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Cardiovascular > Dysrhythmias Part 1 > Flashcards

Dysrhythmias Part 1 Flashcards

1
Q

A cyclic increase in normal HR w/ inspiration and decrease w/ expiration

A

Sinus arrhythmia

Not a pathologic arrhythmia, and therefore, no tx required

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2
Q

sinus arrhythmia results from ?

A

reflex changes in vagal influence on nml pacemaker and disappears w/ breath holding or increase of HR

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3
Q

T/F: sinus arrhythmia is common in both young and elderly

A

troo

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4
Q

sinus brady is defined as a HR slower than?

A

< 60 bpm

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5
Q

sinus brady is due to ?

A

increased vagal influence on nml pacemaker/organic disease of sinus node (sick sinus syndrome, etc)

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6
Q

sinus brady rate usually increases during when?

A

exercise or administration of atropine

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7
Q

Severe sinus bradycardia (< 45 beats/min) may be an indication of ?

A

sinus node pathology, especially in elderly patients and individuals with heart disease
sx - weakness, dizziness, confusion, or syncope

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8
Q

causes of sinus brady

A
  1. drugs
    - Sympatholytics: βB, methyldopa, clonidine
    Cimetidine, digoxin, CCB’s, amiodarone, lithium
  2. increased ICP - Exclude in sinus bradycardia & neurologic dysfunction
  3. AMI - IWMI → RCA supplies SA node in 60% of population
  4. OSA - HR ↓ < 30bpm during apneic episodes; Tx the OSA – not an indication for pacemaker
  5. Other - hypothyroidism, hypothermia
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9
Q

Commonly have recurrent SVA (ex. Afib) and bradycardia (tachy-brady syndrome)

A

sick sinus syndrome

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10
Q

presentation of sick sinus syndrome

A

Sinus arrest occurs on monitoring; persistent sinus bradycardia can also be common presentation
Chronotropic incompetence is another form of SSS

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11
Q

sick sinus syndrome is MC in who

A

elderly – usually indicates more significant conduction disease

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12
Q

what can cause sick sinus syndrome

A

meds
These should be held prior to invasive pacemaker insertion, for at least 24-48 hrs

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13
Q

tx for sick sinus syndrome

A

Symptomatic → PPM
- Withhold possible offending agents
- r/o possible causes
- Determine if symptomatic and if sx correlate with the bradycardia (KEY!)
- Once all of the above are done, and sx are determined to be related to bradycardia = permanent pacemaker implantation (1st line)
- acute - transcutaneous pacing, transvenous pacing, or atropine (ACLS protocol)

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14
Q

sinus tach is defined as a HR of ?

A

> 100bpm (adult) - (220-Age) d/t impulse formation from SA node

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15
Q

causes of sinus tach and which is MC?

A
  • exercise, anger/stress (MC)
  • Others - hyperthyroidism, fever, sepsis, pain, anemia, volume depletion, pheochromocytoma, hypoxia, PE, heart failure, acute coronary ischemia, alcohol/alcohol withdrawal, stimulants
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16
Q

sinus tach at rate > 140 bpm what may be hard to visualize on ecg?

A

P waves - superimposed on preceding T wave
Consider carotid sinus massage or vagal maneuvers

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17
Q

sx of sinus tach

A

Palpitations, lightheadedness

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18
Q

how can high HR affect structural heart disease?

A
  • ↑ myocardial O₂ consumption
  • ↓ coronary blood flow
  • ↓ C.O. by shortening ventricular filling time
  • Exacerbate myocardial/valvular heart disease
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19
Q

what is Inappropriate Sinus Tachycardia

A
  • Occurs in absence of heart disease or secondary causes
  • ↑ resting HR and/or exaggerated HR response to exercise
  • Exact cause unknown; possible abnormal autonomic control
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20
Q

what is Postural orthostatic tachycardia syndrome (POTS)

A

Young women w/o heart disease w/ normal resting HR
Exaggerated sinus tachycardia elicited by upright TTT
Occurs in absence of orthostatic hypotension

