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Anatomic Structures Controlling Heart Activity: The Hearts Conduction System

Automaticity of the heart
Heart pumping blood continuously Dependent upon rhythmic stimulation of cardiac muscle cells Precise electrical events initiated by conduction system Begin with stimulation by pacemaker Transmission of action potential by conduction fibers Ensures atria contracts prior to ventricles

Anatomic Structures Controlling Heart Activity: The Hearts Conduction System

Conduction system
Specialized cardiac muscle cells Initiate and conduct electrical signals Sinoatrial (SA) node
in posterior wall of right atrium adjacent to superior vena cava initiates heartbeat referred to as pacemaker of heart

Anatomic Structures Controlling Heart Activity: The Hearts Conduction System

Conduction system (continued)
Atrioventricular (AV) node
in floor of right atrium between right AV valve and coronary sinus opening

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Figure 19.14a

Sinoatrial (SA) node (pacemaker) Right atrium Atrioventricular (AV) node Right and left bundles Purkinje fibers Purkinje fibers

Atrioventricular (AV) bundle

extends from AV node though interventricular septum divides into left and right bundles

Purkinje fibers
extend from left and right bundles from apex of heart through walls of ventricles

Atrioventricular (AV) bundle

(a) Conduction system

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Anatomic Structures Controlling Heart Activity: The Hearts Conduction System Why is the SA node referred to as the pacemaker?
The SA node initiates the signal of the heartbeat.

Conduction system

Conduction system
Electrical activity initiated at SA node Action potential transmitted through conduction system
Figure 19.15a
SA node

Initiation SA node initiates action potential.

Nodal cell

2 Spread of action potential An action potential is propagated throughout the atria, the conduction system.

(a)

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Cardiac muscle cells

Cardiac muscle cells

Action potential spreads across sarcolemma of cardiac muscle cells First in atria, then in ventricles
Figure 19.15b

1 The action potential initiated in the conduction system is propagated across the sarcolemma of cardiac muscle cells.

Action potential

Cardiac muscle cell

Stimulation of the HeartElectrical Events at the SA Node: Initiation of the Action Potential
Autorhythmicity
Depolarize and fire action potential spontaneously Exhibited by SA nodal cells Depends on a series of events within SA nodal cells

Sarcolemma

2 Muscle contraction Thin filaments slide past thick filaments and sacromeres shorten within cardiac muscle cells. Sarcomeres shorten. (b)

Stimulation of the HeartElectrical Events at the SA Node: Initiation of the Action Potential
Events occurring in SA nodal cells
1) Reaching threshold
opening of slow voltage-gated Na+ channels Na+ flow into nodal cells membrane potential from -60 mV to -40 mV (threshold value)

Stimulation of the HeartElectrical Events at the SA Node: Initiation of the Action Potential
Events occurring in SA nodal cells (continued)
3) Repolarization
closure of calcium channels opening of voltage-gated K+ channels K+ flowing out membrane potential back to resting membrane potential (-60 mV) triggers reopening of voltage-gated Na+ channels
begins process again

2) Depolarization
opening of fast voltage-gated Ca2+ channels triggered entry of Ca2+ into cell membrane potential from -40 mV to just above 0 mV

Figure 19.16b

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Stimulation of the HeartElectrical Events at the SA Node: Initiation of the Action Potential
Heart rate
Process takes about 0.8 sec = HR 75 beats/min Inherent rhythm faster at 100/min Slower rate due to continuous parasympathetic stimulation
by vagus nerve this slowing of heart rate, vagal tone

+10 0 Membrane potential (mV) 10 20 30 40 50 60 70 1

RMP Pacemaker potential

2 3
Threshold voltage Action potential

1 Reaching threshold Slow voltage-gated Na+ channels open. Inflow of Na+ changes membrane potential from 60 mV to 40 mV. 2 Depolarization Fast voltage-gated Ca2+ channels open. Inflow of Ca2+ changes membrane potential from 40 mV to just above 0 mV. 3 Repolarization Fast voltage-gated Ca2+ channels close. Voltage-gated K+ channels open allowing K+ outflow. Membrane potential returns to RMP 60 mV, and K+ channels close.

0.4

0.8

1.2

1.6

Time (seconds) (b)

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Stimulation of the HeartElectrical Events at the SA Node: Initiation of the Action Potential
Comparison of Cardiac Nodal Cells and Neurons
Nodal cells
do not require stimulation (unlike neurons) do not have stable resting membrane potential (RMP) RMP gradually increasing to threshold without stimulation termed pacemaker potential depolarization occurs with entrance of Ca2+ into cells (unlike neurons)

Stimulation of the HeartConduction System of the Heart: Spread of the Action Potential
Action potential through conduction system
1) Action potential distributed throughout atria
relayed to AV node spread through gap junctions allows for almost instantaneous excitation of muscle cells atria contracting at same time

Stimulation of the HeartConduction System of the Heart: Spread of the Action Potential
Action potential through conduction system (continued)
2) Action potential delayed at the AV node
AV nodal cells with smaller fiber diameter and fewer gap junctions slows conduction rate with fibrous skeleton, only moves through AV node delay allows atria to finish contracting force blood into ventricles before ventricular contraction

Stimulation of the HeartConduction System of the Heart: Spread of the Action Potential
Action potential through conduction system (continued)
3) Action potential moving from AV node
moves along AV bundle moves to Purkinje fibers

4) Spreads throughout ventricles via gap junctions

begin to contract within 120 to 200 ms after firing of SA nodal cells

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Sinoatrial node and atrial myocardium 1 An action potential is generated at the sinoatrial (SA) node. SA node It spreads via gap (pacemaker) junctions between cardiac muscle cells throughout the atria AV node to the atrioventricular (AV) node. 3 The AV bundle conducts the action potential along the left and right bundle branches to the Purkinje fibers.

