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Nerve Supply to the Heart / SA & AV Nodes / EKG

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Chapter 19<br />

<strong>Nerve</strong> <strong>Supply</strong> <strong>to</strong> <strong>the</strong> <strong>Heart</strong> /<br />

<strong>SA</strong> & <strong>AV</strong> <strong>Nodes</strong> / <strong>EKG</strong>


<strong>Nerve</strong> <strong>Supply</strong> <strong>to</strong> <strong>Heart</strong> (1 of 3)<br />

Sinoatrial Node (<strong>SA</strong> node) and Atrioventricular Node<br />

(<strong>AV</strong> node) “leak sodium ions”<br />

do not maintain a “static” resting potential<br />

nodal cardiocytes <strong>to</strong> reach threshold first will<br />

depolarize and set <strong>the</strong> rate of depolarization for all<br />

<strong>the</strong> o<strong>the</strong>r myocardiocytes in <strong>the</strong> heart<br />

Sinoatrial Node = Pacemaker (leak sodium faster!)<br />

Atrioventricular Node = Secondary Pacemaker<br />

The rate of depolarization of <strong>the</strong>se nodes are<br />

“modified” by <strong>the</strong> au<strong>to</strong>nomic nervous system<br />

• Sympa<strong>the</strong>tic NS<br />

• Parasympa<strong>the</strong>tic NS


<strong>Nerve</strong> <strong>Supply</strong> <strong>to</strong> <strong>Heart</strong> – Sympa<strong>the</strong>tic <strong>Nerve</strong>s (2 of 3)<br />

• sympa<strong>the</strong>tic nerves<br />

– sympa<strong>the</strong>tic pathway <strong>to</strong> <strong>the</strong> heart originates in <strong>the</strong><br />

lower cervical <strong>to</strong> upper thoracic segments of <strong>the</strong><br />

spinal cord<br />

– continues <strong>to</strong> adjacent sympa<strong>the</strong>tic chain ganglia<br />

– some pass through cardiac plexus in mediastinum<br />

– continue as cardiac nerves <strong>to</strong> <strong>the</strong> heart<br />

– fibers terminate in<br />

• <strong>SA</strong> and <strong>AV</strong> nodes<br />

• in atrial and ventricular myocardium<br />

• coronary arteries (as well as <strong>the</strong> aorta, pulmonary trunk)<br />

– increase heart rate and contraction strength<br />

– dilates coronary arteries <strong>to</strong> increase myocardial blood<br />

flow


<strong>Nerve</strong> <strong>Supply</strong> <strong>to</strong> <strong>Heart</strong> (3 of 3)<br />

• parasympa<strong>the</strong>tic nerves<br />

– pathway begins with nuclei of <strong>the</strong> vagus nerves in<br />

<strong>the</strong> medulla oblongata<br />

– extend <strong>to</strong> cardiac plexus and continue <strong>to</strong> <strong>the</strong> heart by<br />

way of <strong>the</strong> cardiac nerves<br />

– fibers of right vagus nerve lead <strong>to</strong> <strong>the</strong> <strong>SA</strong> node<br />

– fibers of left vagus nerve lead <strong>to</strong> <strong>the</strong> <strong>AV</strong> node<br />

– little or no vagal stimulation of <strong>the</strong> myocardium<br />

• parasympa<strong>the</strong>tic stimulation reduces <strong>the</strong> heart rate<br />

– slows heart rate


Cardiac Rhythm<br />

• cycle of events in heart given special names<br />

– sys<strong>to</strong>le – atrial or ventricular contraction<br />

– dias<strong>to</strong>le – atrial or ventricular relaxation<br />

• sinus rhythm<br />

– normal heartbeat triggered by <strong>the</strong> <strong>SA</strong> node<br />

– set by <strong>SA</strong> node at 60 – 100 bpm<br />

– adult at rest is 70 <strong>to</strong> 80 bpm (vagal <strong>to</strong>ne)<br />

• ec<strong>to</strong>pic focus<br />

– caused by ano<strong>the</strong>r parts of heart that fires before <strong>SA</strong><br />

node discharges<br />

– caused by hypoxia, electrolyte imbalance, caffeine,<br />

nicotine, cocaine and o<strong>the</strong>r drugs<br />

– see next slide


Abnormal <strong>Heart</strong> Rhythms<br />

• spontaneous firing from some part of heart o<strong>the</strong>r than <strong>the</strong> <strong>SA</strong><br />

node<br />

– ec<strong>to</strong>pic foci<br />

• region of spontaneous firing<br />

• nodal rhythm – if <strong>SA</strong> node is damaged, heart rate is set by<br />

<strong>AV</strong> node, 40 <strong>to</strong> 50 bpm<br />

• intrinsic ventricular rhythm – if both <strong>SA</strong> and <strong>AV</strong> nodes are<br />

not functioning, rate set by o<strong>the</strong>r myocardiocytes at 20 <strong>to</strong> 40<br />

bpm<br />

– Arrhythmia<br />

– this requires artificial pacemaker <strong>to</strong> sustain life long term<br />

