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Semiology second semester > Heart Rhythm disorders > Flashcards

Heart Rhythm disorders Flashcards

1
Q

Arrhythmia Presentation

A

• Tachyarrhythmias
– Palpitation, skipped beat

• Bradyarrhythmias
─ Fainting
─ Sincope
─ Dizzy spells

• Other symptoms
– Dizziness
– Chest Pain
– Dyspnea
– Sudden cardiac death
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2
Q

Arrhythmia Etiology

A 
• Physiological
• Pathological
─ Structural heart disease
 Ischemic heart disease
 Hypertensive heart diseases
 Valvular heart disease
 Cardiomyopathies
 Miocarditis, Pericarditis
 Congenital heart disease
 RV dysplasia

─ Drug related
─ Pulmonary diseases
─ Others

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3
Q

Mechanism of Arrhythmogensis

A
  1. Disorder of impulse generation
    a) Automaticity (Automatism crescut)
    b) Triggered Activity (Activitate declansata)
    1) Early after depolarization
    2) Delayed after depolarization
  2. Disorder of impulse conduction
    a) Block – Reentry.
    b) Reflection.
  3. Combined disorder
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4
Q

Mechanism of Arrhythmogenesis

History taking

A

(1) documentation of initial onset of symptoms
(2) complete characterization of symptoms
(3) identifying conditions that initiate symptoms
(4) duration of episodes
(5) frequency of episodes
(6) pattern of symptoms over time→ better or worse
(7) effect of any treatment
(8) family history of a similar problem

►Asses Pt. past medical history

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5
Q

Arrhythmias

Physical Examination

A

─check for orthostatic hypotension
─ findings related to atherosclerosis & CAD
 presence of a carotid bruit
 decreased peripheral pulses

─ findings related to a cardiac cause→presence of

 specific cardiac murmurs or
 S3 or S4 gallop
─ patient’s sex and age

 PSVT that occurs in a 7-year-old boy →AVRT
 PSVT presenting in a 65-year-old woman →AVNRT

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6
Q

Arrhythmias

Clinical Presentations

A

 a wide spectrum of clinical presentations
→ from asymptomatic ECG abnormalities
→ to cardiac arrest

 Related to arrhythmia
 Related to primary condition (the underlying
disease)

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7
Q

Arrhythmias

Diagnosis

A
  • ECG
  • 24h Holter Ecg monitor
  • Head-Up Tilt Table Testing
  • Electrophysiology study
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8
Q

Arrhythmias
Ecg
Normal Sinus Rhythm

A

 P wave

positive in lead II
negative in lead aVR

 heart rate (50) 60-100 bpm
 Constant PP (constant RR)
 Constant PR (normal range)

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9
Q

Ecg

Major Tachyarrhythmias

A 
Narrow QRS complex
• Sinus tachycardia
• Paroxysmal supraventricular tachycardia (PSVTs)
• Atrial flutter
• Atrial fibrillation
Wide QRS complex
• Ventricular tachycardia
• Aberrant ventricular conduction
• Bundle branch block
• Atrioventricular bypass tract
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10
Q

Supraventricular Arrhythmias

Sinus Tachycardia

A

simply Sinus Rhythm + heart rate ≥ 100 bpm

  • P waves have normal morphology, positive in lead II
  • Atrial rate 100-200 beats/min (adults)
  • One P wave precedes every QRS complex
  • Fast rates: P merged with the preceding T wave
  • Ventricular rate 100-200 beats/min
  • Regular ventricular rhythm
  • Symptoms: palpitation, anxiety
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11
Q

Respiratory / Sinus Arrhythmia

A

Normally
 HR increases slightly with inspiration
 HR decreases slightly with expiration

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12
Q

Atrial and Nodal (AV Junctional) Premature

Beats

A

APBs features
- premature atrial depolarization (occur before the next normal P wave

