EMS Update:
Anatomy & Physiology of the Heart
Dispatch
- preload
- afterload
Left ventricular systole produces a surge of blood through the blood vessels that gives rise to two important vital signs. Vital signs are readily available indices used to monitor the general state of health of an individual and include pulse, blood pressure, body temperature, and rate of respirations. In hospitalized patients, these are the measurements the physician or nurse records on the patient's chart and which provide an indication of the patient's general condition. Of the vital signs, two, pulse and blood pressure, are generated by left ventricular systole.
The pulse is a direct result of the surge of blood produced by left ventricular systole. It is a ready means of recognizing the rate of the heart and its regularity. The strength of the pulse is also of importance; a weak, thready pulse may be an indication of a serious problem. The pulse can be taken at any point where a large artery runs close to the skin. Common sites for this are the temple, neck, armpit, groin and foot. For convenience, the pulse is usually "taken" at the wrist at the base of the thumb, where the large radial artery to the hand is close to the skin. In case of doubt, the pulse can be verified by listening to the heart with a stethoscope, a procedure referred to as auscultation.
The blood pressure is the second of the vital signs that is related to the heart. It is a measurement of the outward pressure exerted on arterial walls by the blood and consists of two components; the systolic (SBP) and the diastolic blood pressure (DSP). The systolic blood pressure is the pressure generated by left ventricular systole. The diastolic pressure is the residual pressure in the arterial system during the diastolic phase of ventricular relaxation and refilling. It is important to remember that there is always a supply of blood in the vascular system, both during systole and diastole. Blood pressure is measured by various types of sphygmomanometers which register the pressure in terms of the height of a column of mercury expressed in millimeters - mm/Hg (mercury is a liquid element 13 times heavier than water and provides an easy and useful means of measurement). The blood pressure is expressed as the ratio of systolic to diastolic pressures (systolic/diastolic).
Normally, the systolic pressure is 140 millimeters of mercury (mm/Hg) or less and the diastolic is 90 mm/Hg or less. Hypertension (high blood pressure) exists when either the systolic or diastolic readings are above 140 and 90 respectively. There are no set standards for hypotension (low blood pressure) since it is relative to the patient's known normal blood pressure. Thus a systolic blood pressure of 120 mm/Hg, considered normal under usual conditions, might represent hypotension in an individual who had a systolic blood pressure of 180 mm/Hg. Generally speaking, however, a systolic blood pressure of 100 mm/Hg or below suggests hypotension. The diagnosis is usually made in the presence of other confirmatory signs and symptoms.
According to guidelines set by the JNC (Joint National Committee) on Detection, Evaluation, and Treatment of High Blood Pressure, blood pressure under 140/90 mmHg is considered normal. Systolic readings between 130-139 mmHg and diastolic readings from 85-89 mmHg are high normal, while blood pressure under 120/80 mmHg is optimal.
Arterial blood pressure is determined by two primary factors: the total amount or volume of blood pumped by the heart (cardiac output) and the resistance arterioles present to blood flow (total peripheral resistance). In turn, each of these primary factors is influenced by a number of secondary factors.
Cardiac output (CO) is the volume of blood that is pumped each minute from the left ventricle to the tissues. If all other variables remain equal, increased cardiac output leads to increased arterial blood pressure. Resistance to blood flow is determined by the diameter of every arteriole in the body and is called Total Peripheral Resistance (TPR) or systemic vascular resistance. TPR is controlled by arterioles because their diameters, under control of the autonomic nervous system, can vary according to the body's needs.
If expressed mathematically, the relationship between CO, TPR, and arterial blood pressure can be represented with the following equation:
CO x TPR = BP
According to this equation, a change in cardiac output or peripheral resistance will result in a proportional change in arterial blood pressure (i.e., if CO or TPR increase, BP will also increase). Numerous factors influence cardiac output and peripheral resistance.
Cardiac output can be calculated by multiplying the heart rate by the stroke volume. Heart rate (HR) is the number of ventricular contractions per minute, regulated by the autonomic nervous system. The normal range for heart rate is 60-100 contractions per minute. Stroke volume (SV) is the volume of blood ejected by the left ventricle each time it contracts. It is determined by calculating the difference between the volume of the ventricle at the end of systole and the end of diastole. Stroke volume is influenced largely by venous return, the volume of blood returned to the heart by the veins. The normal range for left ventricular stroke volume is 60-130 mL per contraction.
HR x SV = CO
(It is important not to confuse stroke volume with the term ejection fraction. The ejection fraction is the ratio of the stroke volume to the volume of the left ventricle at the end of diastole. In other words, the ejection fraction is the percentage of the end diastolic volume. That is the volume of blood present in the ventricle at the end of diastole that is actually forced out of the left ventricle into the aorta during contraction. Typically, ejection fraction averages around 67%.)
Since changes in stroke volume or heart rate can alter cardiac output, these variables can also affect arterial blood pressure. For example, an increase in heart rate, with no compensating decrease in other parameters, will increase cardiac output and thus increase overall blood pressure. Similarly, if stroke volume increases, but heart rate does not drop accordingly, overall blood pressure will rise.
