PSL301H – Lecture 2: Cardiac Excitability: Heart Rate and ECG PDF

PSL301H – Lecture 2: Cardiac excitability: heart rate and ECG What is the underlying reason that heart cells contract? What is the cause, the effect, and ways to use that information to study the heart? Silverthorn 7th ed: 453-461 Silverthorn 8th ed: 450-459 Two...

PSL301H – Lecture 2: Cardiac excitability: heart rate and ECG What is the underlying reason that heart cells contract? What is the cause, the effect, and ways to use that information to study the heart? Silverthorn 7th ed: 453-461 Silverthorn 8th ed: 450-459 Two types of Cardiac action potentials Type 1: Non-pacemaker cell (myocyte) action potentials "fast response" action potentials - rapid depolarization in response to AP contractile cells are “soldiers” – need instructions to fire Make up most of the atrial and ventricular muscle wall Two types of Cardiac action potentials Type 2: Pacemaker (autorhythmic) cells Unstable resting potential- causes spontaneous firing Non-contractile cells- “generals”- provide firing instructions to muscular soldiers found in the sinoatrial and atrioventricular nodes Action Potentials in cardiac autorhythmic cells Funny current channels (If) cause unstable resting potential - permeable to both K+ and Na+ 20 Ca2+ channels close, K+ channels open 0 Ca2+ in K+ out Lots of Ca2+ Membrane potential (mV) channels –20 open Threshold –40 Ca2+ in Some Ca2+ channels open, –60 If channels close If channels Net Na+ in If channels open Pacemaker Action open potential potential K+ channels close Time Time Time The pacemaker potential Ion movements during an gradually becomes less action and pacemaker State of various ion channels negative until it reaches potential threshold, triggering an action potential. If; Na influx>K efflux Cardiac action potentials (roles for Na+ and Ca2+) Role of Na+ Cardiac muscle (non-pacemaker) cells Rapid depolarization phase caused by an opening of Na+ channels Cardiac pacemaker cells Slowly depolarizing pacemaker potential (If opening results in net Na+ influx) for autorhythmic cells Role of Ca2+ Cardiac muscle (non-pacemaker) cells Ca2+ influx prolongs the duration of the action potential and produces a characteristic plateau phase. Cardiac pacemaker cells Ca2+ ions are involved in the initial depolarization phase of the action potential. Electrical Conduction to Myocardial Cells How do autorhythmic signals reach muscle cells? Membrane potential of autorhythmic cel Membrane potential of contractile cell Cells of SA node Contractile cell Intercalated disk with gap junctions Depolarizations of autorhythmic cells rapidly spread to adjacent contractile cells through gap junctions.  All cells of the intrinsic conduction system (wiring) have the ability to generate spontaneous action potentials - i.e. they are autorhythmic Copyright © 2009 Pearson Education, Inc. Copyright © 2009 Pearson Education, Inc. Electrical Conduction in the Heart Audiovisual https://www.youtube.com/watch?v=bxKBQqe_Bo0 Electrical Conduction in the Heart 1 1 SA node depolarizes. SA node AV node 2 Electrical activity goes 2 rapidly to AV node via internodal pathways. 3 Depolarization spreads more slowly across THE CONDUCTING SYSTEM atria. Conduction slows OF THE HEART through AV node. 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 Bundle Purkinje branches fibers 5 Nodes (Control Points) SA node Sets the pace of the heartbeat at ~70 bpm AV node (50 bpm) and Purkinje fibers (25-40 bpm) can act as pacemakers under some conditions….slower pacemaker activity AV node Routes the direction of electrical signals Delays the transmission of action potentials  Conductive fibres are often sheathed (separated from myocyte connections) except for in specialized contact regions of atria and ventricles. Note also how atrial and ventricular myocyte syncytia are separated? By an inert fibrous tissue barrier - there are no GAP junctions between them. Why do you think this might be? Copyright © 2009 Pearson Education, Inc.  Heart Rate is Controlled by both Symapthetic and Parasympathetic Nerves Copyright © 2009 Pearson Education, Inc.  