Cardiac Muscle

The third category of muscle is cardiac muscle, which makes up most of the heart. Like skeletal muscle, it is striated. Like smooth muscle, it can propagate action potentials from cell to cell. There are three categories of cardiac muscle: atrial, ventricular, conducting.

Cardiac muscle cells branch. Intercalated disks allow ions to flow through gap junctions, which is how action potentials propagate.

A tissue consisting of cells that are coupled (can propagate action potentials) is called a syncytium. The heart has two syncytia, the atria and the ventricles, separated by connective tissue. Action potentials in any cell in a syncytium eventually reach every cell in that syncytium.

Cardiac action potential: Note that resting potential drifts toward excitation, cardiac cells are leaky. The drift terminates with a rapidly rising depolarization, followed by a more or less constant phase called the plateau, finally, a return to the resting potential.

Because of the drifting potential, every cardiac muscle cell can spontaneously depolarize. The leakiness differs in different parts of the heart, so the spontaneous depolarization rate differs as well.

The plateau phase is about 150 msec in atrial muscle, about 300 msec in ventricular muscle. The cell is refractory during the plateau, so atrial cells can’t depolarize more than 5 or 6 times per second, around 300 per minute. Ventricular cells, because of their longer refractory period, have maximum rates of about half that.

This shows the relation between the cardiac action potential, refractory period, and contraction. One action potential = one contraction. Both have much greater durations than in skeletal muscle (about 1 to 2 msec).

The Path of Circulation

This illustrates the important elements of cardiac anatomy, with arrows showing the direction of blood flow. Blood flows from the left ventricle to the aorta, through the systemic circulation, back to the right atrium -> right ventricle -> pulmonary artery (to lungs), through the pulmonary circulation, back to the left atrium -> left ventricle. The cycle repeats about once per second.

Some Basic Physics of Fluids

First, some basics about fluids (gases and liquids are fluids). If they move, it’s always from where the pressure is higher to where the pressure is lower. No exceptions. When there’s a pressure difference and a path through which fluid can flow, it will flow. No exceptions.

Here’s a mystery: How can blood circulate through the heart? That would require it to be the place in the circulation with the highest and the lowest pressure, right?

Right. It is. But not both at the same time. The left ventricular pressure varies between about 0 mm Hg and 120 mm Hg with every heartbeat. The valves in the system only open in one direction (like doors), which is why the flow is only in one direction.

The Cardiac Cycle

The heart goes through two major phases: contraction (= systole) and diastole (= relaxation). Pressure increases during systole, decreases during diastole. The diagram shows the sequence in which the chambers contract and relax. It is one cardiac cycle.

Start at the beginning of diastole. Atria and ventricles relax, pressure in each falls. As long as it is above 10 mm Hg (pressure in the veins), the valves remain closed. This is the period of isovolumic (= with the same volume) relaxation. Pressure will fall all the way to 0 mm Hg. When it gets below 10 mm Hg, valves from veins to heart open, blood flows through atria and into ventricles. About 70% of the amount entering the ventricle does so during this phase. Then the atria contract. This closes the valve between veins and atria; atria pump the final 30% of the volume into the ventricles.

Now systole begins. Ventricles contract, pressure rapidly rises above that in the atria (ventricle muscle is much thicker than atrial muscle, generates much more tension) shutting the valves from the atria. The valve to the aorta is still shut because aortic pressure is greater than 80 mm Hg. As ventricular pressure increases, volume in ventricle can’t change until pressure exceeds that in aorta. This is the period of isovolumic contraction. When pressure gets to 80 mm Hg, valve to aorta is forced open; ventricular pressure reaches 120 mm Hg. This is the period of ejection. Ventricle then relaxes.

Volume in heart at end of diastole (end diastolic volume) = 125 mlVolume in heart at end of systole (end systolic volume) = 55 mlDifference = amount ejected in one beat = stroke volume = 70 ml

Cardiac output = volume ejected per minute = stroke volume x heart rate = 70 ml x 65 beats per minute = 4,550 ml/min. Usually rounded off to 5 L/min

Cardiac output to systemic and pulmonary circulations are equal: 5 L/min each. How could it be otherwise? Think of the consequences if it was.

Starling’s Law

Starling’s Law = Frank-Starling Law = Law of the heart: Stroke volume will be equal to volume entering heart during last diastole. More commonly stated: cardiac output = venous return

Basis is the length-tension relation in muscle: stretching a muscle -> greater active tension. Increased end-diastolic volume = greater stretch of cardiac muscle -> more forceful contraction. Therefore, Starling’s Law (we’ll come back to how venous return can vary).

