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Block 31 CardioResp > CT 3 Arrhythmia > Flashcards

CT 3 Arrhythmia Flashcards

1
Q

what is arrhythmia

A

abnormal heart rate or rhythm

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2
Q

what are the symptoms of arrhythmia

A

asymptomatic
palpitations
decompensated failure
syncope
sudden death

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3
Q

how can arrhythmias be classified

A

1) bradyarrhythmia (HR <60bpm)

2) tachy-arrhythmias (HR>100bpm)

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4
Q

how can we further split brady-arrhythmias

A

1) sinus arrhythmias or sinus arrest

2) atrioventricular block

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5
Q

give examples of sinus arrhythmias

A

1) sinus bradycardia (slow firing of the SA node leading to slower heart rate

2) sinus pause (transient pathology in which the SA node fails to generate the electrical impulses leading to a skipped heart beat)

3) sick sinus syndrome
(condition in which the SA node alternates between tachycardia and bradycardia (AF is common in this syndrome)

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6
Q

what are causes of sick sinus syndrome

A

age related scarring
IHD
cardiomyopathies
meds like beta blockers, calcium channel blockers and digoxin

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7
Q

what are the different types of heart block

A

1) 1st degree

2) 2nd degree (further split into mobitz type I and II)

3) 3rd degree

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8
Q

what is AV block

A

condition in which electrical signals from the atria are not conducted appropriately through to the ventricles and his-purkinje system.
it can be delayed or completely block

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9
Q

what is first degree heart block

A

electrical impulse is delayed to the ventricles but is still complete ( P wave is followed by complete QRS complex)

PR interval is longer than 5 small squares

asymptomatic

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10
Q

what is second degree mobitz type I heart block

A

Some p waves are conducted to the ventricles whilst others are blocked

PR interval increases until a QRS is dropped

mild dizziness

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11
Q

what is second degree mobitz type II heart block

A

PR interval is fixed but often QRS complexes are dropped

syncope and bradycardia occurs

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12
Q

what is 3rd degree heart block

A

complete heart block in which P waves and QRS complexes are independent of each other (atria and ventricles are beating separately)

presents with severe bradycardia, dizziness, syncope

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13
Q

which forms of heart block require pacing

A

2nd degree mobitz type II
3rd degree

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14
Q

how are tachyarrhythmia’s classified

A
  • narrow complex <120ms
  • broad complex >120ms

in each category consider whether rhythm is regular or irregular

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15
Q

TA>Broad complex> regular rhythm examples:

A
  • VT
  • SVT with BBB
  • Sinus tachycardia with BBB
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16
Q

what is sinus tachycardia

A

🔹 What Happens?

The heart beats faster due to increased SA node activity.
The rhythm is still normal but faster than 100 bpm.
🔹 ECG Findings:
✅ P waves present before each QRS.
✅ Narrow QRS (<120ms).
✅ Regular rhythm.

🔹 Causes:

Physiological: Exercise, stress, fever, dehydration.
Pathological: Anaemia, hyperthyroidism, shock, heart failure.

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17
Q

what is VT

A

🔹 What Happens?

An ectopic focus in the ventricles takes over, bypassing the SA node.
The ventricles beat rapidly, but inefficiently, which can lead to cardiac arrest.
🔹 ECG Findings:
✅ Wide QRS (>120 ms, often >140 ms).
✅ No P waves or AV dissociation (P waves unrelated to QRS).
✅ Regular rhythm (monomorphic VT) or irregular (polymorphic VT, e.g., Torsades de Pointes).
✅ “Capture beats” or “fusion beats” may be present.

🔹 Causes:

Structural heart disease (ischemic heart disease, cardiomyopathy).
Electrolyte imbalances (low K+, low Mg2+).
Drug toxicity (digoxin, tricyclic antidepressants).

