BIOLOGY 238 CLASS NOTES

 The Heart

See also [Anterior Heart] [Posterior Heart]

See also [Coronary Circulation Diagram] and [ Coronary Artery Disease Diagram].

chordae tendineae - attach AV valves to papillary muscles

papillary muscles - muscular extensions from the ventricular walls which attach to chordae tendineae to help hold valve cusps in place.

trabeculae - net-like muscles visible on the inside of the ventricles, pathway for some of the Purkinje fibers.

auricles - external "earlike" structures which increase the volumes of the atria. These landmarks indicate top and sides of heart.

AV valves - The atrioventricular valves, located between each atrium and ventricle, prevent the backflow of blood into the atrium when the ventricle contracts. Their closing causes the first heart sound.

(See Figure 19.8 and [AV Valve])

Semilunar valves - Located at the entrance to the pulmonary trunk and aorta, close to prevent backflow of blood into ventricles when the ventricles relax. Their closing causes the second heart sound.

(See Figure 19.9 and [Aortic Valve])

stenosis - stiffness and narrowing of a valve or vessel, usually caused by disease.

prolapse - a stretched valve resulting in incomplete closure and producing leakage.

heart murmur - the sound produced by a leaking valve. Most murmurs are inconsequential but some indicate severe inadequacy of the valve.

regurgitation - the backflow of blood due to an incompetent (ineffective) valve.

Terms:

systole - the contraction phase; unless otherwise specified refers to left ventricle, but each chamber has its own systole.

diastole - the relaxation phase; unless otherwise specified refers to left ventricle, but each chamber has its own diastole.

1) quiescent period - period when all chambers are at rest and filling. 70% of ventricular filling occurs during this period. The AV valves are open, the semilunar valves are closed.

2) atrial systole - pushes the last 30% of blood into the ventricle.

3) atrial diastole - atria begin filling.

4) ventricular systole - First the AV valves close causing the first heart sound, then after the isovolumetric contraction phase the semilunar valves open permitting ventricular ejection of blood into the arteries.

5) ventricular diastole - As the ventricles relax the semilunar valves close first producing the second heart sound, then after the isovolumetric relaxation phase the AV valves open allowing ventricular filling.

Minute Volume = Heart Rate X Stroke Volume

Heart rate, HR at rest = 65 to 85 bpm (widest range usually quoted)

Each heartbeat at rest takes about .8 sec. of which .4 sec. is quiescent period.

Stroke volume, SV at rest = 60 to 70 ml.

Heart can increase both rate and volume with exercise. Rate increase is limited due to necessity of minimum ventricular diastolic period for filling. Upper limit is usually put at about 220 bpm. Maximum heart rate calculations are usually below 200. Target heart rates for anaerobic threshold are about 85 to 95% of maximum.

End Diastolic Volume, EDV - the maximum volume of the ventricles achieved at the end of ventricular diastole. This is the amount of blood the heart has available to pump. If this volume increases the cardiac output increases in a healthy heart.

End Systolic Volume, ESV - the minimum volume remaining in the ventricle after its systole. If this volume increases it means less blood has been pumped and the cardiac output is less.

EDV - ESV = SV

SV / EDV = Ejection Fraction The ejection fraction is normally around 50% at rest and will increase during strenuous exercise in a healthy heart. Well trained athletes may have ejection fractions approaching 70% in the most strenuous exercise.

Isovolumetric Contraction Phase - a brief period at the beginning of ventricular systole when all valves are closed and ventricular volume remains constant. Pressure has risen enough in the ventricle to close the AV valves but not enough to open the semilunar valves and cause ejection of blood. 

Isovolumetric Relaxation Phase - a brief period at the beginning of ventricular diastole when all valves are closed and ventricular volume is constant. Pressure in the ventricle has lowered producing closure of the semilunar valves but not opening the AV valves to begin pulling blood into the ventricle.

Dicrotic Notch - the small increase in pressure of the aorta or other artery seen when recording a pulse wave. This occurs as blood is briefly pulled back toward the ventricle at the beginning of diastole thus closing the semilunar valves.

