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Medicine Phase 2a CVS > Cardiac Arrhythmias > Flashcards

Cardiac Arrhythmias Flashcards

1
Q

What is a cardiac arrhythmia?

A

abnormality of the cardiac rhythm

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2
Q

*Clinical presentation of cardiac arrhythmias

A
  • Sudden death
  • Syncope
  • Heart failure
  • Chest pain
  • Dizziness
  • Palpitations
  • No symptoms at all
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3
Q

2 main types of arrhythmia

A

Bradycardia

Tachycardia

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4
Q

Features of Bradycardia arrhythmia

A

Heart rate is slow (<60bpm during day and <50bpm at night)
Usually asymptomatic unless the rate is very slow
Normal in athletes owing to increased vagal tone and thus parasympathetic activity

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5
Q

Features of tachycardia arrhythmias

A

HR is fast (>100bpm)

More symptomatic if arrhythmia is fast and sustained

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6
Q

What are 2 types of tachycardia arrhythmias

A

Supraventricular tachycardias - arise from the atrium or the AV junction
Ventricular tachycardias - arise from the ventricles

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7
Q

What is the normal conduction pathway in the heart?

A

SAN → Action potential → Muscle cells of atria → Depolarisation of the AVN → Slow → Interventricular septum → Bundle of His → Right and left bundle branches → Free walls of both ventricles → Purkinje cells → Ventricular myocardial cells

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8
Q

Where is Sinoatrial node

A

Junction between the superior vena cava (SVC) and right atrium

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9
Q

What cell junctions are found between cardiac cells

A

Gap junctions

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10
Q

Where is Atrioventricular node?

A

Lower interatrial septum

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11
Q

Why is there slow spread of action potential between the AVN and ventricles?

A

Allow for complete contraction of atria before ventricles are excited and contract

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12
Q

SAN discharge rate is modulated by autonomic nervous system - is sinus rate faster in men or women

A

Women

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13
Q

What characterised normal sinus rhythm on an ECG?

A

Normal sinus rhythm is characterised by P waves that are upright in leads I & II of the ECG, but inverted in the cavity leads aVR & V1

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14
Q

How does HR change during inspiration

A

Parasympathetic tone falls and the heart rate quickens

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15
Q

How does HR change during expiration

A

Parasympathetic tone increases and so heart rate falls

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16
Q

Define atrial fibrillation

A

A chaotic irregular atrial rhythm at 300-600bpm; the AV node responds intermittently, hence an irregular ventricular rate

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17
Q

Epidemiology of Atrial fibrillation

A

Most common sustained cardiac arrhythmia
Males more than females
Around 5-15% of patients over age of 75

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18
Q

Clinical classifications of atrial fibrillation

A 
Acute
Paroxysmal
Recurrent
Persistent
Permenant
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19
Q

Clinical classifications of atrial fibrillation: Acute

A

onset within the previous 48 hours

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20
Q

Clinical classifications of atrial fibrillation: Paroxysmal

A

stops spontaneously within 7 days

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21
Q

Clinical classifications of atrial fibrillation: Recurrent

A

2 or more episodes of AF

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22
Q

Clinical classifications of atrial fibrillation: Persistent

A

continuous for more than 7 days and not self-terminating

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23
Q

Causes of atrial fibrillation

A
  • Idiopathic (5-10%)
  • Any condition that results in raised atrial pressure, increased atrial muscle mass, atrial fibrosis, or inflammation and infiltration of the atrium may cause atrial fibrillation
  • Hypertension (most common in developed world)
  • Heart failure (most common in developed world)
  • Coronary artery disease
  • Valvular heart disease; especially mitral stenosis
  • Cardiac surgery (1/3rd of patients after surgery)
  • Cardiomyopathy (rare cause)
  • Rheumatic heart disease
  • Acute excess alcohol intoxication
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24
Q

Risk factors of atrial fibrillation

A
  • Older than 60
  • Diabetes
  • High blood pressure
  • Coronary artery disease
  • Prior MI
  • Structural heart disease (valve problems or congenital defects)
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25
Q

Pathophsyiology of atrial fibrillation

A

Atrial fibrillation (AF) is maintained by continuous, rapid (300-600/min) activation of the atria by multiple meandering re-entry wavelets.

