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CardioResp Block > ECG and Arrhythmias > Flashcards

ECG and Arrhythmias Flashcards

1
Q

when might minor R and L axis deviation be considered normal?

A

R in tall and thin people

L in short and fat people

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2
Q

normal cardiac axis?

A

from -30 to + 90 degrees

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3
Q

causes of R axis deviation?

A

RV hypertrophy, PE

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4
Q

causes of L axis deviation?

A

conduction defect

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5
Q

normal time of PR interval?

A

120-200 ms (3-5 small squares)

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6
Q

causes of prolonged PR interval?

A

1st degree heart block-CAD, digoxin toxicity, acute rheumatic carditis, electrolyte disturbances e.g. hyperkalaemia.

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7
Q

define 2nd degree heart block

A

intermittent failed spread of depolarisation through the AVN or bundle of His.

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8
Q

name given to type of 2nd degree heart block in which the PR interval progressively lengthens before failure of conduction of an atrial beat, and then a shorter PR interval than the preceding conducted beat?

A

Mobitz type 1 (Wenckeback phenomenon)

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9
Q

name given to type of 2nd degree heart block in which PR interval relatively constant but occasionally atrial depolarisation without subsequent ventricular depolarisation?

A

Mobitz type 2

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10
Q

name given to type of 2nd degree heart block in which there are alternate conducted and nonconducted atrial beats, producing 2 P waves for every QRS complex?

A

2:1 conduction

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11
Q

appearance of 3rd degree heart block on an ECG?

A

P wave rate regular as atrial contraction normal, but no consistency in PR interval
no relationship between P waves and QRS complexes
QRS complexes abnormally shaped due to abnormal spread of depolarisation from a ventricular focus.

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12
Q

causes of complete heart block (3rd degree)?

A 
MI, usually transient
IHD
chronic e.g. fibrosis around bundle of His, or block of both bundle branches.
aortic valve calcification
congenital
cardiac surgery/trauma
digoxin toxicity
infiltration- abscesses, granulomas, tumours, parasites
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13
Q

how can bundle branch block with a sinus rhythm be distinguished from rhythms beginning in the ventricles?

A

BBB with a sinus rhythm- PR interval constant and normal P waves but this doesn’t happen if rhythm begins in the ventricles.

however, both would show widened QRS complexes= longer time taken for depolarisation to spread through the ventricles.

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14
Q

is RBBB always pathological?

A

no, often indicates R heart problems but can be found in healthy people with a normal QRS complex duration.

LBBB always an indication of heart disease, usually of LV.

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15
Q

why does a second R wave (R1) follow the S wave in V1 in RBBB?

A

the RV depolarises after the LV, and so the depolarisation towards V1 now causes an upward deflection following the downward deflection that occurred due to LV depolarisation away from the lead.

this results in a wide and deep S wave following the R wave in V6, and so a wide QRS complex.

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16
Q

what is partial RBBB?

A

RSR1 pattern in V1 with a QRS complex of normal width

this is a normal variant

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17
Q

explain the appearance of LBBB in V6?

A

septum cannot be depolarised normally from L to R, so instead depolarises from R to L, producing an upward deflection in V6 as depolarisation moves towards the lead (R wave).
RV then depolarises before L and is of a small muscle mass, so produces a small S wave in V6.
LV then depolarises producing a 2nd R wave in V6.

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18
Q

T wave changes LBBB is assoc. with?

A

T wave inversion in lateral leads (I, VL and V5-V6), though not necessarily in all of these.

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19
Q

why does the axis usually remain normal with RBBB?

A

normal depolarisation of LV with its large muscle mass.

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20
Q

when is 2nd degree HB often seen?

A

acute MI

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21
Q

tment consideration in 3rd degree HB?

A

always indicates conducting tissue disease

consider temporary or permanent pacemaker

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22
Q

what can cause RBBB?

A

atrial septal defect

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23
Q

what can cause LBBB?

A

aortic stenosis

ischaemic disease e.g. acute MI

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24
Q

define sinus rhythm

A

depolarisation of the heart has begun in the SA node

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25
Q

why are patients normally in sinus rhythm?

A

SAN has the highest frequency of electrical discharge and the rate of contraction of the ventricles will be controlled by the part of the heart which is depolarising most frequently.

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26
Q

associations and causes of a sinus bradycardia?

