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CVS > ECGs, Heart Sounds and Valve problems > Flashcards

ECGs, Heart Sounds and Valve problems Flashcards

1
Q

What is the difference between stenosis and reguritation?

A

stenosis is valve not opening properly and regurgitation is it not closing properly

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2
Q

What can cause a aortic valve stenosis?

A
  • degenerative (calcification/ fibrosis)
  • congenital (leaflets fuse to make valve bicuspid)
  • chronic rheumatic fever (leads to inflammation and fibrosis)
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3
Q

What would be heard and where for an aortic valve stenosis?

A

a creshendo- decreshendo murmer between S1 and S2 (as blood forced through smaller hole), in the 2nd intercostal space, on the right sternal boarder

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4
Q

What are consequences of aoetic valve stenosis?

A

less blood through- left sided heart failure & LV pressure increases

  • LV hypertrophy
  • syncope and angina
  • microangiopathic haemolytic anaemia
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5
Q

What is heard in an aeortic valve regurgitation?

A

diastolic decreschendo murmer (murmer heard on/ just after S2) as blood flows back into aorta in diastole when the valve should be closed

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6
Q

What can cause an aortic valve regurgitation?

A
  • aoertic root dilitation (common with marfans but as common as any other aneurysm)- pulls leaflets apart
  • Valvular damage (eg by rheumatic fever)
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7
Q

What are the consequences and signs of aortic regurgitation?

A
  • systolic pressure increases leading to LV hypertophy
  • Bounding pulse as diastolic pressure decrease and systolic pressure increases
  • head bobbing
  • qinkes sign
  • dizziness, angina ect
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8
Q

What is qinkes sign?

A

nail bed blanches and flushes with each heart beat

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9
Q

What is heard with a mitral valve regurgitation?

A

holosystolic murmur- constant volume murmur through gap between s1- s2 best heard in 5th intercostal space at midclavicular line

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10
Q

What can cause a mitral valve regurgitation?

A
  • myxomatous degeneration of the chordae teninae and papillary muscles
  • Damage to papillary muscles after heart attack
  • Left sided heart failure leading to LV dilitation stretching valve
  • rheumatic fever
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11
Q

What is heard in mitral valve stenosis?

A

Snap as valve closes (S1 is snapping sound) and diastolic rumble (rumble just after S2, finishes at s1)

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12
Q

What causes 99.9% of mitral stenosis’?

A

rheumatic fever

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13
Q

What are the consequences of mitral valve stenosis?

A
  • LA dilitation
  • atrial fibirillaiton
  • oesophas compression
  • dysphagia (difficulty swallowing)
  • increase LA pressure
  • pulmonary hypertension
  • Pulmonary oedmea
  • dysponea
  • RV hypertophy
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14
Q

When does the S2 heart sound split into two? ( aortic and pulmonary closing seperates)

A

on inspiration

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15
Q

What 4 locations does the diaphragm need to be placed to hear all 4 valves?

A
  • 2nd intercostal space, right boarder of sternum
  • 2nd intercostal space, left boarder of sternum
  • 4th intercostal space, left boarder of sternum
  • 5th intecostal space, midclavicular line
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16
Q

What pneumonic states what valve is being listened to in what location

A

All Prostitutes Take Money

aortic, pulmonic, tricuspid, mitral

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17
Q

If the wave of depolarisation goes towards the + electrode is a positive or negative complex that forms?

A

positive complex

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18
Q

During repolarisation, if the wave goes towards the +ve electrode, will the EGC show a positive or negative complex

A

Negative complex

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19
Q

What does the size of the peak/ trough of an ECG depend on?

A
  • size of the charge

- direction the depolarisation/ repolarisation is going in in relation to the electrodes

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20
Q

Why does the depolarisation not spread from atria to the ventircles?

A

There is a fibrous ring of non conductive tissue around the valves

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21
Q

What creates the q wave of an ecg?