Peripheral resistance can be changed by both chronic and temporary factors. Chronic changes in arteriolar diameter, such as the narrowing caused by atherosclerosis, can produce a constant change in resistance to blood flow. Temporary changes may occur from either vasodilation (relaxation of smooth muscle in the arteriolar walls, which causes the vessel diameter to increase and resistance to blood flow to drop) or vasoconstriction (contraction of smooth muscle in the arteriolar walls, which causes the vessel diameter to decrease and resistance to rise). If peripheral resistance increases or decreases while cardiac output remains unchanged, overall blood pressure will rise or fall accordingly.
The relationship between heart rate and cardiac work is fairly simple. If the heart beats more quickly (during exercise, for example), it performs more work. However, the ways in which cardiac wall tension and myocardial contractility affect cardiac work are somewhat more complex.
Cardiac wall tension is the force cardiac muscle fibers exert to contain the blood and to contract against it. As blood enters the heart, it exerts an outward pressure on the cardiac walls. To prevent the heart from expanding like a balloon filling with air, the heart fibers are able to resist excessive stretching and thus exert the pressure necessary to contain the blood. When the heart contracts to pump the blood, the cardiac walls must exert even greater pressure to expel the blood into the circulation. Increasing the wall tension increases the total effort that must be exerted by the heart muscle and it must work harder to contract.
Two factors play a significant role in determining cardiac wall tension. These factors
are:
Preload and Cardiac Wall Tension
Preload refers to the pressure exerted by the blood against the ventricular wall the instant prior to contraction. Preload is synonymous with venous return to the heart, and this is often monitored as left ventricular end diastolic pressure (LVEDP). Any change in the body that increases the return of blood to the heart will increase the preload.
Increases in preload increase myocardial work. To understand this relationship, imagine two bicycle tires, with one containing more air than the other. If you try to compress each tire with your hand, you must squeeze harder on the tire with the higher air pressure to push the wall inward. In a similar way, the heart must work harder to "push" its walls inward during contraction if the preload has been increased.
Two factors can increase preload: increased blood/fluid volumes and constriction of blood vessels. Increases of blood/fluid volume means that more fluid is available in the cardiovascular system to enter the heart prior to each contraction. Constriction of blood vessels affects preload by reducing the area in the vascular system through which blood can flow. Vasoconstriction decreases the capacity of the veins and venules to hold blood. This reduces the amount of blood that is allowed to pool in the veins, thus forcing more blood back into the heart. Vasoconstriction is primarily controlled by activation of the sympathetic nervous system, which stimulates vasoconstriction through the action of norepinephrine.
Afterload and Cardiac Wall Tension
Afterload is the pressure that the ventricles must work against to pump blood into the aorta and pulmonary artery. It varies with arteriolar resistance to the flow of blood (peripheral resistance). An increase in afterload increases cardiac work by forcing the ventricles to pump against a higher pressure in the arteries.
If afterload remains increased for a long period of time, the heart must work harder to pump the blood through the arterial system. To compensate for this, the muscles of the heart increase in size (hypertrophy). Eventually, this compensatory mechanism fails and the heart is no longer capable of pumping blood against the elevated arterial pressure and its pump action begins to fail. This condition is known as congestive heart failure (CHF), and requires therapy.
Myocardial contractility and cardiac work
Myocardial contractility is the strength or forcefulness of contraction of individual cardiac muscle fibers. Depending on its health, the heart may contract vigorously or weakly. A strong contraction allows expulsion of a greater volume of blood. Thus, if a heart's contractions are strong, it has to pump fewer times (i.e., it does less work) than it would if its contractions were weakened by disease.
Myocardial contractility can be augmented by sympathetic nervous stimulation. This is mediated by the actions of epinephrine (adrenaline) and norepinephrine on muscle fibers. In periods of stress, fright, or other conditions that initiate sympathetic activity, myocardial contractility and the work performed by the heart increase. Certain drugs, called inotropic agents, have the capability of increasing the force of myocardial contraction and are valuable therapeutic agents.
The Frank-Starling Principle and Myocardial Contractility
One further concept important to understanding cardiac function is the Frank-Starling Principle. The Frank-Starling Principle states that the output of the heart increases in proportion to the amount of stretch in the cardiac muscle fibers. In other words, if the heart is forced to stretch to accommodate higher volumes of blood, myocardial contractility will increase. Thus, the amount of blood pumped out of the heart per beat will increase if the amount of stretch of the ventricle increases.
Increased preload can cause cardiac muscle fibers to stretch. An increased volume of blood returning to the heart can fill the heart's chambers to the point where muscle fibers have to stretch more than normal to expel the blood. As the Frank-Starling Principle states, the increased stretch provides increased force for contraction. However, if the myocardium is stretched too far or too frequently, it can lose the ability to return to its original contracted state. If the heart muscle is stretched excessively, it can eventually lose its ability to contract with its normal force.
Anatomy & Physiology of the Heart
Overview of the Cardiovacular System
Hemodynamics of the Cardiac System