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Clin med II exam II Cardio > Arrythmias, Conduction Blocks and EKGs > Flashcards

Arrythmias, Conduction Blocks and EKGs Flashcards

1
Q

Define parameters associated w/ bradycardia and tachycardia

A

brady <60

tachy >100bpm

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2
Q

define Symptomatic Bradycardia and compare it to sleep bradycardia

A

usually below 40 AND does not increase with physiological demand

•During sleep: common HR to drop below 60, even below 50 and sometimes below 40 without consequence

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3
Q

•most common ECG finding with PE is ____ ____

A

sinus tachycardia

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4
Q

si/ sx of sinus tachycardia

include sx in pts w CAD

A

Asymptomatic

Heart palpitations

Shortness of breath (especially with exertion) – feel they cannot catch their breath

CAD:

  • Heart palpitations
  • Shortness of breath – anginal sx
  • Chest discomfort à sinus tach causes cardiac ischemia due to supply/demand mismatch
  • Lightheadedness
  • Fatigue
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5
Q

how do we tx sinus tachycardia

A

tx underlying cause

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6
Q

Si/Sx of SVT

A

••Sudden onset racing heart palpitations ** that fades suddenly

comes on suddenly and fades suddenly

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7
Q

contrast pathophysiologies of AVRT vs AVNRT

A

AVNRT Abnormal re-entrant loop around the AV node

AVRT -

Accessory pathway b/w atria and ventricle –> signal goes around and around causing tachycardia

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8
Q

defne pathophysiology for junctional rhythm

A

AV node is pacemaker -> depolarizing quickly and causing rapid HR

Junctional pacemakers usually 40-60bpm (ventricular rate)

•Differentiate based on junctional rate

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9
Q

recall treatment for stable SVT

first and second line

unstable SVT?

A

first - vagal maneuvers

second adenosine

unstable

vagal maneuvers

if unsuccessful - DC cardioversion

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10
Q

list meds that prolong QTc interval

A

Antiarrhythmic agents

  • Amiodarone
  • Flecainide
  • Sotalol
  • Antipsychotics
  • Chlorpromazine
  • Haloperidol
  • Olanzapine
  • Quetiapine
  • Risperidone
  • Antibiotics
  • Macrolides – azithromycin
  • Quinolones – levo, cipro
  • Antidepressants
  • Citalopram
  • TCAs
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11
Q

length of QTc that puts pts at risk for ventricular arrythmias

A

QTc greater than 500 milliseconds (ms) puts patient at risk for ventricular arrythmias (Torsade de Pointe)

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12
Q

Si/Sx of Vtach

A
  1. Conscious w/ pulse – will show symptoms
  2. Unconscious with pulse
  3. Unconscious w/o pulse
  • Heart palpitations
  • Lightheadedness
  • Chest pain
  • Shortness of breath
  • Diaphoresis (drenching sweat)
  • Near syncope
  • Syncope
  • Sustained LOC
  • Pulseless (death)
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13
Q

tx for vtach

A

Pulse present:

stable - amiodarone 150 mg IV followed by continuous infusion

unstable - cardioversion

long term implantable device

pulselessness:

CPR

  • Defibrillation – as soon as it is available place on chest
  • Epinephrine
  • ICD
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14
Q

tx for torsade de pointe

first and second line

A

Stable

  • First line: give Mg before you check levels
  • Temporary transverse overdrive pacing if no response to Mg –> external pacer

Second line – if persistent or Unstable –> prompt defibrillation

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15
Q

causes of Vfib

A

•Myocardial ischemia / MI

  • HF
  • Hypoxemia or hypercapnia
  • Hypotension / shock
  • Electrolyte imbalances
  • Stimulants (drugs, caffeine)
  • Often preceded by Vtach
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16
Q

tx vfib

A

CPR

Defibrillation – IMMEDIATE (no cardiac output)

