Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

6. Cardiovascular System > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

What is the main pacemaker in the heart?

A

The sinus node.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What controls the sinus node discharge rate?

A

The autonomic nervous system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define sinus rhythm.

A

Sinus rhythm - a P wave precedes each QRS complex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Normal sinus rhythm: characteristics on ECG leads.

A
  • P waves that are upright in leads I & II of the ECG
  • Inverted P waves in the cavity leads, AVR & V1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is sinus arrhythmia? Describe it during inspiration + expiration.

A
  • Fluctuations of autonomic tone result in changes of the sinus discharge rate.
  • During inspiration:
  • Parasympathetic tone falls and the heart rate quickens.

During expiration:
* Parasympathetic tone increases and so heart rate falls.

  • This variation is normal especially in children and young adults.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name 4 causes of sinus tachycardia.

A
  1. Physiological response to exercise.
  2. Fever / sepsis
  3. Anxiety
  4. Anaemia.
  5. Dehydration.
  6. Pneumonia.
  7. Heart failure.
  8. Hypovolemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give 4 causes of sinus bradycardia.

A
  1. Ischaemia.
  2. Fibrosis of the atrium.
  3. Inflammation.
  4. Drugs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What lead(s) would you look in to assess sinus bradycardia/tachycardia?

A

Any - rhythm strip is best.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a cardiac arrhythmia?

A

An abnormality of the cardiac rhythm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the most common cardiac arrhythmia?

A

Atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 2 main types of arrthymias?

A
  1. Bradycardia (slow HR)
  2. Tachycardia (fast HR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is classed as bradycardia?

A

Less than 60 bpm during the day and less than 50 bpm
at night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens in the autonomic nervous system to cause bradycardia?

A

Increased PARASYMPATHETIC TONE or decreased
SYMPATHETIC STIMULATION produces BRADYCARDIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is classed as tachycardia?

A

More than 100 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens in the autonomic nervous system to cause tachycardia?

A

A reduction of PARASYMPATHETIC TONE or an increase in SYMPATHETIC STIMULATION leads to TACHYCARDIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give 3 potential consequences of arrhythmia.

A
  1. Sudden death.
  2. Syncope.
  3. Dizziness.
  4. Palpitations.
  5. Can also be asymptomatic.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give the 2 broad categories of tachycardia.

A
  1. Supra-ventricular tachycardias
  2. Ventricular tachycardias.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where do supra-ventricular tachycardia’s arise from?

A

They arise from the atria or atrio-ventricular junction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where do ventricular tachycardia’s arise from?

A

The ventricles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give the 5 types of supraventricular tachycardias.

A

Supraventricular tachycardias:
1. Atrial fibrillation.
2. Atrial flutter.
3. AV node re-entry tachycardia (AVNRT).
4. Accessory pathway / AVRT (WPW Syndrome).
5. Focal atrial tachycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give the 3 types of ventricular tachycardias.

A

Ventricular tachycardias:
1. Ventricular ectopic
2. Prolonged QT syndrome
3. Torsades de Pointes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Do supra-ventricular tachycardia’s have narrow or broad QRS complexes?

A

Supraventricular tachycardias are often associated with narrow complexes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Do ventricular tachycardia’s have narrow or broad QRS complexes?

A

Ventricular tachycardias are often associated with broad complexes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Name 2 things that may aggravate a supraventricular tachycardia.

A

Exertion, coffee, tea, alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is atrial fibrillation?

A

A chaotic irregularly irregular atrial rhythm at 300-600 bpm.
- The AV node responds intermittently, hence an irregular ventricular rate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Give the 5 clinical classifications of AF.

A
  1. Acute: onset within the previous 48 hours
  2. Paroxysmal: stops spontaneously within 7 days
  3. Recurrent: two or more episodes
  4. Persistent: continuous for more than 7 days and not self terminating
  5. Permanent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Give 5 causes of AF.

A
  1. Idiopathic
  2. Hypertension (most common in developed world)
  3. Heart failure (most common in developed world)
  4. Coronary artery disease
  5. Valvular heart disease; especially mitral stenosis
  6. Cardiac surgery (1/3rd of patients after surgery)
  7. Cardiomyopathy (rare cause)
  8. Rheumatic heart disease
  9. Acute excess alcohol intoxication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Give 3 risk factors of AF.