A

L-> R depolarisation of the interventricular septum (lead is slightly more towards left side of heart, so direction of depolarisation is obliquely away

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22
Q

Why is atrial repolarisation not seen on an ECG?

A

It is hidden by the R wave of ventricular depolarisation

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23
Q

How many electrodes are placed on the body for an ecg?

A

10- but 12 views are given

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24
Q

Where are the 4 upper limb electrodes placed?

A
  • on boney prominences of ankles and wrists
  • Ride Your Green Bike
  • red lead on R arm, yellow on L arm, green on L leg, black on R leg
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25
Q

Where are the 6 chest leads placed?

A
  • 4th R ICS (septal boarder)
  • 4th L ICS (septal boarder)
  • 5th L rib (inch to left)
  • 5th L ICS in line with axilla
  • 2 leads in 5th ICS, one in midclavicular line, one to the left of this
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26
Q

Which leads look at the inferior surfaces of the heart? Which coronary artery supplies this area?

A

2, 3 and aVF

Right coronary artery

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27
Q

Which leads look at the anteroseptal surface of the heart? Which coronary artery supplies this area?

A

v1, v2

Left anterior descending

28
Q

Which leads look at the anteroapical surface of the heart? Which coronary artery supplies this area?

A

V3, V4

distal left anterior descending

29
Q

Which leads look at the anterolateral of the heart? Which coronary artery supplies this area?

A

v5, V6, 1 and aVl

Circumflex

30
Q

If there are problems in v1, v2, v3, v4, v5, v6, 1 and aVl which coronary artery is affected and what surface of the heart is ischaemia/ infarcted?

A

The proximal left coronary artery

Most of the anterior surface

31
Q

Why does the trace for aVr look different to the rest?

A

It is inverted because the positive electrode is facing in the opposite direction to the rest

32
Q

Why is there a transition from upwards to downwards Q waves in leads v1- v6?

A

because V1 is in same direction as septal depolarisation (so positive complex), v2,3,4,5 see different views around it, so complex gets smaller and then by v5 and 6 the depolarisation is away from the electrode so there is a positive complex

33
Q

Why does the wave of depolarisation of the ventricles register as going left towards the v6 electrode when it should be towards V2/3?

A

becuase there are more myocytes on the left so depolarisation is greatest in the leftwards direction

34
Q

How many seconds is 5 large squares (25mm)?

A

1 second

35
Q

How can HR be calculated from and ECG?

A

Take R-R interval, find out how many in 300 large boxes (1 min), so 300 by number of large boxes between R waves

36
Q

How can HR be calculated for an irregular rhythm?

A

number of QRS complexs in 6 seconds (30 large boxes) and times by 10

37
Q

How long should the PR interval be? What does a long PR interval indicate?

A

3-5 small bones (0.12-0.2 s)

1st degree heart block

38
Q

How long should the QRS interval be? what does a long one indicate?

A

less than 3 small boxes

long one indicates ventricular depolarisation not started by AVN

39
Q

How long should the QT interval be?

A
  • This varies with heart rate

- shouldnt be more than 11-12 small boxes by calculation needs to be done that takes into account HR

40
Q

What should the ST segment look like?

A

It should be isoelectric- in line with flatline at P-Q and T-P

41
Q

In supraventricular abnormalities, which part of the PQRST is affected?

A

The P wave

42
Q

If the P wave drops too far down, what is abnormal?

A

the atrial muscle conductance (or rhythm is starting in the atrial muscle) because the impulse is going in the back and forth direction

43
Q

What does an inverted P wave suggest?

A

The impulse is going in the opposite direction, ie it is starting in the AVN

44
Q

What can happen to the P wave if the atrial contraction starts in the mid or lower AVN?

A

It will not be present as it will be lost in the QRS complex as depolarisation will happen later

45
Q

If there is a no P wave and a wide QRS complex, where is the impulse likely to have started from?

A

The right ventricle

46
Q

If there is no P wave and the QRP complex has inverted, where has the impulse likely to have originated from?

