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6. Cardiovascular System > ECGs > Flashcards

ECGs Flashcards

1
Q

What is the mechanism of atrial flutter?

A

a re-entry circuit within right atrium

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2
Q

List some causes of AF

A

ischaemic heart disease

thyrotoxicosis (hyperthyroidosis)

sepsis

valvular heart disease

alcohol excess

PE

hypokalaemia/hpomagnesaemia

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3
Q

What is the mechanism of atrial tachycardia?

A

A single ectopic focus, outside the SAN that’s triggering rapid depolarisation of the atria

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4
Q

List causes of atrial tachycardia

A

digoxin toxicity

atrial scarring

catecholamine excess

congenital abnormatlities

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5
Q

What is the mechanism of junctional tachycardia?

A

AV junctional pacemaker rhythm exceeds that of SAN. There is increased automaticity in AVN coupled with decreased automaticity in SAN.

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6
Q

Describe the ECG changes seen in right bundle branch block

A

broad QRS >120ms

RSR pattern in V1-3 (‘m’ shaped complex)

wide, slurred S waves in lateral leads (I, aVL, V5-6) giving a ‘W’ shaped complex in V6

(MarroW - M in V1, W in V6, rr = right)

possible ST depression in precordial leads (V1-3)

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7
Q

What is the mechanism in RBBB?

A

activation of R ventricle is delayed as depolarisation has to spread across septum from left ventricle due to blockage of R bundle of Purkinje fibres

left ventricle is activated normally, so early part of QRS is unchanged, but delayed R ventricle activation produces a secondary R wave in V1-3 and a slurred S wave in lateral leads

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8
Q

List causes of RBBB

A

RVH / cor pulmonale

PE

IHD

rheumatic heart disease

myocarditis or cardiomyopathy

degenerative disease of conduction system

congenital heart disease

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9
Q

Describe the ECG changes seen in left bundle branch block

A

broad QRS >120ms

dominant S wave in V1 - W

broad, notched R wave in V6 - M

(WilliaM - W in V1, M in V6, ll = left)

no Q waves in lateral leads (I, V5-6, small Q waves in aVL)

prolonged R wave peak time >60ms in V5-6

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10
Q

List causes of LBBB

A

aortic stenosis

ischaemic heart disease

dilated cardiomyopathy

anterior MI

primary degnerative disease (fibrosis) of the conducting system

hyperkalaemia

digoxin toxicity

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11
Q

Describe the mechanisms in LBBB?

A

septum is activated R to L instead of L to R

spreads via right bundle branch, and then via septum to left bundle branch

this extends the QRS duration and removes Q waves in lateral leads

as the venrticles are activated sequentially, broad R waves are produced

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12
Q

Describe the ECG changes seen in junctional escape rhythms

A

no p waves, or p waves completely unrelated to QRS

normal QRS, maybe slightly narrow

slow HR

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13
Q

What is the mechanism of junctional escape rhythms?

A

there are pacemaker cells at various points in the conduction system

junctional escape rhythm occurs when the rate of AV node depolarisation is less than the intrinsic rate of an ectopic pacemaker

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14
Q

list causes of junctional escape rhythms

A

severe sinus bradycardia

sinus arrest

sino-atrial exit block

high-grade second degree heart block (4:1, 5:1 etc)

complete heart block

hyperkalaemia

drugs:

beta blockers

CCBs

digoxin poisoning

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15
Q

Describe the ECG changes seen in a ventricular escape rhythm

A

ventricular rhythm of 20-40bpm

broad QRS complexes, possibly with a LBBB or RBBB morphology

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16
Q

what arteries are likely to be blocked in a lateral STEMI

A

LAD and LCx

17
Q

Describe the ECG changes seen in a lateral STEMI

A

ST elevation in the lateral leads

(I, aVL, V5-6)

reciprocal ST depression in inferior leads (III and aVF)

18
Q

Describe the ECG changes seen in an inferior MI

A

ST elevation in II, III and aVF

progressive development of Q waves in II, III and aVF

reciprocal depression in aVL (±lead I)

19
Q

Which artery most commonly causes an inferior STEMI?

A

right coronary artery

(more ST elevation in lead III than II)

LCx can cause it less commonly

(ST elevation in lead II = lead III)

20
Q

Describe the ECG changes seen in posterior MI

A

In V1-V3:

horizontal ST depression

tall, broad R waves

upright T waves

dominant R wave in V2

21
Q

Occlusion of what artery causes an anterior STEMI?

A

LAD

22
Q

Describe the ECG changes seen in anterior STEMI

A

ST elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL)

reciprocal ST depression in the inferior leads (mainly III and aVF)

23
Q

In what leads would ST elevation be maximal in a septal STEMI?

A

V1-2

24
Q

In what leads would ST elevation be maximal in an anterior STEMI?

A

V2-5

25
Q

In what leads would ST elevation be maximal in an anteroseptal STEMI?

A

V1-4

26
Q

In what leads would ST elevation be maximal in an anterolateral STEMI?

A

V3-6, I + aVL

27
Q

What is seen in an NSTEMI?

A

pathological Q waves only

28
Q

Describe the ECG changes that may be seen in a ventricular tachycardia

A

very broad QRS (>160ms)

no p waves

T waves difficult to identify

rate > 200bpm

29
Q

Describe the ECG changes seen in ventricular fibrillation

A

chaotic irregular deflections of varying amplitude

no identifiable P waves, QRS complexes or T waves

rate 150-500bpm

30
Q

Causes of VF

A

myocardial iscahemia/infarction

electrolyte abnormalities

cardiomyopathy (dilated, hypertrophic, restrictive)

Long QT

Brugada syndrome

Drugs

environmental - electrical shock, drowing, hypothermia

PE

cardiac tampnoade

blunt trauma

31
Q

Describe the ECG changes seen in Wolff-Parkinson-White syndrome

A

sinus rhythm

right axis deviation

short PR interval

sluured upstroke of the QRS complex, best seen in V3 and V4 - wide QRS due to this delta wave

dominant R wave in V1

32
Q

what is the mechanism in Wolff-Parkinson-White?

A

accessory pathway, usually from left atria, allows direct transmission of signal, bypassing AVN (hence short PR)

33
Q

Describe the “digoxin effect”

A

downsloping ST depression with “sagging” appearance

flattened, inverted or biphasic T waves - hockey stick

shortened QT

34
Q

What is the mechanism behind the digoxin effect?

A

shortening of atrial and ventricular refractory periods - producing short QT

increased vagal effects at AVN - prolonged PR interval

35
Q

Describe the ECG changes seen in pericarditis

A

widespread concave ST elevation and PR depression

Reciprocal ST depression and PR elevation in aVR

36
Q

What is P Pulmonale?

A

peaked P waves

37
Q

What is seen in p mitrale?

A

bifid p waves

38
Q

list causes of p pulmonale

A

anything that cause right atrial enlargement

e.g. tricuspid stenosis, pulomnary hypertension

6. Cardiovascular System (24 decks)

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