If pulse regained: coronary arteriography (cardiac catheterization) to tx CAD

Implantable cardioverter-defibrillator for long term management

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17
Q

describe conduction pathway of WPW

A

Accessory pathway (delta wave) creates preexcitation à electoral impulses arrive to ventricle early and bypass AV node

_Orthodromic AVR_T (narrow complex) – more common

•Impulse transmits anterograde down AV to ventricles and retrograde to atria up through accessory pathway

Antidromic AVRT (wide complex) - Opposite of above

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18
Q

complications of WPW in the setting of rapid afib

A

• can lead to dangerous ventricular arrythmias

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19
Q

standard tx for WPW

A

Nonpharmacologic – catheter ablation of accessory pathway

Pharmacologic – to slow ventricular heart rates / prevent arrythmias

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20
Q

differentiate b/w sustained vs nonsustained Vtach

A

Sustained ventricular tachycardia - 3 or more consecutive beats of ventricular origin

•Lead to vfib à death

Non-sustained ventricular tachycardia – less then 3 ventricular beats , <30s

•Asymptomatic

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21
Q

what is Torsades triggerd by?

A
  • Hypokalemia – check levels before administration
  • Hypomagnesemia – ok for emergent administration
  • Drugs that prolong QTc
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22
Q

what type of arrythmia is associated w/ syncope and is a frequent complication of MI and dilated CM

A

SVT

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23
Q

what type of arrythmia is associated w/ severe CAD caused by acute MI

A

VFib

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24
Q

name some narrow complex rhythms

A

sinus tachycardia

SVT

AVNRT

AVRT

WPW - orthodromic AVRT

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25
Q

name some wide complex rhythms

A

sustained ventricular tachycardia

Torsade de pointe

Vfib

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26
Q

define the classes of Afib

Paroxysmal

persistent

long-standing

permanent

“Lone-AF”

refractory

A
  • Paroxysmal (PAF) - intermittent
  • Persistent - fails to self-terminate within 7 days & requires intervention in order to convert
  • Long-standing - >12 months
  • Permanent - >12 months & no longer pursue rhythm control
  • “Lone AF” – without structural heart disease, lowest risk of complications.
  • term not used much anymore
  • Example is if patient underwent heart surgery and developed afib once after as heart was healing
  • Refractory – not responding well to therapy/ keeps returning.
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27
Q

risk factors associated w/ Afib and Aflutter

A
  • >65 y/o
  • Men>women
  • Whites most common
  • Hypertension
  • Elevated BMI
  • Prolonged PR interval
  • Valvular disease
  • CHF
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28
Q

Triggers for Afib

A
  • Sleep deprivation
  • Physical illness
  • Post-surgery
  • Stress
  • Hyperthyroidism
  • Physical exercise
  • Stimulant meds (Sudafed)
  • Alcohol
  • Caffeine
  • Dehydration
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29
Q

workup in pt w/ newly diagnosed Afib

A

Hx and PE

  • ECG – narrow QRS, irregular, no p wave
  • Echo – look at mitral valve – if mitral valve disease put on anti-coagulation
  • Stress test
  • Labs: CBC, BMP, kidney function tests , TSH (new afib ALWAYS get both)
  • Exercise stress test – assess for ischemic heart disease
  • Heart monitors

FIRST Echo TTE –less invasive

•valvular heart disease (MS/ rheumatic heart disease )

SECOND Echo TEE – more invasive

•More sensitive for dx atrial thrombus à prior to cardioversion

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30
Q

describe a TEE echo vs TTE echo

A

FIRST Echo TTE –less invasive

•valvular heart disease (MS/ rheumatic heart disease )

SECOND Echo TEE – more invasive

•More sensitive for dx atrial thrombus à prior to cardioversion

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31
Q

goals of therapy w/ afib

A
  1. Rhythm control
  2. Reduce risk of stroke
  3. Prevent tachycardia mediated cardiomyopathy and ischemia (rate control)
  4. Alleviate symptoms
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32
Q

outline pharmacologic tx for Afib

A

first line - BBs or CCBs

metropolol and diltiazem (preferred in ED)

Adjuncts after maximizing BB or CCB

Digoxin - monior for dig tox

amiodarone (antiarrythmic) added in refractory Afib w/ RVR - lots of side effects

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33
Q

Most common side effect associated w/ amiodarone

A
  • Abnormal LFTs
  • Pulmonary toxicity – several months or years after initiation
  • Most common is chronic interstitial pneumonitis
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34
Q

what are symptoms of digoxi toxicity?

what is digoxin effect?