A

The left ventricle, the impulse then spreads in the opposite direction

47
Q

What happens in atrial fibrillation?

A

The impulse starts from many different foci in the atria causing it to quiver rather than contract properly. Impulses arrive at the AVN at an irregular and rapid rate so only some will be conducted to the ventricles

48
Q

What does atrial fibrillation look like on an ECG?

A
  • No distict p waves
  • wavey baseline
  • irregulalrly irregular QRS waves of normal width
49
Q

Why do atria fibrillate? What is a major complication of them?

A
  • Hypertension, abnormal valves, heart failure, hyperthryroidism, exposure to stimulants or alcohol
  • lead to thrombus forming from stagnant blood in auricles
  • lead to stroke
50
Q

What is heart block? What are the 3 types?

A 
a delay in conductance from the atria to the ventricles due to MI or old age 
- first degree
- 2nd degree:
  mobitz type 1
  mobitz type 2
- 3rd degree 
- 2:1/3:1
51
Q

Describe 1st degree heart block

A
  • P wave normal
  • Prolonged PR interval (more than 5 small squares)
  • QRS normal
52
Q

What is 2nd degree heart block?

A

a complete lack of conductance to the ventricles after some P waves (but not all)
There are 2 types: mobitz type 1 (wenkebatch penomenon) and 2

53
Q

Describe mobitz type 1 heart block

A
  • Progressively prolonged PR interval
  • Until a QRS is missed
  • Then the cycle restarts
54
Q

Describe mobitz type 2 heart block?

A
  • NORMAL PR INTERVAL

- sudden non conductance of a beat meaning not all P waves are followed by a QRS

55
Q

What is 2:1/3:1 heart block?

A
  • regularly 2 or 3 P waves to each QRS complex

- Some P waves may be lost in T wave or seen as U waves

56
Q

What is 3rd degree heart block?

A
  • Atrial depolarisation is normal but impulses are not conducted to the ventricles
  • Ventricular pace maker takes over but this is much slower (30-40 bpm)- slow so that normally SAN can set the pace
  • This HR is too slow to maintain perfusion so pacemaker needed
57
Q

State the key features of 3rd degree heart block on ECG

A
  • P-P intervals normal and regular at 60-100 bpm
  • this has no relationship with QRS complexes
  • R-R intervals regular but only 30-40 bpm
  • QRS complex wider as one of the budles of his looses conductance so slower conductance across ventricles
58
Q

What is a ventricular ectopic beat?

A

Where the focus of the impulse is in the ventricle. QRS is wider and abnormal shape w/ no P wave before it

59
Q

What is the cause of ventricular ectopic beats?

A

Can be MI but if there is only one it is usually benign

60
Q

What is ventricular tachycardia?

A

A run of 3 or more consecutive ventricular ectopic beats, leads to v. fibrillation so dangerous and needs defibrillation

61
Q

What indicates a previous MI/ ischaemic event?

A
  • Abnormally wide or deep Q waves (> 1 small square wide and 2 deep)
62
Q

What are the indicators of unstable angina/ ischaemia on an ECG?

A

ST degment depression

T wave inverison

63
Q

What indicates an MI on an ECG?

A

ST segment elevation- can lead to a tall and broad T wave if they fuse

64
Q

What effects does hyperkalaemia have on an ECG?

A
  • At 7mmol/L you get a high T wave
  • at 8, prolonged PR interval, depressed ST and high T wave
  • at 9, no P wave, inverted QRS
  • at 10 V. fib
65
Q

WHat effects does hypokalaemia have on an ECG?

A
  • below 3.5, low T wave
  • below 3, low T wave and high U wave (wave after T)
  • below 2.5, low T wave, high U wave, depressed ST segment
66
Q

Why does hyperkalaemia make the heart less excitable?

A
  • RMP less negative
  • Some Na+ channels inactivated
  • Action potential cannot spread as well

CVS (7 decks)

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