this?

A

Implantable loop recorders (subcutaneous)
* Usually for pt for a longer period of time

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14
Q

dysrhythmias dx options:

Invasive electrophysiologic studies (EPS)
* Electodes where?
* Done in patients with what?
* Reproduced what?
* Assess what?
* With electrical current, do what?
* Can also be used to detetmine what?

A
  • Electrodes in RA & ventricular chambers
  • Done in patients with documented tachyarrhythmias or syncope suspected to occur with tachyarrhythmias
  • Reproduce tachyarrhythmias
  • Assess effectiveness of pharm agents
  • With electrical current, ablate abnormal focus or pathway
  • Can also be used to determine conduction disorders & mechanism of heart block
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15
Q

Things to Consider When Analyzing Dysrhythmias
* What are the different sites of origin?

A
  • Sinus Node (ST)
  • Atria (PAC)
  • AV junction (junctional escape rhythm)
  • Ventricles (PVC)
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16
Q

Things to Consider When Analyzing Dysrhythmias

  • What are the different rates?
A
  • Accelerated - faster than expected (accelerated junctional rhythm @ 75 bpm)
  • Slower than expected (marked SB @ 40 bpm)
  • Normal (junctional escape rhythm)
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17
Q

What are the different Regularity of ventricular or atrial response?

A
  • Regular (PSVT)
  • Regular irregularity (atrial/ventricular bigeminy)
  • Irregular irregularity (AF or MAT-COPD)
  • Irregular (multifocal PVCs)

MAT is sort of like wandering pacemaker with different rate

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18
Q
  • All narrow QRS complex arrhythmias originate where?
  • Supraventricular arrhythmias can have a wide QRS complex if what?
  • Ventricular dysrhythmias can never have what?
A
  • All narrow QRS complex arrhythmias originate above the His bundle & are called supraventricular.
  • Supraventricular arrhythmias can have a wide QRS complex if there is a concomitant intraventricular conduction defect or aberrant conduction
  • Ventricular dysrhythmias can never have a narrow QRS complex
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19
Q

What are the types of tachycardias?

A
  • Narrow Regular
  • Narrow Irregular
  • Wide Regular
  • Wide Irregular
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20
Q

What are the examples of narrow, regular?

A
  • SINUS TACHYCARDIA
  • SVT
  • Orthodromic WPW
  • Atrial flutter
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21
Q

What are these two examples?

A
  • Top: SVT
  • Bottom: A.Flutter
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22
Q

What are the narrow, irregular?

A
  • Atrial Fibrillation
  • Aflutter w/variable block
  • MAT
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23
Q
A
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24
Q

What are the wide, regular?

A
  • Ventricular Tachycardia
  • SVT w/aberrancy
  • Antidromic WPW
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25
Q

What are the wide, irregular?

A
  • Afib w/aberrancy
  • Polymorphic VT
  • WPW w/afib – essential to review old EKGs if available
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26
Q

What are the different types of bradycardias?

A
  • Sinus bradycardia
  • Slow atrial fibrillation
  • Junctional rhythm (usually)
  • Most AV blocks
  • Idioventricular rhythm
  • 3rd degree AV block (usually)
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27
Q

What is this?

A

Sinus brady
* P waves present
* Narrow QRS

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28
Q
A
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29
Q

What can you give to patients with different heart blocks to increase HR? What heart block will this not work?

A

Atropine
* 3rd will not work because the drug only works on SA node

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30
Q

What is this?

A

Idioventricular

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31
Q

What are Dr. Pepe’s ordering package?

A
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32
Q

What is the most common tachydysrhythmia? How do you treat it?

A

Sinus tachy
* Treat the underlying cause

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33
Q

Approach to Tachycardia
* Consider treatment of rate once above what? Why?
* Wide complex tachycardia is what?

A
  • Consider treatment of rate once above 140. Above this level, further increase in heart rate is rarely adaptive and helpful. This is because CO falls at this level as there is no longer sufficient filling time in diastole.
  • Wide complex tachycardia is VT until proven otherwise and needs to be treated as such
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34
Q

What are the two broad causes of tachycardia?

A

Medication (usually stable, so have time) and electricity (unstable, looks unwell)

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35
Q
  • What is the most common braydysrhythmia? Txt?
  • Rarely has what?
A
  • Most common bradydysrhythmia- sinus bradycardia- treat underlying cause
  • Rarely with symptoms / instability >50 bpm
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36
Q

What are the broad causes of bradycardia?

A

Medications and electricitiy

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37
Q

Vaughn Williams Classification
* What are the different classes of sodium channel blockage? What does it reduce?
* What are the other 3 classes?

A

CAB

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38
Q

What are the classes of flecainide, diliazem, esmolol and sotalol

A
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39
Q

What are the agents of Class 1?

