Physiology
Lec: 5 د. زيـد الاطرقجيCardiovascular system
Contractility:
Is the strength of contraction at any given end-diastolic volume.Sympathetic stimulation to the heart increases the contractility of the heart. On sympathetic stimulation the heart contracts more forcefully and squeezes out a greater percentage of the blood it contains leading to more complete ejection.
This increased contractility is due to the increased Ca+ influx triggered by nor epinephrine and epinephrine. This extra cytosolic Ca+ lets the myocardial fibers generate more force through greater cross-bridge cycling than they would without sympathetic influence.
Normally the EDV is 135ml and the end-systolic volume [ESV] is 65ml for a stroke volume of 70ml, under sympathetic influence for the same EDV of 135ml the ESV might be 35ml and the stroke volume 100ml.
Sympathetic stimulation increases stroke volume not only by strengthening cardiac contractility but also by enhancing venous return. Sympathetic stimulation constricts the veins which squeeze more blood forward from the veins to the heart increasing the EDV and subsequently increasing stroke volume even further.
High blood pressure increases the work load of the heart. The arterial blood pressure is called the after-load which is work load imposed on the heart after contraction has begun. If arterial blood pressure is chronically elevated or if the exit valve is stenotic the ventricle must generate more pressure to eject blood, the end result is heart failure.
Heart failure:
Is the inability of the cardiac output to compensate with the body demand for supplies and removal of wastes. Either one or both ventricles may progressively weaken and fail. When a failing ventricle cannot pump out all the blood returned to it, the veins behind the failing ventricle becomes congested with blood.
The prime defect in heart failure is a decrease in cardiac contractility; that is weakened cardiac muscle contracts less effectively.
Compensatory measures for heart failure:
In the early stages two major compensatory measures help restore stroke volume to normal.
1. Sympathetic activity to the heart is reflexly increased which increases heart contractility toward normal. But sympathetic stimulation can help compensate only for a limited period of time. However because the heart becomes less responsive to nor epinephrine after prolong exposure and furthermore the nor epinephrine store in the hearts sympathetic nerve terminal become depleted.
2. When the cardiac output is reduced the kidneys in a compensatory attempt to improve their reduced blood flow retain extra salt and water in the body during urine formation to expand the blood volume. The increase in circulatory blood volume increases the EDV, the resultant stretching of the cardiac muscle fibers enables the weakened heart to pump out a normal stroke volume. The heart is now pumping out the blood but it is operating at a greater cardiac muscle fiber length.
Nourishing the heart muscle [coronary blood flow]:
Cardiac muscle cells contain an abundance of mitochondria (the O2 dependent energy organelle). In fact up to 40% of the cell volume of cardiac muscle cells is occupied by mitochondria which is an indicative of how much the heart depends on O2 delivery and aerobic metabolism to generate the energy necessary for the contraction. Cardiac muscle also has an abundance of myoglobin which stores limited amounts of O2 within the heart for immediate use.
Most coronary blood flow occurs during diastole because the coronary vessels are compressed almost completely closed during systole. Although all the blood passes through the heart, the heart muscle cannot extract O2 or nutrients from the blood within its chambers for two reasons:
A. the water tight endocardial lining does not permit blood to pass from the chambers into the myocardium.
B. the heart walls are thick to permit diffusion of O2 and other supplies from the blood in the chamber to the individual cardiac cells. Therefore like other tissues of the body heart muscle must receive blood through blood vessels specifically via the coronary circulation.
The heart muscle receives most of its blood supply during diastole. Blood flow to the heart muscle cells is substantially reduced during systole for two reasons:
1. The contracting myocardium especially in the powerful left ventricle compresses the major branches of the coronary arteries.
2. The open aortic valve partially blocks the entrance to the coronary vessels.
Thus most coronary arterial flow [70%] occurs during diastole driven by the aortic blood pressure with flow declining as aortic pressure drops. Only about 30% of coronary arterial flow occurs during systole. This limited time for coronary blood flow becomes especially important during rapid heart rates when diastolic time is much reduced. Just when increased demands are placed on the heart to pump more rapidly it has less time to provide O2 and nourishment to its own musculature to accomplish the increased work load.
