Cardiac output and venous return
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THE CARDIAC OUT PUT AND VENOUS RETURN
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Cardiac output and venous return
- 1. Cardiac Output and Venous Return
- 2. Learning objectives • Define Cardiac Output and Venous Return. • Define the factors that affect cardiac output. • Explain how alteration in (preload,contractility,afterload) change the cardiac output. • Describe the effects of changing total peripheral resistance on cardiac output. • Understand the principles underlying cardiac output measurements using the Fick principle, dye dilution, and thermodilution methods. • Know how cardiac function (output) curves are generated and how factors which cause changes in contractility in the heart can alter the shape of cardiac function curves. • Construct a vascular function curve. Predict how changes in total peripheral resistance, blood volume, and venous compliance influence this curve. • Use the intersection point of the cardiac function curve and vascular function curve to predict how interventions such as hemorrhage, heart failure, autonomic stimulation, and exercise will affect cardiac output and right atrial pressure.
- 3. Cardiac output • Amount of blood ejected by each ventricle per minute is called cardiac output (CO). Its value is almost same for both the ventricles & is about 5L/min. in a normal adult male • Cardiac output = heart beat rate X stroke volume (stroke volume is amount of blood ejected/ventricle/beat or stroke = EDV-ESV) • CO = 72/min X 70ml = 5 L/min (approx.) • Cardiac index: CI is the cardiac output per square meter of body surface area. Normal value is about 3 L/min/m2
- 4. Measurement of Cardiac Output • Calculation of flow through the pulmonary circuit provides a measure of the CO. Required data are: • oxygen consumption of the organ • A – V oxygen content (concentration) difference across the organ (not PO2)
- 7. • In a test subject, oxygen consumption was measured at 700 mL/min.Pulmonary artery oxygen content was 140 mL per liter of blood and brachial artery oxygen content was 210 mL per liter of blood. Cardiac out-put was which of the following? a. 4.2 L/min b. 7.0 L/min c. 10.0 L/min d. 12.6 L/min e. 30.0 L/min
- 9. Regulation of cardiac output • Factors effecting
- 10. 14-14
- 13. Bainbridge Reflex, Atrial Receptors, and Atrial Natriuretic Peptide
- 15. Determinants of Cardiac Output • Venous parameters, not arterial parameters, normally determine cardiac output. • Heart rate does not normally affect cardiac output but very low and very high heart rates impede venous return and cardiac output. • Increased resistance of arteries raises blood pressure but does not affect venous return and cardiac output. • For instance, aortic stenosis, coarc-tion of the aorta, and hypertension do not decrease cardiac output if the heart if able to pump against the increased afterload.
- 17. Stroke Volume • Is determined by 3 variables: – End diastolic volume (EDV) = volume of blood in ventricles at end of diastole – Total peripheral resistance (TPR) = impedance to blood flow in arteries – Contractility = strength of ventricular contraction 14-9
- 18. • EDV is workload (preload) on heart prior to contraction –SV is directly proportional to preload & contractility • Strength of contraction varies directly with EDV • Total peripheral resistance = afterload which impedes ejection from ventricle –SV is inversely proportional to TPR Regulation of Stroke Volume
- 19. Regulation of stroke volume 1. Preload :Passive tension in the muscle when it is being filled during diastole. • End diastolic volume • Venous return • Frank-Starling’s law (Energy of contraction is proportional to the initial length of cardiac muscle fibres)
- 20. Venous Return • Is return of blood to heart via veins • Controls EDV & thus SV & CO • Dependent on: – Blood volume & venous pressure – Vasoconstriction caused by Symp – Skeletal muscle pumps – Pressure drop during inhalation Fig 14.7 14-15
- 21. Preload General features • Preload is the load on the muscle in the relaxed state. • More specifically, it is the load or prestretch on ventricular muscle at the end of diastole. • Preload on ventricular muscle is not measured directly; rather, indices are utilized.
