Cardiac Output and venous return Dr Badri Paudel GMC Definitions Cardiac Output 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 11/13/13 badri@gmc 2 11/13/13 badri@gmc 4 End-Diastolic Volume End-Systolic Volume = Stroke Volume Cardiac Output (CO) Beat = stroke volume (SV) = EDV ESV = 70 ml Volume of blood ejected from one ventricle Minute = Cardiac output (CO) = SV x HR = 5 liters / min End-Diastolic Volume End-Systolic Volume 11/13/13 badri@gmc 5 Minute / square meter of body surface area = Cardiac index = 3.2 liter / min / m2 11/13/13 badri@gmc 6 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% CO%=%HR%x%SV%% If#HR#increases,#what#will# happen#to#cardiac#output?# If#SV#decreases,#what#will# happen#to#cardiac#output?# Ejection Fraction:! Definition: It is the ratio of SV compared to EDV. = SV 70 X 100 X 100 = EDV 135! Value: Normally it is about 50 60 %.! Importance: It is used as indicator for myocardial contractility. 11/13/13' badri@gmc' 7' 11/13/13 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. 11/13/13 badri@gmc 9 11/13/13 badri@gmc 10 IMPORTANT RELATIONSHIPS Determinants of Cardiac Output CONTRACTILITY PRELOAD AFTERLOAD HEART RATE (+) CARDIAC OUTPUT (+) STROKE VOLUME (+) (+) 11/13/13 badri@gmc 11 (-) Some definitions " 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 " Determining factor: # Venous return 11/13/13 badri@gmc 12 Preload Pumps up the heart. 2
Some definitions " Afterload: the force the sarcomere must overcome in order to shorten during systole " Determining factor: # Aortic pressure Measurement of Cardiac Output " Electromagnetic flowmeter " Indicator dilution (dye such as cardiogreen) " Thermal dilution " Oxygen Fick Method " CO = (O 2 consumption / (A-V O 2 difference) 11/13/13 badri@gmc 13 11/13/13 badri@gmc 14 Fick Principle " Cardiac output = O 2 Consumption [O 2 ] pulmonary vein [O 2 ] pulmonary artery " A man has a resting O2 consumption of 250 ml O2/min, a femoral arterial O2 content of 0.20 ml O2/ml blood, and a pulmonary arterial O2 content of 0.15 ml O2/ml blood. " CO = 250 ml O 2 /min = 5000 ml/min 0.20 ml O 2 /ml 0.15 ml O 2 /ml 11/13/13 badri@gmc 15 O 2 Fick Problem " If pulmonary vein O 2 content = 200 ml O 2/ L blood " Pulmonary artery O 2 content = 160 ml O 2 /L blood " Lungs add 400 ml O 2 /min " What is cardiac output? " Answer: 400/(200-160) =10 L/min 11/13/13 badri@gmc 16 Regulation of Cardiac output Extrinsic regulation * It depends on - Nervous supply of the heart. - Hormones or chemical * It adjust both stroke volume and heart rate. Heterometric autoregulation 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 Homeometic autoregulation 11/13/13 badri@gmc 1 7 Intrinsic autoregulation 1-Heterometric autoregulation: Initial Length (Preload): The major determinant of the force of contraction is the initial length of the muscle fiber. The end diastolic volume (EDV) is used instead of length of muscle fiber. The EDV is determined by the preload. The term preload refers to the degree of passive stress exerted by the volume of blood in the ventricle just before its contraction. 11/13/13 badri@gmc 18 3
Characters of heterometric auto-regulation " 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. " End systolic volume slightly increases. " It is usually followed by Homeometric regulation. Preload 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. 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. 11/13/13 badri@gmc 1 9 11/13/13 badri@gmc 2 0 Frank-Starling Relationship 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.% 11/13/13 badri@gmc 21 11/13/13 badri@gmc 2 2 Because we cannot measure sarcomere length directly, we must use indirect indices of preload. LVEDV (left ventricular end-diastolic volume) LVEDP (left ventricular end-diastolic pressure) PCWP (pulmonary capillary wedge pressure) CVP (central venous pressure) Preload'is%directly% affected%by % filling%<me%and% venous%return% 11/13/13 badri@gmc 23 11/13/13 badri@gmc 2 4 4
