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Adult Clinical Medicine > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

Goals of evaluation and treatment of arrhythmias

A
  1. eliminate or attenute sx
  2. prevent death or injury
  3. offset long-term risk
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2
Q

Primary care approach to the patient with an arrhythmia

A
  1. ID of the arrhythmia
  2. Does it cause symptoms?
  3. Does it have prognostic significance?
  4. Is it life-threatening?
  5. Is treatment needed?
  6. Does the patient need to be in the hospital?
  7. Does cardiology need to be involved? How urgently?
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3
Q

Arrhythmia symptoms

A
  1. Can be asymptomatic
  2. Palpitations
  3. Dizziness
  4. Chest pain
  5. Dyspnea
  6. Weakness
  7. Anxiety
  8. Symptoms may be due to underlying heart disease e.g. HF, ischemia
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4
Q

Initial evaluation of arrhythmias consists of:

A
  1. Thorough HX and PE
  2. 12-lead ECG, ideally:
    - in the presence and absence of symptoms
    - in sinus rhythm and during the arrhythmia
  3. In selected patients:
    - Ambulatory monitoring (using a Holter or event monitor)
    - Referral to an electrophysiologist
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5
Q

describe risk assessment in an asymptomatic pt and one w/ known CAD

A
  • Be very careful with arrhythmias in patients with known coronary artery disease
  • Asymptomatic arrhythmias rarely require urgent intervention

*risk assessment often requires a cardiologist

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6
Q

Tissues along the conduction pathway have inherent rates. In the absence of any external stimuli, these tissues will generate spontaneous impulses in the following ranges:
SA node:
AV junction:
Ventricle:

A

SA node: 60-100
AV junction: 40-60
Ventricle: 20-40

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7
Q

describe the phenomenon of “escape”

A

If the SA node drops below its inherent rate, fails, or impulses are blocked, the site with the next-highest inherent rate (e.g. the AV junction) will take over the pacemaking role.

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8
Q

describe the phenomenon of “irritability”

A

“Irritable” conduction site discharges impulses at a faster-than-normal rate and takes over the role of pacemaker.

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9
Q

describe the phenomenon of “reentry”

A

An extra conduction pathway creates a circuit that can lead to rapid cycling, causing a “re-entrant” tachycardia

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10
Q

Types of reentry tachycardias

A
  1. AVNRT (most common type of SVT)
  2. AV reciprocating tachycardia (or AVRT) (2nd most common)
  3. WPW (accessory pathwaying causing pSVT)
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11
Q

due to a circuit created by an abnormal accessory pathway between the atrium and ventricle that is more distant from the AV node

A

AVRT (AV reciprocating tachycardia)

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12
Q

Describe the PR interval

A
  • beginning of the P wave to beginning of QRS

- normal is 0.12-0.2 (3-5 small boxes)

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13
Q

Describe the QRS interval

A

-normal is less than 0.12 sec (3 small boxes)

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14
Q

Describe the ST segment

A

-end of QRS to start of T wave

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15
Q

Describe the QT interval

A

-beginning of QRS To end of T wave

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16
Q

each small box = __

each large box = __

A 
small = 0.04 sec
big= 0.2 sec

*5 big boxes = 1 sec

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17
Q

definition of sinus brady and sinus tachy

A

rate less than 60bpm

rate over 100bpm (rates over 140 may have P waves that are “buried”

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18
Q

causes of sinus bradycardia

A
  1. Can be normal, particularly in athletes– unless accompanied by sx
  2. Sinus node dysfunction (aka SSS if has sx too)
  3. Metabolic (hyper-, hypo-kalemia, hypercalcemia, hyper-, hypo-thyroidism)
  4. Drugs (BB, CCB, lithium)
  5. Neurogenic, vagal stimulation (tight collar, cough, defecation, cold water to face)
  6. Cardiac ischemia, acute MI, AV conduction disturbance
  7. Obstructive sleep apnea
  8. Infection
  9. Increased intracranial pressure
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19
Q

Symptoms of bradycardia

A
  1. Usually asymptomatic
  2. Lightheadedness
  3. Presyncope, syncope
  4. Worsening of angina pectoris
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20
Q