• any abnormal cardiac rhythm<br />

• failure of conduction system <strong>to</strong> transmit signals (heart block)<br />

• bundle branch block<br />

• <strong>to</strong>tal heart block (damage <strong>to</strong> <strong>AV</strong> node)


• atrial fibrillation<br />

– ec<strong>to</strong>pic foci in atria<br />

Cardiac Arrhythmias<br />

– atria beat 200 - 400 times per minute<br />

– May not be fatal<br />

• ventricular fibrillation<br />

– serious arrhythmia caused by electrical signals reaching different regions at<br />

widely different times<br />

– heart can’t pump blood and no coronary perfusion<br />

– kills quickly if not s<strong>to</strong>pped<br />

• defibrillation - strong electrical shock whose intent is <strong>to</strong> depolarize <strong>the</strong><br />

entire myocardium, s<strong>to</strong>p <strong>the</strong> fibrillation, and reset <strong>SA</strong> nodes <strong>to</strong> sinus<br />

rhythm<br />

• premature ventricular contractions (PVCs)<br />

– caused by stimulants, stress or lack of sleep


Pacemaker Physiology<br />

• <strong>SA</strong> node does not have a stable resting membrane potential<br />

– note <strong>the</strong>se cells are different than <strong>the</strong> typical myocyte!<br />

– starts at -60 mV and drifts upward from a slow inflow of Na +<br />

– gradual depolarization is called pacemaker potential<br />

– when reaches threshold of -40 mV<br />

• voltage-gated fast Ca 2+ and Na + channels open <strong>to</strong><br />

depolarize <strong>the</strong> cell (contraction)<br />

• faster depolarization occurs peaking at 0 mV<br />

• K + channels <strong>the</strong>n open and K + leaves <strong>the</strong> cell<br />

– causing repolarization (relaxation of cardiocyte)<br />

– once K + channels close, pacemaker potential starts over<br />

– each depolarization of <strong>the</strong> <strong>SA</strong> node sets off one heartbeat<br />

• at rest, fires every 0.8 seconds or 75 bpm<br />

• <strong>SA</strong> node is <strong>the</strong> system’s pacemaker


<strong>SA</strong> Node Potentials<br />

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.<br />

+10<br />

Membrane potential (mV)<br />

0<br />

–10<br />

–20<br />

–30<br />

–40<br />

–50<br />

–60<br />

–70<br />

Fast<br />

Ca 2+ –Na +<br />

inflow<br />

Slow Na +<br />

inflow<br />

Fast K +<br />

outflow<br />

Threshold<br />

Pacemaker<br />

potential<br />

Action<br />

potential<br />

0 .4 .8<br />

1.2 1.6<br />

Time (sec)


Impulse Conduction <strong>to</strong> Myocardium<br />

• signal from <strong>SA</strong> node stimulates two atria <strong>to</strong> contract almost<br />

simultaneously<br />

– reaches <strong>AV</strong> node in 50 msec<br />

• signal slows down through <strong>AV</strong> node<br />

– thin cardiocytes have fewer gap junctions<br />

– delays signal 100 msec which allows <strong>the</strong> ventricles <strong>to</strong> fill<br />

• signals travel very quickly through <strong>AV</strong> bundle and Purkinje<br />

fibers<br />

– entire ventricular myocardium depolarizes and contracts in<br />

near unison<br />

• papillary muscles contract an instant earlier than <strong>the</strong> rest,<br />

tightening slack in chordae tendineae<br />

• ventricular sys<strong>to</strong>le progresses up from <strong>the</strong> apex of <strong>the</strong> heart<br />

– spiral arrangement of cardiocytes twists ventricles slightly<br />

– like someone wringing out a <strong>to</strong>wel


Cardiac Conduction System<br />

1<br />

<strong>SA</strong> node fires.<br />

Right atrium<br />

Sinoatrial node<br />

(pacemaker)<br />

Atrioventricular<br />

node<br />

Atrioventricular<br />

bundle<br />

2<br />

1<br />

3<br />

2<br />

4<br />

5<br />

Left<br />

atrium<br />

Purkinje<br />

fibers<br />

Bundle<br />

branches<br />

2<br />

3<br />

4<br />

5<br />

Excitation spreads through<br />

atrial myocardium.<br />

<strong>AV</strong> node fires.<br />

Excitation spreads down <strong>AV</strong><br />

bundle.<br />

Purkinje fibers distribute<br />

excitation through<br />

ventricular myocardium.<br />

Purkinje fibers


Electrical Behavior of Cardiocyte<br />

• cardiocytes have a stable resting potential of -90 mV<br />

• depolarize only when stimulated<br />

– depolarization phase (very brief)<br />

• stimulus opens voltage regulated Na + gates, (Na + rushes in)<br />

membrane depolarizes rapidly<br />

• action potential peaks at +30 mV<br />

• Na + gates close quickly<br />

– plateau phase lasts 200 <strong>to</strong> 250 msec, sustains<br />

contraction for expulsion of blood from heart<br />

• Ca 2+ channels are slow <strong>to</strong> close and SR is slow <strong>to</strong> remove<br />

