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mastering the cardiovascular physiology and identifying the pathophysiological cardiovascular physiology concepts are essential if and only. download Cardiovascular Physiology Concepts: Read 37 Books Reviews - site. com. Request PDF on ResearchGate | On Nov 30, , R. E. Klabunde and others published Cardiovascular Physiology Concepts.

Philadelphia, WB Saunders, , pp. Google Scholar 2. Circulatory physiology: Cardiac output and its regulation. Philadelphia: WB Saunders, Google Scholar 3. Effect of ventrlcula. Circ Res ; — Several intracellular mechanisms help to regulate lusitropy, most of which influence intracellular calcium concentrations.

The rate at which calcium enters the cell at rest and during action potentials influences intracellular concentrations. Under some pathologic conditions e. Inhibiting these transport systems can cause intracellular calcium concentrations to increase sufficiently to impair relaxation.

An Introduction to Cardiovascular Physiology

Blood vessels, except capillaries and small postcapillary venules, are composed of three layers: Capillaries and small postcapillary venules do not have media and adventitia. The primary components are given for each layer.

In larger vessels, a region of connective tissue also exists between the endothelial cells and the basal lamina. The media contains smooth muscle cells, imbedded in a matrix of collagen, elastin, and various glycoproteins. Depending on the size of the vessel, there may be several layers of smooth muscle cells, some arranged circumferentially and others arranged helically along the longitudinal axis of the vessel. The smooth muscles cells are organized so that their contraction reduces the vessel diameter.

The ratio of smooth muscle, collagen, and elastin, each of which has different elastic properties, determines the overall mechanical properties of the vessel.

For example, the aorta has a large amount of elastin, which enables it to passively expand and contract as blood is pumped into it from the heart. This mechanism enables the aorta to dampen the arterial pulse pressure see Chapter 5. In contrast, smaller arteries and arterioles have a relatively large amount of smooth muscle, which is required for these vessels to contract and thereby regulate arterial blood pressure and organ blood flow.

The outermost layer, or adventitia, is separated from the media by the external elastic lamina. The smallest vessels, capillaries, are composed of endothelial cells and a basal lamina; they are devoid of smooth muscle. Numerous small invaginations caveolae found in the cell membrane significantly increase the surface area of the cell Fig. The sarcoplasmic reticulum is poorly developed compared with the sarcoplasmic reticulum found in cardiac myocytes.

Contractile proteins actin and myosin are present; however, the actin and myosin in smooth muscle are not organized into distinct bands of repeating units as they are in cardiac and skeletal muscle. Instead, bands of actin filaments are joined together and anchored by dense bodies within the cell or dense bands on the inner surface of the sarcolemma, which function like Z-lines in cardiac myocytes.

N, nucleus. Similar to cardiac myocytes, vascular smooth muscle cells are electrically connected by gap junctions. These low-resistance intercellular connections allow propagated responses along the length of the blood vessels. For example, electrical depolarization and contraction of a local site on an arteriole can result in depolarization at a distant site along the same vessel, indicating cell-to-cell propagation of the depolarizing currents. Vascular smooth muscle tonic contractions are slow and sustained, whereas cardiac muscle contractions are rapid and relatively short a few hundred milliseconds.

In blood vessels, the smooth muscle is normally in a partially contracted state, which determines the resting tone or diameter of the vessel. This tonic contraction is determined by stimulatory and inhibitory influences acting on the vessel. Vascular smooth muscle contraction can be initiated by electrical, chemical, and mechanical stimuli.

Electrical depolarization of the vascular smooth muscle cell membrane using electrical stimulation elicits contraction primarily by opening voltage-dependent calcium channels L-type calcium channels , which causes an increase in the intracellular concentration of calcium. Membrane depolarization can also occur through changes in ion concentrations e. Many different chemical stimuli, such as norepinephrine, epinephrine, angiotensin II, vasopressin, endothelin-1, and thromboxane A2 can elicit contraction.

