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Cardio > Cardiac impulses and ECG > Flashcards

Cardiac impulses and ECG Flashcards

1
Q

where does excitation originate?

A

pacemakers cells within the sino-artial nodal cells in the upper right atrium

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2
Q

do SA nodal cells have a stable membrane resting potential?

A

no they do not - they exhibit a spontaneous pacemaker potential

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3
Q

The pacemaker potential is a slow depolarisation (i.e. slowly becoming becoming more positive working towards the threshold for the action potential). What is this due to?

A

this is due to an decrease in potassium ion efflux with a super-imposed sodium ion influx.

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4
Q

the falling phase of the action potential (i.e. repolarisation) is caused by what?

A

the opening of potassium channels and therefore [K] efflux.

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5
Q

how is the action potential spread from the sino-artial node to the AV node?

A

through Gap junctions in-between myocytes (which allow a low electrical resistance pathway for cell-to-cell communication)

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6
Q

what allows atrial systole to precede ventricular systole?

A

the fact that conduction id delayed in the AV node, allowing ore time of the atria to contract

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7
Q

how does the conduction spread to the ventricles?

A

bundle of his, through the purkinje fibres (the right and left branches), then up through he ventricles via gap junctions, in turn forcing the blood up and out of the heart.

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8
Q

do ventricular muscles cells have a steady resting membrane potential? if so what is it?

A

yes, -90mV, and the ventricular cells will remain at this potential until excited

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9
Q

what occurs when the ventricular cells become excited?

A

rapid sodium influx, causing the rising phase of the action potential

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10
Q

what is the next phase after the rising phase?

A

the plateau phase - the membrane potential rises until +30mV and is maintained close to this value due to the opening of voltage gated calcium channels (and subsequent calcium influx)

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11
Q

what is the falling phase and what causes it?

A

the falling phase immediately precedes the plateau phase, due to the closure of the voltage gated calcium channels and the opening of potassium channels (potassium efflux causing depolarisation)

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12
Q

how long does the whole cycle in ventricular cells take?

A

250ms

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13
Q

how long does the action potential in pacemaker cells within the SA node take?

A

800msec

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14
Q

what does the P wave represent?

A

atrial depolarisation?

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15
Q

what does the QRS complex represent?

A

ventricular depolarisation (its masks atrial repolarisation)

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16
Q

what does the T wave represent?

A

ventricular repolarisation

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17
Q

what does the PR interval represent?

A

largely AV nodal delay

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18
Q

what does the ST segment represent?

A

ventricular systole

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19
Q

what does the TP interval represent?

A

diastole

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20
Q

causes of sinus tachycardia?

A

anxiety, pain, sepsis, hypovolaemia, caffeine, adrenaline

21
Q

treatment for sinus tachycardia?

A

treat the underlying cause, then beta blockers

22
Q

causes of sinus bradycardia?

A

physiological (physical fitness), drugs (beta blockers, digoxin, verapamil) acute MI, hypothermia

23
Q

treatment of sinus bradycardia?

A

atropine if acute, pacing if haemodynamic compromise

24
Q

what are the features of a ventricular tachycardia?

A

no p-waves (so not sinus), regular rhythm, bored QRS complexes, tachycardia

25
Q

what is the treatment for VT?

A

acute: IV amiodarone/lidocaine

IF PULSELESS IT IS A SHOCKABLE RHYTHM

26
Q

features of ventricular fibrillation?

A

no p-waves present (not sinus), very irregular rhythm, tachycardia (hard to calculated HR because of irregularity)

27
Q

treatment for ventricular fibrillation?

A

always shockable (not compatible with life) - cardioversion (a shock to get the heart back to normal sinus rhythm)

28
Q

features of atrial fibrillation?

A

no p-waves, and a irregular baseline is seen

29
Q

possible causes of atrial fibrillation?

