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Module 103, Theme 3: Physiology of the CVS: principles of pathology, diagnosis and treatment of CV diseases. > ECG > Flashcards

ECG Flashcards

1
Q

Heart functional syncytium

A

Many cardiac cells function as one, in sync, due to gap junctions.

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2
Q

The 3 types of cardiomyocytes in the heart

A

Pacemakers- generates the heartbeat

Conducting - transmits rhythm throughout the heart

Contractile- the most numerous cells, muscle fibres that generate contraction to eject blood from the heart chambers.

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3
Q

Conducting cardiomyocytes

A

Modified cardiomyocytes that move current around the heart to reach different locations at the appropriate time to initiate contraction in an orderly fashion.

Includes:
Purkinje fibres
AV node

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4
Q

Syncytium

A

One large cell having many nuclei that are not separated by cell membrane- like a skeletal muscle cell

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5
Q

Cardiomyocytes

A

Muscle cells that includes:

  • Striations, that are not as distinct as skeletal muscles.
  • Branching cells that are connected.
  • Intercalated discs that allow divide cells longitudinally.
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6
Q

Gap junctions and intercalated discs

A

Cardiomyocytes are linked by gap junctions in the intercalated discs.

Intercalated disc: double membrane that separates adjacent cardiomyocytes. They stabilise cells and gap junctions during contraction. This allows electrical coordination.

Gap junctions: gap can open and close allowing specific molecules and ions to pass freely. Action potential depolarised one cell and initiates an AP in the adjacent cell.
Gap junctions do not allow large molecules.

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7
Q

Conduction pathway in the heart

A

Initiation of heartbeat at SAN—> atria contraction —> AVN—-> bundle of His—-> bundle branches in ventricles —-> ventricular contractile myocardium

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8
Q

Spread of impulse from SAN to atria

A

Impulse spreads from SAN to the atria via internodal bundles. The bundles ensure synchronised contraction.

This conducts the impulse quicker than cardiomyocytes- from 0.3-0.5m/s to 1.0 m/s.

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9
Q

Internodal bundles

A

Conduct impulse from SAN to atria.

There are 4 specialised bundles in the atria:

  • Contain purkinje-like cells that conduct impulses.
  • 3 bundles go to the AVN.
  • Bachmann’s bundle goes to the left atrium.
  • These bundles directly contact to contractile cells in the atria, via gap junctions.
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10
Q

The 3 internodal bundles that go from the SAN to AVN

A

Anterior, middle and posterior tracts.

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11
Q

Bachmann’s bundle

A

An internodal bundle that connects the SAN to the left atrium.

Directly connected to the contractile cells in the left atrium via gap junctions.

This allows synchronised contraction in the atrium.

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12
Q

Impulse at AVN

A

There is a delay of signal which allows time for the atrium to contract and empty to fill the ventricles.

The delay- 160 ms (0.16s)
This delay is due to the cardiomyocytes at the AVN having a smaller diameter, which increases electrical resistance.

Resistance is increased due to the smaller cross section and more gap junctions per SA due to its short length.

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13
Q

Time it takes impulse to travel from SAN to AVN

A

30 ms

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14
Q

Delay time at AVN before penetrating AV bundle

A

90 ms

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15
Q

Delay time in penetrating bundle

A

40 ms

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16
Q

Ventricular propagation

A

AVN connects to the bundle of His which is connected to the Purkinje fibre.

Purkinje fibres transmit impulse rapidle to the contractile cells in the ventricles.

There is a slower conduction between contractile myocytes.

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17
Q

Purkinje fibres

A

Conducting fibres that connect the AVN to the contractile cardiomyocytes in the ventricles.

They are very large myocytes with large diameters that transmit impulses very rapidly- up tp 5 m/s.

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18
Q

The basis of ECG

A

Gross electrical measurement of the heart, measured on the skin.

Currents detected from the wrist, ankle and 1m from the heart as the heart is a functional syncytium.