Each of these substances binds to specific receptors on the vascular smooth muscle cell. Different signal transduction pathways converge to increase intracellular calcium, thereby eliciting contraction. This probably results from stretch-induced activation of ionic channels that leads to calcium influx.

Figure 3. An increase in free intracellular calcium can result from either increased entry of calcium into the cell through L-type calcium channels or release of calcium from internal stores e. The free calcium binds to a special calciumbinding protein called calmodulin. The calcium—calmodulin complex activates myosin light chain kinase, an enzyme that phosphorylates myosin light chains in the presence of ATP. Myosin light chains are regulatory subunits found on the myosin heads.

Myosin light chain phosphorylation leads to cross-bridge formation between the myosin heads and the actin filaments, thus leading to smooth muscle contraction. The concentration of intracellular calcium depends on the balance between the calcium that enters the cells, the calcium that is released by intracellular storage sites, and the movement of calcium either back into intracellular storage sites or out of the cell.

Calcium is removed from the cell to the external environment by either an ATP-dependent calcium pump or the sodium—calcium exchanger, as in cardiac muscle see Chapter 2. Several signal transduction mechanisms modulate intracellular calcium concentration and therefore the state of vascular tone.

This section describes three different pathways: Dephosphorylation of myosin light chains by MLC phosphatase also produces relaxation.

Cardiovascular Physiology Concepts, 2nd Edition

ATP, adenosine triphosphate; Pi, phosphate group. The IP3 pathway in vascular smooth muscle is similar to that found in the heart. IP3 then directly stimulates the sarcoplasmic reticulum to release calcium.

The formation of diacylglycerol from PIP2 activates protein kinase C, which can modulate vascular smooth muscle contraction as well via protein phosphorylation. Receptors coupled to the Gs-protein stimulate adenylyl cyclase, which catalyzes the formation of cAMP. The mechanism for this process is cAMP inhibition of myosin light chain kinase see Fig. Adenosine and prostacyclin PGI2 also activate Gs-protein through their receptors, leading to an increase in cAMP and smooth muscle relaxation.

Many endothelial-dependent vasodilator substances e. This activates the IP3 pathway and stimulates calcium release by the sarcoplasmic reticulum, which leads to increased smooth muscle contraction. If the endothelium is intact, stimulation of the NO—cGMP pathway dominates over the actions of the IP3 pathway; therefore, acetylcholine normally causes vasodilation. Ultrastructure of the heart.

Handbook of Physiology, vol 1. American Physiological Society, ; 3— Regulation of cardiac contraction by calcium. American Physiological Society, ; — Physiology from Cell to Circulation.

Rhodin JAG. Architecture of the vessel wall. Handbook of Physiology, vol 2. American Physiological Society, ; 1— Sanders KM. Invited review: J Appl Physiol ; Somlyo AV: Ultrastructure of vascular smooth muscle. American Physiological Society, ; 33— The right atrium is a highly distensible chamber that can easily expand to accommodate the venous return at a low pressure 0 to 4 mm Hg.

Blood flows from the right atrium, across the tricuspid valve right atrioventricular [AV] valve , and into the right ventricle. The free wall of the right ventricle wraps around part of the larger and thicker left ventricle. The outflow tract of the right ventricle is the pulmonary artery, which is separated from the ventricle by the semilunar pulmonic valve. Blood returns to the heart from the lungs via four pulmonary veins that enter the left atrium. Blood flows from the left atrium, across the mitral valve left AV valve , and into the left ventricle.

The left ventricle has a thick muscular wall that allows it to generate high pressures during contraction. The left ventricle ejects blood across the aortic valve and into the aorta. The papillary muscles contract when the ventricles contract. This generates tension on the valve leaflets via the chordae tendineae, preventing the valves from bulging back and leaking blood into the atria i.

The semilunar valves pulmonic and aortic do not have analogous attachments. Autonomic Innervation Autonomic innervation of the heart plays an important role in regulating cardiac function.

