Cardiovascular Physiology: Lecture 2 PDF

Lecture 2 Properties of Cardiac Muscle ( part 1 ) Learning Objectives:  Demonstrate understanding the properties of cardiac muscle  Knowledge about electrical activity of cardiac muscle cell and its action potential  Explaining the pacemaker of the heart 1- EXCITABILITY is defined...

Lecture 2 Properties of Cardiac Muscle ( part 1 ) Learning Objectives:  Demonstrate understanding the properties of cardiac muscle  Knowledge about electrical activity of cardiac muscle cell and its action potential  Explaining the pacemaker of the heart 1- EXCITABILITY is defined as the ability of a living tissue to give response to a stimulus. In all tissues, initial response to a stimulus is electrical activity in the form of action potential. ELECTRICAL POTENTIALS IN CARDIAC MUSCLE Resting membrane potential in:  Single cardiac muscle fiber: – 90 mV  Sinoatrial (SA) node: – 55 to – 60 mV Action Potential Action potential in cardiac muscle is different from that of other tissues such as skeletal muscle, smooth muscle and nervous tissue. Duration of the action potential in cardiac muscle cell is 200 to 350 msec (0.2 to 0.35 sec). Phases of action potential Action potential in a single cardiac muscle fiber occurs in the following phases: Phase 0: Initial Depolarization It is very rapid and it lasts for about 2 msec (0.002 sec). Amplitude of depolarization is about + 20 mV. Phase 1: Initial Repolarization Immediately after depolarization, there is an initial rapid repolarization for a short period of about 2 msec. Phase 2: Plateau or Final Depolarization the muscle fiber remains in depolarized state for sometime before further repolarization. It forms the plateau (stable period) in action potential curve. Due to long plateau in action potential, the contraction time is also longer in cardiac muscle by 5 to 15 times than in skeletal muscle. Phase 3: Final Repolarization occurs after the plateau. It is a slow process and it lasts for about 50 to 80 msec before the re-establishment of resting membrane potential. Phase 4 : The resting membrane potential. IONIC BASIS OF ACTION POTENTIAL 1. Initial Depolarization ( phase 0 ) is a result of rapid opening of fast sodium channels and the rapid influx of sodium ions. 2. Initial Repolarization ( phase 1 ) is due to the transient (short duration) opening of potassium channels and efflux of a small quantity of potassium ions from the muscle fiber. Simultaneously, the fast sodium channels close suddenly and slow sodium channels open, resulting in slow influx of low quantity of sodium ions. 3. Plateau or Final Depolarization ( phase 2 ) Plateau is due to the slow opening of calcium channels. These channels are kept open for a longer period and cause influx of large number of calcium ions. Already the slow sodium channels are opened, through which slow influx of sodium ions continues. Because of the entry of calcium and sodium ions into the muscle fiber, positivity is maintained inside the muscle fiber, producing prolonged depolarization, i.e. plateau. 4. Final Repolarization ( phase 3 ) there is a closure of calcium channels and efflux of potassium ions. Potassium efflux continues until the end of repolarization. 5. Resting membrane potential ( phase 4 ) At the end of final repolarization, all sodium ions, which had entered the cell throughout the process of action potential move out of the cell and potassium ions move into the cell, by activation of sodium-potassium pump. Simultaneously, excess of calcium ions, which had entered the muscle fiber also move out through sodium calcium pump. Thus, the resting membrane potential is restored. SPREAD OF ACTION POTENTIAL THROUGH CARDIAC MUSCLE Action potential spreads through cardiac muscle very rapidly because of the presence of gap junctions between the cardiac muscle fibers. Gap junctions allow free movement of ions and so the action potential spreads rapidly from one muscle fiber to another fiber. 2- RHYTHMICITY is the ability of a tissue to produce its impulses regularly. THE PACEMAKER is the structure of heart from which the impulses for heartbeat are produced. It is formed by the pacemaker cells called P cells. The pacemaker of the heart is the sinoatrial node (SA node). Sinoatrial Node Sinoatrial (SA) node is a small strip of modified cardiac muscle, situated in the superior part of lateral wall of right atrium, just below the opening of superior vena cava. The fibers of this node do not have contractile elements. Other parts of heart such as atrioventricular (AV) node, purkinje fibers also can produce the impulses and function as pacemakers but Still, SA node is called the pacemaker because the rate of production of impulse is more in SA node than in other parts (about 60- 100/minute ). N.B. AV node rate is about 40- 60 / minute Purkinje fiber is about 15- 40 / minute The resting membrane potential in SA node has a negativity of –55 to –60 mV and it is unstable. Action Potential of pacemaker Depolarization starts very slowly and the threshold level of –40 mV is reached very slowly. After the threshold level, rapid depolarization occurs up to +10 mV. It is followed by rapid repolarization. Ionic Basis of Electrical Activity in Pacemaker: Depolarization Resting membrane potential is not stable in the SA node. To start with, the sodium ions leak into the pacemaker fibers and cause slow depolarization( phase 4). This slow depolarization forms the initial part of pacemaker potential ( prepotential ). Then, the calcium channels start opening (phase 0). There is a slow influx of calcium ions causing further depolarization in the same slower rate. It forms the later part of the pacemaker potential. When the negativity is decreased to –40 mV, which is the threshold level, the action potential starts with rapid depolarization. The depolarization occurs because of influx of more calcium ions. Unlike in other tissues, the depolarization in SA node is mainly due to the influx of calcium ions, rather than sodium ions. Repolarization (phase 3) After rapid depolarization, repolarization starts which it is due to the efflux of potassium ions from pacemaker fibers. Potassium channels remain open for a longer time, causing efflux of more potassium ions. It leads to the development of more negativity, beyond the level of resting membrane potential. Autonomic control of the SA node 1- Vagal stimulation  Decrease the rate of nodal discharge ( - ve chronotropic effect )  Release acetylcholine which act on muscarinic receptors leading to increase potassium outflow leading to hyperpolarization. 2- Sympathetic stimulation  Increase the rate of nodal discharge ( + ve chronotropic effect )  Release of norepinephrine acting on B1 receptors leading to increase intracellular c AMP which facilitate the opening of Ca+ channels and Ca+ influx leading to more rapid depolarization.