Lecture 11

what characteristics make action potentials in cardiac muscle different from those in skeletal muscle?

1. action potentials in cardiac muscle can be self-generating 2. action potentials can be conducted directly from cell to cell without the release of neurotransmitter at synapses 3. action potentials in cardiac muscle cells have long duration which prevents fusion of individual twitch contractions

how does the heart specialized excitation and conduction system work? SUMMARY progression of AP

1. start at SA Node - spontaneous depolarization is most rapid here: normal pacemaker 2. Atria - conduction slower than ventricles 3. AV Node - small cells, conduction greatly slowed, latent pacemaker 4. bundle of his (AV bundle) - conveys atrial impulses to purkinje fibers and adds another delay 5. purkinje fibers - large cells, sharply rising AP have very rapid conduction 6. ventricular muscle - last to depolarize are the first to re-polarize

resting potential for heart muscle

85-90 mV

where are the slow response AP? graph of heart

A and D: resting potential is slowly depolarizing and there is no plateau A and D are rounded so no plateau unstable resting potential so slow response AP found in AV node and SA node

The normal electrocardiogram is composed of what

P wave, QRS complex, T wave

P wave PR interval PR segment QRS wave St segment T wave QT interval

P wave: atrial depolarization PR interval: conduction time through atria and AV node to depolarization of ventricle PR segment: plateau phase of atrial excitation QRS wave: ventricular depolarization ST segment: plateau phase of ventricular excitation T wave: ventricular re-polarization Qt interval: approximates ventricular systole

PVCs and ventricular tachycardia

PVCs: not serious ventricular tachycardia: very serious, results from an ectopic focus of excitation

P wave

atrial depolarization

ventricular arrhythmias causes

bundle branch blocks PVCs Ventricular fibrillation

ventricular fibrillation is corrected by

cardiac conversion

abnormal heart excitation can impair

cardiac output

supraventricular tachycardia

caused by ectopic focus of reentry phenomenon

atrial fibrillation

complete loss of synchrony in the firing of atrial muscle cells

ask about ~ 38:30 min

confused about graph and summary / progression of AP

tachycardia

fast heart rate faster than 100 beats per minute in an adult general causes: increased body temp, sympathetic stimulation, toxic conditions of the heart can limit cardiac filling time in between beats

two diff type of action potentials of the heart

fast response slow response they're generated at different sites

what is the cardiac resting potential determined by?

it is mainly determined by membrane permeability to K+ just like skeletal muscle

what does the heart specialized excitation and conduction system promote?

it promotes efficient pumping

key concept

last slide

compared to skeletal muscle, does cardiac muscle have a short or long action potential duration

long duration (0.3 sec)

Ventricular fibrillation

loss of synchrony in excitation and contraction of ventricles and is fatal unless corrected

explain the distribution of potassium, sodium, and calcium of muscle cells of the heart

more potassium inside the cell more sodium and calcium outside the cell

what are fast response action potentials characterized by?

rapid rise and plateau following a stable resting potential

conduction blocks

represent impaired conduction through at AV node

ventricular arrhythmias

result from abnormal conduction of conduction blocks

supraventricular arrythmias

result from abnormal pacemaker activity or conduction blocks

minute 7 of slide explanation of structures of the heart

right atrium sinotrial node is below entrace of superior venacava, this node has specialized cells specialized cells within the atrioventricular node as well, its in the right atrium, right above trcuspid valve, separating right atrium from right ventricle bundle of fibers from atrial ventriclular node to left and right bundle braches is called the nundle of his or the AV bundle AV bundle splits into left and right bundle branches, there are large perkingy fibers

key concept: on slides

slides

bradycardia

slow heart rate fewer than 60 beats per minute general causes: can facilitate athletic conditioning or be a result of vagal stimulation insufficient heart rate impairs cardiac output

what are the differences between fast and slow response action potentials in cardiac muscle?

slow response: unstable resting potential is responsible for pacemaker activity and is caused by changes in membrane permeability to three ions 1. decrease in K+ permeability 2. increase in Na+ permeability 3. increase in Ca2+ permeability potassium permeability slowly decreases while sodium and calcium permeability slowly increases slowly increasing sodium and calcium permeability is described as the membrane being leaky (SA cells have leaky membranes for Na+ and CA2+), this means over time, the cell will slowly depolarize until the cell reaches threshold The SA cell AP have a slow rise primarily from inward Ca2+ with NO plateau, the cell reaches threshold and then initiates a calcium based action potential, there is little fast sodium current re-polarization then occurs, the cell goes back to negative as potassium permeability increases (less potassium flowing out, POSITIVE POTASSIUM FLOWING OUTSIDE CELL?) and Ca2+ and Na+ permeability decreases REMEMBER UNLIKE SKELETAL MUSCLE CELLS, CARDIAC ACTION POTENTIALS CAN BE SELF-GENERATING

how does the heart specialized excitation and conduction system work?

