Cardiac Conduction system
heartbeat is coordinated by this. composed of an internal pacemaker and nervelike conduction pathways through the myocardium. it generates and conducts rhythmic eletrical signals in the following order.
Sinoatrial Node (SA) node
patch of modified cardiocytes in the right atrium, just under the epicardium near the super venae cava. this is the pacemaker that initiates each heartbeat and determines heart rate. signals from this node spread throughout the atria.
Atrioventricular Node (AV) node
located near right AV valve at lower end of interatrial septum. this node acts as an electrical gateway to ventricles; fibrous skeleton acts as an insulator to prevent currents from getting to the ventricles by any other route.
Atrioventricular (AV) bundle (bundle of HiS)
pathway by which signals leave the AV node. AV bundle soon forks right and left bundle branches, which enter interventricular septum and descend toward apex.
nervelike processes spread throughout the ventricular myocardium. these distribute the electrical excitation to cardiocytes of the ventricles. they form more elaborate network in the left ventricle than the right. once these fibers have delivered the electrical signal to their limits, cardiocytes perpetuate it by passing ion flows from cell to cell through gap junctions.
step by step
1. SA node fires
2.excitation spreads through atrial myocardium
3.AV node fires
4. excitation spreads down AV bundle
5. Pukinje fibers distribute excitation through ventricular myocardium.
raises heart rate. flight or fight. originates in the lower cervical to upper thoracic segments of the spinal cord. continues to adjacent sympathetic chain ganglia. some pass through cardiac plexus in mediastinum. continue as cardiac nerves to heart. these fibers terminate in the SA and the AV nodes and in atrial and ventricular myocardium, aorota, pulmonary trunk, and coronary arteries. increases heart rate and contraction strength and dialtes the coronary arteries to increase myocardial blood flow.
slows heart rate. begins with nuclei of the vagus nerves in medulla oblongata. preganglionic fibers extend through vagus nerves to cardiac plexus, where they mingle with sympathetic fibers, and contin to the heart by way of cardiac nerves. fibers of right vagus nerve lead to SA node and fibers from left vagus nerve lead to AV node. there is little or no vagal stimulation of the myocardium. parasympathetic stimulation reduces the heart rate.
atrial or ventricular contraction.
atrial or ventricular relaxation.
normal heartbeat triggerd by SA node. at rest adult heart beats about 70-80 times per min, 60-100 are not unusual. Stimuli such as hypoxia, electrolyte imbalances, caffeine, nicotine, and other drugs can cause other parts of the conduction system to fire before SA node does, setting off an xtra heartbeat called premature ventricular contraction (PCV) or extrasystole.
any region of spontaneous firing other than SA node. if SA node is damaged, this may take over governance of the heart rhythm.
most common ectopic focus in the AV node, which produces slower heartbeat of 40-50 bpm.
region of spontaneous firing.
intrinsic ventricular rhythm
if both SA and AV nodes are not functioning, rate set at 20-40 bpm that requires a pacemaker to sustain life.
an abnormal cardiac rhythm. one cause can be from heart block- the failure of any part of the conduction system to transmit signals, usually as a result of disease and degeneration of conduction system fibers. for ex. bundle branch block is due to damage to one or both bundle branches. damage of AV node causes total heart block, in which signals from the atria fail to reach the ventricles and the ventricles beat at their own intrinsic rhythm of 20-40 bpm.
premature ventricular contractions and ventricular fibrilation are common. occurs when ectopic foci in the atria set off extra contractions and the atria beats 200-400 times per min.
premature ventricular contractions PCVs
occur singly or in bursts as a result of early firing of ectopic focus. often due to irration of the heart by stimulants, emotional stress, lack of sleep,
serious arrythmia caused by electrical signals arriving at different regions of the myocardium at differnt times. fibrilating ventricle exhibits squirming, uncoordinated contractions(feels like a bag of worms). heart cant pump blood, there is no coronary perfusion(blood flow) and myocardium dies of ishcemia. kills quickly if not stopped.
emergency procedure in which the heart is given strong electrial shock with a pair of electrodes. purpouse is to depolarize the entire myocardium and stop fibrilation., w hope that the SA node will resume its sinus rhythm.
SA node does not have a stable resting membrane potential. starting at -60 mV and drifts upward showing a gradual depolarization called the pacemaker potential. this results from a slow inflow of Na+ without a compensating outflow of K+. when reaches threshold of -40 mV, voltage regulated fast calcium sodium channels open and both Ca+ and Na+ flow from the ECF. this produces the rising (depolarization) phase of action potential, which peaks slightly above 0 mV. at that point K+ channels open and K+ leaves the cell. this makes cytosol increasingly negative and creates falling (repolarization) phase of action potential. when repolarization is complete the K+ channels close and the pacemaker potential starts over to produce the next heartbeat. when SA node fires; it excites other components in the conduction system. SA node serves as the systems pacemaker. at rest it serves 0.8 sec, creating a heart rate at about 75 BPM.
impulse conduction to myocardium
firing of SA node excites atrial cardiocytes and stimulates two atria to contract almost simultaneously. signal travels at a speed of about 1 m/sec through the atrial myocardium and reaches the AV node in abiout 50 msec. in the AV node, signal slows down to about 0.05 msec. bcus cardiocytes here are thinner, and have fewer gap junctions over which the signal can be transmitted. this delayes signal so it can allow the ventricles time to fill with blood before contracting. signals travel through AV bundle and purkinje fibers very quickly. entire ventricular myocardium depolarizes within 200 msec after the SA node fires causing ventricles to contract when they are in unison. papillary muscles contract and begin taking up slack in the tendinous chords an instant before ventricular contraction causes blood to surge against AV valves. ventricular systole begins at apex of heart, which is first to be stimulated, and moves upward- pushing blood up toward the SL valves. bcus of spiral arrangement of ventricular cardiocytes, ventricles twist slightly as they contract like someone is wringing a towel.