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18
Q

TA> Broad complex> irregular rhythm examples

A

V Fib

A fib with BBB

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19
Q

TA > narrow complex > regular rhythm examples

A

Sinus tachycardia

AVRT /AVNRT

atrial flutter

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20
Q

TA> Narrow complex > irregular rhythm example

A

A fib

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21
Q

how to assess bundle branch blocks

A

broad QRS complexes

look at leads V1 V2

LBBB = William (prominent deep S waves)

RBBB = marrow M shaped

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22
Q

what is atrial flutter

A

rapid, regular atrial tachyarrhythmia caused by a reentrant circuit in the right atrium. It produces fast atrial contractions (250–350 bpm), but not all impulses conduct to the ventricles due to the AV node’s filtering effect.

ECG Findings in Atrial Flutter
🔹 “Sawtooth” P waves (flutter waves, F-waves) best seen in leads II, III, aVF
🔹 Narrow QRS unless there is a bundle branch block
🔹 Fixed AV conduction ratios (e.g., 2:1, 3:1, 4:1)

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23
Q

How does AVRT and AVNRT look on an ECG

A

No P waves
narrow complexes
regular
tachycardic

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24
Q

Characteristics of Afib

A

multiple electrical foci within the atria leading to erratic contraction.

AV node not able to filter in ratio as seen in Atrial flutter so ventricles contract irregularly

