Cardiology

Question 1

what can influence automaticity?

Answer 1

1. Neurohormonal tone - para/sympathetic stimulation
   
   2. Abnormal metabolic conditions (hypoxia, acidosis, hypothermia)
   3. Electrolyte abnormalities
   4. Drugs
      Local ischaemia/infarction

Question 2

what are early afterdepolarisations?

Answer 2

Occur in the context of AP prolongation
Consequence of the membrane potential becoming more +ve during repolarisation (e.g. not returning to baseline)
Result in self maintaining depolarising oscillations of AP generating a tachyarrhythmia
Basis for degeneration of QT prolongation, either congenital or acquired into Torsades de Pointes

Question 3

what are delayed afterdepolarisations?

Answer 3

Occur after the AP has fully repolarised but before the next usual AP
Commonly occurs in situations of high intracellular calcium (e.g. digoxin intoxication, ischaemia) or during enhanced catecholamine stimulation e.g. twitchy pacemaker cells

Question 4

what are re-entry circuits?

Answer 4

Reentry, which occurs when a propagating impulse fails to die out after normal activation of the heart and persists to re-excite the heart after the refractory period has ended

Question 5

give examples of rhythms for which re-entrant circuits are responsible

Answer 5

atrial fibrillation
atrial flutter
atrial tachycardia
AVNRT (AV node re-entry tachycardia)
AVRT (atrio-ventricular re-entry tachycardia)
ventricular tachycardia

Question 6

causes of conduction block

Answer 6

ischaemia
fibrosis
trauma
drugs

Question 7

what is the most common cause of conduction block?

Answer 7

refractory myocardium

Question 8

name some bradyarrhythmias

Answer 8

sinus brady
SA block
sinus arrest
AV block
junctional rhythm
idioventricular rhythm

Question 9

name some tachyarrhythmias: regular with narrow QRS

Answer 9

SVTs:
sinus tachy
atrial tachy
junctional tachy
AVNRT
AVRT
atrial flutter

Question 10

name some tachyarrhythmias: regular with wide QRS

Answer 10

SVT with aberrancy/BBB
Vent tachy
AVRT

Question 11

name some tachyarrhythmias: irregular with narrow QRS

Answer 11

AF
A flutter with variable block
multifocal atrial tachy
premature atrial contraction

Question 12

name some tachyarrhythmias: irregular with wide QRS

Answer 12

AF with BBB
A flutter with BBB and variable block
polymorphic VT
premature ventricular contraction

Question 13

what may cause sinus brady?

Answer 13

increased vagal tone or vagal stimulation
drugs - bblockers, CCB
ischaemia/infarction

Question 14

major features of first degree heart block

Answer 14

PR >200ms

Question 15

major features of second degree heart block mobitz i

Answer 15

gradual prolongation of PR precedes the failure of conduction of a P wave

Question 16

causes of second degree HB I

Answer 16

increased vagal tone

RCA mediated ischaemia

Question 17

major features of second degree heart block mobitz II

Answer 17

PR constant

abrupt failure of conduction of a P wave

Question 18

where is block usually found in 2nd degree HB I?

Answer 18

in the AVN

Question 19

where is block usually found in 2nd degree HB II?

Answer 19

distal to AVN e.g. bundle of his

Question 20

major features of third degree heart block

Answer 20

no associtaiton between P waves and QRS

R-R intervals constant

Question 21

presentation of SVT and pre excitation syndromes

Answer 21

palpitaitons
dizziness
dyspnoea
chest discomfort
presyncope/syncope

Question 22

causes of sinus tacky

Answer 22

Occurs in normal subjects with increased sympathetic tone (e.g. exercise, emotions, pain), alcohol use, caffeinated beverages, drugs (e.g. b-adrenergic agonists, anticholinergic drugs etc)
Aetiology
Fever, hypotension, hypovolaemia, anaemia, thyrotoxicosis, CHF, MI, shock, PE etc