Heart rate regulation - SA node action potential firing rate is regulated by both and fibres Epi NE Ach Copyright © 2009 Pearson Education, Inc. Parasympathetic Control of Heart Rate Parasympathetic activity lowers heart rate: activates the vagus nerve that innervates the SA node. releases the neurotransmitter acetylcholine (Ach) that binds to muscarinic receptors (M2R) in SA node cells at rest, there is significant vagal tone on the SA node ! resting heart rate is between 60 and 80 beats/min. atropine, a muscarinic receptor antagonist, leads to a 20-40 beats/min increase in heart rate.  Ach Copyright © 2009 Pearson Education, Inc. Control of Heart Rate To increase heart rate (above the intrinsic rate) Need activation of sympathetic nerves innervating the SA node that release the neurotransmitter norepinephrine (NE) that binds to beta- adrenergic receptors (bARs) on SA node cells. Can also be stimulated by circulating catecholamines released from the adrenal gland during a sympathetic response  Epi NE Sympathetic activity in SA node results in increased cAMP, increased PKA activity and increased Cav (L-type Ca2+ channels) and HCN (funny current) channel activity Copyright © 2009 Pearson Education, Inc. Modulation of Heart Rate by the Autonomic Nervous System Membrane potential (mV) Membrane potential (mV) Normal Sympathetic stimulation Normal Parasympathetic stimulation 20 20 0 0 –20 –40 –60 –60 Depolarized More rapid depolarization Hyperpolarized Slower depolarization 0.8 1.6 2.4 0.8 1.6 2.4 Time (sec) Time (sec) Review question Which of the following statements regarding autorhythmic cells is true? a) The depolarization phase requires the movement of K+ out the cell b) They are located on the outside of the heart c) The membrane potential is unstable, drifting between -90mV and – 55 mV d) Increasing the cellular concentration of cAMP will increase their rate of depolarization Control of Heart Rate vs Contraction strength Vagus nerves (Parasympathetic) causes a decrease in the SA node rate (thereby decreasing the heart rate). Parasympathetic fibers cannot change the force of contraction, however, because they only innervate the SA node and AV node. Sympathetic fibers increase SA node rates (thereby increasing the heart rate) and can increase the force of contraction because in addition to innervating the SA and AV nodes, they innervate the atria and ventricles themselves. Can we use what we learned of the heart anatomy and basic electrical properties to gain even more insight into health and disease??? Copyright © 2009 Pearson Education, Inc. The Electrocardiogram Three major waves: P wave, QRS complex, and T wave The electrocardiogram (ECG) is the oldest and the most commonly used cardiology procedure. It is noninvasive, simple to record and its cost is minimal. Electrical Activity - Overview Correlation between an ECG and electrical events in the heart  Figure 14-21 (2 of 9) Copyright © 2009 Pearson Education, Inc.  Figure 14-21 (3 of 9) Copyright © 2009 Pearson Education, Inc.  Figure 14-21 (4 of 9) Copyright © 2009 Pearson Education, Inc. 14-21CorrelateECGHeart_3_L  Figure 14-21 (5 of 9) Copyright © 2009 Pearson Education, Inc.  Figure 14-21 (6 of 9) Copyright © 2009 Pearson Education, Inc.  Figure 14-21 (7 of 9) Copyright © 2009 Pearson Education, Inc.  Figure 14-21 (8 of 9) Copyright © 2009 Pearson Education, Inc. Comparison of ECG and myocardial action potential 1 mV 1 sec (a) The electrocardiogram represents the summed electrical activity of all cells recorded from the surface of the body. 110 mV 1 sec (b) The ventricular action potential is recorded from a single cell using an intracellular electrode. Notice that the voltage change is much greater when recorded intracellularly. Tips for analysis of an ECG QUESTIONS TO ASK WHEN ANALYZING ECG TRACINGS: 1. What is the rate: Is it within the normal range of 60–100 beats per minute? 2. Is the rhythm regular? 3. Are all normal waves present in recognizable form? 4. Is there one QRS complex for each P wave? If yes, is the P-R segment constant in length? If there is not one QRS complex for each P wave, count the heart rate using the P waves then count it according to the R waves. Are the rates the same? Which wave would agree with the pulse felt at the wrist? ECG: Normal and abnormal electrocardiograms Normal P, wide QRS Complete Block: alternate pacemaker in ventricle..Purkinje Fibers. Infarcted? ‘no P’, irregular QRS ‘no P’, no QRS Ventricular fibrillation Normal P, normal QRS P Not triggering QRS…… Problems where?? Second degree heart block: AV node