No P waves

narrow complexes
irregular

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25
what does VT look like on an ECG
No P waves broad complex regular
26
what does V fib look like on an ECG
no P waves broad complex irregular (just looks like scribbles)
27
How is AF classified
1) paroxysmal ( intermittent episodes that resolve spontaneously without intervention) 2) persistent (episode can be terminated but requires intervention) 3) permanent ( med intervention does not re-establish sinus rhythm
28
what scoring system is used for risk of stroke
CHA2DS2VASc score 1) congestive HF 2) hypertension 3) Age 65-74 scores 1 point >75 scores two points 4) Diabetes 5) stroke scores 2 points 6) VA vascular disease (previous MI, PVD) 7) Sex - female scores 1 point
29
what score on the CHA2Ds2VAS score warrants oral anticoag
>2
30
what score is used to assess risk of bleeding
HAS BLED hypertension abnormal renal, liver function, age Stroke (previous) Bleeding predisposition Labile INR Ethanol use Drugs that increase risk of bleeding
31
1st line in AC in Af
1) DOAC 2) warfarin (elderly who have already been on it, metal heart valve replacement) 3) LMWH (used as bridging therapy or in those with sev renal failure
32
examples of DOACs
1) edoxaban 1/day (interacts with erythromycin + ketoconazole) 2) apixaban 2/day 3) rivaroxaban 1/day needs to be taken with food 4) dabigatran
33
what other management is needed for afib
rate control - 1st line BBs bisoprolol rate limiting CCBs like diltiazem digoxin rhythm control - amiodarone or flecanide electrical cardioversion anticoagulation (consider stroke vs bleeding risk before) left atrial ablation (pulmonary veins are often initial source of abnormal electrical impulses so scar tissue is formed) left atrial appendage occlusion (area where most clots form can be closed off)
34
how is atrial flutter managed
same as afib
35
what are the 4 causes of a narrow complex tachycardia
1) Sinus tachycardia 2) SVT 3) AF 4) Atrial flutter `
36
what are different types of SVT
1) AVRT - presence of an accessory pathway that leads to electrical activity looping back to the atria and tachycardia. example is WPWS (bundle of kent) 2) AVNRT (occurs within the AV node itself with a slower pathway with a short refractory period and faster conducting pathway with a longer refractory period. 3) atrial tachycardia (originates from a single ectopic focus in the atria other than the SA node
37
what are the ECG findings of WPW
- shortened PR interval <0.12s - broad QRS >0.1s (should be normally 3 little squares) - a slurred upstroke to the QRS complex (delta wave - indicates ventricular pre-excitation from accessory pathway)
38
How are SVTs managed
episodes are treated with: Valsalva manoeuvre carotid sinus massage (both of these stimulate the vagus nerve to slow down the HR) - adenosine - BB - CCBs eg verapamil - Amiodarone unstable patients are treated with synchronised cardioversion radiofrequency ablation can be curative
39
what are the causes of broad complex tachycardias
- VT - polymorphic VT eg torsades de pointes - associated with prolonged QT interval - SVT with bundle branch block - AF with bundle branch block
40
what is a prolonged QT interval and what does it represent
- > 0.44s in men so 11 little squares - > 0.46s in women so 12 little squares normal is 9-11 little squares - represents prolonged repolarisation
41
causes of prolonged QT interval
1) long QT syndrome (inherited) 2) medications: anti-psychotics, citalopram, flecainide, sotalol and amiodarone + macrolide antibiotics 3) hypo Ca, Mg, K+
42
what is a normal PR interval
(0.12-0.20s) 3 to 5 little squares
43
how is bradycardia treated
atropine inhibits the parasympathetic system having a antimuscarinic effect thus increasing the HR
44
what are the SE of using atropine for bradycardia
anti-muscarinic: pupil dilation dry mouth urinary retention constipation
45
management of unstable bradycardia
IV atropine inotropes like isoprenaline and adrenaline temporary cardiac pacing permanent implantable pacemaker
46
causes of bradycardia
1) normal physiology - athletes have lower resting HRs 2) sinus node dysfunction (sick sinus syndrome) 3) hypothyroidism (reduced metabolism slows the heart) 4) increased ICP slows the HR as a compensatory mechanism 5) heart blocks 6) drugs: - BB - CCBs non-dihydropyridines eg verapamil + diltiazem - amiodarone
47
what are the stages of the AP within the SA node
phase 0 - depolarisation rapid influx of Ca2+ (L type channels) phase 3 - repolarisation = outflow of K+ and slow inactivation of Ca2+ influx phase 4 = spontaneous depolarisation = increase of slow Na influx
48
what are the stages of the AP within cardiac myocyte
Phase 0 (rapid depolarisation) = fast influx of Na⁺. Phase 1 (initial rapid repolarisation) = closure of Na⁺ channels, and outflow of K⁺ - Phase 2 (plateau) = delay repolarisation due to a balance between Ca²⁺ influx and K⁺ outflow. Phase 3 (final repolarisation) = outflow of K⁺ and closure of Ca²⁺ channels. Phase 4 (resting membrane potential) = Na⁺ and Ca²⁺ channels close, while K+ channels stay open, keeping membrane potential at -90mV.
49
what are class 1 anti-arrhythmic drugs
Na+ channel blockers clinical use is SVT + VT affect phase 0 of AP
50
example of 1a anti-arrhythmic drugs
