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Definitions Cardiac Output Cardiac Output and venous return Dr Badri Paudel GMC – The quantity of blood pumped into the aorta each minute – measured in milliliters (mL) per minute (min) or liters (L) per minute – normally around 5,000 mL (5 L) per minute (5,000 mL/min or 5 L/min) Venous Return – The quantity of blood flowing from the veins into the right atrium each minute 4/18/12 badri@GMC 2 4/18/12 badri@GMC 4 Cardiac Output (CO) End-Diastolic Volume – End-Systolic Volume = Stroke Volume Beat = stroke volume (SV) = EDV – ESV = 70 ml Volume of blood ejected from one ventricle End-Diastolic Volume 4/18/12 End-Systolic Volume badri@GMC 5 4/18/12 Minute = Cardiac output (CO) = SV x HR = 5 liters / min Minute / square meter of body surface area = Cardiac index = 3.2 liter / min / m26 badri@GMC 1 Cardiac output (CO) is directly affected by… • heart rate (HR), the number of <mes the heart beats each minute; and • stroke volume (SV), the amount of blood ejected during each beat 4/18/12 Ejection Fraction: Ø Definition: It is the ratio of SV compared to EDV. SV 70 X 100 = = EDV Ø Value: CO = HR x SV X 100 135 Normally it is about 50 – 60 %. Ø Importance: • If HR increases, what will happen to cardiac output? It is used as indicator for myocardial contractility. • If SV decreases, what will happen to cardiac output? badri@GMC 7 4/18/12 badri@GMC 8 Cardiac Reserve • During exercise CO (Cardiac Output) may increase up to 20-25 liters/minute and up to 40 liters/minute during heavy exercise in athletes • Cardiac reserve is the difference between the cardiac output at rest and maximal cardiac output during heavy exercise. 4/18/12 9 badri@GMC 4/18/12 badri@GMC 10 IMPORTANT RELATIONSHIPS Determinants of Cardiac Output CONTRACTILITY PRELOAD (+) (+) HEART RATE Some definitions AFTERLOAD (-) o STROKE VOLUME (+) o (+) o badri@GMC Determining factor: n CARDIAC OUTPUT 4/18/12 Preload: the initial stretching of the cardiac myocytes prior to contraction. End diastolic volume: the volume of blood in a ventricle at the end of filling 11 Venous return Preload Pumps up the heart.badri@GMC 4/18/12 12 2 Measurement of Cardiac Output Some definitions o o o Afterload: the force the sarcomere must overcome in order to shorten during systole Determining factor: n o o o o Aortic pressure 4/18/12 badri@GMC 13 Electromagnetic flowmeter Indicator dilution (dye such as cardiogreen) Thermal dilution Oxygen Fick Method CO = (O2 consumption / (A-V O2 difference) 4/18/12 Fick Principle O2 Consumption Cardiac output = o A man has a resting O2 consumption of 250 ml O2/min, a o [O2] pulmonary vein – [O2] pulmonary artery o femoral arterial O2 content of 0.20 ml O2/ml blood, and a pulmonary arterial O2 content of 0.15 ml O2/ml blood. o o CO = 250 ml O2/min o = 5000 ml/min 0.20 ml O2/ml – 0.15 ml O2/ml 4/18/12 14 O2 Fick Problem o o badri@GMC badri@GMC 15 If pulmonary vein O2 content = 200 ml O2/ L blood Pulmonary artery O2 content = 160 ml O2 /L blood Lungs add 400 ml O2 /min What is cardiac output? Answer: 400/(200-160) =10 L/min 4/18/12 badri@GMC 16 Intrinsic autoregulation Regulation of Cardiac output 1-Heterometric autoregulation: Initial Length (Preload): Extrinsic regulation * It depends on - Nervous supply of the heart. - Hormones or chemical * It adjust both stroke volume and heart rate. Intrinsic regulation (Auto regulation) *It is the ability of the heart to change its stroke volume independent of nervous chemical or hormonal factors. * It include • The major determinant of the force of contraction is the • The end diastolic volume (EDV) is used instead of • The EDV is determined by the preload. • The term preload refers to the degree of passive stress initial length of the muscle fiber. length of muscle fiber. exerted by the volume of blood in the ventricle just 4/18/12 Heterometric badri@GMC autoregulation Homeometic 17 autoregulation before its contraction. 4/18/12 badri@GMC 18 3 Characters of heterometric auto-regulation Preload " It is preload phenomena . " It is of a short duration . " There is an increase in the length of muscle fiber . " End diastolic volume ( E.D.V ) increases . " Stroke volume ( S.V ) increases . • Preload can be defined as the initial stretching of the cardiac myocytes prior to contraction. It is related to the sarcomere length at the end of diastole. " End systolic volume slightly increases . " It is usually followed by Homeometric regulation . Examples of heterometric regulation : " a - In case of changing position from standing into supine position e.g. lying in bed. " b - In the ( early stage ) beginning of muscular exercise . 