These are often driven by rapidly depolarising automatic foci, located
predominantly within the pulmonary veins.

(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.

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26
Q

What does ventricular response depend on?

A

Rate and regularity of atrial activity (particularly at entry to the AV node)
Balance between sympathetic and parasympathetic tone

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27
Q

How much can cardiac output drop if the ventricles are not primed reliably by the atria?

A

10-20%

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28
Q

Why are people with AF at higher risk of thromboembolic events e.g. stroke?

A

When the atria are spasming and some parts are not contracting, it causes blood to POOL in these parts and thus remain still. Here the blood doesn’t move and thus CLOT (or thrombus) begins to form. This could easily result in an EMBOLI and thus a stroke.

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29
Q

As people with AF are at higher risk of thromboembolic events, what can be given to help prevent these TE events?

A

Blood thinner e.g. Warfarin

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30
Q

*Clinical presentation of AF

A
  • Symptoms are highly variable
  • May be asymptomatic
  • Palpitations
  • Dyspnoea and or chest pains following the onset of atrial fibrillation
  • Fatigue
  • Apical pulse rate is greater than the radial rate
  • 1st heart sound is of variable intensity
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31
Q

*Describe ECG of AF (diagnosis of AF)

A

No P Waves

Rapid and irregular QRS complex

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32
Q

*Differential diagnosis of AF

A

Atrial flutter

Supraventricular tachyarrhythmias

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33
Q

Acute management of AF

A

If AF due to acute precipitating event (e.g. alcohol toxicity, chest infection, hyperthyroidism), the provoking cause should be treated.
Cardioversion (conversion to sinus rhythm)
Ventricular rate control (by drugs that block AV node)

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34
Q

What is cardioversion?

A

Treatment of acute AF:

Conversion to sinus rhythm achieved by DC shock e.g. defrillator

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35
Q

What drugs should be given when having cardioversion and why?

A

LMW Heparin

e.g. Enoxaparin or Dalteparin to minimise risk of thromboembolism associated with cardioversion

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36
Q

If cardioversion fails, what can you do instead of cardioversion

A

Medical routes - IV infusion or anti-arrhythmic drug e.g. flecainide or amiodarone

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37
Q

What drugs can be given in acute management of AF to control ventricular rate?

A

Calcium Channel Blocker
Beta-blocker
Digoxin
Anti-arrhythmic

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38
Q

Example of calcium channel blocker

A

Verapamil

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39
Q

Example of Beta-blocker

A

Bisoprolol

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40
Q

Example of Anti-arrhythmic

A

Amiodarone

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41
Q

2 parts of long term and stable patient AF management

A

Rate control

Rhythm control

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42
Q

Long term and stable patient management AF: Rhythm control

A
  • Cardioversion to sinus rhythm and use Beta-blockers e.g. Bisoprolol to suppress arrhythmia.
  • Appropriate anti-coagulation e.g. Warfarin due to thrombo-embolism risk with cardioversion
  • Can use pharmacological cardioversion e.g. Flecainide if no structural heart defect or use IV Amiodarone instead if there is structural heart disease
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43
Q

Long term and stable patient management AF: Rate control

A

AV nodal slowing agents plus oral anticoagulation
Beta-blocker e.g. Bisoprolol
Calcium channel blocker e.g. Verapamil or Diltiazem

If they fail try Digoxin and then consider Amiodarone

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44
Q

Long term and stable patient management AF - who would rhythm control be advocated for?

A

Younger, symptomatic and physically active patients

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45
Q

*What could you use to calculate stroke risk in AF patients (and thus need for anticoagulation)?