  • ectopic atrial pacemaker
  • ventricles depolarized in a normal way

 P wave APB is before QRS APB

  • slightly different shape and/or
  • different PR interval (longer or shorter)
  • may be “buried” in the T wave of the preceding beat
     QRS APB usually identical or very similar to the QRS SR
     slight pause After the APB before the normal sinus beat
     Symptoms: palpitation, extra beat-skipped beat
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13
Q

Atrial bigeminy

A

each sinus beat is followed by an APB

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14
Q

Atrial tachycardia (AT)

A 
 3 or more consecutive APBs
 ectopic pacemaker (nonsinus)
 fires off "automatically" in a rapid way
 atrial rate ~ 200 beats/min
(range: 100 to 250 beats/min)
 Abnormal P wave morphology
 Ventricular rhythm usually regular
 Symptoms: palpitation, light-headedness or even syncope
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15
Q

Paroxysmal Supraventricular Tachycardia

A 
A sudden run of 3 or more beats
- Notsustained (< 30 sec)
(i.e., lasting from 3 beat up to 30 sec)
- Sustained
episodes > 30 sec.- may last minutes, hours, or longer
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16
Q

AV NODAL REENTRANT TACHYCARDIA

AVNRT

A

 Rapid and Regular rhythm
 Rates between 140 - 250 beats/min
 generally initiated by an APB
may occur with normal hearts or with underlying heart disease reentry = a situations in which a cardiac impulse appears to “chase its own tail”

therapy = ↑ vagal tone ( Valsalva maneuver, carotid sinus massage)

(• slow and fast conduction routes
• final common pathway through the
lower part of the AV node and
bundle of His )

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17
Q

A premature atrial impulse finds the

A

fast pathway refractory,
allowing conduction only down the slow pathway (left). By the time the impulse reaches the His bundle, the fast pathway may have recovered, allowing retrograde conduction back up to the atria—the resultant “circus movement” gives rise to slow-fast atrioventricular nodal re-entrant tachycardia (right)

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18
Q

AV Junctional Rhythms

A 
- Retrograde P waves
(+ in lead aVR , - in lead II)
Pattern
1. precede the QRS complex
2. immediately after the QRS
3. Absent P waves (buried in the QRS)
- ventricles normally depolarized → narrow QRS complex
- Mechanism: ectopic pacemaker
- if AV junction=cardiac pacemaker → atria stimulated in a retrograde fashion, from bottom to top
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19
Q

Atrial Flutter

A

F “sawtooth” flutter waves instead of discrete P waves
Atrial Rate is about 300 beats/min (250 - 350 bpm)

*** IF atrial rate < 250 beats/min (eg 200 - 220 beats/min)
→ patient taking drugs that slow atrial conduction

Ventricular Rate:
Constant: 150, 100, or 75 beats/min (150 bpm → 2:1 flutter) variable
Eg
4:1 flutter →1 QRS complex with every 3 flutter wave,
2:1 flutter →1QRS with everyTwo flutter waves,
1:1 flutter → ventricles contract about 300 times a minute → rare

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20
Q

Atrial Fibrillation

A

most commonly seen arrhythmias
• fibrillatory or f waves
• irregular waves replace the normal P waves
• atria depolarized at a very rapid rate 400 - 600 min
• ventricular rate
- irregular
- normal AV junction → 110 - 180/min

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21
Q

Ventricular Premature Beats

A

 premature depolarizations
 arising in the ventricles (right or left ventricle)
 QRS complexes → wide
( the stimulus spreads through the ventricles in an aberrant direction)

22
Q

Ventricular Premature Beats

Characteristics:

A 
 premature
 occur before the next normal beat is expected
 aberrant in appearance
 wide QRS (> 120 ms)
 T wave usually point in opposite
directions from QRS
23
Q

Ventricular Premature Beats

Compensatory Pause

A

 followed by a pause before the next normal beat
 usually but not always > pause after an APB
 fully compensatory pause:
 Interval
 [QRS before - QRS after VPB] = 2x basic RR interval

24
Q

VPBs Clasification:

A
  1. Uniform
  2. Multiform

Uniform VPBs
 arise from the same anatomic site (focus)
 are uni focal
 may occur in normal or pathological hearts

!! VPB
Two in a row are referred to as a pair or couplet
3 or more in a row are, by definition, VT

25
Q

Ventricular Tachycardia

Definition

A

a run of 3 or more consecutive VPBs

26
Q

Ventricular Tachycardia

Classification

A

Duration
 Nonsustained (lasting 3 beats to 30 seconds)
 Sustained (lasting 30 seconds or more)

Morphology
 Monomorphic
 Polymorphic

With long QT(U) syndrome: torsade de pointes
Without long QT(U) syndr.: polymorphic VT with acute ischemia

27
Q 
Ventricular tachycardia
Sustained VT (lasting > 30 seconds)
A

→ potential life-threatening arrhythmia
 hypotension
 may degenerate into VF causing
 cardiac arrest

28
Q

Ventricular Tachycardia

Therapy

A

 Pharmacologic /

 implantable cardioverter defibrillator (ICD)

29
Q

Accelerated Idioventricular Rhythm

A 
 heart rate : 50 - 100 beats/min
 without associated P waves
 wide QRS complexes
 Short duration lasting minutes or less
 no specific therapy required
 common with acute MI
 sign of reperfusion after the use of thrombolytic agents
30
Q

Torsade de Pointes

A

 Form of Polymorphic Ventricular Tachycardia
 direction of the QRS complexes appears to rotate cyclically, pointing downward for several beats and then twisting and pointing upward in the same lead.
 Favored by long QT intervals

31
Q

Ventricular Fibrillation

A

 fibrillatory waves → coarse or fine
 irregular pattern

 Most common cause of sudden cardiac death
 Ventricles
 Do not beat in any coordinated fashion
 Fibrillate or vibrate asynchronously and ineffectively
 No cardiac output occurs
 Patient becomes unconscious immediately

32
Q

Ventricular Fibrillation

There are 3 major ECG patterns in with cardiac arrest

A
  1. Brady-asystolic patterns
  2. Electromechanical dissociation
  3. Ventricular Fibrillation
33
Q

Bradyarrhythmias

Sinus Bradycardia

A

 sinus rhythm + heart rate < 60 beats/min
Many patients tolerate heart rates of 40 beats/min
surprisingly well, but at lower rates symptoms are likely
1. Dizziness
2. Near syncope
3. Syncope
4. Ischemic chest pain
5. Stokes-Adams attacks
6. Hypoxic seizures

  • Some authors define sinus bradycardia as a heart rate of less than 50 bpm
34
Q

Atrioventricular Heart Block

Heart block

A

= general term for atrioventricular (AV) conduction disturbances
 occurs when transmission through the AV junction is impaired transiently or permanently

35
Q

Classification of AV Heart Blocks

A

 First-degree block =Uniformly prolonged PR interval
 Second-degree block = Intermittent conduction failure
 Mobitz type I = progressive PR prolongation
 Mobitz type II: sudden conduction failure
 Third-degree block =No atrioventricular conduction

36
Q

First-Degree Heart Block (Prolonged PR

Interval)

A

 prolonged PR interval

 constant from beat to beat PR >200 msec

37
Q

Second-Degree AV Block

A

Classification
 Mobitz type I block (also called Wenckebach block)
 Mobitz type II block.

