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CVS > Lecture 13 > Flashcards

Lecture 13 Flashcards

1
Q

How do you determine normal sinus rhythm?

A

Look at lead 2

  • is rhythm regular
  • regular HR (60-100 bpm)
  • p waves present and upright, followed by QRS complex
  • is PR interval normal
  • is QRS width normal
  • is corrected QT interval normal
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2
Q

What is an atrioventricular conduction block?

A

Delay/failure of conduction of impulses from atria to ventricles via AVN and Bundle of His

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3
Q

What are the 3 types of atrioventricular heart block?

A
  • first degree heart block
  • second degree heart block (Mobitz type1/2)
  • third degree heart block
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4
Q

What are some causes of heart block?

A
  • degeneration of electrical conducting system with age (sclerosis/fibrosis)
  • medications
  • valvular heart disease
  • acute myocardial ischaemia (blood flow to heart is disrupted)
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5
Q

What is sclerosis?

A

Abnormal hardening of body tissue

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6
Q

What is a first degree AV block?

A

Conduction is slowed without skipped beats

  • all p waves are followed by QRS complexes
  • PR interval is longer than normal (>0.2s)
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7
Q

What is second degree AV blockand the two types?

A

Mobitz type 1/Wenkebach

  • successively longer PR intervals until one QRS is dropped (electrical signal not conducted through to ventricles)
  • cycle starts again

Mobitz type 2
-PR intervals do not lengthen
-sudden drop of QRS complex with no prior changes to PR
-atrial rhythm is regular (p waves)
-ventricular rhythm is irregular
HIGH RISK PROGRESSION TO COMPLETE HEART BLOCK

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8
Q

Which block is high risk to progress to complete heart block?

A

Mobitz type 2 (second degree)

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9
Q

What is a third degree AV block?

A

Atria and ventricles are depolarising independently (complete failure of AV conduction)
-ventricular pacemaker takes over which is slow (20-40 bpm)
-too slow to maintain blood pressure
-wide QRS complex
URGENT PACEMAKER REQUIRED
-random p waves being fired off without QRS following

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10
Q

What heart block requires a pacemaker urgently?

A

Third degree heart block

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11
Q

What is a bundle branch block?

A

Delayed conduction within bundle branches
(LBBB/RBBB)
-p waves and PR intervals are normal
-wide, notched QRS complex because ventricular depolarisation takes longer

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12
Q

What is a symbol of heart disease?

A

LBBB

left bundle branch block

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13
Q

What is arrythmia?

A

Abnormal rhythms from the heart

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14
Q

What are the types of arrythmia?

A

Atria (above ventricles and therefore called SUPRAVENTRICULAR arrythmia)

  • SAN
  • atrium
  • AVN

Ventricular arrythmia

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15
Q

Difference between supraventricular and ventricular arrythmias:

A 
Supraventricular
-normal QRS complex
-HR is altered
Ventricular
-wide/bizarre QRS complexes (ectopic beats)
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16
Q

What is an ectopic beat?

A

When a beat comes too early/there is an extra beat
-beat is out of place
=palpitations

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17
Q

What is atrial fibrillation?

A

A type of supraventricular arrythmia
Atria quiver but you still get blood into ventricles
-arises from many atrial foci (fire in an uncoordinated manner)
-no p waves
-wavy baseline (atria quiver- still get blood to ventricles)
-irregular R-R intervals
-impulses reach AVN at rapid irregular rate- not all conducted
-normal QRS as when conducted, ventricles depolarise normally

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18
Q

What are ectopic foci?

A

Abnormal pacemaker sites in the heart which display automacity (activity normally supressed by SAN)
-in both atria and ventricles

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19
Q

What are the atrial fibrillation variations?

A

SLOW
FAST
Normal rate
Coarse (>0.5mm) vs Fine fibrillation (<0.5mm)

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20
Q

What is tachy brady syndrome?

A

Sometimes the heart is tachycardiac and then bradycardic

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21
Q

Whats an issure with course fibrillation?

A

It may be mistaken for p waves

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22
Q

What are the haemodynamic effects of atrial fibrillation?

A
  • atria quiver
  • ventricles contract normally
  • HR and pulse are IRREGULARLY IRREGULAR
  • loss of atrial contraction leads to increased blood stasis, especially in left atria
23
Q

What does blood stasis in the atria cause?

A

Flow and velocity reduced leading to small clots in LA therefore could lead to ischaemic stroke

24
Q

What are premature ventricular ectopic beats?

A

PVC’s
Impulse does not spread via fast His-Purkinje system
-ectopic focus in ventricles leading to slower depolarisation of ventricles = Wider QRS
-premature as it occurs earlier than would be expected for next sinus impulse
-may cause palpitations without haemodynamic consequences

25
Q

What is ventricular tachycardia?

A

Run of >3 consequetive PVC’s

  • dangerous requiring urgent treatment
  • high risk of developing into ventricular fibrillation
26
Q

What is ventricular fibrillation?

