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Cardiology > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

What is an arrhythmia?

A

Abnormal heart rhythm

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2
Q

What are the two classes of arrhythmias?

A
  • supraventricular

- ventricular

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3
Q

What does a supraventricular arrhythmia refer to?

A

It is a non-specific term that refers to an arrhythmia who’s origin is above the ventricle ie SA node, atrial muscle, AV node or HIS

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4
Q

What does a ventricular arrhythmia refer to?

A

An arrhythmia who’s origin is in the ventricular muscle or fascicles of the conducting system

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5
Q

Which origin of a ventricular arrhythmia is most common?

A

ventricular muscle

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6
Q

What are the two types of supraventricular arrhythmia?

A
  • supraventricular tachycardia

- bradycardia

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7
Q

What are the types of supraventricular tachycardias?

A
  • atrial flutter
  • atrial fibrillation
  • ectopic atrial tachycardia
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8
Q

What are the types of bradycardia?

A
  • sinus bradycardia

- sinus pauses

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9
Q

What are the types of ventricular arrhythmias?

A
  • ventricular ectopic or Premature Ventricular complexes
  • Ventricular tachycardia
  • Ventricular Fibrillation
  • Asystole
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10
Q

What are the types of AV node arrhythmias?

A
  • AV node re-entry tachycardia
  • AV reciprocating or AV re-entrant tachycardia
  • AV block
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11
Q

What are the clinical causes of Arrhythmias?

A
  • abnormal anatomy
  • autonomic nervous system
  • metabolic
  • inflammation
  • drugs
  • genetic
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12
Q

What kinds of anatomical abnormalities cause arrhythmias?

A
  • left ventricular hypertrophy
  • accessory pathways
  • congenital HD
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13
Q

How can the autonomic nervous system cause arrhythmias?

A
  • sympathetic stimulation: stress, exercise, hyperthyroidism

- increased vagal tone causing bradycardia

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14
Q

What kinds of metabolic things can cause arrhythmias?

A
  • hypoxia: COPD, PE
  • Ischemic myocardium : MI, angina
  • electrolyte imbalance: K, Ca, Mg
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15
Q

What genetic causes can cause arrhythmias?

A

mutations of genes encoding cardiac ion channels eg the congenital long QT syndrome

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16
Q

What are ectopic beats?

A

Beats or rhythms that originate in places other than the SA node

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17
Q

What causes ectopic beats?

A
  • altered automaticity eg ischemia

- triggered activity eg digoxin

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18
Q

What is re-entry?

A

requires more than one conduction pathway, with different speed of conduction and recovery of excitability eg accessory pathway tachycardia, prev MI, congenital heart disease

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19
Q

What are the mechanisms of tachycardia?

A
  • ectopic beats may be single beats or may be continuous
  • if they run faster than sinus rhythm then they can take over the intrinsic rhythm
  • re entry may be triggered by ectopic beat which results in a self perpetuating circuit
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20
Q

What is the effect of tachycardia?

A

Tachycardia may or may not be dangerous depending on how they affect the CO

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21
Q

how does altered automaticity work?

A

myocytes increase their gradient (increase phase 4 slope) so they reach the threshold sooner and exhibit action potentials. Therefore are firing spontaneously without regard to the SA node

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22
Q

What three things can alter automaticity?

A
  • changing resting membrane potential
  • changing trigger threshold
  • increasing potential gradient
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23
Q

What effects do increasing and decreasing the phase 4 slopes have?

A
  • increasing slope causes increased HR

- decreased slope causes decreased HR

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24
Q

What can cause an increase in the slope?

A
  • hyperthermia
  • hypoxia
  • hypercapnia
  • hypokalaemia
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25
Q

What can cause a decrease in the slope?

A
  • hypothermia

- hyperkalaemia

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26
Q

What occurs in triggered activity?

A
  • There is an extra depolarisation at the end of the last action potential.
  • if this depolarisation is large enough to reach threshold this will lead to a train of depolarisations
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27
Q

What two things can lead to re-entry?

A
  • structural abnormalities that form accessory pathways ie scars
  • functional abnormalities ie conditions that depress conduction velocity or shorten refractory period
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28
Q

How does a normal conduction pathway occur?