38
Q

Mobitz type I (Wenckebach AV block)

A

 progressive lengthening of the PR interval from beat to beat until a beat is “dropped.”
 The dropped beat is a P wave that is not followed by a QRS complex
 failure of the AV junction to conduct the stimulus from A to V

39
Q

MOBITZ Type II AV block

A

sudden appearance of a nonconducted sinus P wave
severe conduction system disease involving regions below the AV node (i.e., His-Purkinje system)
progressive → complete heart block
indication for a pacemaker may be seen with anterior wall MI

40
Q

Advanced second-degree AV block

A

two or more consecutive nonconducted P waves

example with sinus rhythm and 3:1 block, every 3rd P wave is conducted with 4:1 block, every 4th P wave is conducted

41
Q

Third-Degree (Complete) Heart Block

A

 atria and ventricles are paced independently
 no stimuli are transmitted from the atria to the ventricles
 atria → paced by the or sinoatrial (SA)
 ventricles → paced by an escape pacemaker below the AV junction
 atrial rate > ventricular rate
 resting ventricular rate
 lower than 30 beats/min or
 as high as 50 to 60 beats/min

42
Q

Third-Degree (Complete) Heart Block

Classification

A

 with narrow QRS generally stable

 with wide QRS less stable

43
Q

Sinus breaks, sinus arrest, and escape beats

A

 The sinus impulse does not depolarize the atria
for one or more beats
 An absent beat (without P wave or complex
Sinus break in a patient with sinus node disease

44
Q

Atrioventricular Blocks
Signs and symptoms
1 th-degree AV block

A
  • Generally not associated with any symptoms

* zan incidental finding on Ecg usually

45
Q

Atrioventricular Blocks
Signs and symptoms
2 th-degree AV block

A
  • Asymptomatic usually
  • some: sensed irregularities of the heartbeat, presyncope, or syncope
  • physical examination may manifest as bradycardia (Mobitz II) and/or irregularity of heart rate (especially Mobitz I )
46
Q

Atrioventricular Blocks
Signs and symptoms
3 th-degree AV block

A

• associated with profound bradycardia unless the site of the block is located in the proximal
• Frequently associated with symptoms:
→ fatigue, dizziness, light-headedness, presyncope, and syncope;

47
Q

The Stokes-Adams Syndrome

Definition

A

= an abrupt, transient loss of consciousness due to sudden but pronounced decrease in the cardiac output, which is caused by a sudden change in the heart rate or rhythm
* This definition does not include vasovagal syncope or epilepsy although patients with Stokes-Adams syncope may have seizures during periods of cerebral ischemia.

48
Q

The Stokes-Adams Syndrome

Clinical Features

A

depend upon the duration and type of underlying arrhythmia
depend upon the status of the cerebral circulation
Symptoms
 vary from slight faintness →loss of consciousness
 with or’without convulsions.

49
Q

The Stokes-Adams Syndrome

Attack Description

A
  • Initial pallor
  • A facial flush after the resumption of the normal circulation
  • The abscence of an aura tend to separate seizures during Stokes Adams syncope from seizures of primary cerebral origin
  • Stokes-Adams seizures usually commence and terminate abruptly
  • The patient may resume a previous conversation or
    activity without being aware of the pause produced by the period of arrythmia-induced cerebral ischemia
  • Physical exam.: A slow or a very rapid pulse during the period of unconsciousness
  • Ecg during a syncopal episode demonstrates the responsible rythm
50
Q

Rhythm disturbances Symptoms

Summary

A 
Broad range
• palpitation
• skipped beat
• awareness of heart palpitations
• fluttering sensation in the chest or neck
Long lasting arrhythmias
• Fatigue
• Chest pain
• Dizziness
• Shortness of breath
• Lightheadedness
• Fainting (syncope) or near-fainting spells
• Adam Stokes syndrome
-> AV block
-> Ventricular Fibrillation
• extreme cases→ collapse and sudden cardiac arrest
51
Q

Technical errors during Ecg Recording

A
  1. Errors in electrodes placement
  2. Inadequate filter application
  3. Artifacts due to device or to the pacient (cold
    environement, Parkinson disease)
  4. Misplacement of electrodes determine an incorrect
    diagnosis (e.g.Q wave MI)
  5. Inappropriate use of some filters may amplify ST
    elevation in V1 to V2 or may suppress an otherwise
    visible J wave”
  6. Artifacts generally mimic arrhythmias: flutter or
    ventricular tachycardia

Semiology second semester (13 decks)

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