A 
athletic training
fainting attacks e.g. vasovagal
hypothermia
myxoedema, hypothyroidism
often seen immediately after an acute MI, espec. inferior
drugs- beta blockers, digoxin, amiodarone, verapamil
raised IC pressure
cholestasis
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27
Q

associations of a sinus tachycardia?

A 
exercise
thyrotoxicosis
fear
pain
haemorrhage
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28
Q

define an arrhythmia

A

disturbance of the generation or conduction of the electrical impulses of the heart responsible for atrial and ventricular contraction

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29
Q

how do supraventricular and ventricular rhythms differ in their ECG appearances?

A

supraventricular-depolarisation has begun in either the atrial muscle or the region around the AVN (junctional/nodal), and then spreads to the ventricles in normal way via bundle of His and its branches, so QRS complex normal (narrow) EXCEPT in presence of R or LBBB, or WPW syndrome.

ventricular-depolarisation spreads abnormally through ventricles via the Purkinje fibres, producing a wide QRS complex.

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30
Q

what should the HR exceed for ventricular tachycardia to be diagnosed?

A

120 beats/min

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31
Q

define escape rhythms

A

slow and protective rhythms generated in the heart from a site other than the SAN when secondary sites for initiating depolarisation escape from their normal inhibition by the more active SAN.

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32
Q

what is the difference between an extrasystole and an escape beat?

A

an extrasystole comes early- a part of the heart has depolarised earlier than it should, and an escape beat comes late-secondary site for depolarisation has been released from its inhibition so is controlling depolarisation which occurs later than it should as the site’s depolarising frequency is less than that of the SAN.

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33
Q

why are ventricular extrasystoles potentially dangerous?

A

can occur early in the T wave of the preceding beat and induce VF- ventricles do not have sufficient time to relax normally and fill with blood before the next systole so cardiac output plummets.

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34
Q

cause of an early QRS complex following an early P wave?

A

atrial extrasystole

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35
Q

why might a P wave appear after the QRS complex?

A

this can happen with a junctional extrasystole-depolarisation has originated in the abnormal location of around the AVN, and caused excitation to be conducted both to the atria and the ventricles.

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36
Q

difference in T wave appearance in supraventricular and ventricular beats?

A

ventricular- T wave inverted

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37
Q

why does the next P wave appear at the predicted time with a ventricular extrasystole in contrast to with a supraventricular extrasystole?

A

a ventricular extrasystole doesn’t affect the SAN

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38
Q

name given to a tachycardia which occurs intermittently?

A

paroxysmal

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39
Q

when is atrial flutter present?

A

when atrial rate is greater than 250/min and there is no flat baseline between the P waves.

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40
Q

in atrial flutter with 2:1 block, how can the extra P waves be distinguished from T waves?

A

due to their regularity

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41
Q

when might an ECG be described as having a ‘sawtooth’ appearance?

A

when very high rate of P waves as seen in atrial flutter

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42
Q

how can carotid sinus pressure be useful in some tachycardias?

A

can have a therapeutic effect on supraventricular tachycardias as activates the baroreceptor reflex that leads to vagal stimulation of the SA and AVNs, which will increase delay of conduction in the AVN.

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43
Q

2 possible causes of a tachycardia with broad QRS complexes?

A

ventricular tachycardia

supraventricular tachycardia with BBB

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44
Q

what is ‘fibrillation’?

A

when individual muscle fibres contract independently

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45
Q

will the QRS complex be normal in shape in AF and why?

A

yes
as despite the irregularity of the depolarisation waves passing into the bundle of His and to the ventricles, conduction of these both into and through the ventricles is by the normal route.

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46
Q

atrial rate in atrial flutter?

A

more than 250/min

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47
Q

atrial flutter is described as what type of tachycardia?

A

supraventricular

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48
Q

tment of choice in atrial flutter?

A

catheter ablation- eliminate conduction via the re-entry loop

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49
Q

what is cardioversion?

A

‘shocking’ the heart
may be done for newly diagnosed atrial flutter- helps to put heart back into sinus rhythm
DC cardioversion= direct current

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50
Q

what is wolff-parkinson-white (WPW) sydrome?