- 22. • Indices of left ventricular preload: – Left ventricular end-diastolic volume (LVEDV) – Left ventricular end-diastolic pressure (LVEDP) • somewhat less reliable indices of left ventricular preload are those measured in the venous system. – Left atrial pressure – Pulmonary venous pressure – Pulmonary wedge pressure • Measurement of systemic central venous pressure is an index of preload on the right ventricle
- 24. Frank-Starling Law of the Heart (a) is state of myocardial sarcomeres just before filling Actins overlap, actin- myosin interactions are reduced & contraction would be weak In (b, c & d) there is increasing interaction of actin & myosin allowing more force to be developed
- 25. • The preload effect can be explained on the basis of a change in sarcomere length
- 26. Frank-Starling Law of the Heart • States that strength of ventricular contraction varies directly with EDV – Is an intrinsic property of myocardium – As EDV increases, myocardium is stretched more, causing greater contraction & SV 14-11
- 27. • The Frank–Starling law of the heart states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant.
- 29. The contractility factor in systolic performance (inotropic state) • Contractility is the change in systolic performance at a given preload. • Contractility is a change in the force of contraction at any given sarcomere length. • Acute changes in contractility are due to changes in the intracellular dynamics of calcium.
- 30. Indices of contractility –dp/dt (change in pressure vs. change in time) = rate of pressure development during isovolumetric contraction. –ejection fraction (stroke volume/end-diastolic volume)
- 31. Effects of increased contractility
- 32. • Both an increased preload and an increased contractility will be accompanied by an increased peak left ventricular pressure, but only with an increase in contractility will there be a decrease in the systolic interval.
- 33. Regulation of stroke volume 3 Contractility (Inotropic state)
- 34. Independence of preload and contractility Preload and Contraction in acute situation
- 35. • In summary, A → B increased performance due entirely to preload A → C increased performance due entirely to contractility A → D increased performance due to an increase in both preload and contractility
- 36. Regulation of stroke volume • 3 Afterload – • It is the load on the muscle during contraction • It represents the force that the muscle must generate to eject the blood into the aorta
- 37. Indices of afterload • An approximation for the left ventricle is aortic diastolic pressure, which is primarily determined by the resistance of the arterioles (TPR). • Other acceptable indices of afterload on the left ventricle are the following: a.Mean aortic pressure b.Peak left ventricular pressure
- 38. Regulation of stroke volume 2 Afterload • Usually measured as arterial pressure • ↑PR → ↑BP → ↑Afterload → ↓CO • ↓PR → ↓BP → ↓Afterload → ↑CO
- 39. CHRONIC INCREASE IN AFTERLOAD Systolic dysfunction • An abnormal reduction in ventricular emptying due to impaired contractility or excessive afterload. Diastolic dysfunction • Decrease in ventricular compliance during the filling phase of the cardiac cycle due to either changes in tissue stiffness or impaired ventricular relaxation. • The consequence is a diminished Frank- Starling mechanism
- 40. An increase in afterload can be due to a pressure or a volume overload. Pressure Overload 1.Hypertension and aortic stenosis 2.Initially, increased performance due to (increased contractility); no decrease in CO 3.Chronically, in an attempt to normalize wall tension (actually internal wall stress), the ventricle develops a concentric hypertrophy. There is a dramatic increase in wall thickness and a decrease in chamber diameter.
- 41. • The consequence of concentric hypertrophy (new sarcomes laid down in parallel, i.e., the myofibril thickens) • is a decrease in ventricular compliance and diastolic dysfunction, • followed eventually by a systolic dysfunction and ventricular failure.
- 42. Volume Overload • mitral and aortic insufficiency, patent ductus arteriosus.
- 43. • Chronically, in an attempt to normalize wall tension (actually internal wall stress), the ventricle develops an eccentric hypertrophy (new sarcomeres laid down end-to-end, i.e., the myofibril lengthens. All cardiac volumes increase.) • There is a modest increase in wall thickness that does not reduce chamber size.