A
  • conduction comes down purkinje fibres then splits down two pathways
  • Route one takes the same time and is the same length as route 2
  • leads to ventricle muscle depolarisation and contraction
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29
Q

How does ischemia and re-entry arrhythmia affect the conduction pathway?

A
  • conduction comes down purkinje fibres then splits down two pathways
  • Route one is ischemic and this slows down conduction
  • the electrical current flows down the pathways at different speeds
  • By the time B gets depolarised it si at the end of the action potential for route 2. Therefore causes a second beat.
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30
Q

What are symptoms of cardiac arrhythmias?

A
  • palpitations
  • SOB
  • dizziness
  • LOC
  • faintness
  • sudden cardiac arrest
  • Angina/ HF
  • asymptomatic
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31
Q

What investigations can be done?

A
  • 12 lead ECG
  • CXR
  • stress ECG
  • 24h ECG
  • event ECG
  • EP study
  • echocardiogram
32
Q

How does pre excitation present on an ECG?

A

incline between the P wave and QRS complex

33
Q

What does electro physical study allow?

A
  • trigger the clinical arrhythmia to study its mechanism and pathway
  • it is an opportunity to treat the arrhythmia by delivering radiofrequency ablation to extra pathway
34
Q

What is a normal sinus arrhythmia?

A
  • variation in HR due to breathing
  • when you breath in the HR speeds up and when you breath out it slows down.
  • when this does not occur it i s a sign of a diseased heart
35
Q

What is sinus bradycardia?

A

It is a slow heart rate with a normal sinus rhythm. It can be caused by physiological changes, drugs or ischemia (inferior STEMIs)

36
Q

How is it treated?

A
  • Atropine if it is acute

- Pacemaker if there is haemodynamic compromise ie hypotension, angina, collapse

37
Q

What is sinus tachycardia?

A
  • HR over 100
  • can be caused by physiological causes
  • can be caused by drugs
38
Q

How do you treat sinus tachycardia?

A
  • treat underlying cause

- B blocker

39
Q

What are atrial ectopic beats?

A
  • can have palpitations but can also be asymptomatic
  • no treatment
  • avoid stimulant ie caffeine
  • may be a marker for COPD
40
Q

Describe narrow complex tachycardias

A

-Any tachycardia with a QRS complex shorter than 120ms ie 3 small boxes

41
Q

Describe broad complex tachycardias

A

-Any tachycardia with a QRS complex larger than 120ms ie 3 small boxes

42
Q

What can cause regular supraventricular tachycardia ?

A
  • AV nodal re-entrant tachycardia
  • Av reciprocating tachycardia/ AV re-entrant tachycardia
  • Ectopic atrial tachycardia
43
Q

What is AV re entrant tachycardia?

A

Fast HR caused by electrical signals that loop back on each other.
-There is an accessory pathway locates in the ventricles that causes the conduction from the purkinje fibres to loop back through this pathway back to the atrium. This causes another depolarisation wave despite the SA node not generating one. This loop causes tachycardia.

44
Q

What is AV nodal re entrant tachycardia?

A

Fast HR caused by electrical signals that loop back on each other

  • There are two pathways the alpha which is slow but has a short refractory time and the beta which is fast but has a slow refractory time.
  • Signals that are passed from the SA node to the AV node get looped back around so that both the ventricles and atria are contracting at an increased rate.
  • this occurs close to the AV node.
45
Q

What are the two types of AVNRT?

A

typical and atypical
In typical AVNRT the current goes down the slow pathway and up the fast pathway
-In atypical AVNRT the current goes down the fast pathway and up the slow pathway

46
Q

What is the treatment for AVRT and AVNRT?

A
  • radio-catheter ablation (accessory pathway and slow pathway)
  • vagal manoeuvres ie carotid sinus massage
47
Q

What would you see on an ECG in AVRT and AVNRT?

A
  • AVNRT wont have P waves due to atrial and ventricular contractions being too closely timed
  • AVRT may or may not have P waves depending on the site of the accessory pathway
48
Q

Describe atrial tachycardia

A

fast abnormal heart rhythm in which the electrical impulse originates in atrial tissue different than the sinoatrial node

49
Q

How do you manage supraventricular tachycardia acutely?

A
  • increase vagal tone

- slow conduction in AV node via adenosine and verapamil

50
Q

How do you manage supraventricular tachycardia chronically?