A

presence of an extra or ‘accessory’ conducting bundle, usually on the L side of the heart, forming a direct connection between the atrium and ventricle, without an AV node to delay conduction.
therefore, a depolarisation wave reaches the ventricle early-pre-excitation. PR interval short and QRS complex has an early slurred upstroke= delta wave, but 2nd part is normal as conduction through His bundle catches up.

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51
Q

how can WPW syndrome cause a paroxysmal tachycardia?

A

depolarisation spreading down the His bundle can spread back up the accessory pathway and so reactivate the atrium, setting up a re-entry circuit that allows a sustained tachycardia to occur.

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52
Q

where does adenosine particularly act in the heart?

A

AV node

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53
Q

define tachycardia

A

heart rate more than 100bpm

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54
Q

define bradycardia

A

heart rate less than 60bpm

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55
Q

causes of a sinus tachycardia

A 
exercise
anxiety
PE
sepsis
HF
thyrotoxicosis
CO2 retention
anaemia
pain
raised temp.
pregnancy
phaeochromocytoma
sympathomimetics e.g. caffeine, adrenaline, nicotine

ECG: normal P waves followed by normal QRS, HR more than 100bpm.

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56
Q

causes of SAN block?

A

IHD-RCA- supplies blood to the SAN via SAN branch (in 60% of population?)
infiltrative disease: amyloidosis
sarcoidosis
haemochromatosis

lyme disease

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57
Q

what structural heart disease may be identified on ECHO to help explain origin of an arrhythmia?

A

mitral stenosis

hypertrophic cardiomyopathy

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58
Q

SVT precipitating factors?

A 
IHD
smoking
alcohol
caffeine
thyrotoxicosis
infection?
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59
Q

why do P waves eventually disappear on ECG as hyperkalaemia worsens?

A

atria more sensitive than ventricles to high K+ as as levels increase, atria unable to depolarise.

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60
Q

distinguish between electrical cardioversion and defibrillation

A

electrical cardioversion= used when pt has a pulse but is unstable, or chemical cardioversion has failed or is unlikely to be successful, aiming to convert arrhythmia back to sinus rhythm.
defibrillation= tment of immediately life-threatening arrhythmias with which pt has no pulse e.g. VF or pulseless VT.

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61
Q

why might an occlusion to part of the RCA lead to 2nd degree HB on an ECG?

A

In most people, the RCA gives rise to the AV nodal branch that supplies blood to the AVN so an RCA occlusion can cause ischaemia of the AVN which can cause 2nd degree HB- atrial depolarisation not always transmitted through the AVN to allow for ventricular depolarisation.q

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62
Q

blood supply to inferior heart?

A

RCA

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63
Q

blood supply to lateral heart?

A

circumflex from LCA

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64
Q

what might an ECG revealing deep, symmetric T wave inversions and QT interval prolongation indicate?

A

acute CNS abnormality e.g. SA haemorrhage, intracranial haemorrhage and less commonly severe ischaemic strokes.

also less commonly, carotid end arterectomy can lead to this picture chronically.

65
Q

indications for implantable cardioverter defibrillators (ICDs)?

A

People with previous serious ventricular arrhythmia, so those who, without a treatable cause:
have survived cardiac arrest caused by VT or VF OR
have spontaneous sustained VT (more than 30s) causing syncope or severe haemodynamic compromise OR
have sustained VT without syncope or cardiac arrest, and also have an reduction in LVEF of 35% or less but symptoms no worse than class III in NYHA HF classification.

also those with a familial cardiac condition with a high risk of sudden death e.g. Brugada syndrome, hypertrophic cardiomyopathy, long QT syndrome or arrhythmogenic RV dysplasia OR
have undergone surgical repair of congenital heart disease.

66
Q

recommendations for treating people with CRS-D?

A 
ICDs, CRT (biventricular device- a lead in LV aswell as RV) with defibrillator (CRT-D) or CRT with pacing (CRT-P) recommended as tment options for HF pts with LV dysfunction with LVEF of 35% or less.
if NYHA functional class of IV, only CRT-P recommended and this is for those QRS is prolonged.
for all other classes, ICD ( 1 or 2 leads-always 1 in RV, maybe 1 in RA) recommended if QRS normal and there is risk of sudden cardiac death, if QRS 120-149ms and no LBBB, or NYHA I, prev. QRS and LBBB.
CRT-D considered if NYHA I-III, QRS 150ms or more with or without LBBB, and if NYHA II or III, and QRS 120-149ms with LBBB.
67
Q

most common cause of death in those with mild to moderate HF?

