Abnormal ECG - Arrhythmias Flashcards
(102 cards)
1
Q
How are arrhythmias dangerous?
A
Reduction in cardiac output
2
Q
What allows all parts of the heart to become latent pacemakers?
A
Phase 4 depolarisation
3
Q
Bradyarrhythmia:
A
< 60 bpm
4
Q
Tachyarrhythmia:
A
> 100 bpm
5
Q
Which types of arrhythmias are easiest to treat?
A
Supraventricular rather than ventricular
Those of atrial or AVN origin
6
Q
What is complete (third degree) heart block?
A
Complete dissociation of beating between the atria and the ventricles
7
Q
What dictates the speed of the bradyarrhythmia in third degree heart block?
A
The location of the ectopic pacemaker: slower more distal to the SAN
8
Q
What causes complete (third degree) heart block?
A
Atherosclerosis
CHD
Dilated cardiomyopathy
Idiopathic
9
Q
ECG findings in complete (third degree) heart block?
A
QRS complex and T waves completely dissociated from the P waves as the ventricles beat independently of the SAN firing
10
Q
How does re-entry cause arrhythmia?
A
Because the wave of depolarisation in the heart is no longer homogenous and the rate becomes too rapid
11
Q
How can you treat a unidirectional bundle branch block?
A
Deepen the block to prolong the refractory period with a drug
12
Q
What paradoxically can cause early afterdepolarisations?
A
Anti-arrhythmics e.g. digoxin (also too much calcium and catecholamines)
13
Q
What do both early and delayed after-depolarisations cause?
A
Re-entry
14
Q
In atrial fibrillation, where is the ectopic pacemaker located?
A
Atria / pulmonary artery / pulmonary vein
15
Q
Why does atrial fibrillation cause decreased cardiac output?
A
Ventricles beat too quickly and are not primed with blood
16
Q
What drugs can treat atrial fibrillation?
A
Adenosine and digoxin
17
Q
How do adenosine and digoxin treat atrial fibrillation?
A
Slow AVN conduction
18
Q
How do you describe the rhythm of beating in atrial fibrillation?
A
Regularly irregular
19
Q
Describe the ECG of atrial fibrillation
A
No p waves
F waves of varying amplitudes
Very frequent QRS complexes
20
Q
Why is the QRS complex in ventricular fibrillation broader than in a normal patient?
A
Ectopic site in the ventricle wall and muscle conducts slower than the conduction system
21
Q
Why can ventricular fibrillation occur post-MI
A
MI scar allows re-entry
22
Q
Describe the ECG of ventricular fibrillation
A
Either: Broad QRS which can be regular (monomorphic0 or irregular (polymorphic) and p waves don’t capture
Or: No ventricular beat so disorganised and chaotic activity reflected in the ECG
23
Q
How does an implanted defibrillator work?
A
Cardioversion back to sinus rhythm
24
Q
Class 1 drugs:
A
Na channel blockers, suppress conduction
25
Give an example of a class 1 drug:
Flecainide
26
Class 2 drugs:
Beta receptor blockers, reduce excitability and inhibit AVN conduction (-olol)
27
Give an example of a class 2 drug:
Bisoprolol
28
Class 3 drugs:
Drugs which prolong the AP and refractory period
29
Give an example of a class 3 drug:
Amiodarone
30
Class 4 drugs:
Ca channel blockers, inhibit AVN conduction
31
Give an example of a class 4 drug:
Verapamil
32
Function of adenosine:
Slows AVN conduction
33
Function of digoxin:
Stimulates the vagus and thus slows AVN conduction
34
What drugs could be used to slow AVN conduction as a rate control strategy for treatment?
Class 2 (bisoprolol), class 4 (verapamil), adenosine and digoxin
35
What drugs could be used to block the re-entrant pathway and treat the source of the arrhythmia as a rhythm control strategy for treatment?
Class 1 (flecainide), class 3 (amiodarone)
36
Name class 2 drugs:
```
Carvedilol
Propranolol
Esmolol
Timolol
Metoprolol
Atenolol
Bisoprolol
Nebivolol
```
37
Name class 1 drugs:
1a: Quinidine
Procainamide
Disopyramide
Ajmaline
1b: Lidocaine
Mexiletine
1c: Flecainide
Propafenone
38
Name class 3 drugs:
```
Amiodarone
Dronedarone
Sotalol
Bretylium
Ibutilide
Dofetilide
```
39
Name class 4 drugs:
Verapamil
Diltiazem
Nifedipine
40
The majority of paroxysmal tachycardias are caused by what?
Re-entry
41
Chronic degenerative cause of bradycardia?