Question 23

features of premature atrial contraction

Answer 23

Ectopic supraventricular beat originating in the atria

P wave morphology of the PAC usually differs from that of a normal sinus beat

Question 24

features of junctional premature beat

Answer 24

Ectopic supraventricular beat that originates in the vicinity of the AVN
P wave is usually not seen or an inverted P wave is seen and may be before or closely follow the QRS

Question 25

features of atrial flutter

Answer 25

Saw tooth in inferior leads (II, III, aVF), narrow QRS, commonly seen as a 2:1 block with 150bpm

Question 26

causes of atrial flutter

Answer 26

CAD, thyrotoxicosis, mitral valve disease, cardiac surgery, COPD, PE, pericarditis

Question 27

what is multifocal atrial tachy?

Answer 27

Irregular rhythm caused by presence of 3 or more atrial foci (may mimic aFib) Atrial rate 100-200 bpm - 3 or more distinct P wave morphologies and PR intervals vary, some P waves may not be conduced

Question 28

treatment of multifocal atrial tachy

Answer 28

Underlying cause, CCB may be used B-blockers may be contraindicated because of severe pulmonary disease No role for electrical cardioversion, antiarrhythmics or ablation

Question 29

describe the classification of AF

Answer 29

Lone Occurs in people < 60 yr and in whom no clinical or echo causes are found Nonvalvular Not caused by valvular disease, prosthetic heart valves or valve repair Paroxysmal Episodes that terminate spontaneously Persistent Afib sustained for >7days or that terminates only with cardioversion Permanent/chronic Continuous that is unresponsive to cardioversion or in which clinical judgment has led to a decision not to pursue cardioversion Recurrent >=2 episodes Secondary Caused by a separate underlying condition or event (MI, cardiac surgery, pulmonary disease, hyperthyroidism)

Question 30

describe the initiation of AF

Answer 30

Single circuit re-entry and/or ectopic foci act as aberrant generators producing atrial tachycardia (350-600bpm) Impulses conduct irregularly across the atrial myocardium to give rise to fibrillation In some cases, ectopic foci have also been mapped to the pulmonary vein ostia and can be ablated

Question 31

how does AF become maintained?

Answer 31

Tachycardia causes atrial structural and electrophysiological remodelling that causes further Afib

Question 32

consequences of AF

Answer 32

AV node irregularly filters incoming atrial impulses producing an irregular ventricular response of <200 bpm and the tachycardia leads to suboptimal CO Fibullatory conduction of the atria promotes blood stasis increasing risk of thrombus formation

Question 33

ECG findings in AF

Answer 33

No organised P waves due to rapid atrial activity causing a choatic baseline Irregularly irregular ventricular response (typically 100-180), narrow QRS Wide QRS may occur following a long-short cycle sequence Loss of atrial contraction thus no a wave on JVP

Question 34

management of AF

Answer 34

Major Objectives (RACE) all patients with Afib should be stratified using a predictive index for stroke risk and risk of bleeding, and most should receive anticoagulation 1. Rate Control a. B-blocker, verapamil (HF: digoxin, amiodarone) 2. Anticoagulation a. Warfarin or DOAC 3. Cardioversion (electrical) 4. Etiology a. HTN, CAD, valvular disease, pericarditis, cardiomyopathy, myocarditis, ASD, post-operative, PE, COPD, thyrotoxicosis, sick sinus syndrome, alcohol (holiday heart)

Question 35

features of AVNRT

Answer 35

Re-entrant circuit using dual pathways (fast B-fibres and slow a-fibres) within or near the AVN, often found in the absence of structural heart disease – cause often idiopathic, although familial possible Sudden onset and offset Fast, regular rhythm – 10-250bpm Usually initiated by a supraventricular or ventricular premature beat 60-70% of all paroxysmal SVTs Retrograde P waves may be seen but are usually lost in the QRS

Question 36

describe WPW

Answer 36

Congenital defect Accessory conduction tract (bundle of Kent, can be L or R atrium), abnormally allows early electrical activation of part of one ventricle Impulses travel at a greater conduction velocity across the Bundle of Kent thereby bypassing the AVN Ventricles are activated earlier therefore ECG shows early ventricular depolarisation in the form of initial slurring of QRS (delta wave) Atrial impulses that conduct to the ventricles through both the Bundle of Kent and the normal AVN/His-Purkinje system generate a broad fusion complex