A

sudden cardiac death

68
Q

describe the components of a CRT-P?

A

also known as biventricular pacing
pulse generator in upper chest with 3 leads, to RA and both ventricles, and device resynchronises contraction of the ventricles to improve heart’s pumping efficiency.

69
Q

describe the use of reveal devices (implantable loop recorders ILD/cardiac monitor)

A

SC, single lead ECG monitoring device
used for diagnosis in those with recurrent unexplained episodes of syncope or palpitations
used for monitoring in those at risk of AF or with documented AF
and risk stratification in those who have had an MI and have certain genetic disorders.

70
Q

what does catheter ablation involve?

A

use of an energy source e.g. high frequency radiowaves that generate heat, being transmitted through a catheter inserted into the heart via the venous system to destroy the tissue responsible for abnormal electrical circuits.

71
Q

ECG changes of hypokalaemia?

A

prominent U waves
T wave flattening and inversion
ST depression
prolonged PR interval

72
Q

causes of 1st and 2nd degree HB?

A 
normal
athletes
sick sinus syndrome*
IHD
acute carditis
drugs- digoxin, beta blockers
73
Q

digoxin effect on ECG?

A

ST depression (downward sloping, reversed tick) in V5, V6
1st and 2nd degree HB
toxicity-3rd degree HB, ventricular ectopics

74
Q

how can Ca2+ affect the ECG?

A

high- short QT interval

low- long QT interval, small T waves

75
Q

how long before we know if catheter ablation of arrhythmia has been successful?

A

within 3 mnths, so F/U pt at 3 mnths

if arrhythmia comes back, likely to be very soon post op, and at least within 3 mnths.

76
Q

ECG of sinus arrhythmia and causes?

A

irregularly irregular sinus rhythm- all QRS complexes preceded by P waves, rest of ECG normal. normal sinus P waves, with constant morphology, and constant PR interval.

=normal physiological entity, commonly seen in young healthy people, heart rate varies due to reflex changes in vagal tone occurring during different phases of the respiratory cycle. inspiration increases the HR due to decrease in vagal tone. with expiration, vagal tone is restored. incidence reduces with age as reduction in carotid distensibility and baroreceptor reflex sensitivity.

irregular ventricular rate in sinus rhythm may also be result of frequent premature atrial contractions, type 1 SA exit block and wenckebach phenomenon.

77
Q

most common cause of a short RP tachycardia?*

A

AV nodal reentry tachycardia (AVNRT)

78
Q

EP mechanism behind AVNRT? **

A

AVNRT is due to a congenital abnormality within the AV node that allows for a re-entrant tachycardia. In those susceptible to AVNRT, two conduction pathways exist within the AV node. One pathway conducts fast and has a long refractory period while the second pathway conducts slowly and has a short refractory period. When an ectopic beat occurs (a premature atrial contraction or premature ventricular contraction), a re-entrant loop can be triggered resulting in this narrow-complex tachyarrhythmia.

79
Q

tment of AVNRT?

A

In most cases, AVNRT will spontaneously terminate with no intervention. Simply reducing the amount of sympathetic nervous system stimulation by having the patient relax or by giving sedation may be effective. The re-entrant pathway can be interrupted by blocking the AV node enough to restore sinus rhythm. Enhancing vagal tone by specific maneuvers (Valsalva, carotid massage, ice on face) can cause a physiologic AV blocking affect and terminate the tachycardia. Any of the AV blocking medications may also work (remember the mneumonic “ABCD” for AV blocking agents: Adenosine, Beta-blockers, Calcium channel blockers, Digoxin). Usually adenosine is used in the emergency room due to its short half-life. Very rarely is electrical cardioversion needed. If the severity and frequency of attacks decrease the patient’s quality of life, catheter ablation can be performed to eliminate one of the dual pathways and is more than 90% effective in preventing future episodes of AVNRT.

80
Q

electrolyte disturbances which potentiate digoxin toxicity?

A

hypokalaemia

hypercalcaemia

81
Q

pathogneumonic arrhythmia of digoxin toxicity?

A

bidirectional VT

82
Q

causes of a broad QRS complex?

A

BBB
VT
ventricular ectopics

83
Q

ECG leads for the anterior heart?

A

V1-V4

84
Q

ECG indications ACUTE MI?

