| Question | Answer |
| Excitation contraction coupling | excitation (depolarisation) - first messenger
Rise in cytoplasmic Ca - second messenger
Contraction - target |
| Process of ECC | Depolarisation spreads along membrane
Opens L type VGCC
Calcium induced calcium release from SR via Ryr channels
Activation of contractile apparatus
Restoration of calcium levels |
| Cardiac glycosides | Positive inotropes
Inhibits Na pump
Net gain of Ca |
| How is contraction synchronised | Rapid spread of excitation throughout the atria and ventricles |
| How do the atria contract before ventricles | Transmission from atria to ventricles is slowed
1/10 second delay by AVN |
| Gap junctions | Electrically connect cells - electrical syncytium
Can regulate conduction velocity by altering number of gap junctions to control resistance |
| SAN | Initiated heart beat allowing heart to be myogenic
Highest firing rate
On right - closest to where blood enters to allow changes to be detected |
| Pattern of spread of excitation | Excitation spreads through atria rapidly
Reaches AVN and is delayed by 0.1 s
Excitation spreads rapidly through bundle of his towards the apex
Large pukinje fibres ensure rapid spread across ventricle wall |
| What does ECG record | A recording of potential changes
At the skin surface
Typically 1 mv
Due to extracellular currents
That result from heart electricity
Mainly from atria and ventricles |
| How does and ECG work | Spread of excitation between cells generates a local circuit current
This extracellular current is measured by electrodes
faster the spread bigger the reflection
Current in opposite direction to intracellular AP |
| Transmembrane vs extracellular voltage | Transmembrane - -90mV at rest, one cell depolarises giving a peak, same voltage at plateau then repolarise so graph falls
Extracellular - No difference (isoelectric), Difference produced, lost and reversed |
| Direction of dipole is important | Direction of spread of charge in the heart changes as it moves
If perpendicular - will be seen
If parallel - will not be seen
One axis of measurement is insufficient to map all electrical activities in the heart |
| Einthoven's triangle | Lead 1 - right hand to left hand detects excitation left
Lead 2 - right hand to left foot detects excitation downwards
Lead 3 - left hand to left foot detects excitation right and down |
| What causes deflection | Rapid transmission gives large deflection
Uniform excitation gives no deflection
Slow transmission gives undetectable deflection |
| Cardiac AP and ECG waves | SAN too small to produce ECG deflection
Atria depolarisation - P wave
Ventricular depolarisation - QRS complex
Ventricular repolarisation - T wave |
| Cardiac cycle and ECG | Atrial systole - P-Q
Ventricular systole - R-T
Ventricular diastole - T-R |
| PR interval | Shows AV delay of 1/10 s
If longer than 200ms - 1st degree heart block
2nd degree heart block - not all responses activate ventricles
3rd degree heart block - no communication |
| ST interval | Uniform excitation of the ventricle
Isoelectric
In ischaemia there is non-isoelectric ventricles so ECG raises
ST interval elevation shows myocardial ischaemia |
| Why no downwards deflection during atria repolarisation | Atrial repolarisation is slow
Cannot produce a sharp electrical dipole
There is a significant time when one cell is excited and another non-excited |
| Why is QRS complex not a single upright deflection | During cardiac cycle, ventricles electrical dipole changes its angle
Q wave - away from left arm -ve
R wave - to left side +ve
S wave - upwards to right -ve |
| Why are both the R and T wave upright | Ventricular APs have different durations depending in what depth they are at
Epicardium - short APs
Endocardium - long APs
First to be excited - same dipole is produced at beginning and end of contraction when only this is contracted |