A
  • Older than 60
  • Diabetes
  • High blood pressure
  • Coronary artery disease
  • Prior MI
  • Structural heart disease (valve problems or congenital defects)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Explain the pathophysiology of AF.

A
  1. Atrial fibrillation (AF) is maintained by continuous, rapid (300 600/min) activation of the atria by multiple meandering re-entry wavelets.
  2. These are often driven by rapidly depolarising automatic foci, located predominantly within the pulmonary veins.
  3. The atria respond electrically at this rate, but there is NO COORDINATED MECHANICAL ACTION and only a proportion of the impulses are conducted to the ventricles
    I.E. there is no unified atrial contraction instead there is atrial spasm.
  4. The ventricular response depends on the rate and regularity of atrial activity, particularly at the entry to the AV node, and the balance between sympathetic and parasympathetic tone.
  5. Cardiac output DROPS by 10-20% as the ventricles are not primed reliably by the atria.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the symptoms of AF.

A

Symptoms are highly variable.
- May be asymptomatic
- Palpitations.
- Dyspnoea and or chest pains following the onset of AF.
- Fatigue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Diagnosis of AF.

A

ECG:
1. No P waves
2. Rapid & irregular QRS rhythm
3. Fine oscillation of the baseline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

The ECG taken from someone with atrial fibrillation shows a fine oscillation of the baseline and absent P waves.
Why?

A

The atria fire a lot, it is chaotic.

The AV node and ventricles can’t keep up -> irregularly irregular pulse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What ECG features would you see in atrial fibrillation?

A

Absent P waves.
Irregular QRS complexes.
QRS less than 120 ms.
Atrial rate 300 bpm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Acute management of AF.

A
  • When AF is due to an acute precipitating events e.g. alcohol toxicity, chest infection or hyperthyroidism - the provoking cause should be treated.
  1. Cardioversion:
    - Conversion to sinus rhythm achieved electrically by DC shock e.g. defibrillator
    - NOTE: give low molecular weight heparin e.g. Enoxaparin or Dalteparin to minimise the risk of thromboembolism associated with cardioversion.
    - If this fails, then achieved medically by IV infusion or anti-arrhythmic drugs e.g. flecainide or amiodarone
  2. Ventricular rate control:
    - Achieved by drugs that block AV node:
    * Calcium channel blocker e.g. Verapamil
    * Beta-blocker e.g. Bisoprolol
    * Digoxin
    * Anti-arrhythmic e.g. Amiodarone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Atrial fibrillation treatment: what might you give someone to help with rate control?

A

Beta blockers, CCB and digoxin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Atrial fibrillation treatment: what might you give someone to help restore sinus rhythm (rhythm control)?

A

Electrical cardioversion or pharmacological cardioversion using flecainide.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Long term & stable patient management of AF.

A

2 strategies; which to choose should be decided based on individual patient needs.

  1. Rate control:
    = AV nodal slowing agents + oral anti-coagulation
    - Beta-blocker e.g. Bisoprolol
    - Calcium channel blocker e.g. Verapamil or Diltiazem
    - If above fails, then try Digoxin and then, consider Amiodarone
  2. Rhythm control:
    = Advocated for younger, symptomatic and physically active patients
    - Cardioversion to sinus rhythm and use Beta-blockers e.g.
    Bisoprolol to suppress arrhythmia
    - Can use pharmacological cardioversion e.g. Flecainide if no
    structural heart defect or use IV Amiodarone instead if there is
    structural heart disease
    - Appropriate anti-coagulation e.g. Warfarin due to
    thromboembolism risk with cardioversion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the long term treatment of atrial fibrillation?

A

Catheter ablation - it targets the triggers of AF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What score can be used to calculate the risk of stroke in someone with atrial fibrillation?

A

CHADS2 VASc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What factors does the CHA2DS2-VASc score consider?

A

CHA2DS2-VASc score to calculate stroke risk and thus need for
anticoagulation:

  • Congestive heart failure (1 point)
  • Hypertension (1 point)
  • Age greater or equal to 75 (2 points)
  • Diabetes mellitus (1 point)
  • Stroke/TIA/thromboembolism (2 points)
  • Vascular disease (aorta, coronary or peripheral arteries) (1 point)
  • Age 65-74 (1 point)
  • Sex Category: female (1 point)

Results:
* If score is 1 then it merits consideration of anticoagulation and or aspirin
* If score is 2 and above then oral anticoagulation is required

41
Q

What is atrial flutter?

