Electrical activity of the heart (human phys exam 3)

electrocardiogram

-A record of the overall spread of electrical activity through the heart. -Electrical currents generated by cardiac muscle during depolarization/repolarization spread into tissues around the heart and are conducted through body fluids. A small part of this electrical activity reaches surface of body -> can be detected -> produces ECG.

Arrhythmias

-Abnormal cardiac rhythms (initiation or conduction of impulse) -Consequences: 1) Hemodynamic: rapid rate -> inadequate filling of ventricles -> dec CO 2) Cardiac: increased heart rate increases oxygen consumption-->anginal attacks, myocardial infarction. --Ventricular tachycardia: forerunner of ventricular fibrillation. Tachycardia = rapid heart rate of more than 100 beats per minute. -Underlying causes: 1) Benign causes: excessive coffee, nicotine, lack of sleep 2) heart disease which causes ischemia (dec blood flow -> dec oxygen supply. -Changes in rate: normal rate = 70 bpm; Bradycardia = <60 bpm; tachycardia = > 100 bmp -Extrasystole or premature beat: causes range from benign to ischemic heart disease -Atrial fibrillation: a) rapid uncoordinated depolarization -> pumping = zero b) compatible with life: atrial contraction -> 25% of ventricular filling -Ventricular fibrillation: a) rapid uncoordinated depolarization and contraction: multiple impulses traveling erratically b) stroke volume and cardiac output = zero c) treatment: ---CPR: external cardiac massage ---electrical defibrillation -> simultaneously depolarizes all cells -> recover -> SA node takes over again.

Excitation-Contraction coupling

-Ca++ initiates contraction. -Sources of Ca++: a) AP travels down muscle cell membrane and T-tubule membrane -> releases Ca++ from sarcoplasmic reticulum b) Ca++ enters cell (from ECF) during plateau. -Ca++ binds to troponin-initiates contraction (sliding filaments) -Strength of contraction depends on [Ca++] in cytoplasm -Calcium pumps in cell membrane and SR

Refractory period

-Cardiac muscle has a refractory period. -During refractory period, a second AP cannot be triggered until an excitable membrane has recovered from the preceding AP. -In skeletal muscle: refractory period very short compared w/ duration of resulting contraction, so fiber can be restimulated before the first contraction is complete to produce summation of contractions. -Rapidly repetitive stimulations results in a sustained, maximal contraction known as tetanus. -In contrast, cardiac muscle has a long refractory period that lasts about 250 msec b/c of the prolonged plateau phase of the AP->cardiac muscle cannot be restimulated until contraction is almost over, preventing summation of contractions and tetanus of cardiac muscle. -This is impt b/c pumping of blood requires alternate periods of contraction (emptying) and relaxation (filling).

AV node

-Delays conduction of the impulse (delay = 0.13 seconds) -> allows time for ventricular filling. Delay allows atria to become completely depolarized and to contract, emptying their contents into the ventricles, before ventricular depolarization and contraction can occur. -The AV node is the only normal electrical connection between the SA node and the ventricles: AP must pass through AV node to travel from atria to ventricles.

Effect of sympathetic stimulation on the heart

-Sympathetic NS controls heart action in emergency/exercise situations that require greater blood flow, "revs up" heart -Sympathetic stimulation on the SA node speeds up depolarization so the threshold is reached more rapidly. Permits more frequent APs and a correspondingly faster heart rate: inc rate of SA node discharge -> inc heart rate -Sympathetic stimulation of the AV node reduces AV delay by increasing conduction velocity: inc rate of conduction through AV node.

Action potential in contractile muscle cells

-The action potential in cardiac contractile cells differs considerably from the action potential in cardiac autorhythmic cells. -Resting membrane potential of contractile cells = -90 mV -Once the membrane of a ventricular myocardial contractile cell is excited, the membrane potential rapidly reverses to a positive value of +30 mV as a result of activation of voltage-gated Na+ channels and Na+ rapidly entering the cell. -The membrane potential is maintained close to this peak positive level for several hundred milliseconds, producing a plateau phase of the action potential. -Whereas the rising phase of the action potential is brought about by activation of comparatively "fast" Na+ channels, this plateau is maintained primarily by activation of relatively "slow" voltage-gated Ca++ channels in the cardiac contractile cell membrane. -These Ca++ channels open in response to the sudden change in voltage during the rising phase of the AP. Opening of these Ca channels results in a slow inward diffusion of Ca++ -This continued influx of positively charged Ca++ prolongs the positivity inside the cell and is primarily responsible for the plateau part of the AP. -The rapid falling phase (repolarization) results from inactivation of the Ca++ channels and opening of voltage-gated K+ channels. -The cell returns to its resting potential as K+ rapidly leaves the cell. Phase 1: Resting membrane potential (-90mV) Phase 2: Depolarization phase --SA node -> threshold stimulus --Rapid increase in Na+ permeability: Na+ quickly diffuses into the cells (voltage sensitive, fast Na+ channels) -> depolarization (membrane potential becomes positive). Phase 3: Rapid repolarization: Fast Na+ channels close Phase 4: Plateau phase: slow Ca++ channels open, Ca++ diffuses into the cardiac cells from ECF --Maintains positive membrane potential --Ca++ also contributes to contraction Phase 5: Repolarization --Ca++ channels close --K+ channels open (voltage sensitive, increase in K+ permeability) -> K+ ions diffuse out of cell -> repolarization to RMP.

Summary of pacemaker activity

-When one action potential ends and the funny channels open, the resultant depolarizing net inward Na+ movement starts immediately moving the pacemaker cell's potential toward threshold. Once threshold is reached, the rising phase of the action potential occurs in response to the opening of voltage-gated Ca2+ channels and the resulting entry of Ca2+ (in contrast to nerve and skeletal muscle cells where Na+ entry rather than Ca2+ entry swings the potential in the positive direction). -The falling (hyperpolarizing) phase occurs as usual by K+ leaving the pacemaker cell as a result of opening of voltage-gated K+ channels. -Through repeated cycles of drift and fire, these autorhythmic cells cyclically initiate action potentials, which then spread throughout the heart to trigger rhythmic beating without any nervous stimulation.

Normal pacemaker activity

-autorhythmic cells have different rates of slow depolarization to threshold, so they have different rates of generating action potentials -heart cells with fastest rate of AP initiation are localized in the SA node: 70-80 aps/min -> 70-80 beats/min -SA node drives rest of the heart at its own pace.

Purkinje fibers

-continuous with ventricular muscle fibers -> impulse is transmitted to all sections at once (0.03 sec)

Automaticity: Generation of the Cardiac impulse

-contraction of the cardiac muscle is triggered by action potentials sweeping across the muscle cell membranes. -Heart contracts as a result of APs that it generates by itself-autorhythmicity. -autorhythmic cells do not contract but initiate and conduct the APs responsible for contracting the contractile cells of the heart. -Cardiac autorhythmic cells display pacemaker activity (generate an AP in the absence of nervous stimulation)

pacemaker activity

-generate an AP in the absence of nervous stimulation -membrane potential of autorhythmic cells slowly depolarizes between APs until threshold is reached->membrane fires (has an AP). -pacemaker activity takes place in the SA node (right atrial wall), AV node (base of right atrium), bundle of His (tract of specialized cells that originates at AV nodes), and Purkinje fibers (extend from bundle of His and spread thru ventricular myocardium.

effect of parasympathetic stimulation on heart.

-parasympathetic stimulation dec the SA node's rate of spontaneous depolarization, prolonging the time required to drift to threshold. Therefore, the SA node reaches threshold and fires less frequently, decreasing heart rate. So, dec rate of SA node discharge -> dec heart rate. -parasympathetic stimulation decreases the AV node's excitability, prolonging transmission of impulses to the ventricles even longer than usual AV nodal delay: dec rate of conduction through AV node.

funny channels

-voltage-gated channels typically open when membrane becomes less negative (depolarizes), but these unusual channels open with the potential becomes more negative (hyperpolarizes) at the end of repolarization from the previous action potential.

pacemaker action potential

1. "Resting potential": slow depolarization phase (automatic) due to unstable resting membrane potential -unique channels ("funny channels") that open when the membrane repolarizes to most negative value (response to hyperpolarization). -Na+ and K+ diffuse through channels but greatest diffusion is Na+ (electrochemical gradient favors Na+). -Slow depolarization to threshold. -Pacemaker potential. 2. Depolarization phase: upstroke -Ca++ channels open (and some Na+ channels) -> Ca++ and Na+ move in-->depolarization 3. Repolarization -Ca++ channels close -Increased permeability to K+ -> K+ leaves cell, hyperpolarizing cell. -At the end of repolarization, the spontaneous depolarization process begins again.

Coordinated conduction of the AP

1. Atrial excitation and contraction occur before the ventricles contract -> enables atrial to eject blood into ventricle to complete ventricular filling 2. Each chamber contracts as a unit to eject blood: excite all cells almost simultaneously 3. Bpoth atria contract together and both ventricles contract togehter.

P wave

atrial depolarization

QRS

depolarization of ventricles

PQ or PR interval

increases when AV conduction slows

T wave

repolarization of ventricles

Ventricular muscle

syncytium: AP conducted from cell to cell through intercalated discs (gap junctions).