A
  • Procainamide (IA)
  • Lidocaine (IB)
  • Flecainide (IC)
  • Propafenone (IC)
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40
Q

What are the agents in class 2?

A
  • Esmolol
  • Metoprolol
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41
Q

What are the agents in class 3?

A
  • Bretylium
  • Amiodarone (MC in ER-> unique because acts like all the classes)
  • Ibutilide
  • Sotalol
  • Dofetilide
  • Dronedarone
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42
Q

What are the nonpharmacologic management?

A
  • Direct current cardioversion & defibrillation
  • Implanted cardiac defibrillators(ICD)
  • Radiofrequency catheter ablation
  • Pacemakers
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43
Q

What is cardioversion? What can go wrong?

A
  • Synchronized application of an electric shock to terminate a tachyarrhythmia
  • Synchronized to QRS complex
  • If administer shock during ventricular repolarization (T wave), can cause VF

R on T: if you shock on rel refract period

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44
Q

What is Defibrillation for?

A

Asynchronous delivery of shock to terminate VF or pulseless VT

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45
Q

Pacemakers:
* What do they do?
* What can you do temporary?
* ICD’s also have what?

A
  • Pacemakers deliver an electrical impuse to cause an action potential
  • Temporary transvenous (IV into right heart). Good for about a week at bedside.
  • Permanent
  • ICD’s also have pacemaker capability of responding to slow rates
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46
Q

What is this?

A

Temporary Transvenous Pacemaker Placement
* Place central line in Right internal jugular
* Place a sheath and feed wire and balloon in blood= floats to the heart

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47
Q

What does this show?

A

Ventricular paced rhythm

QRS are wide due to block. We pace ventricles.

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48
Q

What is this?

A

Dual Chamber Pacemaker

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49
Q

Implanatable Cardiac Defibrillators(ICD)
* What are they?
* What do they sense?
* What do they deliver?
* Often also have what?

A
  • Implanted defibrillators
  • Sense fast rates & responds to them
  • Deliver current to try to terminate them
  • Often also have pacemaker capability of responding to slow rates
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50
Q

Radiofrequency Catheter Ablation
* What is it?
* What is it used for?
* Can do what?

A

Application of alternating current electrical energy in radiofrequency range to an arrhythmogenic focus of myocardium to ablate focus
* Increasing use in treatment of AFib, Aflutter, SVT
* Can ablate accessory pathway in WPW or dual pathways in AV node

Burn it off

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51
Q

What is cryoablation?

A
  • Cools tissue instead of heating it
  • Similar outcomes
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52
Q
A
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53
Q

What is this?

A
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54
Q

Sinus Arrhythmia
* Synchronized with what?
* Faster HR when?

A
  • Synchronized with respiratory cycle
  • Faster HR results when there is an inspiratory reflex inhibition of vagal tone
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55
Q

Sinus Bradycardia
* What is the definition?

A

heart rate of <60 beats/min

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56
Q

What are the sxs of sinus bradycardia?

A

Many patients can tolerate heart rates of 50 or even 40 beats/min, but at lower rates symptoms are likely to occur:
* Fatigue
* Dizziness (not vertigo) about to pass out
* Near syncope
* Syncope
* Ischemic chest pain

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57
Q

Sinus bradycardia:
* What does not need to be treated?
* What does does need to be treated?

A
  • Asymptomatic bradycardia does not need treatment
  • Symptomatic Causes: treat underlying cause
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58
Q

Sinus bradycardia:
* What are the underlying causes that can cause symptomatic bradycardia?

A
  • Acute myocardial infarction
  • Drugs—for example: β blockers, digoxin, calcium channel blockers (Verapamil and Diltiazem), amiodarone
  • Raised intracranial pressure
  • Hypothermia
  • Hypothyroidism
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59
Q

What are the different drugs that cause bradycardia?

A
  • alpha 2- agonists
  • B-blockers
  • CCBs
  • Digoxin
  • Ach-I
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60
Q
A
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61
Q

Sinus tachycardia:
* What is the rate?
* What causes catecholamine induced by physiology?
* What are the pharmacologically induced?

A
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62
Q

Premature Atrial Contractions(PAC’s)
* Premature what?
* What is different?
* Occurs in who?
* Can be precipitated by what?
* Isolated PACs seen in what?
* Asymptomatic patients usually only need what?

A
  • Premature discharge of non-sinus atrial pacemaker
  • P waves are different
  • Occur in patients of all ages
  • Can be precipitated by caffeine, alcohol, smoking
  • Isolated PACs seen in patients with healthy hearts are considered insignificant
  • Asymptomatic patients usually only require observation
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63
Q
A
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64
Q
A
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65
Q

Wandering Atrial Pacemaker
* What are the mechanisms and who is it typically seen in?

A
  • 3 or more ectopic pacemakers in atria
  • Typically seen in young healthy persons
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66
Q

Wandering Atrial Pacemaker
* What is the heart rate?