Treatment of bradycardia

A

*Not indicated in asymptomatic patients

  • If symptomatic:
    1. Change or eliminate meds
    2. Long-term drug therapy usually ineffective
    3. May require pacemaker (50% of all pacemakers are for bradycardia)
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21
Q

causes of sinus tachycardia

A
  1. Fever
  2. Sepsis
  3. Anemia (volume change)
  4. Hypotension and shock (volume change)
  5. Acute coronary ischemia and MI
  6. Heart failure
  7. Chronic pulmonary disease
  8. Hypoxia
  9. Pulmonary embolism
  10. Stimulants or illicit drugs (nicotine, caffeine, OTC decongestants, cocaine)
  11. Anxiety
  12. Pheochromocytoma
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22
Q

Symptoms of sinus tachycardia

A
  1. Often asymptomatic
  2. Awareness of a rapid heartbeat (“palpitations“)
  3. shortness of breath,
  4. dizziness,
  5. syncope,
  6. chest pain,
  7. anxiety
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23
Q

Treatment of sinus tachycardia

A
  1. Treat underlying disease
  2. Beta-blockers if underlying diseases ruled-out or treated
  3. Don’t miss acute MI or PE!
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24
Q

how does HR change with inspiration and expiration

A

increase w/ inspiration

decrease w/ expiration

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25
Q

Atrial rhythms

A
  1. wandering pacemaker (WAP)
  2. APBs
  3. AT
  4. Aflutter
  5. Afib
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26
Q

What is a wandering pacemaker (WAP) rhythm?

A

-Pacemaker site wanders between the sinus node, different ectopic sites within the atria (and, in some cases, the AV junction)

  • Rhythm: Typically, slightly irregular 2º to changing atrial pacemaker sites
  • P wave morphology changes (3 or more distinct p waves)
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27
Q

how does one dx WAP

A
  1. Sometimes noted on exam as an irregularly irregular pulse

2. Usually an isolated finding on ECG and does not require treatment

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28
Q

What are APBs?

A
  • An irritable focus within the atrium fires prematurely and produces a single ectopic beat
  • Formerly called PACs
  • P wave: P wave associated with the APB will have a different morphology (or may be hidden in preceding T wave)
  • PRI: .12-.20 sec, may vary slightly in APB

*maybe be preceded by a shorted R-R interval

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29
Q

APBs can be triggered by:

A
  1. caffeine
  2. nicotine
  3. alcohol
  4. sympathomimetics (pseudoephedrine)
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30
Q

symptoms and tx of APBs

A
  1. usually asymptomatic and require no tx
  2. palpitations or ‘skipping a beat”

tx for pt w/ uncomfortable sx, d/c potential triggers, and consider a BB

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31
Q

What are the different types of SVT

A
  1. re-entry
    - AVNRT
    - AVRT (accessory pathway)
  2. abnormal automaticity
    - (unifocal) AT

*can be chronic, persistent, or paroxysmal

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32
Q

How does SVT look like on an EKG

A

Typically a narrow QRS complex tachycardia with a regular rate and no discernable P wave

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33
Q

Describe pSVT

A
  1. Usually benign and self-limited and can be managed conservatively
  2. Episodes begin and end abruptly, last from seconds to hours
  3. Most common symptom is awareness of rapid pulse (also mild chest pain and SOB)
  4. HR is typically 160-220 bpm
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34
Q

treatment of pSVT

A
  1. avoid triggers (caffeine, alcohol, nicotine, stress)
  2. vagal maneuvers to increase parasympathetic tone (valsalva, gag reflex, water on face, coughing, carotid massage)
  3. Meds: best managed under supervision of cadiologist
  4. radiofrequency ablation
  5. pacemaker
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35
Q

Describe what WPW is

A

Accessory pathway from atrium to ventricle that bypasses usual delay at the AV node causing rapid pSVT

EKG: short PR interval w/ slurred QRRS upstroke (delta wave)

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36
Q

Risks of WPW

A
  1. prone to SVT with may lead to Afib
  2. can develop life-threating arrhythmias

*all should be monitored by cardiologists

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37
Q

How does unifocal AT occur

A

when a single irritable focus in the atrium fires repetitively at a rapid rate

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38
Q

How is unifocal AT treated

A
  • meds

- less commonly catheter ablation

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39
Q

describe what AT looks like on EKG

A

Rhythm: Regular
Rate: Typically 150-250 bpm
Atrial and ventricular rates are equal
P wave: Morphology different from sinus P wave, can be “buried” in T waves

-nl PR and QRS interval

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40
Q

How does atrial flutter occur

A

A single irritable focus within the atrium issues an impulse that is conducted in a rapid, repetitive fashion. The AV node blocks some of these impulses from being conducted through to the ventricles.

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41
Q

What is the main distinction between Aflutter and and AT?