Ca 2+ from <strong>the</strong> cy<strong>to</strong>sol<br />

– repolarization phase -Ca 2+ channels close, K +<br />

channels open, rapid diffusion of K + out of cell returns it<br />

<strong>to</strong> resting potential<br />

• has a long absolute refrac<strong>to</strong>ry period of 250 msec<br />

compared <strong>to</strong> 1 – 2 msec in skeletal muscle<br />

– prevents wave summation and tetanus which would s<strong>to</strong>p<br />

<strong>the</strong> pumping action of <strong>the</strong> heart


Action Potential of Myocardiocyte


Electrocardiogram (ECG or <strong>EKG</strong>)<br />

• composite of all action potentials of nodal and<br />

myocardial cells<br />

• detected, amplified and recorded by electrodes on<br />

arms, legs and chest<br />

0.8 second<br />

R<br />

R<br />

+1<br />

Millivolts<br />

0<br />

P wave<br />

T wave<br />

PQ<br />

segment<br />

ST<br />

segment<br />

PR<br />

interval<br />

Q<br />

S<br />

QT<br />

interval<br />

QRS interval<br />

–1<br />

Atria<br />

contract<br />

Ventricles<br />

contract<br />

Atria<br />

contract<br />

Ventricles<br />

contract


ECG Deflections<br />

• P wave<br />

– <strong>SA</strong> node fires<br />

– atria depolarize<br />

0.8 second<br />

• PQ segment<br />

– atrial sys<strong>to</strong>le<br />

– atrial sys<strong>to</strong>le begins 100 msec after<br />

<strong>SA</strong> signal<br />

• QRS complex<br />

– ventricular depolarization<br />

– complex shape of spike due <strong>to</strong><br />

different thickness and shape of <strong>the</strong><br />

two ventricles<br />

Millivolts<br />

+1<br />

0<br />

P wave<br />

PR<br />

interval<br />

R<br />

Q<br />

S<br />

QT<br />

interval<br />

T wave<br />

PQ<br />

segment<br />

R<br />

ST<br />

segment<br />

QRS interval<br />

–1<br />

• ST segment<br />

– ventricular sys<strong>to</strong>le<br />

– plateau in myocardial action<br />

potential<br />

Atria<br />

contract<br />

Ventricles<br />

contract<br />

Atria<br />

contract<br />

Ventricles<br />

contract<br />

• T wave<br />

– ventricular repolarization and<br />

relaxation


Electrical Activity of Myocardium<br />

1) atrial depolarization<br />

begins<br />

2) atrial depolarization<br />

complete (atria<br />

contracted)<br />

Key<br />

Wave of<br />

depolarization<br />

Wave of<br />

repolarization<br />

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.<br />

P<br />

P<br />

R<br />

Q<br />

S<br />

1 Atria begin depolarizing.<br />

4 Ventricular depolarization complete.<br />

3) ventricles begin <strong>to</strong><br />

depolarize at apex; atria<br />

repolarize (atria relaxed)<br />

P<br />

P<br />

R<br />

Q<br />

S<br />

T<br />

4) ventricular depolarization<br />

complete (ventricles<br />

contracted)<br />

5) ventricles begin <strong>to</strong><br />

repolarize at apex<br />

2 Atrial depolarization complete.<br />

3<br />

Ventricular depolarization begins at apex<br />

and progresses superiorly as atria repolarize.<br />

P<br />

R<br />

Q<br />

5<br />

6<br />

Ventricular repolarization begins at apex<br />

and progresses superiorly.<br />

P<br />

R<br />

Q<br />

S<br />

Ventricular repolarization complete; heart<br />

is ready for <strong>the</strong> next cycle.<br />

T<br />

6) ventricular repolarization<br />

complete (ventricles<br />

relaxed)


Normal Electrocardiogram (ECG)<br />

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.<br />

0.8 second<br />

R<br />

R<br />

+1<br />

PQ<br />

segment<br />

ST<br />

segment<br />

Millivolts<br />

0<br />

P wave<br />

T wave<br />

PR<br />

interval<br />

Q<br />

S<br />

QT<br />

interval<br />

QRS interval<br />

–1<br />

Atria<br />

contract<br />

Ventricles<br />

contract<br />

Atria<br />

contract<br />

Ventricles<br />

contract


Diagnostic Value of ECG<br />

• abnormalities in conduction<br />

pathways<br />

• myocardial infarction<br />

• nodal damage<br />

• heart enlargement<br />

• electrolyte and hormone<br />

imbalances


ECGs: Normal and Abnormal<br />

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.<br />

• abnormalities in conduction<br />

pathways<br />

(a) Sinus rhythm (normal)<br />

• myocardial infarction<br />

• heart enlargement<br />

(b) Nodal rhythm—no <strong>SA</strong> node activity<br />

• electrolyte and hormone<br />

imbalances

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