A
  • Atrial rate is 60-100
  • Ventricular response is regular
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67
Q

Wandering Atrial Pacemaker
* What is the ECG morphology?

A
  • There are at least three P wave morphologies
  • There may be moderate variation in atrial & VR’s
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68
Q

What is this?

A

Wandering atrial pacemaker
* At least three different P wave configurations (seen in the same lead) are needed to diagnose a dysrhythmia as wandering atrial pacemaker.

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69
Q
A
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70
Q

SVT:
* Arises from what?
* Generic term referring to what?
* Includes what?

A
  • Arises from above ventricles but cannot be definitively identified as atrial or junctional tachycardia because the P’ waves cannot be seen sufficiently
  • Generic term referring to a tachycardia originating in atrium, AV junction area, etc (ABOVE VENTRICLE)
  • Includes paroxysmal supraventricular tachycardia, (PSVT), non-paroxysmal atrial tachycardia, MAT
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71
Q

SVT:
* What do the QRS complexes look like?
* What is the rate?
* What is paroxysmal?
* Several types of PSVT depending on what?

A
  • Generally regular & has a narrow QRS complex unless has functional aberrancy (R or L BBB)
  • Rates 150-250 BPM
  • Onset sudden, usually initiated by a premature beat, & arrhythmia also stops abruptly - which is why they are called paroxysmal.
  • Several types of PSVT depending on location of reentry circuit.
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72
Q

SVT:
* What are the mechanisms and causes?

A
  • Most examples due to reentry
  • Commonest reentry pathway involves AV node(70%, & called AV nodal reentrant tachycardia[AVNRT])
  • Pathway may be intraatrial or may utilize an accessory pathway as part of reentrant loop
  • PSVT may occur in otherwise completely normal individuals, or may occur as a result of increased atrial pressure or because of presence of an accessory pathway
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73
Q

What is this?

A

SVT

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74
Q

What is the acute treatment of SVT? (stable and instability)

A
  • Adenosine(6-12 mg IV) first line medical therapy(successfully terminates most SVTs
  • NEW- Ca++ blockers being used more often as a first line treatment
  • With non-adenosine sensitive atrial tachycardias, adenosine will increase level of AV block, but atrial tachycardia will persist which allows precise identification of mechanism
  • In presence of hemodynamic instability, electrical cardioversion is treatment of choice
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75
Q

What type

A

SVT then treated with adenosine

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76
Q

Chronic txt of SVT
* What are drugs that slow down AV nodal conduction?

A
  • Beta blocker
  • Verapamil
  • Diltiazem
  • Digoxin will help recurrent AVNRT, AVRT and may have varying effectiveness for atrial tachycardia
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77
Q

What agents may also be used for long term treatment of SVT? But why are they barely needed?

A

Type I or Type II antiarrythmic agents may also be used for long term treatment bur currently are rarely needed because of success of RF ablation

78
Q

Chronic treatment of SVT
* Radiofrequency ablations: What is the success rate?
* What is a risk?
* For patients with an accessory pathway, what is the success rate?
* For atrial tachycardia success rate?

A
  • Success rate > 95% in eliminating or modifying AV nodal slow pathway function
  • 1% risk of inducing CHB
  • For patients with an accessory pathway,85-95% successful elimination of accessory pathway function
  • For atrial tachycardia,~70-80% success depending on site of tachycardia
79
Q

Multifocal Atrial Tachycardia (MAT)
* Pathological condition that presents with what?
* Caused by what?
* Seen most often in who?
* May be what?

A
  • Pathological condition that presents with changing P wave morphology & HR of 120 to 150 BPM
  • Caused by ectopic atrial foci
  • Seen most often in elderly patients with chronic or acute medical problems such as exacerbation of COPD
  • May be intermittent, alternating with periods of NSR
80
Q

What is this?

A

MAT

81
Q
A
82
Q

Atrial Fibrillation
* What is it?
* What type of rhythm?
* Complications include what?

A
  • Chaotic, asynchronous firing of multiple areas within the atria
  • Irregularly irregular ventricular rhythm and absence of distinct P waves
  • Complications include thromboembolism (including stroke) and risk of heart failure. Affected patients may be at increased risk of mortality.
83
Q

Epidemiology of AF
* What are the most common underlying disorders?
* What is is prevalent in certain resource-limited areas and strongly associated with AF?

A
  • Hypertensive heart disease and coronary heart disease are the most common underlying disorders in pts in developed countries.
  • Rheumatic heart disease is prevalent in certain resource-limited areas and strongly associated with AF.
84
Q

If Patient has afib think about what pulmonary issues?

A
  • Pulmonary embolism (PE)
  • Chronic obstructive pulmonary diases (COPD)
  • Obstructive sleep apnea
  • Pneumonia
85
Q

If Patient has afib think about what ingestion issues?