The heart is innervated by parasympathetic vagal and sympathetic efferent fibers see Chapter 6 for details on the origin of these autonomic nerves. Atrial muscle is also innervated by vagal efferents; the ventricular myocardium is only sparsely innervated by vagal efferents.

Sympathetic efferent nerves are present throughout the atria especially in the SA node and ventricles, and in the conduction system of the heart. Vagal activation of the heart decreases heart rate negative chronotropy , decreases conduction velocity negative dromotropy , and decreases contractility negative inotropy of the heart. Vagal-mediated inotropic influences are moderate in the atria and relatively weak in the ventricles. Activation of the sympathetic nerves to the heart increases heart rate, conduction velocity, and inotropy.

Sympathetic influences are pronounced in both the atria and ventricles. As Chapter 6 describes in more detail, the heart also contains vagal and sympathetic afferent nerve fibers that relay information from stretch and pain receptors.

The stretch receptors are involved in feedback regulation of blood volume and arterial pressure, whereas the pain receptors produce chest pain when activated during myocardial ischemia.

The cardiac cycle diagram in Figure 4. Furthermore, the timing of mechanical events in the right side of the heart is very similar to that of the left side. The main difference is that the pressures in the right side of the heart are much lower than those found in the left side. For example, the right ventricular pressure typically changes from about 0 to 4 mm Hg during filling to a maximum of 25 to 30 mm Hg during contraction. A catheter can be placed in the ascending aorta and left ventricle to obtain the pressure and volume information shown in the cardiac cycle diagram and to measure simultaneous changes in aortic and intraventricular pressure as the heart beats.

This catheter can also be used to inject a radiopaque contrast agent into the left ventricular chamber. This permits fluoroscopic imaging contrast ventriculography of the ventricular chamber, from which estimates of ventricular volume can be obtained; however, real-time echocardiography and nuclear imaging of the heart are more commonly used to obtain clinical assessment of volume and function.

In the following discussion, a complete cardiac cycle is defined as the cardiac events initiated by the P wave in the electrocardiogram ECG and continuing until the next P wave.

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The cardiac cycle is divided into two general categories: Systole refers to events associated with ventricular contraction and ejection.

Diastole refers to the rest of the cardiac cycle, including ventricular relaxation and filling. The cardiac cycle is further divided into seven phases, beginning when the P wave appears. These phases are atrial systole, isovolumetric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid filling, and reduced filling.

The events associated with each of these phases are described below. Phase 1. Atrial Systole: This can be observed when a person is recumbent and the jugular vein in the neck expands with blood, which permits pulsations to be visualized. Therefore, ventricular filling is mostly passive and depends on the venous return.

However, at high heart rates e. In addition, atrial contribution to ventricular filling is enhanced by an increase in the force of atrial contraction caused by sympathetic nerve activation. This leads to inadequate ventricular filling, particularly when ventricular rates increase during physical activity.

After atrial contraction is complete, the atrial pressure begins to fall, which causes a slight pressure gradient reversal across the AV valves. At the end of this phase, which represents the end of diastole, the ventricles are filled to their end-diastolic volume EDV.

Cardiovascular Physiology Concepts by Richard E. Klabunde (2011, Paperback, Revised)

The left ventricular EDV typically about mL is associated with end-diastolic pressures of about 8 mm Hg. The right ventricular end-diastolic pressure is typically about 4 mm Hg. A heart sound is sometimes heard during atrial contraction Fourth Heart Sound, S4.

The sound is caused by vibration of the ventricular wall as blood rapidly enters the ventricle during atrial contraction. This sound generally is noted when the ventricle compliance is reduced i. The sound is commonly present in older individuals because of changes in ventricular compliance.

Isovolumetric Contraction: All Valves Closed This phase of the cardiac cycle, which is the beginning of systole, is initiated by the QRS complex of the ECG, which represents ventricular depolarization. As the ventricles depolarize, myocyte contraction leads to a rapid increase in intraventricular pressure.