A

CHA2DS2-VASc score

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46
Q

*What is each part of the CHA2DS2-VASc score and how many points are needed for treatment

A
  • Congestive heart failure (1 point)
  • Hypertension (1 point)
  • A2ge greater or equal to 75 (2 points)
  • Diabetes mellitus (1 point)
  • S2troke/TIA/thromboembolism (2 points)
  • Vascular disease (aorta, coronary or peripheral arteries) (1 point)
  • Age 65-74 (1 point)
  • Scex Category: female (1 point)
  • If score is 1 then it merits consideration of anticoagulation and or aspirin
  • If score is 2 and above then oral anticoagulation is required
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47
Q

Define Atrial flutter

A

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

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48
Q

Epidemiology of Atrial flutter

A
  • Often associated with atrial fibrillation and frequently require a similar initial therapeutic approach
  • Either paroxysmal or persistent
  • Much less common than atrial flutter
  • More common in men
  • Prevalence increases with age
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49
Q

Aetiology of Atrial flutter

A
  • Idiopathic (30%) (means unknown cause)
  • Coronary heart disease
  • Obesity
  • Hypertension
  • Heart failure
  • COPD
  • Pericarditis
  • Acute excess alcohol intoxication
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50
Q

Risk factor for atrial flutter

A

Atrial fibrilation

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51
Q

Clinical presentation of atrial flutter

A 
Palpitations
Breathlessness
Chest pain
Dizziness
Syncope
Fatigue
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52
Q

Differential diagnosis of atrial flutter

A

Atrial fibrillation

Supraventricular tachyarrhythmias

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53
Q

*Diagnosis of atrial flutter

A

ECG

-Regular sawtooth-like atrial flutterwaves (F waves) between QRS complexes due to continuous atrial depolarisation

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54
Q

What can be done to diagnose atrial flutter if think patient has it but F waves are not showing on ECG

A

F waves may be able to be unmasked by by slowing atrioventricular conduction by carotid sinus massage or IV adenosine (AV nodal blocker)

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55
Q

Treatment of A Flutter

A
  • Electrical cardioversion but anticoagulate (low molecular weight heparin e.g. Enoxaparin or Dalteparin) before if acute i.e. atrial flutter started <48 hours ago
  • Catheter ablation - creating a conduction block to try an restore rhythm and block offending re-entrant wave
  • IV Amiodarone to restore sinus rhythm and use a beta-blocker e.g. Bisoprolol to suppress further arrhythmias
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56
Q

Where can heart block occur in the conducting system

A

AV block:
AV node
His bundle

Block lower in conduction system produces a Bundle Branch Block

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57
Q

3 forms of AV block

A

First degree
Second degree
Third degree

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58
Q

Describe features of 1st degree AV block

A

Simple prolongation of the PR interval to greater than 0.22 seconds
Every atrial depolarisation is followed by conduction to the ventricles but without delay

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59
Q

Causes of 1st degree AV block

A

Hypokalemia
Myocarditis
Inferior MI
AV node blocking drugs e.g. Beta-blockers (Bisoprolol), Calcium channel blockers (Verapamil) and Digoxin

60
Q

Treatment of 1st degree AV block

A

Asymptomatic so no treatment

61
Q

2 types of 2nd degree AV block

A

Mobitz I block
Mobitz II block

2nd degree AV blocks generally occur when some P waves conduct and others do not

62
Q

Describe featuers of Mobitz I block (2nd degree AV block)

A

A progressive PR interval prolongation until beat is ‘dropped’ and P wave fails to conduct i.e. excitation completely fails to pass through the AVN/bundle of His
The PR interval before the blocked P wave is much longer than the PR interval after the blocked P wave

63
Q

Causes of Mobitz I block (2nd degree AV block)

A
  • Atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin
  • Inferior MI
64
Q

Symptoms that result from Mobitz I block

A

Light headiness
Dizziness
Syncope

65
Q

Describe features of Mobitz II block (2nd degree AV block)

A
  • PR interval is constant and QRS interval is dropped

- Failure of conduction through the His-Purkinje system

66
Q

Is a pacemaker required for Mobitz I or II block (2nd degree AV block)

A

Mobitz II block
as high risk of developing sudden complete AV block.