- 44. • Compliance of the ventricle is not compromised and diastolic function is maintained. • Eventual failure is usually a consequence of systolic dysfunction
- 45. Effect of Various Conditions on Cardiac Output. No change • Sleep • Moderate changes in environmental temperature Increase •Anxiety and excitement (50–100%) • Eating (30%) • Exercise (up to 700%) • High environmental temperature • Pregnancy • Epinephrine Decrease •Sitting or standing from lying position (20–30%) • Rapid arrhythmias • Heart disease
- 46. The cardiac function (cardiac output) curve • A cardiac function curve is generated by keeping contractility constant and following ventricular performance as preload increases. • depicts the Frank-Starling relationship for the ventricle. • shows that cardiac output is a function of end- diastolic volume.
- 47. The preload dependence of Cardiac output is defined by cardiac function curve
- 49. • Starting at N, which represents a normal, resting individual: • A = decreased performance due to a reduction in preload • B = increased performance due to an increased preload • C represents an increased performance due almost entirely to increased contractility (close to the situation during exercise) • Points C, D, and E represent different levels of performance due to changes in preload only; all three points have the same contractility.
- 50. Q • Haemorrhage and volume overload: how does it affects preload , performance and contractility?
- 51. • Vector I: consequences of a loss in preload, e.g., hemorrhage, venodilators (nitro-glycerin) • Vector II: consequences of a loss in contractility, e.g., congestive heart failure • Vector III: consequences of an acute increase in contractility • Vector IV: consequences of an acute increase in preload, e.g., volume loading the individual going from the upright to the supine position
- 53. Vascular function curves • Defines the changes in central venous pressure that are caused by changes in cardiac output. • The vascular function (venous return) curve depicts the relationship between blood flow through the vascular system (or venous return) and right atrial pressure.
- 81. cardiac failure • What parameter is reduced in cardiac failure? cardiac contractility • How the kidneys are involved in the compensatory mechanism to cardiac failure. Sympathetic NS acts on Beta-1 cells in the kidney to release renin secretion. This increases blood volume and induces venoconstriction.
- 82. • Q. How does cardiac failure affect CO and RAP? slight fall in CO Increase RAP
- 89. Use the diagram below to answer the following three questions. The point marked control represents the state of the cardiovascular system in the resting state. An increase in total peripheral resistance and contractility is repre-sented by a shift from the resting state to point
Editor's Notes
- Answer- C
- The amount of blood pumped out of the heart per beat, the stroke volume, is about 70 mL from each ventricle in a resting man of average size in the supine position. The output of the heart per unit of time is the cardiac output. In a resting, supine man, it averages about 5.0 L/min (70 mL x 72 beats/min).
- Baroreceptor Reflex Sudden changes in arterial blood pressure initiate a reflex that evokes an inverse change in heart rate Baroreceptors located in the aortic arch and carotid sinuses are responsible for this reflex. The inverse relationship between heart rate and arterial blood pressure is generally most pronounced over an intermediate range of arterial blood pressure. Below this intermediate range, the heart rate maintains a constant, high value; above this pressure range, the heart rate maintains a constant, low value
- of changes in pressure in isolated carotid sinuses on neural activity in cardiac vagal and sympathetic efferent nerve fibers
- Intravenous infusions of blood or electrolyte solutions tend to increase the heart rate via the Bainbridge reflex. Bainbridge reflex – stretched rt.atrium – vasomotor center – back to heart by sympathetic & vagi nerve – increase the heart rate Decrease the heart rate via the baroreceptor reflex. The actual change in heart rate induced by such infusions is the result of these two opposing effects.
