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MD2011 > Cardiovascular Medicine - week 4 > Flashcards

Cardiovascular Medicine - week 4 Flashcards

0
Q

Why are dysrhythmia’s important?

A

Because they might indicate an underlying pathology and also can disrupt normal cardiac function

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1
Q

List the three major classes of dysrhythmia’s?

A
  1. abnormal sites of impulse initiation
  2. abnormal rates of sinus rhythm
  3. disturbances in conduction system
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2
Q

Define dysrhythmias?

A

Abnormalities of the rhythm of action potential production and/or the conduction system

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3
Q

List the three mechanisms that may give rise to ectopic sites of impulse initiation?

A
  1. Abnormal automaticity
  2. Triggered activity
  3. re-entry
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4
Q

Name some dysrhythmias relating to abnormal sites of impulse initiation?

A

Premature atrial complexes, premature ventricular complexes, atrial flutter, atrial fibrillation, ventricular tachycardia, ventricular fibrillation

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5
Q

Describe inappropriate automaticity?

A

Where atrial or ventricular cells which should lack automaticity become able to spontaneously depolarise and produce action potentials. Low ATP levels are often associated with an inability to maintain ion gradients due to loss of atp pumps. This means that the membrane is abnormally leaky to sodium or calcium ions therefore producing a spontaneous depolarisation

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6
Q

Define triggered activity?

A

An extra action potential that is triggered spontaneously during or immediately following repolarisation.

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7
Q

Name the two types of triggered activity?

A

Early afterdepolarisations and delayed afterdepolarisations

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8
Q

When do EADs occur?

A

They are second action potentials that are triggered early in the relative refectory period (phase 3)

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9
Q

In what patients might you see early afterdepolarisations occur?

A

In patients with abnormally long repolarisation times, such as people with long QT syndrome

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10
Q

Describe what happens in early afterdepolarisations?

A

Voltage gated calcium (and sodium) channels recover from inactivation due to longer repolarisation time before membrane potential is below its threshold of activation, allowing them to open and depolarise the cell.

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11
Q

When do delayed afterdepolarisations occur ?

A

After the repolarisation phase is complete

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12
Q

What are delayed afterdepolarisations associated with?

A

High intracellular calcium and SR calcium which trigger calcium release and evoke action potentials

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13
Q

List and describe the two types of re-entry?

A
  1. functional re-entry: occurs when part of the electrical conduction in the heart is abnormally slowed
  2. anatomical re-entry: occurs when part of the electrical conduction in the heart is through and unusually long pathway
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14
Q

Name two things that predispose to re-entry?

A

Myocardial infarction and electrolyte imbalance

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15
Q

List three requirements for re-entry to occur ?

A

1.functional or anatomical loop

2.the absolute refractory period of the re-entered segment of muscle must be shorter than the conduction
time around the loop

  1. Unidirectional conduction block within the loop
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16
Q

What does unidirectional conduction block mean?

A

Action potentials can only propagate in one direction

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17
Q

Define premature atrial complexes?

A

Atrial depolarisation is initiated by cells within the atria other then the sa node pacemaker cells

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18
Q

Describe atrial flutter?

A

Atrial depolarisation rate of 240-350 bpm.

Sawtooth pattern of p waves.

QRS is normal and slower than the P rate, as not all atrial depolarisations are conducted.

Re-entry is the most likely source of the abnormality

Acute alcohol toxicity, underlying heart disease, fluid overload and atrial ischaemia predispose to atrial flutter.

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19
Q

Describe atrial fibrillation?

A

Chaotic depolarization of atria accompanied by ventricular depolarisation that is irregular and variable.

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20
Q

What is real fibrillation often caused by?

A

Multiple and constantly changing re-entry waves.

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21
Q

Why is there a high probability of clots forming in atrial fibrillation?

A

The atria contract and relax randomly failing to pump affectively. This leaves the blood being static and prone to clotting.

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22
Q

How is atrial fibrillation treated?

A

Cardioversion (electric shock) and antiarrhythmic drugs (calcium channel blockers, beta-blockers, digitalis, amiodarone)

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23
Q

What is a premature ventricular complex?

A

A ventricle cell is excited independent of normal activation by the conduction system

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24
Q

Is sinus rhythm affected in premature ventricular complexes?

A

No , excitation encompasses the ventricles but not the atria so sinus rhythm is unaffected

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25
Q

What does the QRS complex and T wave look like in premature ventricular complexes?