A
  • Symptoms: fatigue, dizziness, nausea (nonspecific)
  • ECG changes – heart blocks
  • Digoxin effect – normal to see on ECG of patients taking digoxin – Salvador dali mustache (nontoxic levels)
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35
Q

tx for aflutter w/ RVR

A
  1. Control ventricular rate - More difficult to control then afib
  • FIRST LINE – BB or CCB
  • Digoxin can be added, No amiodarone
  1. Convert to NSR / maintain NSR

•Ablation of IVC-TA area to break circuit

  1. Prevention of systemic embolization (stroke)

•Assess stroke risk - add anticoag if necessary

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36
Q

where is ablation performed

for what condition?

A
  • Type 1 aflutter
  • Ablation of macro reentrant pathway in right atrium involving obligatory pathway between inferior vena cava and tricuspid annulus (IVC-TA area)
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37
Q

outline tx for tachycardia in afib w/ RVR in acute and long term settings

A

ACUTE - FIRST line - BB or CCB in ED setting usually diltiazem drip

chronic - discharge on PO BB / CCB

  • Oral metoprolol BID – long-acting Toprol dosed once daily
  • Nadolol PO (liver failure pts / portal HTN)
  • Carvedilol (HF pts)

consider Adjuncts:

  • Digoxin – added if BB insufficient or intolerant
  • Amiodarone – slow rate in refractory Afib

Cardioversion - if necessary

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38
Q

indications for urgent cardioversion

A
  1. Active ischemia
  2. Unstable hemodynamics
  3. Evidence of organ hypoperfusion
  4. Severe manifestations of heart failure (pulmonary edema)
  5. The presence of WPW
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39
Q

indications for nonurgent cardioversion

A
  1. New onset or newly recognized afib –> r/out clots!
  2. Pts with persistent afib who are limited by their symptoms
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40
Q

Reasons NOT TO cardiovert

A
  1. Known afib that is minimal symptomatic
  2. Multiple comorbidities
  3. Unlikely to maintain NSR
  4. Age - Benefits of cardioversion decrease after 80 years old
  5. Paroxysmal afib
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41
Q

describe measures taken before cardioversion is preformed

A

•Prior to cardioversion:

control ventricular rate & provide intravenous heparin

42
Q

when is a full anticoagulation or assessment for atrial thrombus prior to cardioversion indicated

A

Afib >48 hrs

43
Q

How do we assess for stroke

A

CHADs2

CHADs VASc

44
Q

what are the stroke score models called that we use to assess for stroke risk prior to cardioversion

A

CHADS2 Score –assess annual risk of stroke

CHA2DS2-VASc –Considers age, use if score 1 or 2 on CHADS2

45
Q

define CHADS2 Score and what scores are risks for stroke

A
  • 0 – no anticoagulation therapy, low risk
  • 1 or 2 – move onto CHA2DS2-VASc scoring system (i_ntermediate risk_)
  • 2 – get anticoagulation usually
  • >3 – high risk, provide anticoagulation
46
Q

describe how the CHA2DS2-VASc model differs from CHADS2 model and how we use it to assess stroke risk.