A
  • Ethanol
  • Caffeine
  • Nicotine
86
Q

If Patient has afib think about what endocrine issues?

A
  • Hyperthyroidism
  • Diabetes mellitus (DM) (20%)
87
Q

What are the sxs of A.fib?

A
88
Q

How do you dx A.fib?

A

EKG is diagnostic
* AF is always irregularly irregular as opposed to VT (differentiates but sometimes too fast to tell)

You cannot diagnose Afib without proof on monitor or EKG

89
Q

What are some other devices besides EKG for dx of A.fib?

A

Ambulatory cardiac monitoring
* Event monitors
* Insertable cardiac monitors (Loop Recorder)
* Diagnosis or assessment of afib burden

90
Q

What does an echo TTE show?

A
  • Size of atria, size and function of RV and LV
  • Valvular heart disease
  • LVH
  • Pericardial disease
  • Assess RV pressure
91
Q

What is a TEE used for?

A

TEE to identify thrombi in the left atrium or left atrial appendage

92
Q

What is a stress test for?

A
  • For evidence of ischemic heart disease
  • To guide pharmacotherapy
  • Can be used to gauge adequacy of heart rate control in AF during exercise
93
Q

AFib

Rhythm control:
* To prevent what?
* What can you do?

A
  • To prevent AF and maintain NSR (normal sinus rhythm)
  • Cardioversion
  • Antiarrhythmic
  • Ablation
94
Q

A.Fib-Cardioversion
* Who is required to have it?
* Cardioversion by electrical shock using what?
* It In patients with what type of conditions?
* If hemodynamic stable, recommended patients be what?
* What do you need to exclude?

A
  • Required in AF with rapid VR associated with hemodynamic compromise
  • Cardioversion by electrical shock using DC energy between 100 -360 joules
  • It In patients with AF > 48 hours, who are not anticoagulated, a 5% risk for acute embolism associated with cardioversion
  • If hemodynamic stable, recommended patients be anticoagulated for 3 weeks before & after cardioversion from AF to NSR
  • TEE to exclude LA thrombus alternative & acceptable strategy
95
Q

A.fib ablation:
* Great in patients with what?

A

great in patients with COPD/CHF who may not tolerate beta-Blockers

96
Q

what happens with rate control in a.fib?

A

To leave in afib and slow rate down

97
Q

What are some medications that treat a.fib?

A
  • IV Metoprolol Tartrate
  • IV diltiazem
  • IV digoxin
  • IV verapamil
  • IV amiodarone
98
Q

Acute treatment- A.fib
* Urgent cardioversion in who?

A

In hemodynamically unstable patients:
* It is somewhat unusual for Afib alone to cause marked hemodynamic insult; thus, the possibility of a concurrent process should be considered in this setting

99
Q

Acute treatments:
* What else should you give besides HR medications, cardioversion?

A

Anticoagulation

100
Q
A
101
Q

Surgical options for a.fib:
* What are the options?

A

Electrophysiology study and Ablation
* Usually after trial of antiarrhythmics fail although now becoming 1st line in some centers

Percutaneous left atrial appendage (LAA) occlusion with WATCHMAN device
* For those with increased risk of stroke with contraindications to long-term anticoagulation

102
Q

What are the stages for ablations?

A
103
Q

What is a watchman device?

A
104
Q

What is the rate control strategy for a.fib?

A
  • Patient remains in Atrial Fibrillation
  • Protect from Stroke via anticoagulation!
  • Goal HR 80 at rest
  • May not be able to achieve optimal rate control secondary to blood pressure
105
Q

Anticoagulation for a.fib:
* Use what?
* What needs to be weighted? What are the scores?

A
  • Most important management consideration!
  • Long-term use of oral anticoagulants is the most effective means of reducing the risk of stroke
  • Risk of stroke must be weighed against the risk of bleeding from anticoagulation

Scores:
* CHADS VASc
* HAS-BLED

106
Q
A
107
Q

Anticoagulation Recommendation
* What is the risk ranks for the CHADS VASc?

A
  • 0 in males or 1 in females = may be omitted
  • 1 in males and 2 in females (with one non-sex related risk factor) = oral anticoagulant may be considered
  • 2 in males, 3 in females = anticoagulation unless contraindicated
108
Q

Fill in for HAS-BLED score
* What score needs patient need extra care?

A
  • A score of 3 or more is not a contrainidications to ordal anticoagulation but these patients require extra care
109
Q

Anticoagulation of a.fib
* What are the Recommended over warfarin in most patients with nonvalvular afib?

A
  • Dabigatran (Pradaxa)
  • Rivaroxaban (Xarelto)
  • Apixaban (Eliquis)
  • Edoxaban (Savaysa)
110
Q

Anticoagulation for a.fib:
* What is used for patients with mechanical valves or issues with DOACs?
* What does the IRN need to be?