Mobitz I block only requires a pacemaker if poorly tolerated

67
Q

Causes of Mobitz II block (2nd degree AV block)

A
  • Anterior MI
  • Mitral valve surgery
  • SLE and Lyme disease
  • Rheumatic fever
68
Q

Symptoms that result from Mobitz II block

A

Shortness of breath
Mitral valve surgery
SLE and Lyme disease
Rheumatic fever

69
Q

Describe 3rd degree AV block

A

Complete AV block

  • When all atrial activity fails to conduct to the ventricles
  • Ventricular contractions are sustained by spontaneous escape rhythm which originates below the block
  • P waves are COMPLETELY INDEPENDENT of QRS complex
70
Q

Causes of 3rd degree AV block

A
  • Structural heart disease e.g. transposition of great vessels
  • Ischaemic heart disease e.g. acute MI
  • Hypertension
  • Endocarditis or Lyme disease
71
Q

What are 2 types of escape rhythm that can occur from 3rd degree AV block

A

Narrow-complex escape rhythm (QRS complex <0.12 seconds)

Broad-complex escape rhythm (QRS complex >0.12 seconds)

72
Q

If a narrow-complex escape rhythm is shown for 3rd degree AV block, what can be be deduced about the location of the block

A

Implies block originates in the His bundle and thus the region of block lies more proximally in the AV node

73
Q

Treatment of Narrow-complex escape rhythm (3rd degree AV block)

A 
Recent onset (that has transient causes) - IV atropine
Chronic narrow-complex escape rhythm - Permanent pacemaker (if symptomatic)
74
Q

If a broad-complex escape rhythm is shown for 3rd degree AV block, what can be be deduced about the location of the block

A

Implies block originates BELOW the bundle of His and thus the region of
block lies more distally in the His-Purkinje system.

75
Q

Treatment of Broad-complex escape rhythm (3rd degree AV block)

A

Permanent pacemaker implantation is recommended

76
Q

In which type of escape rhythm do you get dizziness and blackouts

A

Broad-complex escape rhythm

77
Q

*Which of these of false:
Bundle Branch blocks are usually asymptomatic
His bundle gives rise to right and left branches
Left branch subdivides into the anterior and inferior divisions of left bundle

A

Left branch subdivides into the anterior and POSTERIOR divisions of left bundle

78
Q

What would be seen on an ECG to suggest incomplete bundle branch block

A

Incomplete block would cause bundle branch conduction delay.

Results in slight-widening of QRS complex (up to 0.11 seconds)

79
Q

How could you tell a complete bundle branch block on an ECG

A

Wide QRS complex (larger than 0.12 seconds)

Shape of QRS depends on whether the right or left bundle is blocked

80
Q

Causes of RBBB

A

Pulmonary embolism
Ischaemic heart disease
Atrial/Ventricular septal defect

81
Q

*Describe physiological features of RBBB

A

Right bundle no longer conducts
Therefore 2 ventricles do not get impulses at the same time and instead spread from left to right
Produces late activation of the right ventricle
Also causes wide physiological splitting of the second heart sound

82
Q

*ECG of RBBB

A 
Deep S wave in leads I and V6
Tall late R wave in lead V1
MaRRoW (R for RightBBB):
-M = QRS looks like an M in lead v1
-W = QRS looks like a w in V5 and V6
83
Q

*Cause of LBBB

A

Ischaemic Heart Disease

Aortic valve disease

84
Q

Describe physiological features of LBBB

A

Late activation of left ventricle
Causes reverse splitting of 2nd heart sound
Left bundle branch conduction is usually responsible for Initial ventricular activation so LBBB may also produce abnormal Q waves

85
Q

*ECG of LBBB

A 
Deep S wave in V1
Tall late R wave in I and V6
WiLLiaM (L for LBBB)
W = QRS looks like a W in leads V1 and V2
M = QRS looks like an M in leads V4-V6
86
Q