A

in atrial flutter, the AV node blocks some of these singular irritable focus impulses from being conducted

42
Q

describe what Aflutter looks like on EKG

A
  • Rhythm: Atrial rhythm is regular. Ventricular rhythm may be regular or irregular.
  • Rate: Atrial rate: 250-350 bpm, ventricular rate depends on conduction of atrial impulses
  • P wave: Sawtooth appearance
  • PRI: Not measured in this condition
  • QRS: normal
43
Q

atrial flutter is caused by/associated with:

A
  1. HF
  2. MV prolapse
  3. ASD
  4. hyperthyroidism
  5. COPD
  6. MI
44
Q

Describe the management of atrial flutter

A
  1. always prompt consult with cardio
  2. DC cardioversion is often very effective at very low energies (less than 50 joules)
  3. Chronic meds rarely effective
  4. Catheter ablation 85% successful (usually the treatment of choice)
45
Q

How does atrial fibrillation occur?

A

when atrial irritability leads to multiple foci initiating impulses, causing the atria to depolarize repeatedly (fibrillate). AV node blocks most of the impulses, allowing a limited number through to the ventricles

46
Q

How does Afib look on an EKG

A
  • Rhythm:Atrial rhythm unmeasurable, ventricular rhythm is irregularly irregular
  • Rate: less than 100 = “controlled” A fib, over 100 = A fib with “rapid ventricular response”
  • P wave: Not discernable
  • PRI: Unmeasurable
  • QRS: nl
47
Q

What is the most common arrhythmia

A

Afib

*more common with advancing age (median age is 75)

48
Q

paroxysmal Afib is characterized by ___ and is exacerbated with ____

A
  1. episodes that self-terminate in less than 7 days

2. associated w/ emotional stress, following surgery, exercise, EtOH, hot tubs, caffeine, nicotine, fever

49
Q

persistent Afib is characterized by __ and associated with ____

A
  1. Fails to self-terminate in 7 days
  2. associated w/ cardiovascular disease (rheumatic heart, mitral valve, hypertensive, chronic lung, ASD, etc.), thyrotoxicosis
50
Q

How does Afib present?

A
  1. Can be asymptomatic, found incidentally
  2. Syncope, weakness, dizziness, fatigue, palpitations, irregularly irregular pulse
  3. CVA
  4. Ischemic heart disease, MI
  5. CHF
51
Q

describe the evaluation of Afib

A
  1. PE: CV focus, signs/sx of CHF, severe hypotension
  2. ECG
  3. CXR
  4. Echo
  5. Thyroid tests, electrolytes
52
Q

describe the management goals of Afib

A
  1. must address associated conditions (ex. organic heart disease, hyperthyroidism)
  2. rate control
  3. rhythm control
  4. prevention of systemic embolization
53
Q

describe appropriate rate control for afib

A
  1. Goal: 70-100 bpm
  2. If severe failure, angina, hypotension–> electrical cardioversion
  3. If stable–> Use drugs (Verapamil, Diltiazem, Beta-blockers)
54
Q

describe appropriate rhythm control for afib (restore NSR)

A
  1. Anti-arrhythmic drugs - IA (e.g. procainamide), IC (e.g. flecainide), and III (e.g. amiodarone)
    OR
  2. Direct-current cardioversion
55
Q

which is more important in rate vs rhythm control in AFib?

A
  • Rhythm control was the preferred approach until the results of several major clinical trials (e.g AFFIRM) found:
  • Embolic events are just as likely with a rhythm control approach
  • Rate control was associated with better mortality outcomes

*Thus, rate control is the preferred initial approach

56
Q

Afib rhythm control approach should be considered it:

A
  1. persistent sx despite rate control
  2. there is an inability to attain rate control
  3. patient prefers this approach
57
Q

describe moderate and high risk factors for thromboembolism with afib

A

moderate: over 75, HTN, HF, DM
high: CVA, TIA, embolism, prosthetic valve

58
Q

Describe the need for anticoagulation for Afib

A

*based on stroke risk

  1. daily ASA (81-325mg) if no RF
  2. ASA or coumadin (warfarin) if 1 moderate RF
  3. coumadin if more than 1 moderate RF or 1 high RF

*coumadin to achieve INR of 2.0-3.0

59
Q

When should you refer Afib?

A
  1. New dx
  2. If RVR: hospital admission for rate control is critical (send by ambulance)
  3. Usually need 2-3 weeks of anti-coagulation before cardioversion
  4. When in doubt: consult, consult, consult
60
Q

when does junctional tachycardia occur?