Sick sinus syndrome / sinoatrial disease
42
What is sick sinus syndrome?
Fibrosis of the SAN (usually idiopathic)
43
Important prophylaxis in tachy-brady syndrome?
Anti-coagulation
44
Drugs used for vasovagal attacks:
Beta-blockers, alpha-blockers (e.g. amiodarone) and myocardial negative inotropes (e.g. disopyramide)
45
First degree AV block =
Prolongation of the PR interval to > 0.22s
| Every atrial depolarisation is followed by ventricular depolarisation but with delay
46
Second degree AV block =
Some p waves conduct and others do not
47
Progressive PR interval prolongation until a p wave fails to conduct is which type of heart block?
PR interval before the p wave fails is broader than after
Second degree AV block: Mobitz I block
48
Dropped QRS complex not preceded by a progressive PR interval prolongation. QRS complex is wide > 0.12s
Which type of heart block?
Second degree AV block: Mobitz II block
49
Every second or third p wave conducts to the ventricles.
| Which type of heart block?
Second degree AV block: 2:1 / 3:1 / advanced block
50
What does a broad complex escape rhythm > 0.12s imply?
That the escape rhythm occurs below the bundle of His more distally in the His-purkinje system
51
Narrow onset escape rhythm is characterised by which differential?
QRS complex < 0.12s
52
Narrow onset escape rhythm suggests what?
Escape rhythm lies in the bundle of His more proximal to the AVN
53
Treatment for narrow onset escape rhythm?
IV atropine for recent and transient onset, pacemaker for for chronic onset AV block
54
Which drugs can induce complete heart block?
Digoxin, beta-blockers, CCBs (non-dihydropyridine) amiodarone
55
What is the commonest cause of re-entry in patients with normal hearts?
AVN re-entry (AVNRT)
56
ECG of AVNRT? (or accelerated junctional tachycardia)
No visible p wave or inverted p wave immediately before or after the QRS complex
57
ECG of AV reciprocating tachcardia?
P wave visible between QRS complex and t wave
58
ECG of atrial flutter?
Flutter waves of 300/min usually with a 2:1 AVN conduction rate
59
ECG of atrial tachycardia?
Organised atrial activity with p wave morphology different to sinus rhythm preceding the QRS
60
ECG of multifocal atrial tachycardia?
P waves of differing morphologies and irregular RR interval
61
Why should amiodarone be reserved until last as a rhythm control treatment in a heart with no significant disease?
Adverse extra cardiac effects
62
When is amiodarone only recommended treatment for rhythm control?
When the patient has heart failure or left ventricular hypertrophy
63
Where are the ectopic triggers for atrial fibrillation typically found?
Pulmonary veins
64
Drug causes of long QT syndrome:
Quinidine, disopyramide, sotalol, amiodarone, TCAs (e.g. amitriptyline)
Phenothiazine drugs (e.g. chlorpromazine)
Antipsychotics (e.g. haloperidol, olanzapine)
Macrolides (e.g. erythromycin)
Quinolones (e.g. ciprofloxacin)
Methadone
65
Cardiac causes of long QT syndrome:
| Other causes: diabetes, fasting and liquid protein diets
Bradycardia
Mitral valve prolapse
Acute MI
66
Treatment for long QT syndrome?
Beta blokade, pacemaker, left cardiac sympathetic denervation
67
Arrhythmogenic right sided cardiomyopathy ECG and treatment?
ECG: abnormality/inverted t waves in V1-3 and terminal notch in the QRS
Treatment: solatolol, ablation, defibrillator
68
What is a differential for ST elevation in inferior ECG leads?
Aortic dissection
69
Adverse complication of beta blockers?
Worsen peripheral vascular disease if this is present
70
Contraindications for beta blockers?
Uncontrolled heart failure
Asthma
Sick sinus syndrome
Concurrent verapamil use; may precipitate severe bradycardia
71
Side-effects of beta-blockers?
```
Bronchospasm
Cold peripheries
Fatigue
Sleep disturbance (nightmares)
Erectile dysfunction
```
72
Indications for beta blockers?
```
Angina
Post-MI
Heart failure
Arrhythmias
Hypertension
Thyrotoxicosis
Migraine prophylaxis
Anxiety
```
73
ECG showing ST wave going down with inverted T wave =
Subendocardial ischaemia
Innermost layer has most resistance due to contraction of the myocardium - this innermost layer is ischaemic so repolarises slower so heart wall depolarises from the outer layer in rather than in-out causing inversion
74
How does ischaemia cause SOB?