Define sinus tachycardia

A

HR >100bpm

87
Q

Causes of sinus tachycardia

A 
Anaemia
Anxiety
Exercise
Pain
HF
Pulmonary embolism
88
Q

Treatment of sinus tachycardia

A

Treat causes

If necessary, then can use Beta Blockers e.g. Bisoprolol

89
Q

In what patients would you see Atrioventricular Junctional Tachycardias

A

Often seen in young patients with little or no structural heart disease.
First presentation is commonly between ages 12-30
AV node essential component to these tachycardias

90
Q

What does AVNRT stand for

A

Atrioventricular nodal re-entrant tachycardia

Type of

91
Q

Are AVNRTachycardias more common in men or women

A

Women

92
Q

Risk factors of AVNRTs

A 
Exertion
Emotional stress
Coffee
Tea
Alcohol
93
Q

*Examples of paroxysmal Supraventricular tachycardias

A

AVNRT - Atrioventricular Nodal Re-entrant Tachycardia

AVRT - Atrioventricular Re-entrant Tachycardia

94
Q

AVNRT - 2 pathways within the AV node

A

Short effective refractory period and SLOW conduction

Longer effective refractory period and FAST conduction

95
Q

What is refractory period

A

window of time where

cells cannot be excited again after they have already been excited

96
Q

*AVNRT - in sinus rhythm, which pathway does atrial impulse that depolarises the ventricles usually conduct through?

A

Fast pathway with longer effective refractory period.

By the time the impulse has been propagated to the ventricles, the FAST pathway has finished its refractory period and once again is able to transmit impulses

97
Q

What happens in AV node if atrial impulse happens early e.g. atrial premature beat, while fast pathway is still in refractory period

A

Slow pathway takes over in propagating impulses of atria to the ventricles.
BUT
by the time the slow impulse has been propagated to the ventricles, the fast pathway would’ve finished its refractory period and is once again able to transmit pulses.

98
Q

*Describe the Re-entrant loop at the AV node in AVNRT

A

2 pathways: Slow conduction but short refractory time
Fast conduction but long refractory time

Sinus rhythm - atria impulse that causes contraction of ventricles usually conducts through fast pathway.
If atrial impulse happens early, while fast pathway is still in refractory period, slow pathway takes over in propagating atrial impulses to the ventricles.
By the time the slow pathway has been propagated to the ventricles, the FAST pathway would’ve finished its refractory period and is once again able to transmit impulses.
This starts a cycle of fast and slow pathways sending signals through AV node and causing contractions at a much faster rate than a normal pacemaker would so you see Tachyarrhythmia

99
Q

In AVNRT, what is expected heart rate due to re-entrant loop

A

100-250bpm

100
Q

*AVNRT - clinical presentation

A
  • Rapid regular palpitations (abrupt onset and sudden termination)
  • Chest pain and breathlessness
  • Neck pulsations (prominent jugular venous pulsations due to atrial contractions against closed AV valves)
  • Polyuria (due to the realise of atrial natriuretic peptide in response to increased atrial pressures during the tachycardia)
101
Q

*AVNRT - diagnosis

A

ECG

  • QRS complexes can show typical BBB
  • P waves are either not visible or are seen immediately before (normal) or after the QRS complex, due to simultaneous atrial and ventricular activation
102
Q

What is AVRT

A

Atrioventricuar Re-entrant Tachycardia
Abnormal connection of myocardial fibres from posterior ventricle to atrium called accessory pathway or Bypass Tract.
Therefore there are 2 circuits: normal AV circuit and Accessory circuit (both transmitting impulses from atria to ventricles)

103
Q

*What causes Accessory pathway in AVRT

A

Incomplete separation of the atria and the ventricles during fetal development.