Extra blood is delivered to the cardiac cells primarily by vasodilatation of the coronary vessels which lets more blood flow through them especially during diastole.
The increased coronary blood flow is necessary to meet the hearts increased O2 requirements because the heart unlike most other tissues is unable to remove much additional O2 from the blood passing through its vessels to support increased metabolic activities.
Most other tissues under resting conditions extract only about 25% of the O2 available from the blood flowing through them leaving a considerable O2 reserve that can be drawn or when a tissues has increased O2 needs that is the tissue can immediately increase the O2 available to it by removing a greater percentage of O2 from the blood passing through it.
In contrast the heart even under resting conditions removes up to 65-75% of the O2 available in the coronary vessels far more than is withdrawn by other tissues. This leaves little O2 in reserve in the coronary blood. Therefore the primary means by which more O2 can be made available to the heart muscle is by increasing blood flow.
Coronary blood flow is adjusted primarily in response to changes in the hearts O2 requirements. Among the proposed links between blood flow and O2 needs is adenosine which is formed from adenosine- triphosphate [ATP] during cardiac metabolic activity. Cardiac cells form and release more adenosine when cardiac activity increases and the heart accordingly needs more O2 and using more ATP as an energy source.
The released adenosine act as a paracrine factor induces dilatation of the coronary blood vessels allowing more O2 rich blood to flow to the more active cardiac cells to meet their increased O2 demand. Matching O2 delivery to O2 needs is crucial because heart muscle depends on oxidative processes to generate energy. The heart cannot get enough ATP through anaerobic metabolism.
As a fuel sources the heart primarily uses free fatty acids and to lesser extent glucose and lactate depending on their availability. Because cardiac muscle is remarkably adaptable and can shift metabolic pathways to use whatever nutrient is available the primary danger of insufficient coronary blood flow is not fuel shortage but O2 deficiency.
Blood pressure
Is the force exerted by the blood against a vessel wall.
It depends on:
1. Volume of blood contained within the vessel.
2. Compliance or dispensability of the vessel walls [how easily they can be stretched].
If the volume of blood entering the arteries were equal to the volume of blood leaving the arteries during the same period , arterial blood pressure would remain constant this is not the case however.
During ventricular systole a stroke volume of blood enters the arteries from the ventricle while only about one third as much blood leaves the arteries to enter the arterioles. During diastole no blood enters the arteries while blood continues to leave driven by elastic recoil.
The maximum pressure exerted in the arteries when blood is ejected into them during systole, The systolic arterial blood pressure averages 120mmHg..
The minimum pressure within the arteries when blood is draining off into the rest of the vessels during diastole is the diastolic arterial pressure which averages 8ommHg. Although ventricular pressure falls to 0mmHg during diastole arterial pressure does not fall to 0mmHg because the next cardiac contraction occurs and refills the arteries before all the blood drains off.
Blood pressure can be measured indirectly by using sphygmomanometer.
The technique involves balancing the pressure in the cuff against the pressure in the artery. When cuff pressure is greater than the pressure in the vessel, the vessel is pinched closed so that no blood flows through it. When blood pressure is greater than cuff pressure the vessel is open and blood flows through.
Pulse-pressure: the pulse that can be felt in an artery lying close to the surface of the skin is due the difference between systolic and diastolic pressures. This pressure difference is known as the pulse pressure when blood pressure is 120\80mmHg pulse pressure is 40mmHg.
Mean arterial blood pressure: is the main driving force for blood flow. It is the average pressure driving blood forward into the tissues throughout the cardiac cycle.
At rest two thirds of the cardiac cycle is spent in diastole and only one third in systole.
Mean arterial blood pressure= diastolic pressure+ 1\3 pulse pressure.