A

reciprocal changes in other leads*

85
Q

differentials for a broad complex tachycardia, with a regular rhythm?

A

VT- always treat as VT until proven otherwise!- possibly beta blocker, can give IV lignocaine with or without amiodarone, then consider DCCV.
SVT with aberrancy
SVT with BBB
WPW antidromic- conduction is down the pathway and back up through the AVN, delta waves present, in contrast to orthodromic WPW- conduction is down the AVN and back up the accessory pathway (superconductor pathway)- this produces a narrow complex.

86
Q

why must we NOT give adenosine to pts with pre-excited AF?

A

giving adenosine will block the AVN, so all conduction from the atria will be shifted down the superconducter pathway, so the ventricle will be receiving impulses from the atria at a really fast rate which increases the risk of going into VF.

87
Q

in which pts must we NOT give adenosine?

A 
brittle asthma (asthma characterised by recurrent, severe attacks, types 1 and 2) as causes bronchoconstriction
also wouldn't give if on rate-limiting drugs, or HB
and don't give if pre-excited AF- broad complex irregular tachyarrhythmia, as can cause VF.
88
Q

in which pts must we NOT give IV fleicanide?

A

CAD

structural cardiomyopathy/heart disease

89
Q

a 44 yr old female with paroxysmal AF and a history of HTN is being considered for anticoag tment. what score is used to assess her risk and should tment therefore be initiated?

A

CHADSVASC score: CHF, HTN, age 75 or older- 2 points, or aged between 65 and 74 then 1 point, DM, previous TIA or stroke or TE- scores 2, vasc disease- PVD, MI, aortic plaque, female sex.
so she scores 1 for female and 1 for HTN history
2 or more highlights need for anticoag, so she would need this e.g warfarin, rivaroxaban or apixaban.

90
Q

how are we able to define from and ECG if an MI is acute?

A

by presence of reciprocal changes

91
Q

why is it important to consider a recent history of diarrhoea in pt presenting with palpitations?

A

arrhythmia may be result of electrolyte disturbance, with loss of K+ in diarrhoea

92
Q

an ICD is recommended as a consideration for which pts?

A 
those with a LVEF of less than 35% and QRS interval less than 120ms with high risk of sudden cardiac death
or QRS 120-149ms and NYHA class I-III HF
or QRS 120-149ms with LBBB and NYHA class I
93
Q

VT causes?

A

previous MI- VT occurs around scar tissue*
hypertrophic cardiomyopathy/dilated cardiomyopathy
congenital heart defect
myocarditis
brugada syndrome- Na+ channelopathy, produces ST elevation and RSR complex in V1 and +ve QRS in V1.
cocaine
diet pills

94
Q

VT treatment?**

A

A to E approach
IV lignocaine and amiodarone

long term: bisoprolol with amiodarone
RISK STRATIFY FOR ICD- EF less than 35% and QRS more than 120ms in presence of ischaemic or dilated cardiomyopathy.

can ablate if fail medical therapy.

95
Q

ECG features that increase likelihood of VT?

A 
fusion beats
capture beats
AV dissociation
atypical RBBB or LBBB pattern
very broad QRS complexes (140ms or more)
positive or negative concordance throughout chest leads
96
Q

AF causes?

A 
IHD
HTN
HF
mitral valve stenosis
hyperthyroidism
obesity
myocarditis
PE
acute infections e.g. pneumonia, espec. in elderly
post-op
alcohol
97
Q

which pts may benefit from use of NOACs in anticoag tment of AF due to difficulty in maintaining appropraite INR/managing dosing?

A

elderly
malignancy- assoc. with fluctuating INR
frequent travel- can’t keep INR checks

98
Q

why must amiodarone IV be given into a large central vein?

A

due to risk of thrombophlebitis

99
Q

most common site of thrombus formation in pts with AF that increases their risk of stroke?

A

L atrial appendage

100
Q

what is wellen’s phenomenon? (LAD coronary T wave syndrome)

A

biphasic T waves in V1-V3 or symmetrical T wave inversion in all precordial chest leads, and indicates severe proximal LAD stenosis- acute or chronic.

Px ma sound similar to unstable angina. features may include intermittent chest pain on exertion leading up to admission, pain like a heaviness, relieved with rest, gradual onset, less than 30mins duration?