104
Q

True or False: The accessory circuit impulse in AVRT can travel from atria to venticle or ventricle to atria

A

True
Atria to ventricle is Anterograde
Ventricle to Atria is Retrograde

Atrial activation can occur after ventricular activation.
Patients more prone to AF or Ventricular Fibrillation

105
Q

*Example of AVRT

A

Wolff-Parkinson-White (WPW) syndrome

106
Q

Pathophysiology of Wolff-Parkinson-White (WPW) syndrome (AVRT) and formation of re-entry circuit

A

SAN depolarises
Impulse travels to AVN via atria or travels by accessory pathway.
Accessory pathway conducts from atrium to ventricle during sinus rhythm and the electrical impulse can conduct QUICKLY over this abnormal connection to depolarise part of the ventricles ABNORMALLY (PRE-EXCITATION).
Accessory pathway would be in refractory period (cant transmit to signal).
Normal impulse will travel down the AVN, down the Intra-ventricular septum via the Bundle of His and through the left and right bundle branches and into the free walls of the ventricles via the Purkinje cells until it meets the Accessory Pathway, the ventricles innervated by abnormal pathway have already contracted and cant again.
At the point the acessory pathway will be out of its refractory period and will thus be able to conduct the impulse BACK to atria.
Once back in the atria the impulse can then travel back to AVN, thereby setting up a re-entry circuit and the signal cycle will repeat resulting in tachyarrhythmia.

107
Q

Describe Pre-Excitation in AVRT

A

Accessory pathway conducts impulse from atrium to ventricles during sinus rhythm.
Electrical impulse can conduct quickly over this abnormal connection to abnormally depolarise part of the ventricles (this is while normal atria is depolarising)

108
Q

Describe what an ECG showing Pre-Excitation would look like

A

Short PR interval

Wide QRS complex (begins as a slurred part called a delta wave)

109
Q

Clinical presentation of AVRT (WFW syndrome)

A

Palpitations
Severe dizziness
Dysponea
Syncope

110
Q

*Diagnosis of AVRT or Wolff-Parkinson-White syndrome

A

ECG:
Short PR interval
Wide QRS complex that begins as a slurred part known as a DELTA wave

111
Q

*Treatment of AVRT or WFW syndrome

A
  • Patients presenting haemodynamic instability require emergency cardioversion
  • If stable then vagal manoeuvres
  • If vagal manoeuvres unsuccessful the IV ADENOSINE - causes complete heart block for a fraction of a second and is highly effective at terminating AVNRT and AVRT
  • Surgery
112
Q

What is meant by haemodynamic instability

A

Hypotension

Pulmonary oedema

113
Q

Describe surgery in AVRT

A

Catheter ablation of accessory pathway

114
Q

Describe surgery in AVNRT

A

Modification of the slow pathway

115
Q

Give example of vagal manoeuvres

A

Breath-holding
Carotid massage
Valsalva manoeuvre - abrupt voluntary increase in intra-abdominal and intra-thoracic pressure by straining - several seconds after the release of the strain, the resulting intense vagal effect may terminate AVNRT or AVRT

116
Q

Examples of ventricular tacharrhythmias

A 
Ventricular ectopics
Ventricular tachycardia
Sustained ventricular tachycardia
Ventricular fibrillation
Some cardiac channelopathies e.g. Long QT syndrome
117
Q

What are cardiac channelopathies

A

Congenital disorders that are caused by mutations of the function of cardiac ion channels and hence the electrical activity of the heart e.g. long QT syndrome

118
Q

What are most common POST-MI arrhythmias

A

Ventricular ectopics

119
Q

What are ventricular ectopics

A

premature ventricular contraction

120
Q

Ventricular ectopic risk factors

A

MI

can occur in healthy patients

121
Q

Pathophysiology of ventricular ectopic

A

(Extra beats, missed beats or heavy beats)

*These premature beats have a broad and bizarre QRS complex (>0.12 seconds) as they arise from an abnormal (ectopic) site in the ventricular myocardium.

Following a premature beat, there is usually a complete compensatory pause because the AV node or ventricle is refractory so can’t accept next sinus impulse - resulting in missed beat.