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19
Q

Diagnoses made by ECG

A

Very accurate, long term heart rate-

Allows the atrial and ventricular rate to be specifically identified.

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20
Q

Holter monitor

A

An ECG equipment that measures heart rate for 24 hours.

This is more accurate and convenient than using the pulse.

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21
Q

Lead

A

A configuration of electrodes placed in an ECG.

The standard lead is a 12-lead ECG, looking at the heart from 12 different angles.

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22
Q

12-lead ECG

A

Standard lead that looks at the heart from 12 angles.

Uses 10 separate electrodes.

The 10th electrode is a ground electrode placed on the right ankle/leg.

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23
Q

Lead II

A

3 electrodes placed in a specific configuartion:

  • 1 Positive electrode on the left leg.
  • Negative electrode on the right arm.
  • Ground electrode on the right leg (or almost anywhere).
24
Q

The 12 standard leads

A

3 Bipolar leads

3 augmented leads

6 precordial

25
Q

Bipolar leads

A

These leads are placed on the frontal/ coronal plane: I, II, III

They contain a positive and negative end, with a grounding lead

26
Q

The augmented leads

A

3 unipolar leads placed at the frontal/ coronal plane:
aVR
aVL
aVF
The positive electrode is compared to a reference electrode made from the two other connected electrodes.

27
Q

The precordial leads

A

6 unipolar leads placed on the transverse plane, spine to sternum:
V1
V2
V3
V4
V5
V6
The electrodes are placed on the thorax near the heart.
The positive electrode is compared to an estimate of what is happening at the heart centre (R-arm, L arm and leg connected).

28
Q

PQRST wave

A

ECG waves represent the action potentials at different stages of the cardiac cycle.

P wave- depolarisation of the atria due to SAN.
QRS complex- depolarisation of ventricles, triggers ventricular contraction.

T wave- ventricular repolarisation.

29
Q

PR segment

A

The segment between the end of the P wave and start of QRS complex.

Represents the AVN delay, which allows time for ventricles to fill.

30
Q

PR interval

A

The sections between the start of the P wave and start of the QRS complex.

In this interval, atrial depolarisation occurs and ventricular depolarisation is about to occur.

Normal duration=
3-5 boxes
120-200 ms

31
Q

ST segment

A

The section between the end of the QRS complex and the start of the T wave.

This section should be flat. It represents the beginning of ventricular repolarisation.

32
Q

QRS complex

A

The section represents the transmission of depolarisation through the myocardium in the ventricles.

Normal duration=
2-3 boxes
80-120 ms

When this complex is WIDE= abnormal ventricular conduction due to cells interrupting conductions- ectopic pacemaker or bundle branch block

Deep Q waves= dead tissue, such as after a MI.

33
Q

Ectopic beat

A

A heart contraction that is initiated at somewhere other than the SAN.

34
Q

Sinus rhythm

A

When the heartbeat is generated from the SAN.

Therefore it shows a ‘normal’ PQRS wave

35
Q

Sinus tachycardia

A

Tachycardia that occurs due to the SAN depolarising too quickly.

The ECG will show normal PR intervals and a P waved matched with QRS complex.

36
Q

QT interval

A

The section between start of the QRS complex and the end of the T wave.

Normal duration=
9-11.5 boxes
360-460 ms

37
Q

The timing in an ECG

A

A little box= 0.04 sec

5 little boxes/ 1 big box= 0.20 secs

5 big boxes= 1 second

38
Q

PR interval normal duration

A

3-5 boxes

120-200 ms

39
Q

QRS complex normal duration

A

2-3 boxes

80-120 ms

40
Q

QT interval normal duration

A

9-11.5 boxes

360- 460 ms

41
Q

Calculating rate from ECH

A

The period between two R waves.

1 big box= 300 bpm
2 = 150 bpm
3= 100 bpm
4 = 75 bpm
5= 60 bpm
6 = 50 bpm
10= 30 bpm
42
Q

Autonomic control of the CVS rate and contractility

A

Parasympathetic:
Vagus nerve (CNX)
Stimulates muscarinic receptors
Decreases: HR, contractility (inotropy) and conduction velocity.