A

Considers age, use if score 1 or 2 on CHADS2

IF CHADS2 score is 1 or 2 – move onto CHA2DS2-VASc scoring system

  • 0 – stroke risk 0%
  • 9- stroke risk 15%
  • >2 – long term anticoagulation
47
Q

if patients are higher risk for stroke what should we always do before performing a cardioversion

A

anticoag for 3 weeks prior

warfarin - usually (monitor INR)

  • Dabigatran (Pradaxa)
  • Rivaroxaban (Xarelto)
  • Apixaban (Eliquis)
48
Q

•Most common sustained arrythmia and is associated with mitral valve disease

A

Afib

49
Q

describe pathogenesis of afib vs aflutter

A

afib

  • Disruption of electrical conduction system usually by infiltration of inflammation of the atria
  • Ectopic foci are most often located at the ostial portion of the pulmonary veins

Disorganized, rapid and irregular loss of atrial activation à loss of atrial contractility

•Results in irregular ventricular response

aflutter

  • Large macro reentrant excitation in circuit of the right atrium
  • Large macro reentrant pathway in right atrium involving obligatory pathways between inferior vena cava and tricuspid annulus
50
Q

•Commonly occurs after initiation of antiarrhythmic drugs for atrial fibrillation

A

aflutter

51
Q

is amiodarone used in aflutter

A

no - only 20-30% effective at maintaining NSR

52
Q

•Atrial enlargement is most likely cause – rogue pacemakers who steal show from AV node

is describing?

A

Afib

53
Q

how does new onset Afib present

A
  • Heart palpitations
  • Fatigue
  • Lightheadedness
  • Dyspnea
  • Angina
  • Incidental
54
Q

afib w/ RVR is differeniated when what symptom is noted?

A

heart palpitations probably noted

55
Q

valular heart disease is associated with?

how do we ALWAYS manage these pts?

A

Afib

life-long anticoags - increased risk for thromboemolism

56
Q

Most common etiologies of first degree heart block

A
  • Progressive Cardiac Conduction Diseases (50% of cases) –> fibrosis and sclerosis
  • Ischemic heart disease (40% of cases) –> after MI resulting in death of cells that cannot conduct properly
57
Q

tx of first degree AVB

A

If PR interval <300msec w/ narrow QRS - no intervention

If assoc wide QRS - delay may be below AV node, between His bundle and ventricles –> uncertain progression

•refer to EP for study and consideration for pacemaker

Treat underlying cause

avoid AV nodal blocking meds –> CCBs or BBs

58
Q

what conduction blocks are indications for pacemakers

A

first degree AVB - if wide QRS complex

Second degree type I - if syncope/ other sx in setting of wide complex

second degree type II - ALL

third degree AVB - ALL

59
Q

tx for second degree AVB type II

A

Tx underlying cause

Avoid AV nodal blocking meds

ALL will need pacemakers

60
Q

tx for third degree AVB

A

Temporary pacer – IMMEDIATELY

•Refer to EP

Tx underlying cause

Avoid AV nodal blocking meds

61
Q

what conuction blocks are likely to lead to complete heart block / worsening prognosis

A

second degree type II

62
Q

heart block that is:

Asymptomatic

Normal (athletes and sick hearts)

Rarely progress to complete heart block

A

Second Degree –

Type I Wenckebache

63
Q

sx in second degree AVB type II if slow rate or frequent dropped beats

A

If slow rate or frequent dropped beats

  • Fatigue
  • Lightheadedness
  • Syncope
64
Q

tx for second degree AVB type I Wenckebache

A

Tx underlying cause

Avoid AV nodal blocking meds

Monitor EKG for progression to Type II

Asymptomatic – no tx

Syncope or other sx – refer to EP for pacemaker

  • Marked prolongation of conduction b/w his bundle and ventricles
  • Wide complex in setting of symptoms
65
Q

si/sx of third degree AVB

A

Chest pain – in setting of MI

Lightheadedness

Fatigue, weakness, exertional dyspnea, bradycardia

•Due to DEC CO bc of dropped beats

Ventricular tachycardia to Vfib then death

•Vtach due to physiologic demand

66
Q

contrast PR interval in second degree heart block type I vs II

A

type I wecke - Progressively lengthening PR interval until dropped beat occurs

type II - PR intervals equal in length until dropped beat occurs

67
Q

define a STEMI equivalent

A
  • New LBBB in setting of chest pain –> cath lab
  • Highly likely it is a MI
68
Q

which arrythmia is associated:

with INC risk of hospitalization for HF in pts w/ stable coronary heart disease

A

first degree AVB

69
Q

arrythmis associated w/ increased mortality in setting of CAD

A

LBBB

if elderly present w/ LBBB find CAD!!