Electrical Behavior of Myocardium
cardiocytes have stable resting potential of -90 mV and normally depolarize only when stimulated, unlike cells of SA node. stimulus opens voltage regulated sodium gates, causing a Na+ inflow and depolarizing the cell to its threshold. threshold voltage rapidly opens additional Na+ gates and triggers a positive feedback cycle. action potential peaks at nearly +30 mV. Na+ gates close quickly. as action potentials spread over the plasma membrane, they open voltage-regulated slow calcium channels, which admit a small amount of Ca2+ from the ECF into the cell. Ca2+ binds to ligand- regulated Ca2+ channels on the sarcoplasmic reticulum, opening them and releasing a greater amount of Ca from the SR into cytosol. second wave of Ca binds to troponin and triggers contraction in the same way as it does in skeletal muscle. SR provides 90% to 98% of Ca needed for myocardial contraction. at end of plateau Ca channels close and K channels open. potassium diffuses rapidly out of cell and Ca is transported back into the ECF and SR. membrane voltage drops and muscle tension declines afterward. cardiac muscle has an absolute refractory period of 250 msec compared with 1 to 2 msec in skeletal muscle. long refractory period prevents wave summation and tetanus which would stop the pumping action of heart.
Action Potential of Cardiocyte
1. Na gates open
2. rapid depolarization
3. Na gates close
4. slow ca2 channels open
5. ca2 channels close, k channels open(repolarization)
composite of all action potentials of nodal and myocardial cells detected, amplified and recorded by electrodes on arms, legs, and chest.
produced when a signal from SA node spreads through atria and depolarizes them. atrial systole begins about 100 msec after P wave begins, during PQ segment. this segment is about 160 msec long and represents the time required for impulses to travel from SA node to AV node.
consists of small downward deflection (Q), tall sharp peak (R), and a final downward deflection (S). produced when signal from AV node spreads through the ventricular myocardium and depolarizes muscle. complex shape is due to the diff thickness and shape of two ventricles.
ventricular systole begins- plateau in myocardial action potential. represents the time during which ventricles contract and eject blood.
generated by ventricular repolarization immediately after diastole. ventricles take longer to repolarize then depolarize; this wave is smaller and more spread out then QRS complex. and has rounder peak. Atria repolarzie and ventricle depolarize.
electrical activity of myocardium
1. atria begin depolarizing
2. atrial depolarizing complete(atria contracted)
3. ventricular depolarization begins at apex and progresses superiorly as atria repolarize(atria relaxed)
4. ventricular depolarization complete(ventricles contract)
5. ventricular repolarization begins at apex and progresses superiorly
6. ventricular repolarization complete; heart is ready for next cycle. (ventricles relaxed)
ECG: normal and abnormal
Abnormalities in conduction pathways, myocardial infarction, heart enlargement, electrolyte and hormone imbalances.
consists of one complete contraction and relaxation of all 4 heart chambers. atrial systole(contraction) occurs while ventricles are in diastole(relaxation) atrial diastole occurs while ventricles in systole. quiescent period- all 4 chambers are relaxed at the same time.
Operation of heart valves
AV valves. when atrial pressure is greater than ventricular pressure, valves open and blood flows. when ventricular pressure rises above atrial pressure, blood in the ventricle pushes the valve cusps closed. SL valves. when pressure in ventricles is greater than the pressure in the great arteries, the SL valves are forced open and blood is ejected. when ventricular pressure is lower than arterial pressure, arterial blood holds these valves closed.
(incompetence) refers to any failure of a valve to prevent reflux- the backward flow of blood.
is a form of insufficiency in which cusps are stiffened and the opening in constricted by scar tissue. results from theumatic fever, an autoimmune disease in which antibodies produced to fight a bacterial infection also attack the mitral and aorotic valves. as valves become scarred and constricted, the heart is overworked by the effort to force blood through the openings and may become enlarged. backflow of blood through valves creates turbulence that can be heard with stethescope as a heat murmur.
Mitral Valve prolapse (MVP)
an insufficiency in which one or both mitral valve cusps bulge into the atrium during ventricular contraction. often hereditary and affects 1 out of 40 ppl, especially young woman. causes no disfunction, but may cause chest pain, fatigue and shortness of breath.
listening to sounds made by the body.
First heart sound
S1 louder and longer "lubb" occurs with closure of AV valves, turbulence in the bloodstream and movements of the heart wall.
Second heart sound
S2. softer and sharper Dupp occurs with closure of SL valves, turbulence in bloodstream, and movements of heart wall.
Third heart sound
S3. rarely heard in people over 30. exact cause of each sound is not known with certainty.