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21
Q

tx for sinus tach

A
  1. Physiologic = None needed
    - Address any underlying cause
  2. In symptomatic pts w/ inappropriate sinus tachycardia, with/w/o correctable cause:
    - βB (1st line)
    - Alt: non-DHP CCBs / ivabradine (Corlanor)
22
Q

PR interval > 0.2 second with all atrial impulses conducted
what is this dysrhythmia

A

1st degree HB

23
Q

the AV conduction time (PR interval) progressively lengthens, with the RR interval shortening before the blocked beat
This phenomenon is almost always due to abnormal conduction within the AV node

what is this dyrrhythmia

A

Mobitz type I (Wenckebach) AV block

24
Q

there are intermittently nonconducted atrial beats not preceded by lengthening AV conduction
It is usually due to block within the His bundle system.

what is this dyrrhythmia

A

Mobitz type II AV block

25
Q

complete heart block; complete A-V dissociation, in which no supraventricular impulses are conducted to the ventricles

what is this dysrrhythmia

A

3rd degree HB

26
Q

causes of 1st-degree and Mobitz type I block: (4)

A
  • nml individuals w/ heightened vagal tone
  • Drugs - esp digitalis, CCB, BB, or other sympatholytic agents
  • lyte abnormalities
  • Organic dz - ischemia, infarction, inflammatory processes (Lyme), fibrosis, calcification, or infiltration
  • May be transient or chronic
27
Q

causes of Mobitz type II block and 3rd degree block:

A

Almost always due to organic disease involving the infranodal conduction system
May be transient or permanent

28
Q

causes of Atrioventricular block

A
  • Idiopathic
  • Degenerative process
  • IHD (inferior wall, septal area, right ventricle)
  • Calcific aortic and mitral valve disease
  • AV nodal/His ablative procedures
  • Meds - Digitalis, βB, CCB (verapamil, diltiazem), sotalol, dronedarone, amiodarone, donepezil
  • Infections (including aortic valve endocarditis)
  • Inflammatory (myocarditis)
  • Infiltrative dz - Amyloidosis, neoplasm, sarcoidosis, hemochromatosis
  • Neuromuscular diseases
  • Trauma
  • Aortic valve surgery
29
Q

s/s of 1st degree block

A

asx
Diagnosed by EKG alone; no PE abnormalities

30
Q

s/s of Mobitz type I block

A

MC asx; possible palpitations, DOE, or dizziness
Cardiac auscultation will reveal irregular rhythm.

31
Q

s/s of Mobitz type II block

A

possible asx; MC palpitations, DOE, weakness, or dizziness
Cardiac auscultation will reveal irregular rhythm.

32
Q

s/s of Third-degree block

A
  • sx vary, and are worse with exertion; palpitations, DOE, weakness, near syncope, syncope, and/or HF
  • PE include bradycardia and possibly signs of HF
33
Q

work-up for Atrioventricular block

A
  1. Review meds list and PMHx
  2. 12-lead EKG
  3. Telemetry monitoring
  4. echo to r/o structural heart disease
  5. If any s/s of ischemia, will need ischemic eval - cardiac cath
  6. Laboratory studies: CBC, CMP, TSH to begin with; any other tests (immunologic, inflammatory markers) if indicated based on H&P
34
Q

management for 1st degree block

A
  • Typically a stable rhythm with good prognosis
  • Avoid meds that may prolong PR interval and slow AV conduction (AAD 1C, BBs)
35
Q

management for Mobitz Type I AV Block:

A
  • Typically a stable rhythm
  • Treat any identifiable causes; avoid AV node conduction slowing drugs
  • Rarely needs a permanent pacemaker
36
Q

management for Mobitz Type II and Third-degree AV Blocks:

A
  • Unstable rhythms; require permanent pacemaker implantation
  • if transient d/t acute organic process = temporary pacing
37
Q
  • Defined as an ectopic focus in the atria that fires before the next sinus node impulse
  • Usually has a different P wave morphology
  • May conduct with a short, normal, or long PR interval; or may not conduct at all
A

Premature Atrial Contractions

38
Q

PACs frequently occur in:

A

Frequently occur in normal hearts

  • Increased frequency with increasing age
  • Also occur with structural changes, like LAA, MVP, MS/MR, TR
  • May also be precursor to atach, afib, aflutter
39
Q

sx of PAC

A

asx; palpitations (“skipped beats”)

40
Q

tx for PAC

A

MC none required
BB if significant sx
Class IC antiarrhythmic is 2nd-line

41
Q

Premature depolarization originating from the ventricles
Results in a wide QRS complex followed by a compensatory pause

A

Premature Ventricular Contractions

42
Q

PVC frequently occurs in? other causes?

