E109 Lecture 10 Fall 2024 PDF

Lecture 9: Cardiac Muscle Contraction Office hours: Nat Sci 2 4201 12-1PM. Come see exam keys Refractory Period: Cardiac Muscle (End of Lecture 9) a summation of force Cardiac Muscle Contraction: role of calcium...

Lecture 9: Cardiac Muscle Contraction Office hours: Nat Sci 2 4201 12-1PM. Come see exam keys Refractory Period: Cardiac Muscle (End of Lecture 9) a summation of force Cardiac Muscle Contraction: role of calcium 10 9 1 Action potential enters 3 Na+ Ca2+ from adjacent cell. Ca2+ 2 K+ Iiiiii ECF 1 ATP NCX Voltage-gated Ca2+ 2 ICF channels open. Ca2+ 3 Na+ enters cell. Ca2+ RyR2 2+ 2+ 2 3 Ca induces Ca release through ryanodine 3 receptor-channels (RyR2). SR L-type Sarcoplasmic reticulum Ca2+ (SR) Ca2+ channel 4 Local release causes Ca2+ stores Ca2+ spark. 4 ATP 2+ 5 Summed Ca2+ sparks 8 create a Ca signal. Ca2+ sparks T-tubule u 2+ 6 Ca ions bind to troponin 5 to initiate contraction. Ca2+ signal Ca2+ Ca2+ 7 Relaxation occurs when Ca2+ unbinds from troponin. 6 7 7 Actin 2+ 8 Ca is pumped back into the sarcoplasmic reticulum for storage. 2+ 9 Ca is exchanged with Na+ by the NCX antiporter. Contraction Relaxation Myosin 9Metal 10 Na+ gradient is maintained skeletalcontraction similar tocardiac remayhff Yalation by the Na+-K+-ATPase. Review Contractile cells within the heart are connected through intercalated disks that contain gap junctions and allow for transmission of force and graded potentials between cells Action potentials of cardiac contractile cells are long lasting with the cell remaining depolarized for substantially longer period of time The long refractory period prevent summation of force The contraction cycle within cardiac muscle has features that resemble both skeletal and smooth muscle contraction E109 Lecture 10: Electrical Conduction in the Heart Lecture 10 Learning Objectives Observe that autorhythmic cells undergo cyclical depolarization setting the rhythm and pace of our heart Learn that sutorhythmic cells are located at the SA node, the AV and the Purkinje fibers Understand that the fastest of the autorhythmic cells (SA node) normally set the pace Observe that ECGs allow us to detect pathologies that affect heart rate, Heart rhythm, conductions blocks, or coordination Two Types of Cardiac Muscle Cells Membrane potential of autorhythmic cell Membrane potential of contractile cell Autorhythmic cells depoiarYting Contractile cells reg r ate Yesaction cau potential causesgraded potential spreadsamongcells Intraction Contractile Cells: resting potential is stable (true of other cells) cells Contractile 1 Resting potential 3 PNa +20 2 Na+ channels open 4 PK PCa Membrane Potential (mV) 0 3 Na+ inactivation gate closes -20 4 Ca2+ channels open fast K+ channels close -40 5 2 PK PCa 5 Ca2+ channels close slow K+ channels open -60 PNa -80 1 1 -100 0 100 200 300 Time (ms) Action potential: Autorhythmic Cells Authorhythmic cells 20 4 1 If channels open Na+ enters cells 2 some Ca2+ channels open; If 0 channels close 3 3 Many Ca2+ channels open larm causing rapid depolarization –20 5 4 Ca2+ channels close; K+ channels open irential Threshold –40 5 K+ moves out of the cell 2 acalciumchannels getting us to open 1 1 1 sonetnto –60 ftp.yahoo Pacemaker Action Potential Potential naturallydepolarizing events always restarts potentialTime 04 Membrane Electrical Conduction in the Heart: coordination of contraction 1 1 SA node depolarizes. SA node AV node 2 2 Electrical activity goes rapidly to AV node via internodal pathways. 3 Depolarization spreads more slowly across THE CONDUCTING SYSTEM atria. Conduction slows through AV node. OF THE HEART 4 Depolarization moves SA node rapidly through ventricular 3 conducting system to the Internodal apex of the heart. pathways 5 Depolarization wave spreads upward from the apex. AV node AV bundle 4 Purkinje fibers 5 Setting the Pace: synced-up with SA node, or out of sync own candepolarize ontheir SA Node AV Node Purkinje 70 bpm 50 bpm 30 bpm Contractile Cells wee AV Node Purkinje 50 bpm 30 bpm Contractile Cel Purkinje 30 bpm Contractile Cell Electrocardiogram Right arm Left arm I Electrodes are attached to the skin surface. II III Left leg Electrocardiogram ECGs can help assess: Heart rate Heart rhythm Conduction blocks Coordination (fibrillation) Atrial Ventricular Ventricular depolarization depolarization repolarization SAnode avnode pjF Heart rate R 5 sec P T Normal ECG R P T Pathology Terrat Sinus tachycardia is a condition in which the sinoatrial node fires and the electrical impulse travels through the normal conduction pathway but the rate of impulse firing is faster than 100 beats per minute. Coordination (fibrilation) R 5 sec T Normal ECG P R Pathology T P disorganized Atrial fibrillation: A condition that causes uncoordinated contraction of the atria causing a disorganized contraction. Conduction Block R 5 sec T Normal ECG P Pathology P P P P P P AV Conduction block: Signals from SA node are blocked before reaching the AV node causing the ventricle contractions to be paced by the AV node or Purkinje fibers. Review Autorhythmic cells undergo cyclical depolarization setting the rhythm and pace of our heart Autorhythmic cells are located at the SA node, the AV and the Purkinje fibers Under normal conditions the fastest of the autorhythmic cells (SA node) set the pace ECGs allow us to detect pathologies that affect heart rate, Heart rhythm, conductions blocks, or coordination E109 Lecture 10: Control of Cardiac Output Control of Cardiac Output CO (mL/min) = SV(mL) x HR (BPM) Autonomic Control: target the autorhythmic cells Autonomic Control makingchannels moresensitive notsensitive Normal 20 Parasympathetic stimulation ACH + permeability causing 0 hyperpolarization 2+permeability slows the –60 rate of depolarization Hyperpolarized Slower depolarization 0.8 1.6 2.4 Time (sec) Normal Sympathetic stimulation norepinephrine 20 If channels open earlier and stay open longer 0 + permeability) –20 –40 2+ permeability increases –60 the rate of depolarization Depolarized More rapid depolarization 0.8 1.6 2.4 Time (sec) raising wherefunnychannelsopen Control of Cardiac Output muscles nervoussystem pressure increasing bloodreturnsfaster Intrinsic Control: Frank-Starling Mechanism Control of Cardiac Output Extrinsic Control of Stroke Volume Ca2+ ECF 1 ICF RyR2 2 3 SR L-type Ca2+ Ca2+ channel 4 Ca2+ sparks T-tubule 5 Ca2+ signal 6 Contraction Review Cardiac output (volume of blood expelled from the heart per minute) is determined by the product of Stroke volume (mL) and Heart rate (BPM) Heart rate is controlled through antagonistic branches of the autonomic nervous system The autonomic nervous system alters the membrane potential and rate of depolarization in autorhythmic cells Stroke volume is regulated by intrinsic properties of contractile cells and modulated by the sympathetic branch