Physiology
Lec: 3 د. زيــد الأطـرقجيCardiac output:
Is the volume of blood pumped by each ventricle per minute.
Cardiac output depends on the heart rate and the stroke volume.
Cardiac output= heart rate X stroke volume = about 5 liters.
Because the body's total blood volume averages 5 liters each half of the heart pumps the equivalent of the entire blood volume each minute. In other words each minute the right ventricle normally pumps 5 liters of blood through the lungs and the left ventricle pumps 5 liters through the systemic circulation.
During exercise cardiac out put increase to 20 to 25 liters per minute and out-put as high as 40 liters per minute have been recorded in trained athletes during heavy endurance type exercise.
Cardiac reserve= maximum volume of blood the heart can pump per minute cardiac output at rest.
So the cardiac reserve is the difference between the cardiac output at rest and the maximum volume of blood the heart can pump at exercise.
Heart rate:
Is determined primarily by autonomic influences on the S-A node.
Membrane potential of the S-A node is due to a complex interplay of ion movements involving a reduction in K+ permeability, a constant Na+ permeability and an increased Ca+ permeability. When the S-A node reaches threshold an action potential is initiated that spreads throughout the heart.
Para-sympathetic nerve to the heart [the vagus] primarily supplies the atrium especially the S-A node and A-V nodes. Para-sympathetic innervations of the ventricle are sparse.
The cardiac sympathetic nerves also supply the atria including the S-A and A-V node and richly innervate the ventricle as well.
Both the para-sympathetic and sympathetic nervous system brings about their effects on the heart by altering the activity of the cyclic AMP second messenger system in the innervated cardiac cells.
Acetyl-choline released from the vagus nerve bind to a muscarinic receptor and is coupled to an inhibitory G protein that reduces activity of the cyclic AMP pathway.
Sympathetic neurotransmitter norepinephrine binds with a Beta 1 adrenergic receptor and is coupled to a stimulatory G protein that accelerates the cyclic AMP pathway in the target cells.
Effect of para-sympathetic stimulation on the heart:
Acetyl choline released on increased para-sympathetic activity increases the permeability of the S-A node to K+ by slower the closure of K+ channels. As a result the rates at which spontaneous action potential are initiated is reduced through two ways:
A. Enhanced K+ permeability hyperpolarizes the S-A node membrane because more positive potassium ions leave than normal making the inside even more negative.
B. the enhanced K+ permeability induced by vagal stimulation also opposes the automatic reduction in K+ permeability responsible for initiating the gradual depolarization of the membrane to reach threshold.
This countering effect decreases the rate of spontaneous depolarization prolonging the time required to drift to threshold. Therefore the S-A node reaches threshold and fire less frequently decreasing the heart rate.
Para-sympathetic influence on the A-V node decreases the node excitability, prolonging transmission of impulses to the ventricles even longer than the usual AV nodal delay.
This effect is brought about by increasing K+ permeability which hyperpolarizes the membrane thereby retarding the initiation of excitation in the A-V node.
Para-sympathetic stimulation of the atrial contractile cells shorten the action potential reducing the slow inward current carried by Ca+ that is the plateau phase is shortened . As a result atrial contraction is weakened.
The para-sympathetic system has little effect on ventricular contraction because of the sparseness of para-sympathetic innervation to the ventricles.
Thus when the heart under para-sympathetic influence it beats less rapidly ,the time between atrial and ventricular contraction is stretched out and atrial contraction is weaker these actions are appropriate considering that the para-sympathetic system controls heart action in rest situations when the body is not demanding an enhanced cardiac output.
Effects of sympathetic stimulation on the heart:
The sympathetic nervous system control heart action in emergency or exercise situations when there is a need for greater blood flows.
The main effect of sympathetic stimulation on the S-A node is to speed up depolarization so that threshold is reached more rapidly.
Nor epinephrine released from the sympathetic nerve endings decreases K+ permeability by accelerating inactivation of the K+ channels with fewer positive potassium ions leaving the inside of the cell. This swifter drift to threshold under sympathetic influence permits more frequent action potential and a correspondingly faster heart rate.
Sympathetic stimulation of the A-V node reduces the A-V nodal delay by increasing conduction velocity presumably by enhancing the slow inward Ca+ current.
Sympathetic stimulation speeds up spread of the action potential throughout the specialized conduction pathway.
Sympathetic stimulation increases contractile strength so the heart beats more forcefully and squeezes out more blood. This effect is produced by increasing Ca+ permeability which enhances the slow Ca+ influx and intensifies Ca+ participation in excitation contraction coupling.
The overall effect of sympathetic stimulation on the heart is to improve its effectiveness as a pump by increasing heart rate, decreasing the delay between atrial and ventricular contraction, decreasing conduction time throughout the heart and increasing the force of contraction.
The para-sympathetic and sympathetic effects on heart rate are antagonist [oppose each other]. At any given moment heart rate is determined largely by the balance between inhibition of the S-A node by vagus nerve and stimulation of the cardiac sympathetic nerves .under resting conditions para-sympathetic effect dominates.
Heart rate is speeded up by simultaneously increasing sympathetic and decreasing para-sympathetic activity.
Heart rate is slowed by a concurrent rise in para-sympathetic activity and decline in sympathetic activity. The relative level of activity in these two autonomic branches to the heart in turn is primarily coordinated by the cardiovascular center in the brain stem.
Stroke-volume:
Is the volume of blood pumped out by each ventricle during each beat [single beat].
Stroke volume can be controlled:
1. Intrinsic control which is related to the extent of venous return.
2. Extrinsic control which is related to the extent of sympathetic stimulation of the heart.
Both factors increase stroke volume by increasing the strength of heart contraction.
Intrinsic-control:
Increased end-diastolic volume results in increased stroke volume. For cardiac muscle the resting cardiac muscle fiber is less than optimal length. That is within physiologic limits cardiac muscle does not stretched beyond its optimal length to the point that contractile strength diminishes with further stretching. The cardiac muscle fibers length which is determined by the extents of venous filling is normally less than the optimal length for developing maximal tension. Therefore an increase in end-diastolic volume that is an increase in venous return by moving the cardiac fiber length closer to optimal length increases the contractile tension of the fibers on the next systole.
A stronger contraction squeezes out more blood, thus as more blood is returned to the heart and the end diastolic volume increases, the heart automatically pumps out a correspondingly larger stroke volume.
The main determinant of cardiac muscle fiber length is the degree of diastolic filling.
The extent of filling is referred to as the preload because it is the work load imposed on the heart before contraction begins. Therefore the heart is stretched when more blood is pouring in it.
The longer the initial cardiac muscle fiber length before contraction [produced by more filing] the greater the force of subsequent cardiac contraction and thus a greater stroke volume.
Advantage of the cardiac length-tension relationship:
1. Equalizing output between the right and left sides of the heart so that blood pumped out of the heart is equally distributed between the pulmonary and systemic circulation. If such equalization did not happen too much blood would be dammed up in the venous system before the ventricle which has the lower output.
2. When a larger cardiac output is needed such as during exercise. Venous return is increased through action of the sympathetic nervous system. The result is increase in end-diastolic volume [EDV] automatically increases stroke volume correspondingly. Also the exercise increase the heart rate these two factors act together to increase the cardiac output so more blood can be delivered to the exercising muscles.