A

Irritable focus in the AV junction overrides the SA node. Atria depolarized via retrograde conduction, ventricular depolarization is normal.

61
Q

how does junctional tachycardia look on an EKG?

A
  1. rate: 100-180
  2. P waves can be before, buried within, or after QRS
    - if before QRS, PRI is less than 0.12 (SHORT)
62
Q

How are AV blocks acquired?

A
  1. rarely congenital
  2. MI
  3. surgery
  4. RFA trauma
  5. meds (digoxin, CCBs, BB, Class 3 antiarrhythmics)
  6. infections
  7. common in trained athletes

*rarely of prognostic significance

63
Q

symptoms of AV blocks

A
  1. asymptomatic
  2. weakness
  3. fatigue
  4. syncope
  5. exercise intolerance
64
Q

What is 1st degree AV block

A

Not a true block, actually a delay at the AV node. Each atrial impulse is conducted to the ventricles.

65
Q

describe what 1st degree AV block looks like on an EKG

A
  • Rhythm: Depends on underlying rhythm
  • Rate: Depends on underlying rhythm
  • P wave: Upright, uniform, each followed by a QRS
  • PRI: Over .20 sec** (LONG and Fixed)
  • QRS: less than .12 sec (nl)
66
Q

tx of 1st degree AV blocks

A

Does not require treatment but in some individuals can progress to 2nd degree AV block

67
Q

Describe 2nd degree AV block type 1

A

Wenckebach

Each impulse is delayed at the AV node a little longer than the preceding impulse, until one impulse is blocked completely

68
Q

how does 2nd degree AV block type 1 look on an EKG?

A
  • Rhythm: Irregular R-R**
  • Rate: Atrial rate is usually normal (60-100), ventricular rate is usually slow**
  • P wave:Upright, uniform, some not followed by a QRS
  • PRI: Get progressively longer until one P wave is not followed by a QRS***
  • QRS: less than .12 sec (nl)
69
Q

Describe the management of Wenckebach

A
  1. Unlikely to progress or lead to asystole
  2. Medication review and appropriate changes
  3. Thorough cardiac evaluation
  4. Patients with symptomatic bradycardia (syncope, pre-syncope, hypotension) usually benefit from pacing
70
Q

describe 2nd degree AV block type 2

A

AV node selectively allows conduction of some impulses to the ventricles while blocking others

71
Q

how does 2nd degree AV block type 2 look on an EKG?

A
  • Rhythm: Atrial rhythm usually regular, ventricular rhythm can be regular or not, depending on conduction ratio*
  • Rate: Atrial rate usually 60-100, ventricular rate typically bradycardic (less than 60bpm)*
  • P wave:Upright, uniform, more P waves than QRS
  • PRI:Constant on conducted beats
  • QRS: less than .12 sec
72
Q

What is 2nd degree AV block type 2 associated with?

A
  1. Almost always due to disease within the AV node

2. High risk of progression and can lead (sometimes rapidly!) to asystole

73
Q

Management of 2nd degree AV block type 2

A

all pts need pacers

74
Q

describe 3rd degree heart block

A

Complete block of impulses at the AV node. The atria and ventricles function independently

-Complete AV dissociation
Impulses originate at SA and -AV node separately

75
Q

how does 3rd degree heart block look on an EKG

A
  • Rhythm: P-P and R-R intervals are constant but not related
  • Rate: Atrial rate is typically 60-100, Ventricular rate can be junctional (40-60) or ventricular (20-40)**
  • P wave: Upright, uniform, more P waves than QRS**
  • PRI: None
  • QRS: less than .12 sec if controlled by a junctional focus, .12 sec or greater if a ventricular focus**
76
Q

3rd degree AV block can lead to ___. Tx includes ___

A

failure if significantly decreased CO from bradycardia

-tx: pacing

77
Q

What is a BBB

A
  • Abnormal ventricular depolarization
  • Normal conduction down unblocked branch; opposite branch slowly depolarized via myocardial tissue (slower than conductive pathways)
78
Q

causes of RBBB

A
  1. Degenerative conduction system disease (fibrosis),
  2. ischemic cardiac disease,
  3. acute PE (big ones)
  4. can be seen in a normal heart
  5. RBB is a thin bundle of fibers, block can be due to a small lesion
79
Q

What are the EKG characteristics of a RBBB

A
  1. QRS greater than 0.12 sec
  2. wide S wave in lead I, V5, and V6
  3. R-S-R’ in V1
  4. “M” in V2
80
Q