- The heart rate typically accelerates during inspiration and decelerates during expiration . Stretch receptors in the lungs are stimulated during inspiration, and this action leads to a reflex increase in heart rate. The afferent and efferent limbs of this reflex are located in the vagus nerves. Intrathoracic pressure also decreases during inspiration and thereby increases venous return to the right side of the heart .The consequent stretch of the right atrium elicits the Bainbridge reflex. After the time delay required for the increased venous return to reach the left side of the heart, left ventricular output increases and raises arterial blood pressure. This rise in blood pressure in turn reduces the heart rate through the baroreceptor reflex
- Ejection fraction is SV/ EDV (~80ml/130ml=62%) Normally is 60%; useful clinical diagnostic tool
- Ejection fraction EF=(SV/EDV) X 100%
- Pulmonary wedge pressure, sometimes called pulmonary capillary wedge pressure, is measured from the tip of a Swan-Ganz catheter, which, after passing through the right heart, has been wedged in a small pulmonary artery. The tip is pointing downstream toward the pulmonary capillaries, and the pressure measured at the tip is probably very close to pulmonary capillary pressure. Since the vessel is occluded on inflating the balloon and assuming minimal flow, the pressure is probably very close to left atrial pressure as well. A rise in pulmonary capillary wedge pressure is evidence of an increase in preload on the left ventricle. In some cases, such as in mitral stenosis, it is not a good index of left ventricular preload.
- Stroke volume is the amount of blood pumped by each ventricle during systole. Unlike the resting length of skeletal muscle where a sarcomere length is close to the optimum for maximal cross-bridge linking between actin and myosin during contraction (Lo), heart muscle at the end of diastole is below this point. Thus, in a normal heart, increased preload increases sarcomere length toward the optimum actin-myosin overlap. This results in more cross-linking and a more forceful contraction during systole
- More calcium increases the availability of cross-link sites on the actin, increasing cross-linking and the force of contraction during systole.
- When contractility increases, there are other changes in addition to an increased force of contraction.
- The solid line represents left ventricular pressure before (and the dashed line after) an increase in contractil-ity via increased sympathetic stimulation. he overall changes induced by increased contractility can be summarized as follows: 1. Increased dp/dt: increased slope, thus increased rate of pressure development 2. Increased peak left ventricular pressure due to a more forceful contraction 3. Increased rate of relaxation due to increased rate of calcium sequestration 4. Decreased systolic interval due to effects #1 and #3 Both an increased preload and an increased contractility will be accompanied by an increased peak left ventricular pressure, but only with an increase in contractility will there be a decrease in the systolic interval
- Changes in inotropy are unique to cardiac muscle
- Assume X represents a normal preload and point A the force generated at this preload under normal resting conditions. If preload is increased to point Y, what is observed is an increased force of contraction during systole, point B. Thus, we conclude that preload is one factor that determines the overall force of ventricular contraction. Further, we can generalize that when preload is increased, a normal heart will respond with an increased force of contraction If we return to our original preload X but in this case simply increase sympathetic activity to the ventricle, we also observe an increased force of contraction, point C, but at the same preload. Thus, we must conclude that preload was not responsible for the increased performance and that, therefore, by default, it must have been an increase in contractility. This is because there are two factors that determine the overall force of ventricular contraction: preload and contractility. If we increase preload to Y and also increase sympathetic activity, we obtain a very large increase in the force of contraction, point D.
- Hypertension: increased afterload Hypotension: decreased afterload
- Cardiac failure or more specifically congestive failure is a syndrome with many etiologies. Excluded would be valvular heart disease, afterload problems, and coronary heart disease
- Ventricular dilation with only a modest hypertrophy that is less than appropriate for the degree of dilation.
- Any point above a ventricular function curve means increased contractility. Any point below a ventricular function curve means decreased contractility.
- It is venous return creating a filling pressure and preload that normally determines cardiac output. yaxis:indexofsystolicperformance, e.g.,strokework,strokevolume, strokepower(cardiacoutput);all are indices of the force of ventricular contraction xaxis:indexofventricularpreload, e.g.,ventricularend-diastolicvolume or pressure, atrial or venous pressure
- Return supports output: The preload-dependence of CO is dened by the cardiac function curve (Figure 20.22). Increases in left-ventricular lling pressure increase CO through length-dependent activation, and lling pressure is dependent on CVP. Changes in ventricular inotropy modify this relationship: Positive inotropes shift the curve upward and to the left, whereas negative inotropes shift the curve downward and to the right
- Answer- A
- Defines the changes in central venous pressure that are caused by changes in cardiac output In this curve, central venous pressure is the dependent variable (or response), and cardiac output is the independent variable (or stimulus).