- Procainamide - quinidine - disopyramide lengthen duration of AP potential
51
example of class 1b drug
lidocaine shortens duration of AP It works by blocking sodium channels, which raises the depolarisation threshold, and makes the heart less likely to initiate or conduct early action potentials that may cause an arrhythmia
52
example of class 1c drug
Flecanide has no effect on duration of Ap
53
What are class II anti-arrhythmic drugs
beta blockers affect phase 4 of the AP use= SVT
54
Example of Class II drugs and how they work
atenolol bisoprolol they work by slowing conduction through the SA and AV node
55
what are class III anti-arrhythmic drugs
K channel blockers affect phase 3 of the AP act to prolong the AP by slowing down efflux of K+ out of the cell
56
examples of class III anti-arrhythmic drugs
amiodarone sotalol
57
what are class IV anti-arrhythmic drugs
calcium channel blockers that affect phase 2 of the AP slows conduction through the SA and AV node
58
examples of class IV anti-arrhythmic drugs
verapamil diltiazem
59
what are the 4 drugs included in class V of the anti-arrhythmic drug classification
adenosine digoxin magnesium atropine
60
MOA of adenosine
Termination of Supraventricular Tachycardia (SVT) First-line drug for AVNRT (most common SVT) Blocks the AV node, interrupting the reentry circuit opens the K+ channels causing rapid efflux of K+ leading to hyperpolarisation of cell.
61
how does digoxin work
reduces rate of conduction through AV node: inhibits Na/K/ATpase pump leading to increased intracellular Na and subsequently increased Ca. this strengthens ventricular contractions so heart pumps with more force (ionotropic effect)
62
SE of digoxin
abnormal cardiac rhythms, GI effects, visual effects, gynaecomastia, CNS effects (e.g. confusion, agitation, nightmares), and digoxin also interacts with diuretics, as well as amiodarone (class III) and verapamil (class IV)
63
beta blockers
Beta blockers are class II anti-arrhythmic drugs used in hypertension, ischaemic heart disease They work as beta adrenergic receptor antagonists, and inhibit sympathetic stimulation (i.e. blocks the effects of adrenaline). This reduces heart rate, reduce contractility of the left ventricle, reduce blood pressure, and reduces excitability of cardiac tissue to prevent arrhythmias Beta blockers shouldn’t be used with in people with asthma, cardiogenic shock, hypotension, AV block, or people with tumours at their adrenal gland Side effects include fatigue, cold extremities, bronchospasm, nightmares, and impotence
64
amiodarone
It works as a potassium channel blocker, to extend an action potential and delay repolarisation. This blocks transmission of abnormal signals, and stops arrhythmia. It works in a similar way to beta blockers Side effects include abnormal cardiac rhythm (e.g. bradycardia, heart block, ventricular arrhythmia etc), corneal microdeposits, hypo- and hyperthyroidism, photosensitivity reactions, blue-grey skin discolouration, abnormal liver function, abnormal liver function tests, and lung fibrosis
65
CCBs
They work by slowing movement of calcium into the heart and blood vessel walls, which reduces heart rate, reduces left ventricular contraction, and reduces blood pressure It shouldn’t be used in people that are pregnant, are in cardiogenic shock, have severe bradycardia, or mod-sev HF SE: lightheadedness, hypotension, slower heart rate, drowsiness, flushing, ankle oedema, increased appetite, and gastro-oesophageal reflux disease (GORD
66
BB's
β1 receptors (heart & kidneys) → Blockade leads to: ↓ Heart rate (negative chronotropic effect) ↓ Contractility (negative inotropic effect) ↓ Renin release (less angiotensin II = less vasoconstriction & fluid retention) B2 receptors in lungs normally vasodilate so blocking these causes constriction
67
activation of alpha receptors in vasculature normally leads to what
vasoconstriction + muscle contraction blocking this causes vasodilation which is helpful in lowering BP beta receptors on the other hand when stimulated cause vasodilation and muscle relaxation
68
Selective (β1 only) – "Cardioselective" BB examples
Examples: Metoprolol, Atenolol, Bisoprolol, Esmolol Preferred in heart disease (less effect on lungs
69
Non-selective (β1 & β2)
Examples: Propranolol, Nadolol, Timolol
70
mixed beta and alpha blockers
Examples: Carvedilol, Labetalol Cause additional vasodilation (due to α1-blockade
71
CCB MOA
CCBs block L-type calcium channels, which are responsible for calcium entry into: Vascular smooth muscle (causing vasodilation) Cardiac muscle cells (reducing contractility and heart rate) Cardiac conduction system (SA & AV nodes) (slowing heart rate)
72
Dihydropyridines (DHPs) – "Vessel Selective"
Examples: Amlodipine, Nifedipine, Nicardipine, Felodipine Effect: Strong vasodilation, mild effect on heart rate Uses: Hypertension, Angina, Raynaud’s
73
Non-Dihydropyridines (Non-DHPs) – "Heart Selective"
Examples: Verapamil, Diltiazem Effect: Reduce heart rate, contractility, and BP Uses: Arrhythmias (Atrial fibrillation), Angina, Hypertension
74
6 causes of prominent R waves
1) LV pacing 2) RVH 3) RBBB 4) posterior MI 5) WPWS 6) dextrocardia 7) HOCM

Block 31 CardioResp (12 decks)

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