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Year 4 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

what can influence automaticity?

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

what are early afterdepolarisations?

A

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

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3
Q

what are delayed afterdepolarisations?

A

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

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4
Q

what are re-entry circuits?

A

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

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5
Q

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

A 
atrial fibrillation
atrial flutter
atrial tachycardia
AVNRT (AV node re-entry tachycardia)
AVRT (atrio-ventricular re-entry tachycardia)
ventricular tachycardia
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6
Q

causes of conduction block

A

ischaemia
fibrosis
trauma
drugs

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7
Q

what is the most common cause of conduction block?

A

refractory myocardium

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8
Q

name some bradyarrhythmias

A 
sinus brady
SA block
sinus arrest
AV block
junctional rhythm
idioventricular rhythm
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9
Q

name some tachyarrhythmias: regular with narrow QRS

A 
SVTs:
sinus tachy
atrial tachy
junctional tachy
AVNRT
AVRT
atrial flutter
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10
Q

name some tachyarrhythmias: regular with wide QRS

A

SVT with aberrancy/BBB
Vent tachy
AVRT

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11
Q

name some tachyarrhythmias: irregular with narrow QRS

A

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

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12
Q

name some tachyarrhythmias: irregular with wide QRS

A

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

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13
Q

what may cause sinus brady?

A

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

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14
Q

major features of first degree heart block

A

PR >200ms

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15
Q

major features of second degree heart block mobitz i

A

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

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16
Q

causes of second degree HB I

A

increased vagal tone

RCA mediated ischaemia

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17
Q

major features of second degree heart block mobitz II

A

PR constant

abrupt failure of conduction of a P wave

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18
Q

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

A

in the AVN

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19
Q

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

A

distal to AVN e.g. bundle of his

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20
Q

major features of third degree heart block

A

no associtaiton between P waves and QRS

R-R intervals constant

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21
Q

presentation of SVT and pre excitation syndromes

A 
palpitaitons
dizziness
dyspnoea
chest discomfort
presyncope/syncope
22
Q

causes of sinus tacky

A

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

23
Q

features of premature atrial contraction

A

Ectopic supraventricular beat originating in the atria

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

24
Q

features of junctional premature beat

A

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

25
Q

features of atrial flutter

A

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

26
Q

causes of atrial flutter

A

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

27
Q

what is multifocal atrial tachy?

A

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

28
Q

treatment of multifocal atrial tachy

A

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

29
Q

describe the classification of AF

A

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)

30
Q

describe the initiation of AF

A

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

31
Q

how does AF become maintained?

A

Tachycardia causes atrial structural and electrophysiological remodelling that causes further Afib

32
Q

consequences of AF

A

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

33
Q

ECG findings in AF

A

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

34
Q

management of AF

A

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)
35
Q

features of AVNRT

A

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

36
Q

describe WPW

A

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

37
Q

ECG Features in WPW

A 
PR interval <120ms
	Delta wave
	Wide QRS
	Secondary ST segment and T wave changes
Tachyarrhythmias may occur – most often AVRT and Afib
38
Q

discuss AFib in WPW

A

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

39
Q

treatment of AF in WPW

A

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

40
Q

what is AVRT

A

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

41
Q

describe orthodromic AVRT

A

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

42
Q

describe antidromic AVRT

A

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

43
Q

treatment of AVRT

A 
Acute 
		Similar to AVNRT except avoid long acting AVN blockers (digoxin and verapamil)
	Long term
		ablation
	Drugs 
Flecainide and procainamide
44
Q

describe premature ventricular contractions

A

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

45
Q

describe accelerated idioventricular rhythm

A

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

46
Q

ECG features of VT

A

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)

47
Q

monomorphic VT

A

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

48
Q

causes of monomorphic VT

A

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

49
Q

polymorphic VT

A

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

50
Q

causes of polymorphic VT

A

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

51
Q

treatment of VT

A

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

Year 4 (5 decks)

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