101
Q

what does a short PR interval and delta waves on an ECG indicate?

A

Wolff-Parkinson-White (WPW) syndrome

102
Q

which drugs should be avoided in pts with WPW syndrome?

A 
AV nodal blocking agents: ABCD=
adenosine
beta blockers
Ca2+ channel blockers
digoxin
103
Q

ECG identification of Brugada syndrome?

A 
RBBB with coved ST elevation in V1-V3
this can be provoked by giving a class 1 antiarrhythmic e.g. IV fleicanide
104
Q

what is Brugada syndrome?

A

an inherited Na+ channelopathy that accounts for part of a group of pts with idiopathic VF who have no evidence of causative structural cardiac disease, and is more common in young male adults and in SE Asia.

can present with sudden death in sleep, resuscitated cardiac arrest and syncope, or may be asymptomatic and diagnosed incidentally or during familial assessment.

105
Q

only successful tment in Brugada syndrome?

A

ICD

106
Q

causes of long QT syndrome?

A

congenital= Romano-Ward (autosomal dominant) and Jervell-Lange-Nielsen- may be assoc. with congenital deafness (autosomal recessive)
acquired=
electrolyte abnormalities: hypokalaemia, hypomagnesaemia, hypocalcaemia
drugs: amiodarone, sotalol, amitriptyline, quinidine, chlorpromazine, erythomycin, ciprofloxacin, methadone.
poisons: organophosphate

also bradycardia, mitral valve prolapse, acute MI, DM, CNS diseases e.g. dystrophia myotonica.

107
Q

clinical features of long QT syndrome?

A

syncope and palpitations- as a result of polymorphic VT or torsades, usually terminate spontaneously
may degenerate to VF- resulting in sudden death.

QTc usually more than 500ms.

108
Q

describe appearance of torsades de pointes on ECG?

A

rapid irregular sharp complexes that continuously change from an upright to an inverted position.

109
Q

acute management of acquired long QT?

A 
stop causative drugs
correct electrolyte disturbances
maintain HR with atrial or ventricular pacing
Mg sulphate
IV isoprenaline
110
Q

LT tment of congenital long QT syndrome?

A

beta-blockage
pacemaker therapy
occasionally L cardiac sympathetic denervation

ICD therapy if remain symptomatic, have marked prolongation or strong FH of sudden death.

111
Q

tment of normal heart VT?

A

monomorphic VT in those with structurally normal hearts is usually benign, and arises from a focus in RV outflow tract or in LV septum.
symptom tment usually with beta blockers.
some very sensitive to verapamil.
catheter ablation very effective in symptomatic pts.

112
Q

when might catheter ablation be very effective in ventricular premature beats?

A

if origin is a single focus, espec in RV

if highly symptomatic, beta-blockers may be helpful.

113
Q

why is there a pause before the next sinus beat after a ventricular extrasystole?

A

the ventricle or AVN is refractory to the next sinus impulse

114
Q

when are ventricular premature beats dangerous?

A

if occur simultaenously with upstroke of peak of preceeding T wave (early R on T), as can induce VF in pts with heart disease, part. in those following MI.

115
Q

when does pulsus bigeminus occur?

A

when premature ventricular beats occur regularly after every normal beat.

116
Q

AF treatment?**

A

A to E approach
acute management- e.g. address any features of the unwell pt/life-threatening features
rate and rhythm control- rate with beta blocker e.g. bisoprolol, rhythm- IV fleicanide (NOT if CAD or structural HD) 2mg/kg over 10mins, to a max of 150mg or IV =tment of choice
amiodarone 300mg- must be into large central vein due to thrombophlebitis risk.
if complications were to arise from this medical management e.g. BP drop, then electrically cardiovert pt (DCCV).
if pres. within 48hrs of symptom onset, and not anticoag already, start LMWH.
LT: beta blocker-1st line for rate control, consider amiodarone if LV impairment or HF for rhythm control.
ANTICOAG- due to risk of stoke with LA appendage clot formation. decision made on basis of CHADSVASC score- 2 or more, or male and 1 RF then consider. Must also consider bleeding risk- HAS-BLED, and see if can make alterations to reduce risk e.g. give PPI if gastric bleed.
LA catheter ablation or surgical ablation if failed medical therapy. In permanent AF (usually more than 1yr) consider pacing and AV node ablation if symptomatic or LV dysfunction thought to be due to high LV rates.