A
  • Warfrain For those with mechanical valves or issues with DOACs (Cost primary)
  • INR 2-3 (unless already 2.5 – 3.5 for valve)
111
Q

A. flutter:
* Usually associated with what?
* What is shown on EKG?
* What is the atrial rate?
* Ventricular rate depends on what?

A
  • Usually associated with organic heart disease
  • Sawtooth pattern on EKG (F waves or Flutter waves)
  • Atrial rate typically 300 bpm (range 250-350)
  • Ventricular rate depends on conduction through the AV node
112
Q

What is this?

A
113
Q

What is this?

A

In this ECG rhythm strip, arrows point to atrial flutter waves @ 280 bpm with ventricular rate @ 140bpm (atrial flutter with 2:1 block)

114
Q

What are the sxs of A.flutter?

A
115
Q

Treatment of a.flutter:
* What do you need to control?
* What happens if unstable?
* What can be used first line for?
* What for stroke prevention?

A
116
Q
A
117
Q
A
118
Q
  • Mechanisms and causes of junctional escape rhythm?
  • May indication what?
  • Slow rate may adversely affect what?
A
  • Sequence of 3 or more junctional escapes occurring by default at a rate of 40-60 bpm.
  • May indicate that patient’s primary pacemaker is not functioning. These patients may require placement of a pacemaker.
  • Slow rate may adversely affect CO.
119
Q
A
120
Q
A
121
Q
A
122
Q

Accelerated junctional Rhythm
* Accelerated Junctional rhythm is a common rhythm seen following what?
* The rate is increased because of what?

A
  • Accelerated Junctional rhythm is a common rhythm seen following cardiac arrest resuscitation until SA node awakens & takes control of rate.
  • The rate is increased because of either high sympathetic tone or the effects of adrenergic agents such as epinephrine used during resuscitation
123
Q
A
124
Q

Ventricular Dysrhythmias
* QRS?
* T waves?
* P Waves?

A
  • Wide ( > 0.12 seconds in duration), bizarre QRS complexes
  • T waves in opposite direction of R wave
  • Absence of P waves
125
Q
A
126
Q

Premature Ventricular Contractions
* Originate where?
* What is uniform?
* What is multiform? What is going on with these?

A
  • Originate anywhere in the ventricles
  • Uniform PVCs originate from the same foci and look the same
  • Multiform PVCs have different morphologies and originate from different ventricular foci
    * These are more concerning because they suggest that ventricles are more irritable as early beats are arising from more than one location
127
Q

What does this show?

A

Multiform PVCs

128
Q

What are these?

A
129
Q

Premature Ventricular Complexes (PVCs)
* What happens?
* Occur for what?
* Incidence of PVCs increase with what?

A
  • Early ectopic beats that interrupt normal rhythm
    * Spontaneous depolarization of ventricle
  • PVCs can occur for no apparent reason in individuals who have healthy hearts & usually of no significance.
  • Incidence of PVCs increases with age & can occur during exercise or at rest.
130
Q

Premature Ventricular Complexes (PVCs)
* May produce what?
* Patients frequently experience what?

A
  • PVCs may produce a palpable pulse but they may also produce a diminished or nonpalpable pulse (called a nonperfusing PVC).
  • Patients frequently experience sensation of “skipped beats.”
131
Q

What is the txt of PVCs?

A

Can be observed if asymptomatic
Beta Blockers

132
Q

What is this?

A

Multifocal PVCs

133
Q

Ideoventricular Rhythm:
* What is the cause?
* What is the rate?

A
  • A “passive” escape rhythm that occurs by default whenever higher-lever pacemakers in AV junction or sinus node fail to control ventricular activation.
  • Escape rate is usually 20-40 bpm (slower than a junctional escape rhythm).
134
Q

Idioventricular Rhythm:
* What are the sxs? What causes that?
* Idioventricular dysrhythmias are also common during what?

A
  • Decreased CO associated with this dysrhythmia will likely cause patient to be symptomatic (hypotension, syncope, etc.).
  • Idioventricular dysrhythmias are also common during cardiac arrest as they represent final escape rhythm to be generated in an attempt to perfuse the body
135
Q
A
136
Q
A
137
Q

Ventricular Tachycardia:
* What should be considered VT until proven otherwise?
* Most examples are due to what?
* Rarely in who?
* usually indicates what?
* Can occur with or without what?
* ALWAYS what?

A
138
Q

What are these?

A
139
Q

Risk factors of VT:
* VT is a frequent complication of what?
* VT is commonly associated with what?
* What are 15-20% of patients?

A
  • VT is a frequent complication of acute MI and dilated cardiomyopathy
  • VT is commonly associated with structural heart disease
  • 15-20% in patients without structural heart disease; known as idiopathic
140
Q

What are some other risk factors of V.tach?