70
Q

management of LBBB

A

Young, asymptomatic w/ no CAD -> no tx

STEMI equivalent to cath lab

Tx underlying conditions

Manage risk reduction in CAD

  • Well controlled BP
  • Well controlled diabetes
71
Q

describe EKG findings

A

sinus tachy

Narrow QRS complex

  • Fast and regular
  • P-waves are seen
72
Q

identify EKG arrythmia

next steps?

A

Sinus Tachycardia. Treat underlying cause (if you even need to)

73
Q

identify arrythmia and next steps

A

Atrial fibrillation.

Consider cardioversion if onset <48hrs.

Get an echo if it’s a new diagnosis.

Calculate CHADS 2 score for consideration of anticoagulation for stroke prevention.

74
Q
A

Afib with RVR

Rapid afib puts a patient at risk for pulmonary edema due to poor forward contractile forces and fluid gets backed up in lungs.

It also puts patients at risk for demand ischemia in CAD as the rate is too fast to adequately perfuse the myocardium itself

It is common to see rate related ischemic changes such as ST depressions in rapid afib.

Treat: Rate control with AV nodal blocking CCB (diltiazem) or BBs (metoprolol).

75
Q
A

Slow Aflutter

Note the classic _saw toothed pattern of the p wave_s (aka flutter waves).

This patient has bradycardia so you want to know if he is symptomatic and if he is on medications that lower heart rate, perhaps you need to back off those a bit.

Aflutter, like a fib, has a propensity to go fast.

If rapid, tx with nodal blocking agents and if meds are not effective consider ablation or cardioversion.

76
Q
A

(SVT).

It is a regular rhythm so it’s not afib.

You can not see p waves so it is not sinus tach.

SVT usually originates either from the AV node itself (a junctional rhythm) or from a reentrant circuit around the AV node (AVNRT) (most common).

SVT can happen in normal hearts and sick hearts.

It is usually sudden onset and has sudden cessation.

To treat: perform vagal maneuvers, carotid massage (listen for carotid bruits first) and if those don’t work, then give adenosine first dose is 6mg, then 6mg, then 12mg. (In real life, my advice is don’t do carotid massage in patients over 50, the risk of causing a stroke from dislodging carotid plague is not worth it)

77
Q
A

1st degree AV block (1˚ AVB).

Can be found in normal hearts.

Don’t worry about the patient.

78
Q
A

Ventricular fibrillation. T

his patient has no cardiac output because the ventricles are not adequately contracting.

He will be unconscious and pulseless.

Do ACLS protocol:

  1. Call for help (call a code).
  2. Start CPR,
  3. defibrillate as soon as the defibrillator is available.
  4. epi (epinephrine)
79
Q
A

3rd degree heart block.

The first clue is the variable PR intervals which are not following the Wenckebach pattern.

Note how the p waves march out at a certain rate (consistent intervals between p waves) and the QRS complexes march out at a certain rate, but they have nothing to do with each other (AV dissociation).

They are each, “marching to a different drummer.”

Treat: pacemaker

80
Q
A

Inferior ST elevation myocardia infarction (STEMI).

  1. Active cath lab (door to balloon time <90min.)
  2. Provide Aspirin.
  3. Quick physical exam
  4. Quick history, ask about bleeding disorders.
  5. Heparin gtt, NTG, morphine if needed.

(Within 24 hours patient also needs beta-blocker and high dose Lipitor). Of course you might use the BB early for blood pressure, or other meds as well.