117
Q

what is the HAS-BLED score?

A

score for major bleeding risk in pts with AF on anticoag tment
HTN-uncontrolled, more than 160mmHg systolic
age over 65
stroke history
prior major bleeding or predisposition to bleeding
liver disease
renal disease
drugs- antiplatelets, NSAIDs
labile INR
alcohol/drug usage history

1 point for each
score more than 3 indicates pts at higher risk

118
Q

why are NOACs preferred to warfarin?

A

less risk of intracranial haemorrhage
no INR monitroing
more predictablr half life and elimination
fewer food and drink interactions e.g. should avoid grapefruit juice if on warfarin as CYP450 inhibitor, so would reduce warfarin met., making risk of bleeding with warfarin more likely.

119
Q

site of AF origin most commonly?

A

around pulmonary veins in LA, so can ablate pulm vein muscular parts.

120
Q

when might we use NOACs instead of warfarin in tment of AF?

A

when managing dosing is difficult to achieve desired INR e.g. travel, malignancy, elderly
if pt due for cardioversion as don’t have to stop 3 wks prior to cardioversion- may stop less than 1 wk before cardioversion
non-valvular AF-do ECHO
high risk pts
warfarin CI or significant ADRs

121
Q

adenosine t1/2 and time taken to act?**

A

t1/2= 5 to 10s, but slight delay before onset of action as must travel through venous system to R side of heart, into L side and then into the CAs to travel through the AV nodal artery to reach the AVN.
takes around 20s to act.

122
Q

acute management of AVNRT?

A

reassure the pt
vagal manourvres= carotid sinus massage, valsalva, ice bucket
IV adenosine- must warn pt about short duration chest discomfort and dyspnoea.

123
Q

LT management of AVNRT?**

A

may give AVN blocking agents e.g. bisoprolol, with fleicanide
may give amiodarone
consider catheter ablation if recurrent symptoms e.g. syncope.

124
Q

pts we would be worried about if have a broad complex tachycardia?

A

previous MI
structural heart disease
family history

125
Q

how might atrial flutter 1:1 ( a regular broad complex tachycardia) be converted to 2:1 (regular narrow complex tachy)?

A

vagal manouver or adenosine

126
Q

site of atrial flutter ablation?

A

between the tricuspid valve annulus and IVC

127
Q

tment of pre-excited AF?

A

shock them-electrically cardiovert, as risk of sudden death.

128
Q

management of atrial flutter?

A

same as AF
but rate more difficult to control- can try IV flecainide
from 48hrs onward, there is increased risk of CLOT,
can proceed to catheter ablation.

129
Q

define capture beats and fusion beats

A

these may characterise VT
capture beat=narrow QRS complex owing to normal ventricular activation via AVN adn conducting system.
fusion beat= interemdiate between VT beat and capture beat.

130
Q

why must we NOT use flecainide in VT?

A

can cause VF

BUT may be used if rpt VT in pt with a defibrillator.

131
Q

best tment of short QT?

A

ICD
as ventricular arrhythmias and sudden death may occur
result of genetic abnormality leading to faster repolarisation.

132
Q

tment of WPW antidromic- regular broad complex tachycardia?

A

AVN blocking techniques e.g. carotid massage and valsalva, and IV adenosine, as conduction is going down the accessory pathway and back up through the AVN so we can stop this by blocking the AVN.

133
Q

causes of poor R wave progression?

A 
old anteroseptal infarct
LV hypertrophy
L anterior fascicular block
LBBB
clockwise rotation of heart
WPW
134
Q

why is anticoag so important in pts with atrial fibrillation or atrial flutter?

A

to reduce stoke risk and disordered contraction of the atriapredisposes to blood stagnation and therefore thrombus formation, part. in the L atrial appendage in AF, which can then travel out of the L side of the heart, through the carotids and to the cerebral arteries.

135
Q

what does a J wave represent?

A

early repolarisation
often seen in hypothermia
may be linked to VF development and risk of sudden cardiac death*

136
Q

3 main mechanisms of tachyarrhythmia production?**

A

accelerated automaticity- are of myocardial cells depolarises faster than SAN
triggered activity-myocardial damage e.g. VT around scar tissue following MI
re-entry- propagating AP keeps meeting excited myocardium, must be 2 pathways around an area of conduction block.