A
  • Dilated cardiomyopathy
  • Chronic coronary disease
  • Hypertrophic cardiomyopathy
  • Myocarditis
  • Infiltrative cardiomyopathy
  • Complex congenital heart disease
141
Q

What are the sxs of V.tach? (5)
* Can be triggered by what?
* Can present with or without what?
* Patient can be what what?

A
142
Q

Acute treatment of V.tach
* Known or suspected structural heart disease, hemodynamically unstable?

A

Immediate synchronized direct current cardioversion

143
Q

Acute Treatment hemodynamically stable V. Tach:
* What do you give IV?
* What do you give if fails to terminate or symptoms worsen?
* What needs to be replaced? Less likely to help what?
* Increased HR with? Shortens what?
* Overdrive pacing through what?

A
144
Q

Long-term treatment V. Tach:
* Treat what first?
* What do you if it is not reversible, no underlying fixable cause, risk of recurrence?
* Catheter ablation for what?
* What is considered for secondary prevention?

A
145
Q

Long-term management V. tach:
* What is common and what is recommended?
* What is the mainstay of medical management?
* What does antiarrhythmic medications do?
* What is preferred? What can be considered?
* What should be done if recurrence on medication?

A
146
Q

Polymorphic VT - Torsade de pointes
* What is it?
* What is the HR? What is the consequence?
* What does it cause?
* Can be provoked by what?

A
  • A polymorphic VT associated with long-QT syndromes characterized by phasic variations in polarity of QRS complexes around baseline.
  • VR often > 200 bpm & VF is a consequence.
  • Causes symptoms & death in patients with rare congenital long QT syndromes
  • Can be provoked by antiarrhythmic drugs(proarrhythmia effect) or electrolyte imbalance
147
Q

Torsade de Pointes Treatment
* What do you with hemodynamically unstable patients?

A

Prompt defibrillation is indicated in patients with hemodynamically unstable torsades de pointes.

148
Q

In the conscious patient with recurrent episodes of torsades de pointes:
* What is first line?
* Temporary what?
* In those with congenital long QT syndrome, what can be used?

A
  • Intravenousmagnesium sulfate is first-line therapy
  • Temporary transvenous overdrive pacing (atrial or ventricular) at about 100 beats per minute is generally reserved for patients who do not respond to intravenous magnesium.
  • In those with congenital long QT syndrome, beta blockers may be used to reduce the frequency of premature ventricular contractions and shorten the QT interval.
149
Q

Ventricular Fibrillation (VF)
* Results from what?
* What does it look like on cardiac monitor?

A
  • Results from chaotic firing of multiple sites in ventricles
  • On the cardiac monitor, VF appears like a wavy line, totally chaotic, without any logic.
  • There is disorganized, chaotic activity of ventricle without any effective contraction
150
Q

V. Fib:
* Causes what to heart muscles?
* What happens if not promptly treated?
* MCC of what?

A
  • Causes heart muscle to quiver rather than contract efficiently, producing no effective muscular contraction & no CO.
  • Death occurs if patient not promptly treated (defibrillation)
  • Most common cause of prehospital cardiac arrest in adults
151
Q

What is this?

A

V.fib

152
Q

Ventricular Fibrillation
* Patient CANNOT have what with V.fib
* What is sudden cardiac death?
* What is sudden cardiac arrest?

A
  • Patient CANNOT have a pulse with V. Fib
  • Sudden cardiac death: unexpected nontraumatic death in clinically well or stable patients who die within 1 hour after onset of symptoms. Causative rhythm in most cases is ventricular fibrillation
  • Sudden cardiac arrest: term reserved for the successful resuscitation of ventricular fibrillation, either spontaneously or via intervention (defibrillation)
153
Q

What is the treatment of V. fib?

A

Only treatment: Immediate defibrillation(200-300-360 joules)

154
Q

Asystole:
* What is it?
* What does it look like?
* Presence of asystole should always be verified how?
* COmmplete cessation of what?
* _ rhythm
* Chances of recovery is extremely low?

A
155
Q

Sudden Cardiac Dealth
* Preseumed to start with what?
* What may also cause sudden death?
* Analyze all what?

A
  • Presumed to start with monomorphic VT, polymorphic VT, or primarily VF.
  • Complete heart block and sinus node arrest may also cause sudden death
  • ANALYZE ALL SYNCOPE PATIENTS EKGS CLOSELY!
156
Q

In patients younger than 35, most SCD caused by what?

A

inherited heart disease
* Long QT syndrome
* Brugada syndrome
* HCM
* Arrhythmogenic RV cardiomyopathy
* Cardiomyopathy

157
Q

Sudden Cardiac Death
* Prompt evaluation to exclude reversible causes of sudden cardiac arrest should begin when? What are some causes?