Sympathetic:
Stellate nerve
Increases: HR, contractility and conduction velocity.

43
Q

Beta-1 adrenoreceptors

A

Receptors on the heart that when activated by an agonist, like adrenaline:
Increases ionotropism and chronotropism (interferes with HR)

44
Q

Beta-2 adrenoreceptors

A

Receptors that when activated by an agonist, like, adrenaline:
Causes vasodilation in the skeletal muscles.

This results in a wider blood pressure- increase in systolic, decrease in diastolic

45
Q

Atropine

A

Muscarinic antagonist against parasympathetic activity.

This causes parasympathetic withdrawal- which has the same effect as the sympathetic system without activating the system.

46
Q

AV heart block

A

Dysrhythmia caused by impulse conduction block in the AV.

Symptoms:
Palpitations
Other symptoms similar to hypotension- dizziness, syncope, malaise

Causes:
Ischaemia of AVN of AV bundle
Compression of AV bundle by scarring of calcified tissue.
Inflammation of AVN or AV bundle

47
Q

First degree heart block

A

Occurs when the PR interval is greater than 5 littles boxes.

All P waves are still followed by a QRS complex.

This causes delayed AVN transmission.

Almost always asymptomatic and often in young people.

48
Q

Mobitz Type 1 (Wenckebach) heart block

A

Second degree heart block

Some P waves are blocked and NOT followed by QRS complexes, therefore some QRS complexes are missing.

PR intervals gets longer until there is not QRS complex, then the cycle repeats.

Causes: Mainly AV damage
No treatment usually given.

49
Q

Second degree AV heart block

A

When one or more of the atrial impulses fail to conduct to the ventricles due to impaired conduction.

50
Q

Mobitz Type II heart block (Hay)

A

Occurs when some P waves are blocked an not followed by a QRS complex.

In an ECG, the PR intervals are normal and followed by QRS in intervals, before no QRS wave appears.

This can progress to a complete heart block and lead to:
Adams-Stoke attack (periodic fainting spell)
Cardiac arrest
Sudden cardiac death

Treatment- Implanted pacemaker.

51
Q

Third degree heart block

A

Occurs when atrial signals fail to arrive at the ventricles.

Ventricular rate is still constant but slow (<60, 40) but time between atrial and ventricular beats are variable.
Atrial beats are also consistent.
Some P waves are NOT followed by QRS

PR intervals vary and can be very long.

52
Q

Ways to differentiate between second and third degree heart block.

A
  1. In 3rd degree ventricular rate is 30-40 bpm whilst in 2nd degree, it is >50 bpm.
  2. In 3rd degree, QRS is misshaped and upside down- due to ventricular beat being an escape beat. In 2nd degree, QRS is normal as it is AVN initiated.
53
Q

Atrial fibrillation

A

Disorganised electrical activity in the atria:
No P wave- only flatline or wiggly line.

Fast and irregular ventricular rate.

Consequence:
Thrombotic formation due to slow blood flow.

Treatment:
Anti-coagulents

54
Q

Regularly irregular rhythms

A

Rhythms that have missing heart beats from an otherwise regular rhythm.

Example- Mobitz Type II 2nd degree heart block.

55
Q

Irregularly irregular rhythms

A

Rhythms with no consistent pattern in the time between QRS waves.

Example- Atrial fibrillation

56
Q

Respiratory sinus arrhythmia

A

When the heartbeat is slightly faster during inspiration and slower during expiration.

This is normal in healthy hearts like children and athletes

Cause:
Respiratory centres in the brain’s medulla.

57
Q

ST-segment elevation

A

Raised ST segment, above the isoelectric baseline, that should be flat.

Sign of acute MI

Module 103, Theme 3: Physiology of the CVS: principles of pathology, diagnosis and treatment of CV diseases. (20 decks)

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