The abrupt rise in pressure causes the AV valves to close as the intraventricular pressure exceeds atrial pressure. Contraction of the papillary muscles with their attached chordae tendineae prevents the AV valve leaflets from bulging back or prolapsing into the atria and becoming incompetent i. This heart sound is generated when sudden closure of the AV valves results in oscillation of the blood, which causes vibrations i.

During the time between the closure of the AV valves and the opening of the aortic and pulmonic semilunar valves, ventricular pressures rise rapidly without a change in ventricular volumes i.

During this phase, some individual fibers shorten when they contract, whereas others generate force without shortening or can be mechanically stretched as they are contracting because of nearby contracting cells.

Ventricular chamber geometry changes considerably as the heart becomes more spheroid in shape, although the volume does not change. Early in this phase, the rate of pressure development becomes maximal. Phase 3.

Rapid Ejection: Aortic and Pulmonic Valves Open; AV Valves Remain Closed When the intraventricular pressures exceed the pressures within the aorta and pulmonary artery, the aortic and pulmonic valves open and blood is ejected out of the ventricles. Ejection occurs because the total energy of the blood within the ventricle exceeds the total energy of blood within the aorta.

The total energy of the blood is the sum of the pressure energy and the kinetic energy; the latter is related to the square of the velocity of the blood flow. In other words, ejection occurs because an energy gradient is present mostly owing to pressure energy that propels blood into the aorta and pulmonary artery.

During this phase, ventricular pressure normally exceeds outflow tract pressure by only a few millimeters of mercury mm Hg. Although blood flow across the valves is high, the relatively large valve opening i. Maximal outflow velocity is reached early in the ejection phase, and maximal systolic aortic and pulmonary artery pressures are achieved, which are typically about and 25 mm Hg in the aorta and pulmonary artery, respectively. While blood is being ejected and ventricular volumes decrease, the atria continue to fill with blood from their respective venous inflow tracts.

Although atrial volumes are increasing, atrial pressures initially decrease x' descent as the base of the atria is pulled downward, expanding the atrial chambers. No heart sounds are ordinarily heard during ejection. The opening of healthy valves is silent. The presence of a sound during ejection i.

Reduced Ejection: This causes ventricular active tension to decrease i. Ventricular pressure falls slightly below outflow tract pressure; however, outward flow still occurs owing to kinetic or inertial energy of the blood that helps to propel the blood into the aorta and pulmonary artery. Atrial pressures gradually rise during this phase owing to continued venous return into the atrial chambers. The end of this phase concludes systole.

Phase 5. Isovolumetric Relaxation: All Valves Closed As the ventricles continue to relax and intraventricular pressures fall, a point is reached at which the total energy of blood within the ventricles is less than the energy of blood in the outflow tracts. When this total energy gradient reversal occurs, the aortic and pulmonic valves to abruptly close. At this point, systole ends and diastole begins.

Valve closure causes the Second Heart Sound S2 , which is physiologically and audibly split because the aortic valve closes before the pulmonic valve. Normally, little or no blood flows backward into the ventricles as these valves close. Valve closure is associated with a characteristic notch incisura in the aortic and pulmonary artery pressure tracings. Unlike in the ventricles, where pressure rapidly falls, the decline in aortic and pulmonary artery pressures is not abrupt because of potential energy stored in their elastic walls and because systemic and pulmonic vascular resistances impede the flow of blood into distributing arteries of the systemic and pulmonary circulations.

Ventricular volumes remain constant isovolumetric during this phase because all valves are closed. The residual volume of blood that remains in a ventricle after ejection is called the end-systolic volume ESV. For the left ventricle, this is approximately 50 mL of blood. Although ventricular volume does not change during isovolumetric relaxation, atrial volumes and pressures continue to increase owing to venous return.

Phase 6. Rapid Filling: Initially, the ventricles are still relaxing, which causes intraventricular pressures to continue to fall by several mm Hg despite ongoing ventricular filling. The rate of initial filling is enhanced by the fact that atrial volumes are maximal just prior to AV valve opening.

Once the valves open, the elevated atrial pressures coupled with declining ventricular pressures ventricular diastolic suction and the low resistance of the opened AV valves results in rapid, passive filling of the ventricles.