Question 37

ECG Features in WPW

Answer 37

``` PR interval <120ms Delta wave Wide QRS Secondary ST segment and T wave changes Tachyarrhythmias may occur – most often AVRT and Afib ```

Question 38

discuss AFib in WPW

Answer 38

Intermittent rather than persistent Rapid atrial depolarisations in Afib are conducted through the bypass tract which is not able to filter impulses like the AVN Therefore ventricular rate becomes extremely rapid >200bpm and QRS widens

Question 39

treatment of AF in WPW

Answer 39

DC cardioversion IV procainamide or IV amiodarone Do not use drugs that slow AVN conduction (digoxin, b-blockers) as this may cause preferential conduction through the bypass tract and precipitate VF Long term – ablation of bypass tract if possible

Question 40

what is AVRT

Answer 40

Re-entrant loop via accessory pathway and normal conduction system Initiated by a premature atrial or ventricular comple

Question 41

describe orthodromic AVRT

Answer 41

Stimulus from a premature complex travels up the bypass tract (ventricles to atria) and down the AVN with narrow QRS (no delta wave because travels through normal tract) Comprises 95% of re-entrant tachycardia associated with WPW

Question 42

describe antidromic AVRT

Answer 42

More rarely the stimulus goes up the AVN and down the bypass tract, wide abnormal QRS as ventricular activation is only via bypass

Question 43

treatment of AVRT

Answer 43

``` Acute Similar to AVNRT except avoid long acting AVN blockers (digoxin and verapamil) Long term ablation Drugs Flecainide and procainamide ```

Question 44

describe premature ventricular contractions

Answer 44

QRS > 120ms, no preceding P wave, bizarre QRS morphology Origin: LBBB morphology of VT = RV origin, RBBB morphology of VT = LV origin PVCs may be benign; however significant if: Consecutive (3 or more = VT) or multiform (Varied origin) PVC falling on the t wave of the previous beat may precipitated ventricular tachycardia or VF

Question 45

describe accelerated idioventricular rhythm

Answer 45

Ectopic ventricular rhythm with rate 50-100bpm More frequently occurs in the presence of sinus brady and easily overdriven by a faster supraventricular rhythm Frequently occurs in patients with acute MI or other types of HD (cardiomyopathy, hypertensive, valvular) but does not affect prognosis and does not usually require treatment

Question 46

ECG features of VT

Answer 46

3 or more consecutive ectopic ventricular complexes Rate > 100bpm (140-200) Ventricular flutter if rate >200 and complexes resemble a sinusoidal pattern Sustained VT if it lasts longer than 30s ECG Wide regular QRS (usually >140ms) AV dissociation, bizarre QRS Left or right axis deviation, nonspecific intraventricular block pattern, monophasic or biphasic QRS in V1 with RBBB, QRS concordance in V1-6 Occasionally, during VT supraventricular impulses may be conducted to the ventricles generating QRS complexes with normal or aberrant supraventricular morphology (Ventricular capture) or summation pattern (fusion complexes)

Question 47

monomorphic VT

Answer 47

Identical complexes with uniform morphology More common than polymorphic VT Typically result from intraventricular re-entry circuit

Question 48

causes of monomorphic VT

Answer 48

Chronic infarct scarring, acute MI/ischaemia, cardiomyopathies, myocarditis, arrhythmogenic right ventricular dysplasia, idiopathic, drugs (cocaine), electrolyte disturbances

Question 49

polymorphic VT

Answer 49

Complexes with constantly changing morphology, amplitude and polarity More frequently associated with haemodynamic instability due to faster rates (typically 200-250) vs monomorphic

Question 50

causes of polymorphic VT

Answer 50

Acute MI, severe or silent ischaemia and predisposing factors for QT prolongation

Question 51

treatment of VT

Answer 51

Electrical cardioversion lidocaine amiodarone Type Ia agents (procainamide, quinidine)