Bundle branches and Purkinje fibers

Atria

AV bundle

Figure 19.17

Figure 19.17 (continued)

Left and right bundle branches Purkinje fibers

Atrioventricular (AV) node 2 The action potential is delayed at the AV node before it passes to the AV bundle within the interventricular septum. AV node 4 The action potential is spread via gap junctions between cardiac muscle cells throughout the ventricles.

Ventricular myocardium

Purkinje fibers AV bundle Ventricles

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Stimulation of the HeartConduction System of the Heart: Spread of the Action Potential
Specialized Features Associated with Ventricles
Purkinje fibers larger in diameter than other cardiac fibers
action potential extremely rapid ensures ventricles contract at same time

Stimulation of the HeartConduction System of the Heart: Spread of the Action Potential What is the path of an action potential through the conduction system of the heart?
SA node, AV node, AV bundle, Purkinje fibers, through ventricles

Papillary muscles stimulated to contract immediately

muscles anchor chordae tendinae to AV cusps start to pull on cusps just prior to increase in pressure in ventricles

Stimulation beginning at heart apex

ensures blood efficiently ejected toward arterial trunks

Stimulation of the HeartConduction System of the Heart: Spread of the Action Potential
Clinical View: Ectopic Pacemaker
Pacemaker other than SA node Conduction system cells other than SA node
also have ability to spontaneously depolarize depolarize at slower rates than SA node

Stimulation of the HeartConduction System of the Heart: Spread of the Action Potential
Clinical View: Cardiac Arrhythmia
Abnormality in the rate, regularity, or sequence of cardiac cycle Atrial flutter
atria attempting to contract at 200-400 times per minute may persist for many years may degenerate into atrial fibrillation

AV node the default pacemaker if SA node impaired

AV node with inherent rhythm of 40 to 50 beats/min fast enough to sustain life

Atrial fibrillation
action potential more chaotic irregular heart rate may lead to serious disturbance in rhythm

Cardiac muscle with rate of 20 to 40 beats/min

usually too slow to sustain life

Stimulation of the HeartConduction System of the Heart: Spread of the Action Potential
Clinical View: Cardiac Arrhythmia (continued)
Premature ventricular contractions
result from stress, stimulants, or sleep deprivation abnormal action potential within AV node or ventricles not detrimental unless they occur in large numbers

Cardiac Muscle Cells: Repolarization and the Refractory Period

Skeletal and cardiac excitation similarities
Both with refractory period
time after depolarization when muscle cannot be restimulated

Ventricular fibrillation
life-threatening arrhythmia rapid, repetitious movement of ventricular muscle contractions not coordinated; heart unable to pump cardiac arrest shock applied to synchronize hearts electrical activity

Both with depolarization and repolarization Both with muscle contraction and relaxation Both with lag time between action potential and contraction

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Cardiac Muscle Cells: Repolarization and the Refractory Period

Skeletal and cardiac excitation differences
Refractory period longer in cardiac cells
has extended plateau phase needs resting membrane potential for restimulation 250 ms compared to 1-2 ms makes sustained contraction impossible in cardiac cells allows heart to always contract and relax and continue pumping

Cardiac Muscle Cells: Repolarization and the Refractory Period What is the significance of the extended refractory period in cardiac muscle?
It ensures sustained contraction does not occur (which might cause the heart to stop pumping).

Cardiac Muscle Cells: The ECG Recording

Electrocardiogram (ECG/EKG)
Monitoring electrodes attached to skin
at wrist, ankles, and chest locations

Cardiac Muscle Cells: The ECG Recording

Waves and Segments
Has three principle deflections P wave
reflects electrical changes of atrial depolarization originates in SA node

Electrical signals collected and charted Provides assessment of electrical changes of heart Provides composite tracing of all cardiac action potentials Utilized during routine physical exam

QRS complex
electrical changes associated with ventricular depolarization atria simultaneously repolarizing but masked by above

T wave
electrical change associated with ventricular repolarization

Cardiac Muscle Cells: The ECG Recording

Waves and Segments (continued)
Two segments between waves
no electrical change

Cardiac Muscle Cells: The ECG Recording

Intervals
Two intervals P-R interval
period from beginning of P wave to beginning of QRS deflection atrial depolarization to beginning of ventricular depolarization time to transmit action potential through entire conduction system

P-Q segment
associated with atrial plateau at sarcolemma cardiac muscle cells within atria contracting

S-T segment
ventricular plateau cardiac muscle cells in ventricle contracting

Q-T interval
time from beginning of QRS and end of T wave from ventricular depolarization to repolarization interval depends upon heart rate

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Figure 19.20a

Cardiac Muscle Cells: The ECG Recording

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R P-Q segment S-T segment

What events in the heart are indicated by each of the following: P wave, QRS complex, and T wave?
T P T Q

Q S P-R interval

S Q-T interval

P wave: atrial depolarization QRS complex: ventricular depolarization T wave: ventricular repolarization

QRS complex (a)

Cardiac Muscle Cells: The ECG Recording

Clinical View: Heart Blocks
Involve impairment within hearts conducting system May result in syncope (fainting), irregular heartbeats, and palpitations First-degree AV block
lengthened PR interval action potential slowed between atria and ventricles asymptomatic

Cardiac Muscle Cells: The ECG Recording

Clinical View: Heart Blocks (continued)
Second-degree block
exists along path between atria and ventricles failure of some action potentials to be conducted to ventricles

Third-degree block
complete heart block no action potentials from SA node received by ventricles life-threatening