ECG Word Scramble
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| 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 |
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