Electrical properties of the heart and ECG

Question 1

Describe the functional syncitium in cardiac muscle.

Answer 1

There are thin actin filaments and thick myosin filaments. The membrane is called sarcolemma and T-tubules run down the muscle to make sure that the impulse is spread. Cells in cardiac muscle aren’t fused but act as 1 big cell. They are electrically connected via gap junctions and physically connected via desmosomes.

Question 2

Describe excitation-contraction coupling in the heart.

Answer 2

Cardiac muscle has a long AP: 250 milleseconds (vs 2 ms in skeletal muscle). This is due to Ca2+ entering and means contraction can be regulated. As there is a long refractory period, cardiac muscle cannot exhibit tetanic contraction - heart cannot contract again until it has relaxed.

Question 3

How is strength of contraction varied?

Answer 3

Ca2+ entering myocytes - Ca2+ entry does not saturate the troponin and so regulation of Ca2+ release is used to vary strength of contraction.

Question 4

What special function to cells with unstable RMP have?

Answer 4

Act as pacemakers.

Question 5

Describe the non-pacemaker AP.

Answer 5

High resting PK+ (permeability to K+). In initial depolarisation, > PNa+ then Na+ channels close really quickly. Then pleteau when there is an > of PCa2+ (L-type) and PK+.

Question 6

Describe pacemaker AP.

Answer 6

> PCa2+ (L-type). The pacemaker potential in complicated. Due to gradual PNa+ and late > in Pca2+ (T-type) - this nudges the cell towards threshold.

This is contrasted with L-type Ca2+ channels which let lots of Ca2+ and cause the AP.

Question 7

What is explained by the pacemaker potential?

Answer 7

Auto-rhythmicity. Can take the heart out of the body and it will still fire AP’s.

Question 8

Give examples of modulators of electrical activity.

Answer 8

1) Drugs: CA2+ channel blockers block L-type Ca2+; decrease amount of X-bridges made and force of contraction.
2) Temperature: >10 bpm/degree.
3) Hyperkalaemia: fibrillation and heart block; cause cells to spontaneously reach threshold.
4) Hypokalaemia: for unknown reasons all cells start to depolarise and reach threshold; fibrillation and heart block.
5) Hypercalcaemia: > HR and force of contraction.
6) Hypocalcaemia:

Question 9

What is heart block?

Answer 9

Failure in conduction from atria to ventricles.

Question 10

Where are the fastest pacemakers located?

Answer 10

SA node (sianoatrial) - this is classed as the pacemaker of the heart. Conducts at 0.5 m/sec. Wave of contraction goes across the atria and squeezes blood into the ventricles.

Question 11

What is the only part of the heart without gap junctions?

Answer 11

Annulus fibrosis - non-conducting. L and R.

Question 12

What is the function of the AV node?

Answer 12

Delay box - gives time for the atria to contract and push blood into ventricles. Speed is 0.05 m/s.

Question 13

What is the Bundle of His?

Answer 13

Breaks down into individual Purkinje fibres. A rapid conduction system that gets excitation to all parts of the ventricle at the same time. Fastest conductor at 5 m/s.

Question 14

What does an ECG record?

Answer 14

An AP in a single myocyte evokes a very small extracellular electrical potential. However, lots of small extracellular potentials evoked by many cells depolarising/repolarising at the same time can summate to large extracellular electrical waves. These can be recorded in the periphery as an ECG.

Question 15

What are the waves of an ECG and what do these correspond to?

Answer 15

P QRS T.

P: atrial depolarisation

QRS: ventricular depolarisation

T: ventricular repolarisation

(Sometimes there is a U wave which is capillary muscle repolarisation.

Question 16

What isn’t there a wave for atrial repolarisation?

Answer 16

This occurs at the same time as ventricular depolarisation which swamps any signal from artial repolarisation.

Question 17

What does an ECG tell you?

Answer 17

About the speed of depolarisation - doesn’t tell you about the pumping ability of the heart.

Question 18

Describe supraventricular tachycardia.

Answer 18

HR is so high that P wave is always superimposed on previous T wave. A disorder of rhythm.

Question 19

Describe atrial fibrillation.

Answer 19

No P waves, just QRS and T. Not lethal. A disorder of rhythm. Causes irregular and abnormally fast HR.

Question 20

Describe ventricular fibrillation.

Answer 20

Can be lethal as there is no blood flow. Use a d-fib.

Question 21

What do the SLL’s (standard limb leads) look at?

Answer 21

Events in the vertical or frontal plane. Typical ECG’s recorded from SLL2 (from the left leg with respect to the right arm). When atria and ventricles depolarise this goes towards the left leg.

Question 22

What is the PR interval?

Answer 22

Time from atrial depolarisation to ventricular depolarisation. This is mainly due to transmission through the AV node and takes 0.1-0.2 seconds.

Question 23

What does the QRS show?

Answer 23

Time it takes for the whole ventricle to depolarise - 0.8 seconds.

Question 24

What is the QT interval?

Answer 24

Time spend while the ventricles are depolarised - first bits to last bits. Varies depending on HR but usually 0.42 seconds at 60 bpm.

Question 25

Why is the QRS complex so complex?

Answer 25

Different parts of the ventricle depolarise at different times in different directions.

1) (Q) Interventricular septum depolarises from L to R
2) (R) Bulk of ventricle depolarises from endocardial to epicardial surface
3) (S) Upper part of IV septum depolarises

Q and S are smaller bits of tissue and go in the opposite direction from R.

Question 26

Why is the T-wave positive?

Answer 26

AP is longer in epicardial then endocardial cells - wave of repolarisation runs in opposite direction to wave of depolarisation. Cells that depolarised last repolarise first.

Question 27

Why is the R-wave bigger in SLL2 than 1 or 3?

Answer 27

Main vector of depolarisation is in line with the axis of recording of left leg with respect to right arm. Wave biggest when depolarisation is in the same plane?

Question 28

What would happen if the heart was rotated to the left?

Answer 28

Causes axis deviation - bigger SLL1 R wave as it is more in line. If there was more muscle dur to hypertension, bigger R wave in SLL1.

Question 29

What extra information do augmented limb leads give you?

Answer 29

By recording from 1 limb lead with respect to the other 2 it gives you 3 different perspectives on the heart. SLL1, SLL2, SLL3, aVR, aVL and aVF: 6 different perspectives. aVL is in the middle as it is at a right angle. aVR is the biggest negative going wave. aVF is the biggest positive going wave.

Question 30

What extra information is given by pre-cordial (chest) leads?

Answer 30

Arranged in front of the heart and so look at the same events, but in the horizontal plane. Main vector of depolarisation going from LV so negative from V1, positive from V6 and flip over somewhere between V3 and V4.

Question 31

What is the difference between LL’s and pre-cordial leads?

Answer 31

LL’s look at the spread of depolarisation and repolarisation from 6 angles in the frontal plane, pre-cordial same but in transverse plane. Changes in spread of depolarisation are predictable from an ECG.

Question 32

How can HR be calculated by the rhythm strip?

Answer 32

Paper should run at 25 mm/sec. Count R waves in 30 large squares (6 seconds) and X by 10. 60 bpm normal, 60 tachycardia.

Question 33

What is the difference between STEMI and NSTEMI?

Answer 33

STEMI is ST elevated MI. NSTEMI is non-ST elevated MI. STEMI is worse than NSTEMI.