Preload - This is the pressure at the end of ventricular diastole, at the beginning of ventricular systole. It is proportional to the End Diastolic Volume (EDV), i.e. as the EDV increases so does the preload of the heart. Factors which increase the preload are: increased total blood volume, increased venous tone and venous return, increased atrial contraction, and the skeletal muscular pump.

Afterload - This is the impedence against which the left ventricle must eject blood, and it is roughly proportional to the End Systolic Volume (ESV). When the peripheral resistance increases so does the ESV and the afterload of the heart. 

The importance of these parameters are as a measure of efficiency of the heart, which increases as the difference between preload and afterload increases. 

branched - connects to other cells through intercalated disks to form a network called a syncytium.

intercalated disks - gap junction intercellular connections which allow the impulse to pass to all cells connected to form the syncytium.

syncytium - a connected network of cells which function as a unit.

The heart has two syncytia (pleural of syncytium), the atrial myocardium is one, the ventricular myocardium is the other. They are separated from one another by a fibrous septum. An impulse cannot pass from one to another directly, but must travel through the heart's conduction system.

endocardium - smooth endothelial lining of the heart and entire cardiovascular system. This helps to reduce friction of blood flow and prevent clotting.

epicardium - the fibrous covering of the heart. This layer is the visceral layer of the pericardium.

pericardium - the double layered membrane sack around the heart. The inner visceral layer of this sack is bound to the surface of the heart as the epicardium. The outer parietal layer forms a sack around the heart and secretes serous fluid which acts as a lubricant to reduce friction when the heart beats.

Skeletal Muscle:

polarization is maintained by the sodium-potassium pump until a stimulus causes ion gates (channels) to open:

fast sodium channels open to produce the depolarization spike associated with an action potential

short refractory period as potassium channels open to re-establish membrane polarity

polarization is maintained by the sodium-potassium pump. In myogenic cells the ion gates are leaky producing spontaneous depolarization.

fast sodium channels open to produce a spike at the beginning of the action potential.

Slow calcium-sodium channels open to produce a prolonged depolarization called the plateau. This produces a long refractory period which ends as potassium channels open to produce repolarization.

(See calcium channel blockers)

Myogenicity is the property of spontaneous impulse generation. The slow sodium channels are leaky and cause the polarity to spontaneously rise to threshold for action potential generation. The fastest of these cells, those in the SA node, set the pace for the heartbeat.

Autorhythmicity - the natural rhythm of spontaneous depolarization. Those with the fastest autorhythmicity act as the 1. heart's pacemaker.

Contractility - like skeletal muscle, most cardiac muscle cells respond to stimuli by contracting. The autorhythmic cells have very little contractility however. Contractility in the other cells can be varied by the effect of neurotransmitters.

Inotropic effects - factors which affect the force or energy of muscular contractions. Digoxin, epinephrine, norepinephrine, and dopamine have positive inotropic effects. Betal blockers and calcium channel blockers have negative inotropic effects.

1) SA node depolarizes and the impulse spreads across the atrial myocardium and through the internodal fibers to the AV node. The atrial myocardium depolarizes resulting in atrial contraction, a physical event.

2) AV node picks up the impulse and transfers it to the AV Bundle (Bundle of His). This produces the major portion of the delay seen in the cardiac cycle. It takes approximately .03 sec from SA node depolarization to the impulse reaching the AV node, and .13 seconds for the impulse to get through the AV node and reach the Bundle of His. Also during this period the atria repolarize.

3) From the AV node the impulse travels through the bundle branches and through the Purkinje fibers to the ventricular myocardium, causing ventricular depolarization and ventricular contraction, a physical event.

4) Ventricular repolarization occurs.

The P wave results from electrical activity in the atria, 1) above.

The QRS complex results from 2) and 3) above, plus atrial repolarization.

The T wave results from ventricular repolarization.