A

Abnormal and prolonged and t wave is often inverted

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26
Q

Which dysrhythmia has a diagnostic compensatory pause before sinus Rhythm resumes?

A

Premature ventricular complex

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27
Q

What is often associated with Premature ventricular complexes?

A

Coronary heart disease, drug overdose and electrolyte imbalances (Particularly hypokalaemia and hypomagnesiumia) which make phase 4 more depolarised than normal

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28
Q

What is the clinical significance of Premature ventricular complexes that only occur rarely?

A

Nothing- often can be left untreated

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29
Q

What’s can be the implications of frequent Premature ventricular complexes AND how are they treated?

A

May diminish cardiac output and/ or progress to ventricular tachycardia and ventricular fibrillation. Treated with antiarrythmic drugs such as amiodarone

30
Q

What is indicative of ventricular tachycardia on an ECG?

A

3 or more consecutive QRS complexes at a rate exceeding 100bpm. QRS complexes blend into the ST segments and T waves at higher heart rates which produces a series of large, wide undulating waves.

31
Q

What is the most common underlining mechanism for ventricular tachycardia?

A

Re entry

32
Q

What problems are commonly associated with/ cause ventricular tachycardia?

A

Associated with myocardial infarction and ischaemia. High catecholamine levels and electrolyte imbalances predispose to it

33
Q

Can ventricular tachycardia be a serious problem and what is used to treat it?

A

Yes it can be serious and potentially fatal due to compromised cardiac output. It can be treated with antiarrhythmic drugs Cardiopulmonary Resuscitation and electrical cardioversion.

34
Q

What is tornado de pointes?

A

Meaning twisting of the points. Is a form of polymorphic ventricular tachycardia presenting as varying amplitudes of the QRS complex as if the complexes are twisting about at the baseline/ isolectric line. It can be produced by early after depolarisations as well. It may degenerate into ventricular fibrillation

35
Q

Describe what happens to the heart muscle in ventricular fibrillation and its affect on cardiac output?

A

Heart muscle quivers rather than contracting in a coordinated manner. Rapid , chaotic rhythm . Cardiac output is severely compromised

36
Q

What’s conditions produce/ cause ventricular fibrillation?

A

Re entry , myocardial infarction, ischaemia, high catecholamine levels and electrolyte imbalance (same as things that produce VT)

37
Q

How do you treat ventricular fibrillation?

A

CPR and defibrillation.If the heart converts then you can administer any arrhythmic drugs

38
Q

What is the normal rate for sinus rhythm?

A

60-100 bpm

39
Q

How long is the normal PR interval in seconds?

A

0.12-0.2 seconds

40
Q

How long is the normal QRS complex in seconds?

A

0.04-0.1 seconds

41
Q

When is a heart rate (sinus rhythm) tachycardia?

A

When the rate is >100 bpm

42
Q

What is sinus tachycardia commonly associated with?

A

Increased sympathetic NS activity, decreased parasympathetic ns activity, fever, pain, hyperthyroidism ,low blood pressure, increased metabolic rate

43
Q

What happens if the heart rate is too high?

A

May not allow time for ventricles to fill , cardiac output decreases and treatment is necessary

44
Q

Treatment of tachycardia?

A

Drugs that block sympathetic ns tone (sympatholytics) and calcium channel blockers

45
Q

When is a heart rate (sinus rhythm) bradycardia?

A

When it is less than 60bpm

46
Q

Why does SA node pacemaker potential slow in bradycardia?

A

Many reasons including: parasympathetic activity, sleep, drugs, increased stroke Volume, Acute hypertension

47
Q

If Bradycardia leads to insufficient cardiac output what type of treatment is recommended?

A

Sympathomimetic drugs or parasympatholytic drugs

48
Q

What does an ECG look like with sinus bradycardia?

A

Normal QRS complexes and P waves but far apart at regular intervals.

49
Q

What is sick sinus syndrome?

A

Where the Sino atrial node oscillates between periods of tachycardia
and bradycardia. This illness is something that requires an artificial pacemaker

50
Q

What is sinus arrest?

A

Where there is an absence of SA node activity and so electrical activity in the heart. It results in no contraction and no cardiac output. Usually after a period of sinus arrest, slower parts of the conduction system takeover (AV node followed by the bundle of his, bundle branches and purkinje fibers. This restores excitation at a slower rate.