Once the ventricles are fully relaxed, their pressure begins to rise as they fill. The opening of the AV valves causes a rapid fall in atrial pressures.

The v wave and y descent are transmitted into the proximal venous vessels such as the jugular vein on the right side of the heart and pulmonary veins on the left side. Clinically, changes in atrial pressures and jugular pulses are useful in the diagnosis of altered cardiac function see Chapter 9. If the AV valves are functioning normally, no prominent sounds will be heard during filling. When a Third Heart Sound S3 is audible during ventricular filling, it may represent tensing of chordae tendineae and the AV ring, which is the connective tissue support for the valve leaflets.

This S3 heart sound is normal in children, but it is considered pathologic in adults because it is often associated with ventricular dilation. Reduced Filling: The reduced filling phase is the period during diastole when passive ventricular filling is nearing completion.

This is sometimes referred to as the period of ventricular diastasis. As the ventricles continue to fill with blood and expand, they become less compliant i. This causes the intraventricular pressures to rise, as described later in this chapter. Increased intraventricular pressure reduces the pressure gradient across the AV valve the pressure gradient is the difference between the atrial and ventricular pressure so that the rate of filling declines, even though atrial pressures continue to increase slightly as venous blood continues to flow into the atria.

Aortic pressure and pulmonary arterial pressure continue to fall during this period as blood flows into the systemic and pulmonary circulations.

It is important to note that Figure 4. At low heart rates, the length of time allotted to diastole is relatively long, which lengthens the time of the reduced filling phase. High heart rates reduce the overall cycle length and are associated with reductions in the duration of both systole and diastole, although diastole shortens much more than systole.

Without compensatory mechanisms, this cycle length reduction would lead to less ventricular filling i. Compensatory mechanisms are important for maintaining adequate ventricular filling during exercise see Chapter 9.

Summary of Intracardiac Pressures It is important to know normal values of intracardiac pressures, as well as the pressures within the veins and arteries entering and leaving the heart, because abnormal pressures can be used to diagnose certain types of cardiac disease and dysfunction.

Figure 4. The higher of the two pressure values expressed in mm Hg in the right ventricle RV , left ventricle LV , pulmonary artery PA , and aorta Ao represent the normal peak pressures during ejection systolic pressure , whereas the lower pressure values represent normal end of diastole pressure ventricles or the lowest pressure diastolic pressure found in the PA and Ao.

Pressures in the right atrium RA and left atrium LA represent average values during the cardiac cycle. Note that the pressures on the right side of the heart are considerably lower than those on the left side of the heart, and that the pulmonary circulation has low pressures compared to the systemic arterial system. The pressures shown for the right and left atria indicate an average atrial pressure during the cardiac cycle—atrial pressures change by several mm Hg as they fill and contract.

Ventricular Pressure—Volume Relationship Although measurements of pressures and volumes over time can provide important insights into ventricular function, pressure— volume loops provide another powerful tool for analyzing the cardiac cycle, particularly ventricular function.

Pressure—volume loops Fig. In Figure 4. The area within the pressure—volume loop is the ventricular stroke work. The filling phase moves along the end-diastolic pressure—volume relationship EDPVR , or passive filling curve for the ventricle. The slope of the EDPVR at any point along the curve is the reciprocal of ventricular compliance, as described later in this chapter.

The maximal pressure that can be developed by the ventricle at any given left ventricular volume is described by the end-systolic pressure—volume relationship ESPVR. The pressure—volume loop, therefore, cannot cross over the ESPVR, because the ESPVR defines the maximal pressure that can be generated at any given volume under a given inotropic state, as described later in this chapter. The changes in pressures and volumes described in the cardiac cycle diagram and by the pressure—volume loop are for normal adult hearts at resting heart rates.