specialized conduction system involves the synoatrial node and atrioventricular node which is where we normally have slow response action potentials, which can serve as pace makers for the rest of the heart at atrial ventricular node, the specialized conduction system continues through atrial ventricular bundle aka bundle of his key thing about specialized conduction system is that separating atria from ventricles is a thick fibrous ring that acts like an insulator so the only way to get AP conducting from atria to ventricles is over the AV node and AV bundle important thing about AV bundle is when AV bundle pierces the fibrous ring, the diameter of the fibrous ring is small so slowing occurs (slowing of what) once pulse spreads over atria and fires slowing adds delay so towards end of diastole, more blood can be filled in ventricles for optimal filling before ventricles contract during systole Av bundle splits into left/right bundle branches AV bundle branches are referred to as purkinje fibers 1. impulse generation normally occurs at SA node 2. delay occurs at AV node and AV bundle, which increases filling of ventricles 3. rapid spread of action potentials across left and right ventricles by bundle branches and purkinje fibers result in synchronous contractions

resting membrane potential of fast response action potentials

stable inside negative 85-90mV mainly due to K+ conductance resting potential will be at potassium equilibrium potential which is negative (true for fast and slow action response action potentials)

what are the steps of cardiac muscle fast response action potential?

stable resting potenital that's due to potassium permeability there is then a rapid depolarization of the cell meaning the cell is moving from negative to positive rapid depolarization / rise is due to increased permeability for Na+ / fast sodium current (fast Na+ channel) so pretty much sodium is rapidly entering the cell making the cell less negative there is then a plateau phase due to increased Ca2+ into the cell, the influx of Na+ being inactivated, and decreased K+ permeability re-polarization (going from positive and back to negative resting potential, which is where it wants to be) due to increased K+ permeability (less potassium flowing out) and decreased Ca2+ permeability

cardiac conversion

stimulating outside of chest to electrodes get charged up to a few thousand volts and it gets applied for a few millasecond it depolarizes most of the heart so its in refratory period, once everything is in the refractory, if the heart is not damaged enough the heart will resume normal rhtyhm and an action potential will be fired in sinoatrial node, then heart resumes normal rhythm

abnormal heart rhythms can impair

stroke volume

supraventricular arrythmias causes

supraventricular tachycardia conduction blocks atrial fibrillation

what do the (Autonomic innervation) sympathetic and parasympathetic nerves do for pacemaker generation?

sympathetic activation: release of norepinephrine by sympathetic system binds with beta 1 receptors in the heart which increases heart rate and force of contraction -the binding increases Na+ and Ca2+ inward currents and rate of depolarization (increasing flow of positively charged ions) parasympathetic activation: release of ACh of vagus nerve binds with cholinergic receptors and decreases heart rate -the binding increases K+ outward current and hyper-polarization (increases flow of positive ions outside the muscle cell and in SA and AV node, loss of positive ions will slow down depolarization so it takes cells longer to depolarize and fire AP?? confused) -decreases inward Na+ current and rate of depolarization (slower depolarization = slower HR)

the heart is supplied with that kind of nerves

sympathetic and parasympathetic nerves

what do the sympathetic and parasympathetic nerves supply in the heart?

sympathetic nerves: distributed to all parts of the heart parasympathetic nerves: the Vagus nerve supplies mainly the SA and AV nodes

What is the ECG (electrocardiogram)

the ECG is a field potential caused by the electrical activity of the heart recorded from the surface of the body your heart is generating electriicty and with ECG youre picking up extracellular currents produced by the heart

where does impulse generation normally begin in the heart specialized excitation and conduction system?

the SA node specialized conduction system involves the synoatrial node and atrioventricular node which is where we normally have slow response action potentials, which can serve as pace makers for the rest of the heart

what explains rhythmic contractions

the heart has both fast and slow action potential

slow response action potential are located where?

the sinoatrial node (SA) and sometimes atrioventricular node

fast response action potentials is located where

the ventricle and also in the atria, but not at the sinoatrial node or atrioventricular node

3 important waves, P, QRS, and T

these mean there is change in potential

during fast response action potentials, action potentials in ventricular cells result from what?

they result from changes in membrane permeability to ions

how do fast response AP spread through the heart?

unlike skeletal muscle, cardiac AP are conducted directly from cell to cell heart muscle is a "syncytium" or meshwork of muscle cells (AP can quickly spread over entire heart because there are direct connections between one heart muscle to the next, the arrangement makes it easy to spread as well-syncytium)) muscle cells are connected end to end by intercalated disks -intercalated discs are cell membranes that separate individual muscle cells -intercalated disks provide low resistance electrical connections called "gap junctions" because of extensive branching, an AP initiated at any site will be conducted from cell to cell throughout the heart ex: cell A conducts an action potential, there are gap junctions between cells, in response to AP in cell A, there's local depolarization in cell B that happens fast, effectively, and safely cuz of direct electrical connection, that depolarization in cell B triggers an AP in cell B, which results in local depolarization of cell C, and cell D and then trigger AP within cell C and D as well (PICTURE IN SLIDES) gap junctions, meshwork, syncytium, make AP spread rapidly over entire heart

Pacemaker Potentials Summary (Slow response action potentials)

unstable resting membrane potential of conductive muscle leads to spontaneous depolarization and generation of action potential sinoatrial node reaches threshold for action potential first and normally controls the rhythm of contraction of the heart (serves as pacemaker because the cells there reach threshold first) cells with slow-response action potentials are also found in the atrioventricular node Slow AP have leaky membranes which result in gradual depolarization during resting so they can serve as pacemakers slow response AP have no plateau

QRS wave

ventricular depolarization so sharp and large because of large number of ventricle cells tht depolarize, so sharp because of synchornous of depolarization of ventriclular muscle cells

T wave

ventricular repolarization

bundle branch blocks

widen QRS complex