A
158
Q

What are the pre-excitation syndromes?
* May be what?
* What does it give rise to?

A
  • Wolff-Parkinson-White Syndrome
  • Lown-Ganong-Levine Syndrome
  • May be sustained or intermittent
  • Gives rise to SVTs
159
Q

What is this?

A

Wolff-Parkinson-White Presentation
* Delta wave

160
Q

Wolff-Parkinson-White Syndrome (WPW)
* What is the patho?

A

Accessory pathways (Bundle of Kent) or bypass tracts : Congenital bands of tissue that can conduct impulses but lie outside of the normal conduction system.

161
Q

Wolff-Parkinson-White Syndrome (WPW)
* What is the onset?
* What is the HR?
* PR?
* What wave is present?

A
  • Onset and termination: sudden
  • Heart rate: 140-250 bpm
  • PR: short
  • Delta wave on baseline ECG
162
Q

Epidemiology of WPS:
* What is prevalent?
* Just because there’s bypass tract, does not mean that they will definitely experience what? Present when? What is peak incidence?

A

Accessory pathways are prevalent in the general population

Just because there’s bypass tract, does not mean that they will definitely experience a tachyarrhythmia.
* Less than half of persons with documented bypass tracts ever sustain an arrhythmia!
* often present at birth (congenital), but may not be detected until adolescence or later.
* Peak incidence has been reported in individuals between 30 and 40 years old in otherwise healthy adults.

163
Q

Epidemiology of WPS
* Approximately 5-10% of patients with documented bypass tracts have what?
* Familial tendency toward bypass tracts, fourfold to tenfold increase in what?

A
  • Approximately 5-10% of patients with documented bypass tracts have concomitant structural heart disease.
  • Familial tendency toward bypass tracts, fourfold to tenfold increase in incidence among first-degree family members
164
Q

Pathophysiology: Anatomy WPWS
* What is going on?
* What is the pattern called?

A
  • Wolff-Parkinson-White syndrome: Paroxysmal tachycardias mediated by accessory pathways that cross the AV groove and electrically link the atria and ventricles, when combined with a short P-R interval (<0.12), a wide QRS, and secondary repolarization abnormalities.
  • When this ECG pattern is seen without the tachycardia, it is called WPW pattern or Ventricular preexcitation.
165
Q

Wolff-Parkinson-White (WPW) Syndrome
* PR interval?
* QRS?
* What wave is seen?
* Vulnerable to what?

A
  • PR interval < 0.12 seconds
  • Wide QRS complexes
  • Delta wave seen in some leads
  • Patients with WPW are vulnerable to PSVT
166
Q

Pathophysiology: Mechanism of WPWS
* Accessory pathways have inherent property to conduct what?
* AV node conducts more what?
* Most tacycardia initiated by what?

A
  • Accessory pathways have inherent property to conduct in a retrograde direction more easily than antegrade.
  • AV node conducts more efficiently in antegrade
  • Most tachycardia initiated by a PVC or PAC
167
Q

WPWS

AV node conducts more efficiently in antegrade. For this reason, reentrant rhythms most commonly use what?
* What is this termed?
* Accounts for 70-80% of arrhythmias of accessory tracts with HR of what?

A

For this reason, reentrant rhythms most commonly use the AV node to go from the atrium to the ventricle and the bypass tract to return to the atrium.
* Termed Orthodromic AVRT (antegrade conduction over the AV node)
* Accounts for 70-80% of arrhythmias of accessory tracts with HR 140-250.

168
Q

WPSW

What is Antidromic AVRT?

A

Antidromic AVRT, atrial impulse carried to ventricle over the bypass tract and reenters the atrium via retrograde conduction over the AV node.
* Rare, 5-10% of cases.

169
Q

What are the sxs of WPWS?

A
  • Palpitations
  • Episodes of sustained tachycardia
  • Dizziness
  • Presyncope
  • Syncope
170
Q

Treatment- DANGER with WPWS?

A
171
Q

Treatment warning of WPWS
* Can precipiate into what?
* Blocking AV node promotes conduction down what?

A
  • Can precipitate Ventricular fibrillation
  • Blocking AV node promotes conduction down the bypass tract, making all the complexes wide; bypass can conduct faster than the AV node increasing ventricular rates to >200 bpm. This aberrant conduction and rapid rate can lead to disorganized ventricular conduction resulting in VF.
172
Q

Treatment of WPWS
* What is 95% cure? (can be first line)
* If occasional or rare bouts of minimal or mildly symptomatic palpitations (orthodromic or antidromic AVRT) can be treated with what? Do not use when?

A
  • Catheter ablation 95% cure
  • If occasional or rare bouts of minimal or mildly symptomatic palpitations (orthodromic or antidromic AVRT) can be treated with Bblockers or CCB to prevent recurrent episodes.
    * Do not use if also has afib or flutter
173
Q

Treatment of WPWS
* What can be dx and currative? Can be used to avoid what?