A

Usually an ORGANISED atrial rhythm with an atrial rate
typically between 250-350 bpm.

42
Q

What pathophysiological mechanism can cause atrial flutter?

A

The re-entry mechanism - there is blockage of the normal circuit.

Another pathway forms, takes a different course and re-enters the circuit within the right atrium -> tachycardia.

43
Q

What are the 3 clinical classifications of atrial flutter?

A
  1. Paroxysmal
  2. Persistent
44
Q

Give 4 causes of atrial flutter.

A
  • Idiopathic (30%)
  • Coronary heart disease
  • Obesity
  • Hypertension
  • Heart failure
  • COPD
  • Pericarditis
  • Acute excess alcohol intoxication
45
Q

Describe the clinical presentation of atrial flutter.

A
  • Palpitations
  • Breathlessness
  • Chest pain
  • Dizziness
  • Syncope
  • Fatigue
46
Q

Diagnosis of atrial flutter.

A

ECG:
* Regular sawtooth-like atrial flutter waves (F waves) between QRS complexes due to continuous atrial depolarisation

47
Q

Describe what you would see on an ECG trace in atrial flutter.

A

‘Sawtooth’ flutter waves between QRS complexes.

300 bpm

Negative flutter waves in II, III and aVF (inferior)
Positive flutter wave in V1 (septal)
Narrow QRS

48
Q

Treatment of atrial flutter.

A
  1. Electrical cardioversion but anticoagulate before
    e.g low molecular weight heparin
    e.g. Enoxaparin or Dalteparin if acute
    I.E. atrial flutter started less than 48 hours ago
  2. Catheter ablation
    - creating a conduction block to try an restore rhythm and block offending re-entrant wave
  3. IV Amiodarone + Beta-blocker (bisoprolol)
    - To restore sinus rhythm and to suppress further arrhythmias
49
Q

Amiodarone is used for pharmacological cardioversion, but it also chemically resembles a hormone made naturally by the body - what is this and what can this cause?

A

Thyroxine - can cause hyperthyroidism

50
Q

What is the difference between atrial fibrillation and atrial flutter?

A

Atrial fibrillation = irregular ventricular conduction of atrial beats.

Atrial flutter = atrial rate of 300 bpm (same as AF), but ventricles conduct every other atrial beat - 150 bpm.

51
Q

How does digoxin work in AF/atrial flutter?

A

Reduces heart rate and increases force of contraction (-vely chronotropic, +vely inotropic).

Works via indirect pathway - increased vagal tone, reduced contraction at AVN and preventing dome impulses travelling to the ventricles.

52
Q

What are the 2 types of paroxysmal supraventricular tachycardia?

A
  1. AVRNT
  2. AVRT (accesory pathway)
53
Q

What is AVRNT?

A

Atrioventricular Nodal Re-entrant Tacycardia

The most common type of supraventricular tachycardia. People with AVNRT have episodes of an irregularly fast heartbeat (more than 100 beats per minute) that often start and end suddenly.

54
Q

Explain the pathophysiology of AVRNT.

A

2 pathways in the AVN in AVRNT:
1) Slow pathway:
- A short effective refractory period and SLOW conduction

2) Fast pathway:
- A longer effective refractory period (RFP) and FAST conduction

  1. Normal sinus rhythm: electrical impulse from atrium conducts through the fats pathway to the ventricles
  2. Early atrial impulse
    - Happens when the fast pathway is still finishing the long RFP
  3. Slow pathway takes over in electrical impulse propagation
  4. By the time the slow pathway has sent the impulse to the ventricles, the fast pathway has finished its long RFP.
  5. So, the fast pathway then sends the same impulse down to the ventricles + back up.
  6. At the same time, the slow pathway would have recovered from its slow RFP, and so the signal goes down the slow pathway as well.
  7. Sets up a RE-ENTRANT LOOP at the AV NODE
  8. This loop sends signals through the AVN at a MUCH FASTER RATE than a normal pacemaker would

= TACHYARRHYTHMIA with a HR of 100-250 bpm

  1. Signal goes back via the fast pathway (recovers from its RFP)
  2. Initiates the slow-fast AVNRT:
    = the atria contract SLOWLY in 1 cycle and then FAST in the next
55
Q

Give 4 symptoms of AVNRT.