4/18/12 19 badri@GMC Frank-Starling Relationship 4/18/12 badri@GMC 21 20 4/18/12 badri@GMC 22 badri@GMC 24 Preload is directly affected by… • filling <me and • venous return – LVEDV (left ventricular end-diastolic volume) – LVEDP (left ventricular end-diastolic pressure) – PCWP (pulmonary capillary wedge pressure) – CVP (central venous pressure) badri@GMC badri@GMC Preload … • stretches the myocardium so that the myofibers are lengthened before contrac<on resul<ng in a stronger contrac<on, up to a point (above which strength decreases), according to the Frank-‐Starling law of the heart. • Because we cannot measure sarcomere length directly, we must use indirect indices of preload. 4/18/12 4/18/12 23 4/18/12 4 Frank-Starling Mechanism Frank-Starling Mechanism • Allows the heart to readily adapt to changes in venous return. • When venous return to the heart is increased, ventricular filling increases, as does preload. This stretching of the myocytes causes an increase in force generation, which enables the heart to eject the additional venous return and thereby increase stroke volume. • The Frank-Starling Mechanism plays an important role in balancing the output of the 2 ventricles. • In summary: Increasing venous return and ventricular preload leads to an increase in stroke volume. • Simply stated: The heart pumps the blood that is returned to it 4/18/12 badri@GMC 25 4/18/12 badri@GMC 26 Length-tension curve (Frank-Starling ) Frank-Starling Mechanism Stroke volume (SV) (ml) (related to muscle tension) Optimal length Increase in SV (Cardiac muscle does not normally operate within the descending limb of the length– tension curve.) B1 A1 Normal resting length Increase in EDV 4/18/12 badri@GMC 27 4/18/12 End-diastolic volume (EDV) (ml) (related to cardiac-muscle fiber length) badri@GMC 28 Frank-Starling Mechanism • There is no single Frank-Starling Curve for the ventricle. Instead, there is a family of curves with each curve defined by the existing conditions of afterload and inotropy. The muscle developed tension is increased upon increasing the initial length ( preload ) up to certain limit .Further increase in muscle length beyond this limit depresses the muscle developed tension and this is not seen in the normal heart but only 4/18/12 in heart failure 29 badri@GMC 4/18/12 badri@GMC 30 5 Frank-Starling Curves Frank Starling o o o 4/18/12 badri@GMC Intrinsic regulation of heart pumping Increased venous return leads to increased stroke volume CO=SV x HR 4/18/12 31 badri@GMC 2-Homeometic autoregulation 32 Afterload q It follows the heterometric regulation. • Afterload can be viewed as the "load" that the heart must eject blood against. q It can occur for long time. q It is an after load phenomenon. q It is initiated by the increase in aortic pressure. • In simple terms, the afterload is closely related to the aortic pressure. q The increase in myocardial contraction increase SV by the decrease in ESV. q EDV returns to the normal value (not changed). 4/18/12 33 badri@GMC 4/18/12 • LaPlace’s Law • More precisely defined in terms of ventricular wall stress: Wall Stress Wall Stress σ∝ – LaPlace’s Law: Wall stress = Pr/h • P = ventricular pressure • R = ventricular radius • h = wall thickness badri@GMC 34 Afterload is better defined in relation to ventricular wall stress Afterload 4/18/12 badri@GMC Pr h P r h 35 4/18/12 badri@GMC 36 6 Effects of Afterload Afterload • Afterload is increased by: – Increased aortic pressure – Increased systemic vascular resistance – Aortic valve stenosis – Ventricular dilation 4/18/12 badri@GMC 37 4/18/12 badri@GMC 38 AFerload… • inversely affects stroke volume; and • directly affects end systolic volume; ESV • What effect will hypertension have on a=erload? • What effect will hypertension have on stroke volume? 4/18/12 badri@GMC 39 Heterometric Homeometeric q Sequence Occurs at first (followed by homeometic regulation). Following the heterometric regulation. q Onset Rapid (Immediate after increase in VR) Slow (after few min) Short (few minutes) Long (Maintain the elevated stroke volume for long time). No change q Duration q EDV Increase 4/18/12 badri@GMC Heterometric q ESV 40 Homeometeric Constant (or slightly increased) Decrease q SV Increase Increase q Stretch of ventricular muscle fibers. Present Absent q Mechanism Starling law Increase of the aortic pressure Pre load After load. q Phenomenon 7 Extrinsic regulation Anrep Effect • An abrupt increase in afterload can cause a modest increase in inotropy. Ø It is the adjustment of CO via change of heart rate (HR) and/or stroke volume (SV). • The mechanism of the Anrep Effect is not fully understood. Ø It acts through either autonomic nerve supply of the heart and/or hormones (chemicals) in the blood. 