Download After atrial excitation, impulse travels through the AV node

After atrial excitation, impulse travels through the AV node & specialised conduction system to excite the ventricle. Simultaneously atria are contracting, and by the time ventricular activation is complete, atrial contraction is already over (QRS ECG). Ventricular pressure curve sharply increases shortly after QRS complex, signalling onset of ventricular systole. As ventricle contraction begins ventricular pressure immediately exceeds atrial pressure, closing AV valve. Isovolumetric ventricular contraction occurs where no valves are open, therefore ventricle volume is constant, as is muscle fibre length. Ventricle pressure then increases until exceeds aortic or pulmonary pressures, where the aortic valve opens (pulmonary semilunar valve in right side) where blood is then ejected, causing a rise in pressure curves of the blood new location. The amount of blood pumped out is called stroke volume, and ventricular systole includes both isovolumetric contraction and ventricular ejection. The ventricle does not empty completely during ejection, which is normally half diastole blood volume is pumped out. The remaining blood volume is called ESV and averages 65mL. Ventricle repolarisation occurs (T on ECG) at the end of ventricle systole. When ventricle pressure falls below aortic pressure (pulmonary trunk pressure right side) the aortic valve closes, which causes a dicrotic notch in the pressure curve. Isovolumetric ventricular relaxation then occurs, as ventricle pressure still exceeds atrial pressure, so no blood can enter ventricle from atrium. Muscle fibre length and chamber volume remain constant, as the ventricle relaxes and the pressure continues to fall. Ventricular filling occurs when atrial pressure exceeds ventricle pressure, opening the Av valve. Ventricular diastole includes ventricular relaxation and ventricular filling. *Systolic volume = EDV – ESV *Heart sounds-­‐ LUB = closure of AV valves DUM = closure of semilunar valves. * Cardiac output – volume of blood pumped by each ventricle per min / not total blood pumped by heart, as pulmonary blood volume is same as systemic blood volume. * Cardiac output depends on stroke volume and heart rate, with average resting 70 BPM. *Stroke volume average is 70 mL * Cardiac output = heart rate x stroke volume 70 BPM x 70mL = 4900mL/min = 4.9 L / min * Influences that determine cardiac output by influencing heart rate or stroke volume fig 9.25 p 332. Heart rate modulation by innervation of ANS Para-­‐ SA and AV node innervation – Ach from Vagus bind muscarinic – reduce CAMP activity. Also Ach increase K+ permeability of pace maker cells in SA node-­‐ K+ channel open = hyperpolarisation and decrease in AV node excitability (thus adding to the Av nodal delay), as the automatic reduction in K+ permeability that contributes to development of pacemaker potential is opposed. This prolongs the time for the SA node to reach threshold, by inhibiting CAMP pathway together with depressing NA+ and Ca2+ movement, therefore slowing Heart rate. In addition, Ach also supresses sympathetic activity by inhibiting the release of noradrenaline. Symp – SA and AV and ventricle innervation – adrenaline-­‐ bind B1 adrenergic receptor-­‐ G protein accelerate CAMP = channels stay open for longer. SA node and pacemaker cell depolarisation speeds up, allowing more NA+ and Ca2+, resulting in more frequent AP and faster heart rate. AV node stimulation reduces AV nodal delay by increasing conduction velocity as a result enhancing the slow inward Ca2+ current. Increases contractile strength in atrial and ventricle contractile cells, as Ca2+ permeability is increased, whilst also speeding up relaxation by