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Transcript
Cardiac cycle CV III Today – cardiovascular continued Friday – 11am-noon CV IV – noon -1pm Tutorial on membrane potentials Each phase is further subdivided to: 1. Systole a) Isovolumetric ventricular contraction b) Ventricle ejection The rhythmic contraction & relaxation of the heart Cycle divided into 2 phases with respect to ventricle action 1. Systole – ventricle contraction and blood ejection 2. Diastole – ventricle relaxation and blood filling • Note – Atria contract at the end of diastole, but most blood (~80%) moves from the atria to the ventricle prior to atrial contraction. 2. Diastole a) Isovolumetric relaxation b) Ventricle filling 1 Heart Valves Permit blood flow in only one direction When right atrial pressure > right ventricle pressure, blood fills ventricle If right ventricle pressure>right atrial pressure, AV valve closes – no flow back into atria • For blood ejection – Pressure in ventricles must > pressure in aorta and pulmonary artery • Pressure & volume changes during cardiac cycle • After contraction, as ventricles relax, backpressure from the vessels closes the aortic and pulmonary valves 2 ECG Pressure and volume changes 110 in the left heart during a contraction cycle. Aortic Pressure mm Hg Left Ventricle Left Atria End diastolic volume 0 130 End systolic volume Volume (ml) AV valves open 65 D S D Aortic & pulmonary valves open Pressure changes in the right heart during a contraction cycle. Isovolumetric ventricle contraction Isovolumetric ventricle relaxation Pressure-volume curve 120 Left Ventricle Preesure (mm Hg) E D C Left Ventricle Volume (ml) Diastolic filling isovolumetric contraction aortic valve opens rapid ejection slow ejection aortic valve closes isovolumic relaxation Cardiac Output = Heart Rate X Stroke Volume At rest: CO = 72 beats / min X 0.07 L/beat =5.0 L/min Stroke Volume = EDV – ESV = 135 ml – 65 ml = 70 ml B A 0 A–B B–C C C–D D–E E E–A Cardiac Output 200 i.e about ½ the volume remains in the left ventricle 3 Control of Heart Rate by Autonomic Nervous system Understanding cardiac output (CO) • What controls HR? • What controls SV? • SNS ↑ HR via β adrenergic receptors • PNS ↓ HR via muscarinic Ach receptors • Normal rhythm of the SA node is 100 beats/min • But, resting heart rate ~70 beats/min ¾PNS activity dominant at rest Effect of epinephrine on pacemaker potential Effect of Ach on Pacemaker potential 250 ms Epi Control 0 cont -50 Ach 0.01 μm 4 Evidence for involvement of cAMP • Conclusion Probability of Na+ channel being open – “funny” Na+ channel opening is regulated by the level of cAMP (in addition to hyperpolarization) open probability Increase this much with cAMP Membrane voltage At this voltage SA node cell Na+ β mAch Adeylate cyclase Gs Gi “funny” Na+ channel • Therefore, HR controlled by autonomic regulation of “funny” Na+ channel • As channel opening ↑, slope of pacemaker potential ↑ ATP cAMP ↑cAMP ↑ channel opening ↓cAMP ↓ channel opening 5 Other factors that can influence HR 1. Arterial pressure receptors (Baroreceptors) 2. Atrial pressure receptors • What controls Stroke Volume? • SV = End Diastolic Volume – End Systolic Volume EDV Blood flowing back to heart (venous return) ESV Effectiveness of heart pump We’ll come back to these later in blood pressure regulation EDV & SV: Frank-Starling Mechansim Stroke Volume (ml) • Thus, any factor that ↑ venous return will increase cardiac output 200 100 0 100 200 300 400 Ventricular end diastolic volume (ml) 6 Length-tension relationship of muscle 1 • Ventricle contracts more forcefully when it is filled to a larger volume 2 3 – Length-tension relationship of cardiac muscle 4 Relative tension • Why? 1.0 2 3 4 0.5 1 5 1.25 5 1.65 2 2.25 3.65 Sarcomere length (μm) Contractility • Therefore, filling ventricles with more blood stretches the sarcomeres – They produce more force • Sympathetic nervous system control – ↑ SNS activity → ↑ force production at any EDV ↑ SNS activity Stroke Volume (ml) • At rest, cardiac muscle sarcomere length is less than optimal (about position 4 on previous graph) 200 rest 100 0 100 200 300 400 Ventricular end diastolic volume (ml) 7 • How does SNS affect muscle contractility? In myocytes cAMP/Protein kinase A: L-type Ca++ Channel (dihdryopyride receptor) β Adeylate cyclase Gs 1. Increase L-type Ca++ channel opening 2. Increase RyR opening Both serve to increase cytoplasmic Ca++ and increase contraction Protein kinase A 3. Increase Ca++ pump activity Serves to increase Ca++ clearance and increase relaxation cAMP ATP Ca++ Ca++ pump SR Ryanodine receptor baroreceptors End Diastolic Volume (Frank-Starling Mech) ↑ Sympathetic activity ↑ Blood Epinephrine ↓ Parasympathetic activity Heart Rate Stroke volume Relative Contributions of SNS and PNS to Heart Function PNS primarily to SA node, AV node and Atria → Mainly effect HR, smaller effect on atrial contractility SNS to all areas of heart → effects HR and contractility Cardiac Output 8