81
Q
A

Torsade de Pointe (a type of ventricular tachycardia). It is caused by QTc prolongation. It is less likely to degrade into V-fib although it can. Tx with Magnesium 2gm IVP. Review the patient’s med list to determine what needs to be discontinued (which meds cause QTc prolongations; ie antipsychotics and antibiotics – namely fluoroquinolones (Levofloxacin) and macrolides (Azithromycin).

82
Q
A

Second degree AV block Type I (Wenckebach or Mobitz Type I).

No tx necessary unless symptomatic from bradycardia such as fatigue or syncope then treat with pacer.

This can be seen in normal hearts but it can also degrade into Mobitz Type II.

83
Q
A

Normal sinus rhythm develops into ventricular tachycardia.

Call a code whether the patient is conscious or not.

ACLS protocol:

If conscious and otherwise stable, and HR <150 give Amiodarone (antiarrhythmic) otherwise proceed to synchronous cardioversion.

If conscious and unstable; synchronous cardioversion.

If unconscious and pulseless, CPR and defibrillate

84
Q
A

Second degree AV block Mobitz Type II –

Note the PR intervals are consistent duration throughout but dropped beats occur.

This is likely to degrade into third degree heart block.

Treat: pacemaker

85
Q
A

Right bundle branch block (RBBB).

Note the r-Rˡ in V1 and the wide S waves in V5.

no treatment. Can be found in normal hearts.

86
Q
A

Left bundle branch block. (LBBB).

If new LBBB is discovered in a pt presenting with CP, assume ACS.

LBBB is often associated with CAD so get echo, stress test even if not symptomatic

87
Q
A

Tachy-brady syndrome. (Sick sinus syndrome with tachy/brady)

(SSS)- often you’ll see actual bradycardia, not just long pauses, but pauses are part of the deal.

Treat with Pacemaker

88
Q
A

Sinus bradycardia –

Do you need to treat? Depends if patient is symptomatic.

If you need to treat, atropine immediately and referral to EP for pacemaker.

89
Q

if new diagnosis Afib what diagnostic test is important to order

A

echo

90
Q

Afib puts you at risk for what conditions?

A

pulmonary edema due to poor forward contractile forces and fluid gets backed up in lungs.

demand ischemia in CAD as the rate is too fast to adequately perfuse the myocardium itself

91
Q

torsades is caused by

A

QTc prolongation.

It is less likely to degrade into V-fib although it can.

92
Q

can Second degree AV block Type I degrade into type II?

A

yes

93
Q

tx vtach in:

concious stable pt w/ HR <150

concious unstable

unconcious and pulseless

A

If conscious and otherwise stable, and HR <150 give Amiodarone .

If conscious and unstable; synchronous cardioversion.

If unconscious and pulseless, CPR and defibrillate

94
Q

tx for RBBB

A

none

can be found in normal hearts

95
Q

how do we work up LBBB?

A

LBBB is often associated with CAD so get echo

stress test even if not symptomatic.

96
Q

treatment of bradycardia

A

pacemaker if symptomatic

97
Q
A

WPW - “delta wave”

  • A delta wave is slurring of the upstroke of the QRS complex.
  • This occurs because the action potential from the SA node is able to conduct to the ventricles very quickly through the accessory pathway
  • thus the QRS occurs immediately after the P wave, making the delta wave.
98
Q

tx of persistent bradycardia

A

atropine

99
Q

SVT is most commonly due to:

A

AVNRT

100
Q

what does ablation target in

AVNRT

AVRT

junctional

A
  • AVNRT – cause scarring and prevent circuit from going
  • AVRT – ablate accessory pathway
  • NO junctional
101
Q
A

LBBB

V1 - t wave goes up

V6- notches appearance

102
Q
A

RBBB

look at V1 and V6

V1 - T goes down

V6 - t wave goes up

Clin med II exam II Cardio (3 decks)

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