Pressure— volume loops appear very differently in the presence of valve disease and heart failure as described in Chapter 9. The heart achieves this by contracting its muscular walls around a closed chamber to generate sufficient pressure to propel blood from the left ventricle, through the aortic valve, and into the aorta. Each time the left ventricle contracts, a volume of blood is ejected into the aorta. Obviously, this approach cannot be used in humans; therefore, indirect techniques are used.

The most commonly used is the thermodilution technique, which uses a special multilumen, thermistor-tipped catheter Swan-Ganz that is inserted into the pulmonary artery from a peripheral vein. A cold saline solution of known temperature and volume is injected into the right atrium from a proximal port on the catheter.

The cold injectate mixes into the blood and cools the blood, which then passes through the right ventricle and into the pulmonary artery. The thermistor at the catheter tip measures the blood temperature, and a cardiac output computer is used to calculate flow cardiac output. Doppler echocardiography can be used to estimate real-time changes in flow within the heart, pulmonary artery, or ascending aorta. Echocardiography and various radionuclide techniques can also be used to measure changes in ventricular dimensions during the cardiac cycle in order to calculate SV, which, when multiplied by heart rate, gives cardiac output.

This method is based on the following relationship Fick Principle: Sarcomere length cannot be determined in the intact heart, so indirect indices of preload, such as ventricular EDV or pressure, must be used.

These measures of preload are not ideal because they may not always reflect sarcomere length because of changes in the structure and mechanical properties of the heart. Despite these limitations, acute changes in end-diastolic pressure and volume are useful indices for examining the effects of acute preload changes on SV.

Normally, compliance curves are plotted with volume on the Y-axis and pressure on the X-axis, so that the compliance is the slope of the line at any given pressure i. For the ventricle, however, it is common to plot pressure versus volume Fig. Plotted in this manner, the slope of the tangent at a given point on the curve is the reciprocal of the compliance. Therefore, the steeper the slope of the pressure—volume relationship, the lower the compliance.

The relationship between pressure and volume is nonlinear in the ventricle as in most biological tissues ; therefore, compliance decreases with increasing pressure or volume.

When pressure and volume are plotted as in Figure 4. Ventricular compliance is determined by the physical properties of the tissues making up the ventricular wall and the state of ventricular relaxation.

For example, in ventricular hypertrophy, the increased muscle thickness decreases the ventricular compliance; therefore, ventricular end-diastolic pressure is higher for any given EDV. This is shown in Figure , in which the filling curve of the hypertrophied ventricle shifts upward and to the left. From a different perspective, for a given end-diastolic pressure, a less compliant ventricle will have a smaller EDV i. If ventricular relaxation lusitropy is impaired, as occurs in some forms of diastolic ventricular failure see Chapter 9 , the functional ventricular compliance will be reduced.

This will impair ventricular filling and increase enddiastolic pressure. If the ventricle becomes chronically dilated, as occurs in other forms of heart failure, the filling curve shifts downward and to the right. This enables a dilated heart to have a greater EDV without causing a large increase in end-diastolic pressure.

The length of a sarcomere prior to contraction, which represents its preload, depends on Decreased Compliance e. The slope of the tangent of the passive pressure—volume curve at a given volume represents the reciprocal of the ventricular compliance. The slope of the normal compliance curve is increased by a decrease in ventricular compliance e.

LV, left ventricle. This, in turn, depends on the ventricular end-diastolic pressure and compliance. Although end-diastolic pressure and EDV are sometimes used as indices of preload, care must be taken when interpreting the significance of these values in terms of how they relate to the preload of individual sarcomeres. An elevated end-diastolic pressure may be associated with sarcomere lengths that are increased, decreased, or unchanged, depending on the ventricular volume and compliance at that volume.

For example, a stiff, hypertrophied ventricle may have an elevated end-diastolic pressure with a reduced EDV owing to the reduced compliance. Because the EDV is reduced, the sarcomere length will be reduced despite the increase in end-diastolic pressure. As another example, a larger than normal EDV may not be associated with an increase in sarcomere length if the ventricle is chronically dilated and structurally remodeled such that new sarcomeres have been added in series, thus maintaining normal individual sarcomere lengths.