A

-avoid stimulants ie coffee
-EP study and radiofrequency ablation
-B blockers
-antiarrhythmic drugs
(drugs used in older patients where surgery is not an option)

51
Q

What is radiofrequency catheter ablation?

A

selective cautery of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re entry circuit

52
Q

What does an EP study involve?

A
  • ECG catheter placed in heart via femoral veins
  • ECG recorded at different times through different manoeuvres to find location and mechanism of tachycardia
  • can remove pathways
53
Q

what are some causes of heart block?

A
  • ageing
  • acute MI
  • myocarditis
  • some drugs ie B blockers
  • calcific aortic valve disease
  • post aortic valve surgery
  • genetics
54
Q

What are the types of AV block?

A
  • 1st degree
  • 2nd degree
  • 3rd degree
55
Q

What is first degree AV block?

A
  • prolonged PR interval longer than 0.2 seconds ie one big square
  • No treatment
  • asymptomatic
  • long term follow up to ensure doesn’t develop into anything sinister
56
Q

What is second degree AV block?

A

There are two types of second degree AV block: type one and type 2.
-Prolonged PR interval resulting in dropped beats

57
Q

What is type 1 second degree AV block?

A
  • progressive lengthening of the PR interval eventually resulting in a dropped beat
  • usually vagal in origin
58
Q

What is type 2 second degree AV block?

A
  • pathological as it may progress to complete heart block
  • usually 2 P waves to :1QRS complex or 3:1
  • needs a permanent pacemaker
59
Q

What is third degree heart block?

A
  • complete heart block
  • no action potentials from the SA node/atria get through the AV node
  • needs a pacemaker urgently
60
Q

What are the two things the heart does in third degree heart block?

A
  • stops

- goes through the escape rhythm

61
Q

What is the escape rhythm involve?

A
  • due to phase 4 of the action potential
  • Ventricular myocytes have Automatic drift to action potential so that they have their own automaticity.
  • Rather than conducting via the purkinje fibres, the signal spreads across gap junctions. –hence why it goes very slow at around 30bpm but allows you to live for a while until interventions can be made
62
Q

What is a pacemaker and what does it do?

A

-an artificial device that is implanted which can deliver currents to set the pace of the heart.

63
Q

What are the types of pacemaker?

A
  • single chambers (paces RA or RV)

- dual chamber (paces RA and RV) to maintain synchronicity

64
Q

What are the causes of ventricular ectopics?

A
  • structural cuases: LVH, HF, myocarditis
  • metabolic : ischemic heart disease
  • may be a marker for inherited cardiac conditions
65
Q

When should you further investigate ventricular ectopics?

A

if worse on exercise

66
Q

What can be used to treat ventricular ectopics?

A
  • B blockers

- Ablation of focus

67
Q

What are ventricular tachycardias?

A
  • fast heart rate initiating in the ventricles. they are often life threatening and require immediate intervention.
  • Mostly occur in patients with a history of disease
68
Q

What happens to the blood pressure in ventricular tachycardia?

A

large, sustained reduction of arterial pressure

69
Q

What are the two types of VT?

A

monomorphic and polymorphic

70
Q

What are the characteristics of VT on an ECG?

A
  • rapid, wide, distorted QRS complex
  • large T waves
  • regular rhythm
  • P waves not visible
  • PR interval not measurable
71
Q

What is VF?

A

chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump

72
Q

What is the treatment for VF?

A
  • CPR

- defibrillation

73
Q

What is the acute treatment for VT?

A
  • direct current cardioversion if unstable
  • If stable: pharmacologic cardioversion with AAD
  • if unsure if it is VT then consider adenosine to make diagnosis
  • stop trigger factors
74
Q

What is the long term treatment for VT?

A
  • correct ischemia
  • optimise CHF therapies
  • VT catheter ablation
  • implantable cardiovertor defibrillators if life threatening
75
Q

What is good about a ICD?

A
  • pacemaker with defib function
  • terminate VT or VF
  • anti- tachycardic pacing
76
Q

What is anti-tachycardic pacing?

A

Overtakes the VT by speeding up the heart from what the VT was to take over and then slows it down back to normal

Cardiology (32 decks)

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