A
  1. Sudden onset/offset palpitations.
  2. Neck pulsation - prominent jugular venous pulsations due to atrial contractions against closed AV valves
  3. Chest pain.
  4. Shortness of breath.
  5. Polyuria - (due to the realise of atrial natriuretic peptide in response to increased atrial pressures during the tachycardia)
56
Q

What is seen on the ECG for AVRNT?

A

No P wave.
Narrow QRS

57
Q

Do you see P waves in AVNRT?

A

No - the P waves are within the QRS complex.

58
Q

What is AVRT?

A

Atrioventricular Re-entrant Tachycardia

AKA Accessory pathway; Wolff-Parkinson-White sydrome

59
Q

What happens in AVRT?

A

Atrial activation occurs after ventricular activation

60
Q

Describe the pathophysiology of accessory pathway arrhythmias (AVRT).

A

Congenital muscle strands connect the atria and ventricles - accessory pathway.
This can result in pre-excitation of ventricles.

61
Q

Describe 3 characteristics of an ECG taken from someone with accessory pathway arrhythmia (AVRT).

A
  1. Delta wave.
  2. Short PR interval.
  3. Slurred QRS complex.
62
Q

What is an example of AVRT?

A

Wolff-Parkinson-White syndrome.

63
Q

What is Wolff-Parkinson-White syndrome (WPW)?

A

Pre excitation accessory pathway - AVRT

64
Q

What causes Wolff-Parkinson-White?

A

Congenital accessory conduction pathway between atria and ventricles.

65
Q

What is the mechanism in Wolff-Parkinson-White?

A

Accessory pathway, usually from left atria, allows direct transmission of signal, bypassing AVN (hence short PR)

66
Q

Give 4 symptoms of AVRT and WPW.

A
  • Palpitations
  • Severe dizziness
  • Dysponea
  • Syncope
67
Q

Describe the features of a resting ECG in a patient with WPW.

A
  • Short PR interval
  • Wide QRS complex that begins as a slurred part known as a delta wave
    (Best seen in V3 + V4)
68
Q

Treatment of stable AVRT and AVRNT.

A

Vagal manoeuvres:

  1. Breath-holding
  2. Carotid massage
  3. Valsalva manoeuvre
    - Abrupt voluntary increase in intra-abdominal and intrathoracic pressure by straining
    - Several seconds after the release of the strain, the resulting intense vagal effect may terminate the AVNRT or AVRT
69
Q

How to treat AVRT/AVRNT when vagal manoeuvres fail?

A

IV adenosine
- Causes complete heart block for a fraction of a second and is highly effective at terminating AVNRT and AVRT

70
Q

What are the surgical options for AVRT + AVRNT?

A

Surgery:
* Catheter ablation of the accessory pathway in AVRT
* Modification of the slow pathway in AVNRT

71
Q

How do you treat sudden episodes of supraventricular tachycardia?

A

Carotid sinus massage
IV adenosine

72
Q

In supraventricular tachycardia, adenosine is administered IV to bring the heart back into normal rhythm.
How does it work on the heart?
What type of arrhythmias should it be used for?

A

It works via the A1 receptor, which reduces cAMP - so causes cell hyperpolarisation by pushing potassium out of the cell.
also relaxes the smooth muscle of the heart causing vasodilation.

Only used for ventricular tachycardias.

73
Q

Why do you need to warn the patient that they may get a sense of ‘impending doom’ after you administer adenosine?

A

Because it induces transient heart block in the AV node so the heart stops for a beat or so.

74
Q

What are ventricular ectopic premature beats?

A

A premature beat arising from an ectopic focus in the ventricles - this focus depolarises before the SAN, leading to a premature and inefficient beat.
Premature ventricular contraction.

75
Q

What is a risk factor for ventricular ectopic beats?

A

MI
- These are the most common POST-MI arrhythmia

76
Q

Explain the pathophysiology of ventricular ectopic beats.