(LV dysfunction can develop from frequent ectopics)

122
Q

Clinical presentation of ventricular ectopic

A

May be uncomfortable (especially if frequent)
Irregular pulse owing to premature beats
Usually are asymptomatic
Can feel faint or dizzy

123
Q

Diagnosis of ventricular ectopic

A

ECG

Widened QRS complex >0.12 seconds

124
Q

Treatment of ventricular ectopic

A

Reassure patient

Give Beta-blockers e.g. Bisoprolol if symptomatic

125
Q

Define (differential diagnosis of) ventricular tachycardia

A

Pulse >100bpm with at least 3 irregular heart beats in a row

126
Q

What patients can have ventricular tachycardia

A

Patients with structurally normal hearts commonly have this (idiopathic ventricular tachycardia)

In these cases it’s usually a benign condition with an excellent long-term prognosis

127
Q

What can result from untreated ventricular tachycardia

A

Cardiomyopathy

Ventricular tachycardia aka Gallavardin’s tachycardia

128
Q

Pathophysiology of ventricular tachycardia

A

Rapid ventricular beating results in inadequate blood filling of ventricles since they are filled in between beats and if beating was
faster there would be less time to fill (thus less blood fills).
Results in decreased cardiac output and thus a decrease in the amount of
oxygenated blood that is circulated around the body

129
Q

*Symptoms of ventricular tachycardia

A
  • Breathlessness (lack of lung perfusion)
  • Chest pain (lack of heart perfusion)
  • Palpitations
  • Light headed or dizzy (lack of brain perfusion)
130
Q

*Treatment of ventricular tachycardias

A

Beta-blockers e.g. Bisoprolol

131
Q

What is sustained ventricular tachycardia

A

Ventricular tachycardia for longer than 30 seconds

132
Q

Symptoms of sustained ventricular tachycardia

A
  • Dizziness (pre-syncope)
  • Syncope
  • Hypotension
  • Cardiac arrest
133
Q

What is syncope

A

Temporary loss of consciousness usually related to insufficient blood flow to the brain

134
Q

Pulse rate of someone with sustained ventricular tachycardia

A

120-220bpm

135
Q

Diagnosis or ECG of sustained ventricular tachycardia

A

ECG:

  • Rapid ventricular rhythm
  • Broad and abnormal QRS complex (>0.14 seconds)
136
Q

Treatment of sustained ventricular tachycardia

A

Emergency electrical conversion if haemo-dynamically unstable (e.g. hypotensive or pulmonary oedema)

IV beta-blocker e.g. esmolol
IV Amiodarone

Prevented by the use of beta-blockers and implantable cardiac defibrillator

137
Q

Example of an IV beta-blocker

A

Esmolol

138
Q

What can cause ventricular fibrillation

A

a ventricular ectopic beat

139
Q

Pathophysiology of ventricular fibrillation

A

Rapid and irregular ventricular activation with NO MECHANICAL
EFFECT i.e NO CARDIAC OUTPUT
Patient is pulseless and becomes unconscious and respiration ceases (CARDIAC ARREST)

140
Q

ECG of patient with ventricular fibrillation

A

Shapeless
Rapid oscillations
No hint of organised complexes

141
Q

Treatment of ventricular fibrillation

A

ELECTRICAL DEFIBRILLATION
(only effective treatment)
Management of survivors:
Give long-term, implantable cardioverter-defibrillators

142
Q

Congenital causes of long QT syndrome

A

Jervell-Lange-Nielsen syndrome (autosomal recessive) - mutation in cardiac potassium and sodium-channel genes.

Romano-Ward syndrome (autosomal dominant)

143
Q

*Acquired causes of long QT syndrome

A 
Hypokalemia
Hypocalcaemia
Bradycardia
Acute MI
Diabetes
Drugs
144
Q

What drugs can give you a long QT interval

A

Amiodarone

Tricyclic anti-depressants e.g. Emitriptyline

145
Q

*Clinical presentation of long QT syndrome

A

Syncope
Palpitations
Patient may have had Polymorphic ventricular tachycarida that has degenerated into ventricular fibrillation this (or terminates spontaneously)

146
Q

Diagnosis of long QT

A

ECG

147
Q

Treatment of long Qt syndrome

A

Treat underlying cause

If ACQUIRED long QT, then give IV Isoprenaline (contraindicated for congenital long QT)

Medicine Phase 2a CVS (17 decks)

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