A

Electrophysiology study and concomitant radiofrequency ablation
* Can be diagnostic and currative
* Can be used to avoid drug therapy

174
Q

Prolonged QT Syndromes
* Normal QT interval should not exceed what?
* Results from what?
* What are the two syndromes?
* What is a electrolye issue?

A
  • The normal QT interval should not exceed half the R-R interval
  • Results from a defect in cardiac K+ and Na+ channels
  • Romano-Ward syndrome- heart only
  • Lange-Nielsen syndrome- hearing
  • Hypocalcemia
175
Q

What is this?

A

R on T

176
Q

AV blocks:
* What is first, second and third degree?

A
177
Q

Heart block causes:
* What happens in 50%?
* What happens in 40%?
* What happens with the rest of patients?

A
  • Idiopathic fibrosis and sclerosis of the conduction system in about 50% of patients
  • Ischemic heart disease in 40% of patients
  • The Rest: Drugs (eg, β-blockers, Ca channel blockers, digoxin, amiodarone); increased vagal tone; or other disorders
178
Q

Signs and Symptoms of AV blocks:
* Symptoms resulting from what?
* Can be what?
* Better or worse over time?

A
  • Symptoms resulting from conduction disorders reflect cerebral hypoperfusion, low cardiac output at rest or during exercise, and rarely, hemodynamic collapse.
  • Can be episodic or chronic
  • Can worsen over time
  • Can be disabling
179
Q

Signs and Symptoms of AV blocks:
* Patient often adapts what?
* Must closely question about what?
* Can be confused with what?

A
  • Patient often adapts activity levels to compensate for the impairment in heart rate.
    * “oh, I’m just getting old”
  • Must closely question about specific activities and effort tolerance
  • Can be confused with other conditions such as hypothyroidism, medications, underlying heart disease, deconditioning, or old age.
180
Q

What are the sxs of AV blocks?

A
181
Q

Treatment of AV blocks:
* Major reversible causes what?
* Vagally mediated bradycardia are usually what?
* Even if pauses are prolonged and symptomatic, what is not indicated?

A
  • Major reversible causes high vagal tone and medications
  • Vagally mediated bradycardia are usually transient and no treatment needed!
    * Even if pauses are prolonged and symptomatic, permanent cardiac pacing is not indicated if vagally mediated!
182
Q

Treatment of AV blocks:
* Treat what?
* Stop what?
* Implant what?

A
  • Treat underlying process (such as OSA)
  • Stop causative agent (if possible)
  • Implant permanent pacemaker
183
Q

What is this? Txt?

A

Type one
* Regular narrow-complex rhythm at 40-60 beats/minute
* Prolonged PR Interval >0.20 seconds
* Rarely symptomatic and no treatment is required

184
Q

What is this? Txt?

A

Second Degree AV Block: Mobitz Type I AKA Wenckebach
* Progressive increase in PR interval until beat dropped
* Cycle repeats after beat dropped
* Treatment (pacemaker) is unnecessary unless the block causes symptomatic bradycardia and transient or reversible causes have been excluded.

185
Q

What is this? What can is progree into?

A

Second Degree AV Block: Mobitz Type II
* No change in PR interval
* Regularly dropped beats at consistent interval
* Patterns: 2 to 1, 3 to 1 or 4 to 1
* Worse than Mobitz type I (May progress to 3rd degree HB)

186
Q

2nd Degree AV block Mobitz Type II
* Always what? Where does the block occur?
* Patient may be what?
* Patients are at risk of developing what?
* What is indicated?

A
  • Always pathologic; the block occurs at the His bundle in 20% of patients and in the bundle branches in the rest.
  • Patients may be asymptomatic or experience light-headedness, pre-syncope, and syncope
  • Patients are at risk of developing symptomatic high-grade or complete AV block
  • A Pacemaker is indicated.
187
Q

What is this?

A

Third Degree Heart Block

188
Q

How do you place a transcutaneous pacing?

A
189
Q

Common indications for Temporary Cardiac Pacing
* Why is it therapeutic

A
  • To provide adequate heart rate in patients with symptomatic bradycardia from sinus node dysfunction or advanced second-degree and complete AV block while awaiting definitive therapy
  • To attempt to terminate some supraventricular and ventricular tachycardias by overdrive suppression or entrainment (eg, atrial flutter, monomorphic ventricular tachycardia)
190
Q

Common indications for Temporary Cardiac Pacing
* How it is prophylactic?

A
  • To prevent advanced second-degree and complete AV block in some patients with acute myocardial infarction and in some patients after cardiac surgery (eg, aortic valve replacement)
  • To prevent bradycardia-dependent ventricular tachycardia

Clinical Medicine 3 (27 decks)

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