Note that Starling’s Law ignores the pressure against which the heart pumps. Up to arterial pressures of about 170 mm Hg (normal is 100 mm Hg), pressure has nearly no effect on cardiac output. That’s very different than most mechanical pumps. If you doubt this, shop for a water pump. The sales person (if he knows what he’s doing) will ask: 1. What flow rate do you want the pump to be able to generate? 2. How high must the water be raised during pumping?

Factors that Modify Cardiac Output

Venous return (via Starling’s Law)Autonomic input Sympathetic stimulation can increase heart rate to more than 250 beats/min; also increases cardiac contraction, which increases stroke volume. Parasympathetic stimulation (via vagus nerve) can decrease heart rate to below 30 beats/min

Spread of Depolarization in the Heart

Four special systems in heart for excitation and conduction: 1. Sino-atrial (S-A) node, generates normal rhythm of heart 2. Atrio-ventricular (A-V) node, delays action potentials as they pass from atrial to ventricular syncytia 3. A-V bundle, conducts action potentials to ventricles 4. Purkinje fibers, distribute action potentials through ventricles

All cardiac muscle cells are leaky to Na, so all have resting potentials (around -85 mV) that drift toward zero. Thus, every cardiac muscle cell can spontaneously depolarize and contract at a frequency that depends on how fast the drift reaches threshold (about -45 mV).

The leakiest cardiac cells are in the S-A node. They depolarize about once per second (60/minute). Action potentials that arise in the S-A node are propagated, so their neighbors depolarize at 60/min before their drifting resting potential depolarizes them spontaneously. That process continues through the entire atrial syncytium. Every atrial cell depolarizes at that rate. Thus, the S-A node sets the heart rate. That’s why it’s called the pacemaker.

The duration of the action potential is about 150 msec, and the action potential that began in the S-A node gets back to it in about 90 msec. Since the S-A node cells are still refractory, the action potential goes no further. Thus, every cell in the atrial syncytium is simultaneously contracted for about 60 msec.

There’s a conducting fiber pathway from the S-A node to the A-V node. The action potential is delayed in the A-V node for about 40 msec before being passed on to them.

This shows the path of conduction of action potentials through the heart. So far, we’ve gotten it through the atria and to the A-V node. Now to cross into and through the ventricles.

Conducting fibers leave the A-V node, travel into the septum and then through the walls of the ventricles. These fibers conduct very rapidly, and the action potential reaches every ventricular cell within 60 msec after it reaches the first one. Since ventricular action potentials last for about 300 msec, there’s a long period during which every ventricular cell is simultaneously contracted.

Why is the Rate of Spread of Depolarization Important?

The fact that there is a period during which every ventricular cell is simultaneously relaxed means that the end diastolic volume is maximized. The fact that there is a period during which every ventricular cell is simultaneously contracted means that the end systolic volume is minimized.

Since stroke volume = end diastolic volume – end systolic volume, this maximizes stroke volume and makes the heart very efficient.

Imagine the result if half the cells were relaxed, half were contracted at every instant, with the only moment-to-moment change being which cells were in each state. Stroke volume would be zero, so cardiac output would be zero.

The Electrocardiogram (ECG)

As a wave of depolarization spreads through the heart, stray currents from it can be recorded with electrodes on the skin. The recording is called an electrocardiogram (= ECG), sometimes called an EKG because of the German spelling (Elektrokardiogram).

The P wave is the result of atrial depolarization, the QRS complex derives from ventricular depolarization (and atrial repolarization, which is within it), the T wave results from ventricular repolarization.

The ventricular events are much larger because the ventricular muscle mass is much greater than that of the atria. The peculiar shape of the QRS complex reflects the fact that the ventricle depolarizes first down the septum, then up through the outer walls.

The ECG is a very useful diagnostic tool.

Abnormal Cardiac Rhythms

Cardiac rhythm abnormalities can have many causes:1. S-A node abnormality2. Hyperactivity in a region other than the S-A node, making that

region the pacemaker3. Blocked points of transmission4. Anomalous transmission paths5. Abnormal impulses originating almost anyplace in the heart

Flutter = heart rates of 200 – 300 beats/min, with coordinated beatsFibrillation = beats of 200 – 300 beats/min, uncoordinated.

Causes of flutter and fibrillation:6. Conduction path is lengthened to where action potentials never

reach refractory cells, but get propagated continuously7. Conduction velocity decreases due to damaged Purkinje fibers,

muscle damage, hyperkalemia

Atrial fibrillation reduces pumping by about 30%. Can be compensated via sympathetic activity.

Ventricular fibrillation can reduce cardiac output to nearly zero. Usually results from an ischemic area (region receiving little or no blood) becoming hyperexcitable and initiating high frequency action potentials.

Defibrillator depolarizes entire heart simultaneously, making all cells simultaneously refractory. With luck, hyperexcitable area quiets down and a new S-A rhythm takes over.