4/18/12 badri@GMC 43 4/18/12 Heart Rate is directly affected by factors called chronotropic agents (or factors). These factors may be positive or negative. Extrinsic regulation Hormonal (chemical) regulation Nervous regulation Parasympathetic NS 4/18/12 PosiKve chronotropic agents… • increase heart rate and • include epinephrine, norepinephrine and beta agonists (e.g., isoproterenol). 4/18/12 Sympathetic NS badri@GMC 45 4/18/12 NegaKve chronotropic agents… • decrease heart rate and • include acetylcholine (ACh) and beta antagonists (e.g., propranolol). • What effect will sympathe@c nerve impulses have on heart rate? badri@GMC 44 badri@GMC 47 4/18/12 badri@GMC 46 • What effect will parasympathe@c nerve impulses have on heart rate? badri@GMC 48 8 Effects of Heart Rate on Cardiac Output Heart Rate Cardiac Output • Changes in heart rate are generally more important quantitatively in producing changes in cardiac output than are changes in stroke volume • Changes in heart rate alone inversely affect stroke volume Heart Rate 4/18/12 badri@GMC 49 Heart Rate – The decrease in SV is greater than the increase in HR (decreased filling time) • At low HR – decrease in HR is greater than decrement in SV badri@GMC 51 Heart rate regulation: The SA node is the normal pace maker of the heart that set the heart rate during rest at average rate=70 beats/minute The autonomic nervous system supply of the heart: • The atria (SA node and AV node) are supplied by the parasympathetic nervous system (The vagus nerve) and the sympathetic nervous system (Dual supply from both divisions of A.N.S) • The ventricles are mainly supplied by the sympathetic nervous system. There is very little Parasympathetic supply of the ventricles 4/18/12 badri@GMC badri@GMC 50 Bowditch (Treppe) Effect • At high HR 4/18/12 (Increased by Pacing) 4/18/12 53 • An increase in heart rate will also cause positive inotropy (Bowditch effect, Treppe or “staircase” phenomenon). • This is due to an increase in intracellular Ca++ with a higher heart rate: – More depolarizations per minute – Inability of Na+/K+-ATPase to keep up with influx of Na+, thus, the Na+-Ca++ exchange pump doesn’t function as well 4/18/12 badri@GMC 52 Area affected: Parasympathetic stimulation Sympathetic stimulation 1-SA Node Decrease heart rate Increase heart rate 2-Atrial muscle Decrease contractility Increase contractility 3-AV Node Decrease excitability (increase AV node delay) Increase excitability (decrease AV node delay) 4-Ventricles conductive system No effect Increase conduction through His bundle and purkinje cells 5-Ventricle muscle No effect Increase contractility 6-Adrenal medulla No effect Increase epinephrine secretion which enhance sympathetic stimulation on heart 7-Veins Increase venous return (by vasoconstriction of veins) which increase cardiac contraction 54 (Frank-Starling mechanism) 4/18/12 No effect badri@GMC 9 Effect Of ANS on HR: Threshold potential Heart rate Sympathetic activity (and epinephrine) Parasympathetic activity Threshold potential = Inherent SA node pacemaker activity 4/18/12 badri@GMC 55 4/18/12= SA node pacemaker activitybadri@GMC on parasympathetic stimulation 56 = SA node pacemaker activity on sympathetic stimulation Stroke volume The parasympathetic and sympathetic nervous systems act together on heart rate in antagonistic (opposing) way, during rest the parasympathetic nervous system dominate more than the sympathetic nervous system Extrinsic control Strength of cardiac contraction What happen if all autonomic nerves to the heart are cut? The heart rate will be 100/minute,which is he inherent rhythm of the SA (which is the SA Node discharge when it is free from the normal inhibitory dominant parasympathetic effect at rest) Intrinsic control Sympathetic activity (and epinephrine) A Cardiovascular control center in the brain stem coordinates the autonomic activity to the heart, if heart rate is to be increased this center control the increase in sympathetic activity and at same time decrease the parasympathetic activity and vice versa End-diastolic volume Intrinsic control 4/18/12 badri@GMC 57 4/18/12 badri@GMC Venous return 58 Resting heart without sympathetic: End-diastolic volume 135 ml Sympathetic stimulation can increase stroke volume and cardiac output by: A-Increase force of contraction: -Under sympathetic stimulation with the EDV=135 ml___The Stroke volume will be 100 ml and End Systolic Volume(ESV)=35 ml only -Sympathetic stimulation shift the Frank-Starling curve up and to the left and according to the degree of sympathetic stimulation is the degree of the shift up to a maximal increase in strength of contraction 100% greater than resting strength Stroke volume 70 ml B-Increase