The ECG can be used to diagnose abnormalities in the functioning of the heart's components and conduction system. Several easily recognized abnormalities are shown in Figure 19.18. Another abnormality is atrial tachycardia, (see paroxysmal atrial tachycardia also sinus tachycardia), rapid heartbeat resulting from abnormal rhythm in the atria. A typical form of atrial tachycardia involves the AV node and results in an inverted or obscured P wave. Atrial tachycardia tends to occur in young people and generally disappears with age without heart damage. A new surgical technique isolates and destroys the offending cells to restore normal rhythm.

Atrial fibrillation is a short-circuiting electrical spasm in the atria. Though more serious than atrial tachycardia, it is rarely life-threatening. Since it interferes with the filling action of the atria, the heart's efficiency is reduced and may cause symptoms of weakness. In addition the sluggish blood flow in the atria may cause clots which can subsequently form emboli (clots which move and lodge in another location downstream).

Ventricular tachycardia is much more serious, resulting from severe ischemia and damage to the ventricular myocardium and often preceding ventricular fibrillation. Ventricular fibrillation results from electrical spasm in the ventricular myocardium. It prevents normal depolarization and therefore normal contraction of the ventricles. Defibrillators are used to reset the myocardium by depolarizing it all at once. There are now defibrillators which are implanted, much like a pacemaker, that sense the electrical spasm and shock the heart internally.

Artificial Pacemakers are used to compensate for damage to the SA node, Bundle branches or other parts of the heart's conducting system. Some pacemakers stimulate only the ventricles, but more two chamber pacemakers are now being used which stimulate both the atria and ventricles. These devices have complex sensing capability to sense the heart's own electrical activity and coordinate the pacemaker's stimulation of the atria and ventricles. They can even respond to the increased demand of exercise and compensate by increasing heart rate.

Outputs:

The cardioacceleratory center sends impulses through the sympathetic nervous system in the cardiac nerves. These fibers innervate the SA node and AV node and the ventricular myocardium. Effects on the SA and AV nodes are an increase in depolarization rate by reducing the resting membrane polarization. Effect on the myocardium is to increase contractility thus increasing force and therefore volume of contraction. Sympathetic stimulation increases both rate and volume of the heart.

The cardioinhibitory center sends impulses through the parasympathetic division, the vagus nerve, to the SA and AV nodes, but only sparingly to the atrial myocardium, and not at all to ventricular myocardium. Its effect is to slow the rate of depolarization by increasing the resting potential, i.e. hyperpolarization.

The parasympathetic division controls the heart at rest, keeping its rhythm slow and regular. This is referred to as normal vagal tone. Parasympathetic effects are inhibited and the sympathetic division exerts its effects during stress, i.e. exercise, emotions, "fight or flight" response, and temperature.

Inputs to the Cardiac Center:

Baroreceptors in the aortic and carotid sinuses. The baroreceptor reflex is responsible for the moment to moment maintenance of normal blood pressure.

Higher brain (hypothalamus): stimulates the center in response to exercise, emotions, "fight or flight", temperature.

Right Heart Reflex - Pressoreceptors (stretch receptors) in the right atrium respond to stretch due to increased venous return. The reflex acts through a short neural circuit to stimulate the sympathetic nervous system resulting in increased rate and force of contraction. This regulates output to input. [Venous return from the systemic division is related to exercise and enhanced by the skeletal muscular pump and semilunar valves in the large veins (See Figure 20.6). This mechanism also helps return lymph to the circulation for the same reasons.]

The Frank-Starling Law - (Starling's Law of the Heart) - Like skeletal muscle the myocardium has a length tension curve which results in an optimum level of stretch producing the maximum force of contraction. A healthy heart normally operates at a stretch less than this optimum level and when exercise causes increased venous return and increased stretch of the myocardium, the result is increased force of contraction to automatically pump the increased volume out of the heart. I.e. the heart automatically compensates its output to its input.

An important relationship in cardiac output is this one:

Blood Flow =  D Pressure / Resistance to Blood Flow      

The top number on the right side of the equation is the difference in pressure or drop in pressure along the cardiovascular system, i.e. the pressure gradient. Blood flow depends on this pressure gradient and is proportional to it. The bottom number is the Peripheral Resistance. Blood flow is inversely proportional to this value. Examining this formula can explain the effect of vasoconstriction and other factors as they affect cardiac output.