A
  1. normal hearts
  2. Other causes:
    - Caffeine, stress, alcohol
    - Structural heart disease – CAD, Valvular disease, LVH
    - lyte abnormalities
    - Thyroid disease
43
Q

PVCs normally diminish in frequency with ?

A

exercise (suppressed by increased HR)
However, if increase in frequency during exertion, associated with higher risk of CV mortality

44
Q

sx of PVC

A
  1. MC asx
  2. Palpitations MC complaint – “skipped beats”
  3. Symptoms vary based on frequency of PVCs (ex: trigeminy, bigeminy)
    - Dizziness, near syncope or syncope possible, especially with exertion
45
Q

tx for PVCs

A
  1. Manage any underlying causes
  2. If sx - BB 1st line - (Lopressor)
    - mild - reassurance
  3. If BB fails - Class IC / III AAD
  4. Catheter ablation, esp w/ significant ectopy burden
46
Q

A common cause of paroxysmal tachycardia
Most often occurs in patients with normal structured hearts

A

Paroxysmal Supraventricular tachycardia

47
Q

MC mechanism of Paroxysmal Supraventricular tachycardia

A

reentry
Typically initiated by a PAC or PVC

48
Q

2 types of reentry in paroxysmal supraventricular tachycardia

A
  1. AVNRT (AV nodal reentrant tachycardia) – MC
  2. AVRT (AV reciprocating tachycardia)
    - WPW – Accessory pathway
49
Q

```

~~~

s/s of Paroxysmal Supraventricular tachycardia

A
  1. Sx vary:
    - Awareness of rapid heart beat
    - Chest pain, shortness of breath
    - Dizziness, syncope
    - Abrupt onset and termination, last seconds to several hours or longer
  2. EKG
    - Tachycardia (140 to 240 bpm)
    - Regular rhythm
    - QRS MC narrow-complex, can be wide
    - P wave buried in QRS complex
50
Q

management for Paroxysmal Supraventricular tachycardia

A

depends on patient’s stability
- Acute management includes mechanical measures, drug therapy, and cardioversion
- Preventative therapies include catheter ablation and AADs

Acute Management:

  1. Mechanical Measures:
    - Valsalva
    - Stretching arms and body, lowering the head between knees
    - Coughing, breath holding
    - Splashing cold water on the face, placing ice or frozen peas on the face
    - Carotid sinus massage – SHOULD ONLY BE DONE BY A PROVIDER
  2. Initial Drug Therapy (ALL IV):
    - Adenosine – 1st line
    - CCB – Diltiazem, Verapamil
    - BB – Esmolol, Lopressor
  3. Refractory SVT Drug Therapy:
    - Amiodarone
    - Procainamide for antidromic SV (wide-complex tach)
  4. Cardioversion - 1st-line if hemodynamically unstable
    - indicated if meds are CI/ineffective
    - Synchronized electrical cardioversion, beginning at 100 J
51
Q

prevention/long-term management for Paroxysmal Supraventricular tachycardia

A
  1. Catheter Ablation -1st line therapy for recurrent, sx PSVT
  2. Meds
    - AV nodal blocking agents 1st line - BB & CCBs
    - If continued sx - add Class IC (flecainide, propafenone) / ClassIII (amiodarone, sotalol)
52
Q

The one exception of adding an AAD to AV nodal blocking agent for prevention/long-term management in Paroxysmal Supraventricular tachycardia

A
  1. Patient’s w/ AVRT (WPW) are also prone to afib, aflutter.
    - AV nodal blocking agent do not affect refractoriness of the accessory pathway…… Therefore, ventricular rates in afib/aflutter can be even FASTER
    - Tx: Class IC or III AAD + BB/CCB

Cardiovascular (24 decks)

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