A

ischaemic heart disease, hypertension, familia, mitral valve disease, can be lone/idiopathic

30
Q

what are the 3 types of atrial fibrillation?

A

paroxysmal - lasting less than 48hours, often recurrent

persistant - lasting longer than 48 hours - can be cardioverted back to NSR - unlikely to go back to NSR itself

permanent - inability of pharmacologic or non-pharmacologic methods to restore NSR

31
Q

management of atrial fibrillation?

A

rhythm control - to maintain sinus rhythm predominantly

rate control - accept the AF but control the ventricular rate

NB - anticoagulation is needed for both styles of treatment as there is a high risk of thromboembolism

32
Q

what are examples of rate controlling drugs used in AF?

A

beta blockers, digoxin and verapamil are all used to slow down AV nodal conduction - and they can be used alone or in combination

33
Q

what are the rhythm controlling drugs used in AF?

A

methods of pharmacological cardioversion include, anti-arrhythmic drugs such as amiodarone

(NB - direct current cardioversion is also used)

34
Q

what are the 4 classes of antiarrhythmic drugs?

A

Class 1 (IA, IB, IC)
Class 2
Class 3
Class 4

35
Q

where do Class 1 act? give an example.

A

the rising phase (0) as they block sodium channels (sodium channel antagonist)
e.g. lignocaine

use in AF - rhythm control

36
Q

where do Class 2 act? give an example

A

the resting potential phase (4) as they block beta-receptors
e.g. propranolol

use in AF - rate control

37
Q

where do Class 3 act? give an example

A

the falling phase (3) as they block potassium channels (and prolong the action potential)
e.g. amiodarone

use in AF - rhythm control

38
Q

where do Class 4 act? give an example

A

the plateau phase (2) as they block calcium channels (calcium channel antagonists)
e.g. verapamil

Use in AF - rate control

39
Q

how do you judge whether someone needs anticoagulation in AF?

A

CHADSVASC

C - congestive heart failure
H - hypertension 
A - age >= 75
D - diabetes mellitus 
S - stroke 
V - vascular disease**
A - ages 65-74 years 
S - sex (female)

**previous MI, aortic plaque

40
Q

what is ablation and what is it used for?

A

Ablation involves the destruction of re-entry circuits, which are often caused by a myocardial scar or a developmental anomaly

used to maintain the SR (ablating AF focus) and also for rate control (ablating AVN focus to stop fast conduction to the ventricles)

41
Q

features of atrial flutter?

A

classic sawtooth pattern due to continuous atrial depolarisation. (macro-reentrant circuit)

42
Q

treatment of atrial flutter?

A

RF ablation (80-90% long term success)

pharmacological - slow ventricular rate, restore sinus rhythm + maintain it

cardioversion

warfarin for prevention of thromboembolism

43
Q

what are the different types of hear block?

A 
1st degree
2nd degree
- mobitz 1
- mobitz 2
3rd degree
44
Q

features of 1st degree heart block?

A

the PR interval is longer than the normal 0.2s

not really a “block” and doesn’t require any treatment just long term follow up

45
Q

features of 2nd degree heart block (mobitz type I)?

A

is the progressive lengthening of the PR interval until eventually a beat is dropped
usually vagal in origin

46
Q

features of 2nd degree heart block (mobitz type II)?

A

ratio of AV conduction varies from 2:1 to 3:1 (i.e. every 2nd or third P wave is not follow by a ventricular contraction)

it is pathological (IHD, acute carditis) and may progress to 3rd degree

therefore, PERMENANT PACEMAKER IS INDICATED

47
Q

features of 3rd degree heart block?

A

no action potentials from he SA node get through to the AV node - complete heart block

on ECG there is complete dissociation between the P-wave and the QRS complexes

48
Q

causes of complete heart block and how is it treated?

A

idiopathic, congenital, IHD, aortic valve calcification, digoxin

treated with ventricular pacemaker

Cardio (6 decks)

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