Causes of LBBB

A
  1. widespread cardiac disease
  2. LVH
  3. degenerative disease
  4. Aortic stenosis
  5. ischemic disease
  6. cardiomyopathy
    * * cannot rule out infarctio in the presences of LBBB– need other studies
81
Q

What are the EKG characteristics of a LBBB

A
  1. QRS: over 0.12 s
  2. Wide S wave in leads V1 and V2
  3. Wide R wave in V5 and V6, usually seen as R-R’
82
Q

Management of BBB

A
  1. newly dx, needs thorough eval
  2. all new LBBB deserve stress test (persantine thallium)
  3. tx underlying disease
  4. if accompanied by syncope, will likely require pacemaker
83
Q

what are VPBs

A

premature ventricular beats

  • single irritable focus in the ventricle that fires prematurely
  • Very common, increased incidence with age
  • usually benign ectopic ventricular impulses
  • May alternate with sinus beats (bigeminy) or after every two sinus beats (trigeminy)
84
Q

how do VPBs appear on EKGS

A
  • Rhythm: Depends on underlying rhythm
  • Rate: Determined by underlying rhythm
  • P wave: VPB not preceded by a P wave
  • PRI: None associated with VPB
  • QRS: Premature, bizarre, wide (over .12 sec) QRS with compensatory pause (early -QRS penetrates AV node, making it refractory to next impulse.)
85
Q

___ or more consecutive VPBs is Vtach

A

3

86
Q

VPBs are associated with

A
  1. increased caffeine
  2. EtOH
  3. nicotine

*VPBs in the post-MI patient can influence prognosis

87
Q

Management of VPBs

A
  1. thorough H/P
  2. VPBs and non-sustained Vtach (terminates in less than 30 sec) and no structural heart disease: no therapy is needed. Treat symptoms if desired (beta-blockers for 2 weeks)
  3. if occurs during exercise– cardiology referal (sudden cardiac death can occur w/ VPBs in the setting of ischemic heart disease)
88
Q

describe what Vtach is

A

Irritable focus in the ventricle that fires regularly at a rate of 150-250 bpm and overrides higher sites

*difficult to differentiate from SVT w/ aberrancy

89
Q

How does Vtach appear on an EKG

A

-Rhythm: Regular or slightly irregular

  • Rate: 150-250 bpm
  • P wave: None discernable
  • PRI: None
  • QRS: over .12 sec and bizarre, often cannot distinguish between QRS and T wave
90
Q

what is considered slow VT and ventricular flutter

A

slow VT: less than 150bpm

Vflutter: over 250

91
Q

Management of Vtach

A
  1. often requires emergent treatment
  2. thorough cardiac eval
  3. ID Presence, type, severity of cardiac disease
  4. Medication use is very important: proarrhythmics (digoxin, diuretics, erythromycin, class I antiarrhythmics, others)
92
Q

tx of hemodynamically unstable VT

A

synchronized cardioversion (ACLS protocol)

93
Q

tx of hemodynamically stable VT

A
  1. meds: state w amiodarone.. if no response, procainamide.. if no response, lidocaine
    * *NO verapamil
  2. consider synchronized cardioversion
  3. some will require ICDs
94
Q

Why can you not use verapamil w/ VT

A

it can initiate Vfib in VT

-should only be considered if you are certain that it is SVT w/ abberancy

95
Q

What is VFib

A

Multiple irritable foci in the ventricles generate chaotic, uncoordinated impulses that cause the heart to fibrillate rather than contract

96
Q

how does vfib look on an EKG

A
  • Rhythm: Baseline is chaotic, no discernable waves
  • Rate: Can not be determined
  • P wave: None discernable
  • PRI: None
  • QRS: None discernable
97
Q

what is vfib associated w/

A
  1. no effective pumping= death

2. most commonly seen w/ acute MI

98
Q

tx of vfib

A
  1. shock w/ electrical current

2. treat underlying disease

99
Q

what is an idioventricular rhythm

A

A ventricular escape rhythm. In the absence of a higher pacemaker, the ventricles initiate a regular impulse.

100
Q

what does an idioventricular rhythm look like on an EKG

A
  • Rhythm: Usually regular, can gradually slow as death nears
  • Rate: 20-40 bpm, can gradually slow as death nears
  • P wave: None
  • PRI: None
  • QRS: over .12 and bizarre

Adult Clinical Medicine (26 decks)

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