A
  1. Patient complains of extra beats, missed beats or heavy beat
  2. Following a premature beat, there is usually a complete compensatory pause because the AV node or ventricle is refractory (i.e. cannot accept new impulses) to the next sinus impulse - resulting in missed beat.
  3. Can provoke VENTRICULAR FIBRILLATION - potentially fatal
77
Q

Describe the clinical presentation of ventricular ectopic beats.

A
  • May be uncomfortable especially when frequent
  • Pulse is irregular owing to the premature beats
  • Usually are asymptomatic
  • Can feel faint or dizzy
78
Q

What does a ventricular ectopic beat look like on ECG?

A

Broad or double waved QRS
- > 0.12 s

79
Q

Why do ventricular ectopic beats have a broad QRS on an ECG?

A

Because they arise from an abnormal (ectopic) site in the
ventricular myocardium.

80
Q

Describe the clinical and ECG features of a premature ventricular ectopic beat.

A

Broad, abnormal QRS complex before you would expect it.
Patient complains of extra/missed beats/heavy beats - palpitations

81
Q

Treatment of ventricular ectopic beats.

A
  • Reassure patient
  • Give beta-blockers e.g. Bisoprolol if symptomatic
82
Q

How would you treat a symptomatic ventricular ectopic beat?
What are patients with ventricular ectopic beats at a higher risk of?

A

Beta blockers.
Ventricular fibrillation.

83
Q

Causes of ventricular tachycardia?

A

Ventricular fibrosis or dilatation

84
Q

Describe the ECG changes that may be seen in a ventricular tachycardia.

A

Very broad, abnormal QRS (>160ms)
No P waves
T waves difficult to identify
Rate > 200bpm (rapid).

85
Q

What is the treatment for ventricular tachycardia in an urgent situation?

A

DC cardioversion.

86
Q

How do sodium channel blockers work in the treatment of ventricular tachycardia?

A

They block the inactivation gate of the sodium channel.

87
Q

What is the long term treatment for ventricular tachycardia in high risk patients?

A

Implantable defibrillator.

88
Q

What is ventricular fibrillation (VF)?

A

Involves very rapid and irregular ventricular activation with NO MECHANICAL EFFECT i.e NO CARDIAC OUTPUT

89
Q

Causes of VF

A

Myocardial iscahemia/infarction
Electrolyte abnormalities
Cardiomyopathy (dilated, hypertrophic, restrictive)
Long QT
Brugada syndrome
Drugs
Environmental - electrical shock, drowing, hypothermia
PE
Cardiac tampnoade
Blunt trauma

90
Q

Describe the ECG changes seen in ventricular fibrillation (VF).

A

Chaotic irregular deflections of varying amplitude

No identifiable P waves, QRS complexes or T waves

Rate 150-500bpm

91
Q

What is torsaides des pointes?

A

Ventricular tachycardia with long QT
Normally caused by mutations in ion channels or drugs – ventricular depolarisation is longer

92
Q

What is long QT syndrome?

A

Describes an ECG where the ventricular repolarisation - QT interval is greatly prolonged

93
Q

Give 2 signs of long QT syndrome.

A
  1. Palpitations.
  2. Syncope.
94
Q

Give 3 causes of long QT syndrome.

A
  1. Congenital
  2. Electrolyte disturbances
    - Hypokalaemia
    - Hypocalcaemia
    - Hypomagnesaemia
  3. A variety of drugs
    - Tricyclics
    - Macrolides
95
Q

Name 2 drugs that can prolong the QT interval.

A
  1. Sotalol.
  2. Amiodarone.
96
Q

Give 5 potential side effects of drugs that prolong the QT interval.

A
  1. Pro-arrythmic effects.
  2. Interstitial pneumonitis.
  3. Abnormal liver function.
  4. Hyper/hypothyroidism.
  5. Sun sensitivity.
  6. Grey skin discolouration.
  7. Corneal micro-deposits.
  8. Optic neuropathy.
97
Q

Treatment of long QT syndrome.

A
  • Treat underlying cause
  • If acquired long QT: then give IV isoprenaline (contraindicated for congenital long QT)
98
Q

Describe the pathophysiology of focal atrial tachycardia.

A

Another area of the atrium becomes more autonomic than the sinus node and so sinus node function is taken over -> focal atrial tachycardia.

99
Q

What might you see on an ECG taken from someone with focal atrial tachycardia?

A

Abnormal P waves appear before a normal QRS.

6. Cardiovascular System (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions