Cardiac Muscle and Heart Function Cardiac muscle fibers are striated – sarcomere is the functional unit Fibers are branched; connect to one another at intercalated discs. The discs contain several gap junctions Nuclei are centrally located Abundant mitochondria SR is less abundant than in skeletal muscle, but greater in density than smooth muscle Sarcolemma has specialized ion channels that skeletal muscle does not – voltage-gated Ca2+ channels Fibers are not anchored at ends; allows for greater sarcomere shortening and lengthening

How are cardiac contractions started? Cardiac conduction system Specialized muscle cells “pace” the rest of the heart; cells contain less actin and myosin, are thin and pale microscopically Sinoatrial (SA) node; pace of about 65 bpm Internodal pathways connect SA node to atrioventricular (AV) node AV node could act as a secondary pacemaker; autorhythmic at about 55 bpm Bundle of His Left and right bundle branches Purkinje fibers; also autorhythmic at about 45 bpm ALL CONDUCTION FIBERS CONNECTED TO MUSCLE FIBERS THROUGH GAP JUNCTIONS IN THE INTERCALATED DISCS

Why are fibers of the conducting system autorhythmic?autorhythmic Membrane potential of SA nodal cells I f channels How does the depolarization in these cells affect cardiac muscle cells? Superimpose changes in the muscle cell’s membrane potential on this graph

Changes in ion concentrations in a cardiac muscle fiber following depolarization What causes the muscle resting membrane potential to change initially? What would be happening with a skeletal muscle at this point?

The refractory period is short in skeletal muscle, but very long in cardiac muscle. This means that skeletal muscle can undergo summation and tetanus, via repeated stimulation Cardiac muscle CAN NOT sum action potentials or contractions and can’t be tetanized

Autonomic nervous system modulates the frequency of depolarization of pacemaker Sympathetic stimulation (neurotransmitter = ); binds to  1 receptors on the SA nodal membranes Parasympathetic stimulation (neurotransmitter = ); binds to muscarinic receptors on nodal membranes; increases conductivity of K+ and decreases conductivity of Ca2+ How do these neurotransmitters get these results?

If a wavefront of depolarization travels towards the electrode attached to the + input terminal of the ECG amplifier and away from the electrode attached to the - terminal, a positive deflection will result. If the waveform travels away from the + terminal lead towards the - terminal, a negative going deflection will be seen. If the waveform is travelling in a direction perpendicular to the line joining the sites where the two leads are placed, no deflection or a biphasic deflection will be produced. ECG examines how depolarization events occur in the heart

The electrical activity of the heart originates in the sino-atrial node. The impulse then rapidly spreads through the right atrium to the atrioventricular node. (It also spreads through the atrial muscle directly from the right atrium to the left atrium.) This generates the P-wave The first area of the ventricular muscle to be activated is the interventricular septum, which activates from left to right. This generates the Q-wave Next the bulk of the muscle of both ventricles gets activated, with the endocardial surface being activated before the epicardial surface. This generates the R-wave A few small areas of the ventricles are activated at a rather late stage. This generates the S-wave Finally, the ventricular muscle repolarizes. This generates the T-wave

Since the direction of atrial depolarization is almost exactly parallel to the axis of lead II (which is from RA to LL), a positive deflection (P wave) would result in that lead. Since the ventricular muscle is much thicker in the left than in the right ventricle, the summated depolarization of the two ventricles is downwards and toward the left leg: this produces again a positive deflection (R-wave) in lead II, since the depolarization vector is in the same direction as the lead II axis. Septal depolarization moves from left to right, the depolarization vector is directed towards the - electrode of lead II (RA), and therefore a negative deflection (Q-wave) is produced.

Arhythmias can be detected with an ECG draw the others Normal Bradycardia Tachycardia Atrial fibrillation Ventricular fibrillation Compounds that increase or decrease rate are called chronotropic agents Compounts that increase or decrease force of contraction are called inotropic agents

Cardiac Cycle

Atrial volume (ml)

Cardiac Output = Q = volume of blood ejected from the heart each minute What would I have to know to be able to determine what the cardiac output is at rest? What is the stroke volume? What determines the stroke volume? How can I alter cardiac output?

What causes this increase in stroke volume?