137
Q

VT precipitating factors?

A

IHD, MI
cardiomyopathy
metabolic
cocaine

138
Q

SVT precipitators?

A 
alcohol
smoking
caffeine
thyrotoxicosis
IHD
139
Q

why might we proceed straight to electrical CV in a pt with an SVT e.g. AVNRT?

A

if unstable e.g. hypotension, pulmonary oedema, chest pain with ischaemia.
perform under GA or sedation.

140
Q

adenosine dosage in terminating SVTs?

A

6mg stat followed by 12mg if unsuccessful and then a further 12mg if still unsuccessful. follow with 0.9% sodium chloride flush.

141
Q

complications of ablation therapy?

A

need for pacemaker as SAN damage
vascular damage e.g. to femoral vein
DVT or PE
heart perforation and pericardial effusion with need for chest drain

142
Q

3 possible origins of SVT?

A

nodal (around SAN)
accessory pathway
random site within the atrial muscle e.g. that which causes ectopic atrial tachy.

143
Q

how might RBBB affect the heart sounds?

A

can cause persistent splitting of S2 as delayed RV contraction produces delayed pulmonary valve closure.

144
Q

mitral valve prolapse may be confused with what when listening to the heart sounds?

A

a split S2

if the 1st sound is of higher frequency and shorter duration then 2nd, then this indicates mitral valve prolapse.

145
Q

why does presence of a BBB make ST/T interpretation difficult?

A

BBB means depolaisation is abnormal, and so subsequent repolarisation will also be abnormal*

146
Q

investigations for sick sinus syndrome?

A

blds: Us and Es, TFTs, drug levels e.g. digoxin
ECG
ambulatory ECG- assoc. arrhythmias with symptoms
ECHO

147
Q

tment of choice for pts with symptomatic bradyarrhythmias assoc. with sick sinus syndrome?

A

pacemaker

148
Q

give 1 disadvantage of using rivaroxaban over wafarin in LT anticoag tment of AF?

A

no antidote so if serious bleeding unable to give something that reverses this e.g. Vit K and berriplex when warfarin induced bleeding.

149
Q

describe the process of re-entry**-check other cards

A

this is 1 mechanism of arrhythmia production
it occurs when a ‘ring’ of cardiac tissues surrounds an inexcitable core e.g. in region of scarred myocardium post MI.
tachycardia occurs if an ectopic beat finds 1 limb refractory, producing a unidirectional block, and the other limb excitable. As long as conduction is slow enough through the excitable limb, the other will have recovered and will allow retrograde conduction to complete the re-entry loop. if time for conduction around ring is longer than recovery times of tissue within the ring then circus movement is maintained producing a tachycardia.

150
Q

what is sick sinus syndrome/SA disease?

A

usually results from idiopathic fibrosis of the SAN.
may also be caused by IHD, cardiomyopathy or myocarditis which can cause fibrosis.
Episodes of sinus brady or sinus arrest occur, and commonly because of diffuse atrial disease there are paroxysmal atrial tachyarrhythmias (tachy-brady syndrome).

151
Q

name given to the ECG pattern of LA enlargement?

A

P-mitrale

152
Q

most likely diagnosis when pt presents with new LBBB and shock?

A

acute STEMI with cardiogenic shock, usually from thrombosis of left mainstem CA or sometimes proximal LAD.

153
Q

why might an occlusion of the RCA not always be responsible for an acute inferior MI?

A

may be result of left circumflex artery occlusion if pt is L coronary artery dominant so part of circuflex supplies part of inferior wall of myocardium.

154
Q

incomplete RBBB on an ECG?

A

RSR1 pattern in V1 but QRS duration less than 120ms*

155
Q

what can cause early offset ST segments on an ECG?

A

early repolarisation

156
Q

what is trifascicular block?

A

most commonly means RBBB and block of one of the left bundle branches, and 1st degree AV block (PR interval prolongation)

157
Q

causes of an irregular pulse?

A

AF
sinus arrhythmia
ectopics

158
Q

why does mitral regurge frequently occur with an inferior MI?

A

inferior MI results from occlusion of the RCA which is the sole supply of blood for the posteromedial papillary muscle that keeps the mitral valve apparatus working properly, so with an inferior MI the mitral valve often becomes dysfunctional.

CardioResp Block (11 decks)

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