51
Q

Name the two types of escape rhythms?

A
  1. junction escape rhythm

2. ventricular escape rhythm

52
Q

What is a Junctional escape rhythm ?

A

When The SA node is unable to conduct an impulse, escape rhythms can emerge from the more distal pacemakers. Junctional escape beats arise from the AV node or proximal bundle of his. They are characterised by a normal narrow QRS complex, and when they occur in sequence appear at a rate of 40 to 60 bpm.

53
Q

Why is there no P wave on an ECG for a Junctional escape rhythm?

A

Because the impulse originates below the atria. Retrograde p waves may be observed as an impulse propagates from the more distal pacemaker backward to the atrium. Retrograde P-waves typically follow the QRS complex in a inverted in leads II , III and aVF indicating activation of the atria from an inferior direction.

54
Q

Where do ventricular escape rhythms arise from?

A

The bundle of his, bundle branches, or the purkinje fibers (15-40 action potentials per minute)

55
Q

Why are widened QRS complexes typical in ventricular escape rhythms?

A

Because the ventricles are not depolarised by normal rapid simultaneous conduction over the right and left bundle branches, but rather from a more distal point in the conduction system.

56
Q

What is atrioventricular block?

A

Disturbance of conduction of the sinus impulse from the right atrium to the ventricles. Conduction may be slowed or lost all together. Function or pathological defect in the AV node, bundle of his or bundle branches

57
Q

What types of AV block are there?

A

1st degree, second-degree (type one or type two) or 3rd degree

58
Q

What would an ECG that indicated a 1st degree AV block look like?

A

The PR interval is prolonged (more than 0.2 seconds). The rhythm is normal and each QRS complex is associated with the P-wave.

59
Q

What are some causes of 1st degree AV block?

A

It is the most common AV block. It occurs without evidence of any heart disease. However, drugs myocardial infarction and congenital heart defects may produce 1st degree AV block

60
Q

Generally described second-degree AV block?

A

Where not all of the P-waves are conducted to the ventricles (not all P-waves are associated with QRS complexes)

61
Q

Describe the type one/wenkebach second-degree AV block

A

On ECG, the PR interval progressively increases until a P-wave is not conducted (dropped beat). The pattern then repeats. QRS complexes appear clustered.

62
Q

What usually causes type I 2nd degree block?

A

Reversible ischaemia of the AV node, associated with acute myocardial infarctions. Treatment is only required if it progresses to the type II second degree block

63
Q

Describe what an ECG would look like in a patient that had the 2nd degree AV block, type II?

A

Blocked P-waves occur with this consistent PR interval (no PR prolongation, as seen in type I).there are often many p waves in a row before a QRS complex is initiated.

64
Q

Where often is the damage located in second-degree AV block type II?

A

Bundle of his, the right bundle branch or both

65
Q

Why is the QR S complex abnormally wired in second-degree AV block type I I?

A

Due to bundle branch failure

66
Q

Is second-degree AV block type II or type I more serious?

A

Type II is more serious. It is associated with anterior septal myocardial infarction or fibrosis of the conduction system. It may progress to a 3rd degree AV block. Treatment may involve the implantation of an artificial pacemaker.

67
Q

Describe third-degree AV block?

A

Where there is a complete block where no conduction occurs between the atria in the ventricles. No P-waves are conducted through to the ventricles.

68
Q

What controls the rhythm of the QRS complexes in third-degree AV block?

A

Ventricular escape controls the rhythm (Purkinje fibres take over).

69
Q

List some causes of the degree block?

A

Damage to the AV node, bundle of his, and/or bundle branches (width of QRS complex reveals the site of damage) this means that if the damage was in the right bundle branch is the ECG would indicate this

70
Q

Describe Wolff Parkinson White syndrome?

A

Where accessory pathways pass from a tree up to the ventricles without passing through the AV node. This means that there is no delay by the AV node as this pathway bypasses it. The accessory pathways may allow re-entry, VT and VF

71
Q

What would ECG look like in Wolff Parkinson white syndrome?

A

Short PR interval, delta waves (abnormal start of QRS complex more like a upward slant) and Wide QRS complex

72
Q

What is the treatment for wolff Parkinson white syndrome?

A

Treatment includes antiarrythmic drugs, surgical ablation of the accessory pathway, and destruction of the conduction pathway.

MD2011 (32 decks)

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