Effects of Preload on Tension Development Length—Tension Relationship We have seen how ventricular EDV, which is determined by ventricular end-diastolic Muscle L pressure and ventricular compliance, can alter the preload on sarcomeres in cardiac muscle cells. This change in preload will alter the ability of the myocyte to generate force when it contracts.

The length—tension relationship examines how changes in the initial length of a muscle i. To illustrate this relationship, a piece of cardiac muscle e. One end of the muscle is attached to a force transducer to measure tension, and the other end is attached to an immovable support rod Fig.

The end that is attached to the force transducer is movable so that the initial length preload of the muscle can be fixed at a desired length. The muscle is then electrically stimulated to contract; however, the length is not permitted to change and therefore the contraction is isometric. By stretching the muscle to a longer initial length, the passive tension will be increased prior to stimulation.

The left side shows how muscle length and tension are measured in vitro. The right side shows how increased preload initial length increases both passive and active developed tension. The greater the preload, the greater the active tension generated by the muscle. When the muscle is stimulated at the increased preload, there will be a larger increase in active tension curve b than had occurred at the lower preload.

If the preload is again increased, there will be a further increase in active tension curve c. Therefore, increases in preload lead to an increase in active tension.

Not only is the magnitude of active tension increased, but also the rate of active tension development i. The duration of contraction and the time-to-peak tension, however, are not changed. If the results shown in Figure 4. In the top panel, the passive tension curve is the tension that is generated as the muscle is stretched prior to contraction. Points a, b, and c on the passive curve correspond to the passive tensions and initial preload lengths for curves a, b, and c in Figure 4.

The total tension curve represents the maximal tension that occurs during contraction at different initial preloads. The total tension curve is the sum of the passive tension and the additional tension generated during contraction active tension.

The active tension, therefore, is the difference between the total and passive tension curves; it is plotted separately in the bottom panel of Figure The active tension diagram demonstrates that as preload increases, there is an increase in active tension up to a maximal limit.

The maximal active tension in cardiac muscle corresponds to a sarcomere length of about 2.

Because of the passive mechanical properties of cardiac myocytes, their length seldom exceeds 2. The top panel shows that increasing the preload length from points a to c increases the passive tension. Furthermore, increasing the preload increases the total tension during contraction as shown by arrows a, b, and c, which correspond to active tension changes depicted by curves a, b, and c in Figure 4.

The length of the arrow is the active tension, which is the difference between the total and passive tensions. The bottom panel shows that the active tension increases to a maximum value as preload increases.

Cardiac muscle fibers, however, normally shorten when they contract i. If a strip of cardiac muscle in vitro is set at a given preload length and stimulated to contract, it will shorten and then return to its resting preload length Fig. If the initial preload is increased and the muscle stimulated again, it will ordinarily shorten to the same minimal length, albeit at a higher velocity of shortening. Substances transported throughout the cardiovascular system can be categorized as 1 materials entering the body from the external environment e.

The exchange of materials between blood and interstitial fluid occurs across capillaries in the microcirculation. The two atria serve as reservoirs for blood returning to the heart. The two ventricles are pumps that propel blood through the circulation Figure A septum divides the heart into right and left sides.

The right atrium is the reservoir serving the right ventricle, which pumps blood to the pulmonary circulation via the pulmonary artery.ECG Leads: Within proteins troponin complex, TN having three sub- the cell, and in close association with the units: High heart rates reduce the action potential duration and therefore the QT interval. A cold rate is elevated. Normally, little or velocity is reached early in the ejection phase, no blood flows backward into the ventricles as and maximal systolic aortic and pulmonary these valves close.

One major difference is the for sodium to pass through the channel, effec- duration of the action potentials.

The heart has other important functions besides pumping blood. Examples of brane protein channel, and they undergo con- voltage-gated channels include several sodium, formational changes in response to changes potassium, and calcium channels that are in voltage. In the resting closed state, the m-gates activation gates are closed, although the h-gates inactivation gates are open.

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