A
  • abnormal fast ventricular depolarisation
  • impulses from numerous ectopic sites in ventricle
  • no coordinated contraction
  • ventricles quiver
  • no cardiac output so if sustained it lead to CARDIAC ARREST=MEDICAL EMERGENCY
27
Q

What does coronary artery narrowing/occlusion lead to?

A

Ischaemia/infarction of area supplied by that artery

can be viewed by leads facing the affected areas

28
Q

What is released when myocytes die?

A

Troponin

Released in MI due to cardiac muscle necrosis= STEMI/NSTEMI

29
Q

What is myocardial ischaemia?

A

Lack of oxygen, but no muscle necrosis

-blood tests negative for cardiac troponins

30
Q

What is myocardial infarction?

A

Muscle necrosis so blood tests will be positive for cardiac troponins

31
Q

What is a STEMI?

A

ST segment elevation myocardial infarction

  • complete occlusion of coronary artery
  • full thickness of myocardium involved
  • ST elevation (cause unknown) but is the earliest sign of a STEMI
32
Q

How does scar tissue lead to pathologic Q waves?

A

Following STEMI pathological Q waves develop

No electrcial activity in dead tissue

33
Q

What is the heart rate described as in atrial fibrillation?

A

Irregularly irregular

34
Q

Why does atrial fibrillation lead to ischaemic stroke?

A

Loss of atrial contraction leads to increased blood stasis.
Stasis most evident in left atrium
=leading to small clots in LA
=ischaemic stroke

35
Q

WHy learn about premature ventricular ectopics?

A

Sustained series can lead to ventricular tachycardia and then ventricular fibrillation

36
Q

Will troponin be positive in ischaemia?

A

No, because ischaemia is different from infarction. There is lack of oxygen but no muscle necrosis, so no dead cardiomyocytes to release troponin

37
Q

Where are normal Q waves seen in an ECG?

A

Small Q waves: LATERAL leads: 1 and aVL, V5-V6

Deeper Q waves: leads 3, aVR

38
Q

In what leads should you not see a Q wave?

A

Leads V1-V3

39
Q

What may lead to a Q wave in V3 lead, and what else may you see?

A

Pulmonary embolism

  • S waves in lead 1
  • inverted T wave in lead 3
40
Q

What are pathological Q waves?

A

> 1 small square WIDE
2 small squares DEEP (except leads 3 and aVR)
-depth more than 1/4 the height of the susequent R wave

41
Q

What is another name for severe ischaemia?

A

Unstable angina

42
Q

Which 2 diseases have the same ECG changes?

A

Unstable angina and NSTEMI

43
Q

What is the difference between a NSTEMI and unstable angina and how do you differentiate them?

A

UA: an acute coronary syndrome. Angina at rest, increasing in frequency, longer in duration
NSTEMI: actual cardiac muscle damage NOT through entire wall (sub-endocardial)

Blood test for myocyte necrosis: troponin

44
Q

What are the ECG changes in NSTEMI and unstable angina?

A

ST segment depression

T wave inversion

45
Q

In which leads are T waves normally not upright?

A

V1 and aVR

46
Q

In what leads do T wave inversions occur?

A

In leads consistent with anatomical regions perfused by a specific coronary artery
e.g. inferior wall of heart supplied by right coronary artery, via posterior descending artery, atheroslcerosis here will lead to changes in leads facing inferior aspect of heart (leads 2,3 and aVF)

47
Q

What happens to an ECG during stable angina?

A

ST depression during exercise due to stable atherosclerotic plaque causing fixed narrowing of coronary artery
-ECG changes will reverse at rest

48
Q

What are the tests to see if a patient has stable angina?

A

Exercise stress test (treadmill)

Dobutamine stress test (chemically induced)

49
Q

What are the signs and symptoms of someone with hypokalaemia?

A
  • muscle weakness (can’t repolarise as fast)
  • respiration depression
  • ascending paralysis
  • palpitations
  • cardiac arrest
  • arrythmias
  • myocardial hyperexcitability
50
Q

What is the ranges for moderate/severe hypokalaemia?

A

Moderate: <3 mmol/L
Severe: <2.5 mmol/L

51
Q

What do you see in an ECG of someone who has hypokalaemia (low potassium outside the cells)?

A

-peaked P waves
-T wave flatenning/inversion
-U waves
Takes longer for repolarisation due to inactivation of K+ channels

52
Q

What is hyperkalaemia?

A

> 5mmol/L of potassium

53
Q

What are the pathophysiological effects of hyperkalaemia?

A

-resting membrane potential becomes less negative
-causes some voltage gated Na channels to be inactivated
-heart becomes less excitable
-conduction problems can occur
Lead to:
-generalised muscle weakness
-respiratory depression
-ascending paralysis
-palpitations/arrythmia/cardiac arrest

54
Q

What do you see in an ECG of someone who has hyperkalaemia?

A
  • tall tented t waves
  • loss of p wave as you lose atrial depolarisation
  • widening of QRS
  • QRS continues to widen

CVS (16 decks)

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