Slower relaxation in diastole so pressure in LA increases as not properly relaxed and blood is entering from lungs so this pressure is backed up to the lungs
75
What do pathologic Q waves indicate?
Previous MI
76
Detecting ischaemia?
Look for abnormal signs of repolarisation such as ST segment abnormalities or T wave inversion
77
Test for left bundle branch block?
Cannot trust ECG, must move on to CTCA as cannot properly assess ST and T wave as depolarisation is already delayed so repolarisation follows in an inverted direction
78
When do you offer CTCA?
If clinical assessment includes typical or atypical angina
or if assessment indicates non-anginas chest pain but the 12-lead resting ECG has been done and indicates ST-T changes or Q waves
79
What is CTCA?
Perfusion X-ray imaging that allow you to visualise contrast in the coronary arteries
Anatomical assessment, not a functional assessment
Give stressor e.g. bicycle or vasodilatory/inotropic drug a d image again
80
Second-line non-invasive functional testing?
MPS with SPECT
| (first pass contrast enhanced MRI perfusion or MRI for stress induced wall motion abnormalities
81
Invasive functional assessment:
>20% drop in perfusion pressure will be angina causing
| If a positive fractional flow reserve is measured from the pressures, this is an indication for re-vascularisation
82
Anatomical assessment of CAD:
CTCA
| Invasive angiography
83
Functional assessment of CAD:
```
ECG, exercise ECG
Nuclear medicine: SPECT and PET
Stress ECHO
Stress MRI
CT FFR
Invasive coronary physiology
```
84
What drug is used for functional wall motion testing?
Dobutamine which causes inotropic stimulation
| Induces true ischaemia
85
Which drugs are used to measure perfusion?
Vasodilators: adenosine, regadenoson, dipyridamole
| Induction of true ischaemia is exceptional
86
Side effects of adenosine?
Bronchospasm
AV block I, II and III
Hypotension
Hyperventilation
87
Side effects of dobutamide?
```
Sustained or non-sustained VT
Paroxysmal AF
Transient 2:1 block
Severe hypertensive reaction
Hypotension
Nausea
```
88
Mechanism of amiodarone:
```
Class III anti-arrhythmic, blocks K channels and thus prolongs the AP
(also has a class I effect and blocks Na channels)
Used in the treatment of atrial, nodal and ventricular tachycardias
```
89
S1:
Closure of mitral and tricuspid valves
Soft if long PR or mitral regurgitation
Loud in mitral stenosis
90
S2:
Closure of aortic and pulmonary valves
Soft in aortic stenosis
Splitting during inspiration is normal
91
S3 (third heart sound):
Caused by diastolic filling of the ventricles
Normal <30 (up to 50 in women maybe)
Heard in dilated cardiomyopathy (aka left ventricular failure), constrictive pericarditis (aka pericardial knock) and mitral regurgitation
92
S4 (fourth heart sound):
Heard in aortic stenosis, HOCM and hypertension
Caused by atrial contraction against a stiff ventricle
In HOCM a double palpable pulse may be felt as a result of S4
93
Problems with amiodarone?
Interacts with warfarin, increasing warfarin concentration
May cause statin-induced rhabdomyolysis (raised CK)
Pro-arrhythmic affect of prolonging QT interval
Pulmonary/liver fibrosis, thyroid dysfunction, bradycardia, myopathy, neuropathy
94
Which coronary artery blockage would present ECG changes in leads V1 to V4? (anteroseptal)
Left anterior descending
95
Which coronary artery blockage would present ECG changes in leads II, III and aVF? (inferior)
Right coronary
96
Which coronary artery blockage would present ECG changes in leads V4-6, I and aVL? (anterolateral)
Left anterior descending or left circumflex
97
Which coronary artery blockage would present ECG changes in leads I, aVL +/- V5-6? (lateral)
Left circumflex
98
Which coronary artery blockage would present ECG changes in leads V1-2 with tall R waves? (posterior)
Usually left circumflex, also right coronary
99
S1:
Closure of mitral and tricuspid valves
Soft if prolonged PR or mitral regurgitation
Loud in mitral stenosis
100
S2:
Closure of aortic and pulmonary valves
Soft in aortic stenosis
Splitting during inspiration is normal
101
S3 (third heart sound):
Caused by diastolic filling of the ventricle
Normal if <30 y/o (women up to 50)
Left ventricular failure e.g. dilated cardiomyopathy
Constrictive pericarditis
Mitral regurgitation
102
S4 (fourth heart sound):
Atrial contraction against a stiff ventricle
Aortic stenosis, HOCM, hypertension
HOCM may have palpable double apical pulse due to S4
