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Flashcards in CPT1: Dysrhythmias 1 Deck (31)
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1
Q

What is dysrhythmia?

A

An abnormality in the physiolocical rhytm of the heart

2
Q

What are the statics relating to dysrhythmia?

A
  • 15% of stroke patients have dysrhytmia
  • 2-8% of patients with transient ischaemic attacks
  • 2-year incidence increases with age:
    • 0.1% (30-39 YO)
    • >1% (70-79)
  • Prevalance ~10% in males >70’s
  • 7% of all hopsital admissions have an arrythmia
3
Q

What are Aetiologies (CAUSES) of dysrhytmias?

hint: unspecific

A
  1. Infarcation
  2. Conduction disorder (fibrosis)
  3. Changes in autonomic nervous output (Stress, anxiety, exercise, smoking)
  4. Electroylte imbalance (hypo/hyperkalaemia)
  5. Circulating drugs (antiarrhythmias, caffeine, alcohol)
4
Q

What are causes of dysrhythmias?

Hint: Specific

A
  • Hypoxia myocardium - pumlomary embolus, chronic pulmonary disease
  • Ischaemia myocardium - acute MI, expanding MI, angina
  • Bradycardia - Slow HR predisposes one to dysrhytmias
  • Enlargement of atria or ventricles - producing stretch in the pacemakers
5
Q

Describe the ECG of the heart

A
  • P - atrial depolarization
    • P-R ~120-200ms
  • QRS complex - ventricular depolarization
    • QRS ~120ms
  • T - ventricular repolarization
    • Q-T ~3-400ms
  • P-R - interval -slowing through AV node
6
Q

Describe electrical flow through the heart

A
  1. Depolarisation begins at the SA node and spreads rapidly across the atria through internodal conductin fibres/ pws
  2. It slows at the AV node to allow time for the atria to complete contraction before starting ventricular contraction
  3. Electrical singal enters the ventricular conducting system (his and purkinje fibres) and first goes to the apex of the ventricles before spreading upwards (ventircular contraction)
7
Q

Arrhythmia or dysrhytmia?

A
  • Dysrhythmia accurate, arrhythmia most widely used
  • Arrhythmia is generally the name for the anatomical site or chamber of origin
8
Q

What are terms used to describe the location of the origin of the arrhytmia?

A
  • Supraventricular: Origin above the ventricles e.g. SA, atrial AV or HIS origin
  • Ventricular origin: Origin is in the ventircles
9
Q

How sereve are cardiac arrhymias

A
  • May be bengin or life-threatening
  • Mat be paraoxysmal (sudden outbursts) or continous and may cause sudden death, heart failure, syncope (tempory loss of conciousness), light headedness, palpatations or no symptoms at all
10
Q

What does the description of dysrhytmia depend on?

A
  • The rate, pattern, origin
  • All descriptions depend on ECG
  • BUT - this does not refer to how well the heart functios as a pump. Other parameters important (BP, pulse)
11
Q

What are 2 dysrhymia termomologies based on rate?

A

Trachycardia - more than 100 bpm

Bradycardia - less than 60 bpm

12
Q

What are 2 causes of Trachycardia?

A
  • Increased automacity:
    • sustained by repeated spontanreous depolaisations of an ectopic focus or single cell
  • Re-entery:
    • When it is initated by a ectopic beat and sustained by a closed loop circuit or re-entery circuit. Most common cause.
13
Q

What are the potential causes of bradycardia?

A
  • Reduced automacity (e.g. sinus bradycardia)
  • Abnormally slow conduction (e.g. AV block)
14
Q

What do the following terms mean:

  1. Sinus
  2. Atrial
  3. Nodal
  4. Supraventricular
  5. Ventricular
  6. Re-entrant
A
  1. SA node
  2. Atrial tissue but not SA node
  3. AV node
  4. Usually, but not necessarily, from the AV node
  5. Ventricular tissue
  6. Circuit involving retograde conduction. Also accessory pws e.g. Wolff-Parkinsons White Syndrome

Retograde conduction - backwards conduction of the heart

15
Q

Where might the follwing re-entry circuit be seen?