venous return: Sympathetic stimulation also cause vasoconstriction of the veins which squeezes more blood from the veins to the heart (=more filling) which in turn increase EDV and stroke volume 4/18/12 badri@GMC 59 End-systolic volume 65 ml 4/18/12 badri@GMC 60 10 Shift of Frank-Starling curve up and to the left by sympathetic stimulation: Sympathetic stimulation: End-diastolic volume 135 ml Frank-Starling curve on sympathetic stimulation Normal Frank-Starling curve Stroke volume 100 ml End-systolic volume 35 ml 4/18/12 badri@GMC 61 Effects of increased sympathetic stimulation on Cardiac output 4/18/12 badri@GMC 62 Effects of increased parasympathetic stimulation on Cardiac output Increased venoconstriction Increased venous return Increased preload Increased force of ventricular contraction Increased slope of Pace maker potential Increased heart rate decreased force of atrial contraction decreased slope of Pace maker potential decreased heart rate Increased stroke volume Decreased ventricular filling Increased decreased cardiac output cardiac output 4/18/12 63 badri@GMC 4/18/12 badri@GMC 64 Cardiac output Heart rate • Filling Kme is inversely related to heart rate; as heart rate increases, filling <me decreases. • Chronotropic agents affect filling <me, thus they affect EDV. However, these agents may also affect contrac<lity such that the effects on stroke volume are less straighMorward. Stroke volume Extrinsic control Intrinsic control Parasympathetic activity Sympathetic activity (and epinephrine) End-diastolic volume Intrinsic control 4/18/12 badri@GMC Venous return 65 4/18/12 badri@GMC • What effect will increased heart rate have on stroke volume (if other factors stay the same)? 66 11 2- Hormonal (chemical) regulation q Glucagon hormone: Causes increase of CO. It has +ve inotropic action (increases SV and CO). q Catecholamine: Causes increase CO (Its actions similar to sympathetic stimulation). q Digitalis drug: Causes increase of CO (It has +ve inotropic action). q Thyroxin hormone: Causes increase CO by increasing the number and sensitivity of B1 receptors to catecholamine. q Acetyl choline: Causes decrease CO (Action similar to parasympathetic stimulation). q Insulin hormone: Causes increase of CO. It has +ve inotropic action (increases SV and CO). 4/18/12 67 badri@GMC 4/18/12 68 badri@GMC Contractility Extrinsic factors Affecting Myocardial Contraction Force ( Inotropic Factors ) Contractility • The inherent capacity of the myocardium to contract independently of changes in afterload or preload. • Changes in contractility are caused by intrinsic cellular mechanisms that regulate the interaction between actin and myosin independent of sarcomere length. • Increased rate and/or quantity of Calcium delivered to myofilaments during contraction • Alternate name is inotropy. 4/18/12 badri@GMC 70 PosiKve inotropic agents… • increase contrac<lity and • epinephrine, norepinephrine and cardiac glycosides (e.g., digitalis) • What effect will epinephrine have on stroke volume? 4/18/12 badri@GMC 71 4/18/12 badri@GMC 72 12 NegaKve inotropic agents… • decrease contrac<lity and • include calcium channel blockers (e.g., verapamil). • What effect will blocking calcium channels have on stroke volume? 4/18/12 badri@GMC 73 4/18/12 Extrinsic factors Affecting Myocardial Contraction Force ( Inotropic Factors ) 1) Nervous Factors: Sympathetic stimulation increases strength of contraction (positive inotropic factor ) through its Ca ++ raising effect . b) Parasympathetic stimulation has a negative inotropic effect due to its intracellular Ca++ lowering action (opposite to sympathetic). 2) Neurohormones: a. Epinepherine & norepinepherine : are povitive inotropic factors (similar to sympathetic) . b. Acetyl choline : is negative inotropic factor (similar to parasympathetic). 4/18/12 75 badri@GMC badri@GMC 74 3) ECF ions: Effects of variations in Ca++ and K + ions: a. Ca++ infusion (intravenous) may stop the heart during systole (Ca++ rigor). b. Effects of hyperkalaemia: Depresses cardiac contractility and may stop the heart during diastole so increased K + ions have a negative inotropic effect 4) Drugs : Digitalis used in the treatment of heart failure is the most important of all; it acts through inhibition of Na+ K+ ATP ase & thus Na+ ions accumulate inside the cells & stimulate Na+ Ca++ exchanger (between intracellular Na+ & extracellular Ca++) which increases the intracellular Ca++ concentration 4/18/12 badri@GMC 76 Factors Regulating Inotropy (+) (-) Parasympathetic Activation (+) Afterload (Anrep) Sympathetic Activation Inotropic State (Contractility) (-) (+) Catecholamines (+) Heart Rate (Treppe) Systolic Failure 4/18/12 badri@GMC 77 13