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ECG

Physiology and Pharmacology

QuestionAnswer
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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