- Dependence of central venous pressure on cardiac output. Quantifying how CO affects CVP requires that the heart and lungs be replaced with an articial pump whose output can be controlled (Figure 20.23A). Prior to turning the pump on, normal circulating blood volume (5 L) must be restored. The vasculature stretches when accommodating this much blood, cre-ating a pressure of approximately 7 mm Hg (see Figure 20.23B) known as mean circulatory lling pressure (MCFP). MCFP is dened as the pressure that exists in the vasculature when the heart is arrested, and all parts of the system have come into equi-librium. When the pump is turned on, it translocates blood from the veins to the arteries. Because the arterial compartment has a relatively small volume and outow is limited by resistance ves-sels, translocation generates signicant pressure within the arte-rial system. It simultaneously causes CVP to fall because blood is being withdrawn. Driving the pump faster causes CVP to fall fur-ther until it nally becomes negative (see Figure 20.23B). At this point, the great veins collapse and limit any additional increases in CO. The plot shown in Figure 20.23B is known as a vascular function curve.
- When the pump is turned on, it translocates blood from the veins to the arteries. Because the arterial compartment has a relatively small volume and outow is limited by resistance ves-sels, translocation generates signicant pressure within the arte-rial system. It simultaneously causes CVP to fall because blood is being withdrawn. Driving the pump faster causes CVP to fall fur-ther until it nally becomes negative (see Figure 20.23B). At this point, the great veins collapse and limit any additional increases in CO. The plot shown in Figure 20.23B is known as a vascular function curve.
- The vascular function curve is depen-dent on circulating blood volume (Figure 20.24). If blood volume increases, then MCFP necessarily increases also because the vasculature stretches to a greater degree to accommodate the extra volume. When the pump is turned on, CVP falls as before, but, because overall pressure in the system is higher, collapse of the large veins is delayed. Conversely, if circulating blood volume is decreased, then MCFP decreases, and collapse of the great veins occurs at lower output levels.
- Venoconstriction and venodilation caused by changes in SNS activity produce similar effects to changes in circulating blood volume. Initiating a baroreex reduces venous system capacity and MCFP rises. Venodilation reduces system capacity, and MCFP falls.
- Why does arteriolar tone not have much of an effect on MSFP? MSFP is mostly determined by venous pressure because most of the blood is on the venous side.
- Systemic vascular resistance: Constriction and relaxation of resistance vessels has little or no affect on MCFP because the contribution of the small arteries and arterioles to overall vascu-lar capacity is small. Changes in SVR do impact CVP, however. When resistance vessels constrict, they reduce ow through the capillary beds. This translates into less VR, and CVP falls (Fig-ure 20.25). Conversely, vasodilation allows blood to surge through capillary beds and into the venous system, which raises CVP.
- The two plots overlap at an equilibrium point that denes how much CO can be supported by the vasculature for any given contractility and blood volume.
- The two plots overlap at an equilibrium point that denes how much CO can be supported by the vasculature for any given contractility and blood volume.
- How do +ve inotropic agents affect the Guyton cross plot? CO upward, leftVF curve unchanged
- Changes in blood volume do not directly affect myocardial contractility
- Increasing myocardial inotropy allows the ventricle to pump out more blood on every stroke, even though CVP falls as a consequence. A new equilibrium point is created, as shown in Figure 20.28. Increases in inotropy are typically seen during exercise, for example. Conversely, an infarcted myocar-dium translocates less blood from the right atrium to the arte-rial system on every stroke. The new equilibrium point settles at a higher CVP.
- Does right atrial pressure change in the case of arteriolar vasodilation/venodilation? NO!