A
  • Tissues with these type of circuits may exist:
  • • in microscopic size in the SA node, AV node, or any type of heart tissue
  • • in a “macroscopic” structure such as an accessory pathway in WPW
16
Q

Describe what happens during re-entry conduction

A
  1. An arrhythmia is triggered by a premature beat
  2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only
  3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway
  4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit
17
Q

Re-entery picture 2

A

Re-entery Picture 3

18
Q

Give some examples of specific types of Re-entry conditions

A
  • Atrial Re-entry
    • Atrial flutter
    • Atrial fibrililation
    • Atrial trachycardia
  • AV nodal re-entry
    • Supraventricular Trachycardia
  • AV Re-entry
    • Supraventricular trachycardia
  • Ventrical Re-entry
    • Ventricualar trachycardia
19
Q

What is Wolf Parkinons White Syndrome

A
  • An abnormal band of atrial tissue connects the atria and ventircals and can electrically by pass the AV node
  • ECG shows shorted PR interval and slurred QRS complex called delta wave
  • As AV node and bypass tract have different conduction speeds and refractory periods, a re-entry circuit can develop causing bursts of trachycardia events
20
Q

What do the ECG waves for:

  1. Atrial fibrillation
  2. Atrial Flutter
  3. Ventricular fibrillation
  4. Ventricular premature beats
A
21
Q

What are do the following terms mean?

  1. Paroxysmal
  2. Fibrillation
  3. Flutter
  4. Block
  5. Torsades de pointes
  6. Electromechanical dissociation
A
  1. Paroxysmal = Occurs in bursts
  2. Fibrillation = Rapid chaotic rhythm. Multiple foci
  3. Flutter = Rapid regular rhythm. Single focus
  4. Block = delay or absence of conduction via AV node
  5. Torsades de pointes = complex ventricular tachycardia
  6. Electromechanical dissociation = ECG recording not reflected in mechanical activity (pulse)
22
Q

So what is paroxysmal supraventricular trachycardia?

A

A fast rhythmic burst (> 100 bt/min) originating within either the AV node, the SA node or the atrial tissue itself.

23
Q

What is the danger with arhythmias?

A

Increases risk of mortality and morbidities

Mortality = death

Morbidity = predisposition to disease

24
Q

What are the increased risks with atrial fibrillation?

A
  • 2x more likely to have stroke
  • 3x more likely to have Heart failure
  • 2x mortality risk
25
Q

What are the symptoms of arrhythmias?

A
  • Pain (including Angina)
  • Shortness of breath
  • Dizziness/ Syncope
  • Palpatations (awareness of Heart beat)
26
Q

What is the difficulty with diagnosis?

A

Symptoms not unique to arrhytmias and intermittant arhythmias difficult to diagnosis. Therefore use 24hr ECG.

80% of CO from ventricular output regardless of atrial discoordination therefore may be unaffected or only slightly

27
Q

What does:

  1. Slow Atrial fibrillation and effective AV block
  2. Fast AF and ineffective AV block mean?
A

With slow AF + effective AV conduction block = small conduction of fibrillative events in the atria stimulate the ventricles.

With fast AF + ineffective AV conduction block = rapid and irregular heart beat, poor filling of ventricles prior to contraction and so inefficient circulation.

28
Q

What is the treatment criteria?

A
  1. The arrhythmia causes poor circulation (haemodynamic failure)
  2. Haemodynamic failure has not occurred BUT arrhythmia is a predictor of more serious arrhythmia.
    e. g. After MI, ventricular tachycardia increases risk of dying within 1 year by 30%.
  3. Patient distress (palpitation awareness).
29
Q

What are aims of treatment?

A
  1. Restore satisfactory circulation
  2. Prevent further episodes of haemodynamic failure and palpitations.
30
Q

NOTE

A

Arrhythmia implicated in sudden death

However,

Much of the evidence comes from patients having ECG monitored continuously. These may NOT be representative of general population. Evidence DOES support notion that ventricular tachyarrhythmia is a more common cause of death than bradyarrhythmia

31
Q

What are hazzards of treatmetn

A

Arrhythmia may occur with no symptoms.

\ Presence does NOT automatically require treatment.

Antiarrhythmic drugs may make condition WORSE!!

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