Frank-Starling Mechanism 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. Simply stated: The heart pumps the blood that is returned to it 11/13/13 badri@gmc 25 Frank-Starling Mechanism Allows the heart to readily adapt to changes in venous return. 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. 11/13/13 badri@gmc 2 6 Frank-Starling Mechanism Length-tension curve (Frank-Starling ) Optimal length Stroke volume (SV) (ml) (related to muscle tension) Increase in SV B1 A1 (Cardiac muscle does not normally operate within the descending limb of the length tension curve.) Normal resting length Increase in EDV 11/13/13 badri@gmc 27 End-diastolic volume (EDV) (ml) 11/13/13 (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 11/13/13 in heart failure badri@gmc 29 11/13/13 badri@gmc 3 0 5
Frank-Starling Curves Frank Starling " Intrinsic regulation of heart pumping " Increased venous return leads to increased stroke volume " CO=SV x HR 11/13/13 badri@gmc 31 11/13/13 badri@gmc 32 2-Homeometic autoregulation $ It follows the heterometric regulation. $ It can occur for long time. $ It is an after load phenomenon. $ It is initiated by the increase in aortic pressure. $ The increase in myocardial contraction increase SV by the decrease in ESV. $ EDV returns to the normal value (not changed). Afterload Afterload can be viewed as the "load" that the heart must eject blood against. In simple terms, the afterload is closely related to the aortic pressure. 11/13/13 badri@gmc 3 3 11/13/13 badri@gmc 3 4 Afterload More precisely defined in terms of ventricular wall stress: LaPlace s Law: Wall stress = Pr/h P = ventricular pressure R = ventricular radius h = wall thickness Afterload is better defined in relation to ventricular wall stress LaPlace s Law Wall Stress σ Pr h h Wall Stress P r 11/13/13 badri@gmc 35 11/13/13 badri@gmc 3 6 6
Afterload Effects of Afterload Afterload is increased by: Increased aortic pressure Increased systemic vascular resistance Aortic valve stenosis Ventricular dilation 11/13/13 badri@gmc 37 11/13/13 badri@gmc 3 8 What#effect#will#hypertension#have#on#a=erload?# ADerload %% inversely%affects%stroke%volume;%and% directly%affects%end'systolic'volume;'esv% What#effect# will# hypertension# have#on# stroke# volume?# 11/13/13 badri@gmc 39 11/13/13 badri@gmc 4 0 Heterometric Homeometeric Heterometric Homeometeric $ Sequence Occurs at first (followed by homeometic regulation). Following the heterometric regulation. $ ESV $ SV Constant (or slightly increased) Increase Decrease Increase $ Onset Rapid (Immediate after increase in VR) Slow (after few min) $ Stretch of ventricular muscle fibers. Present Absent $ Duration $ EDV Short (few minutes) Increase Long (Maintain the elevated stroke volume for long time). No change $ Mechanism $ Phenomenon Starling law Pre load Increase of the aortic pressure After load. 7
Anrep Effect An abrupt increase in afterload can cause a modest increase in inotropy. The mechanism of the Anrep Effect is not fully understood. Extrinsic regulation! It is the adjustment of CO via change of heart rate (HR) and/or stroke volume (SV).! It acts through either autonomic nerve supply of the heart and/or hormones (chemicals) in the blood. 11/13/13 badri@gmc 43 11/13/13 badri@gmc 44 Extrinsic regulation Hormonal (chemical) regulation Nervous regulation Heart Rate is directly affected by factors called chronotropic agents (or factors). These factors may be positive or negative. Parasympathetic NS Sympathetic NS 11/13/13 badri@gmc 4 5 11/13/13 badri@gmc 4 6 PosiIve' chronotropic' agents ' increase%heart% rate%and%% include% epinephrine,% norepinephrine% and%beta%agonists% (e.g.,% isoproterenol).%% What#effect#will#sympathe@c# nerve#impulses#have#on#heart# rate?# NegaIve' chronotropic' agents ' decrease%heart% rate%and% include% acetylcholine% (ACh)%and%beta% antagonists%(e.g.,% propranolol).% What#effect#will# parasympathe@c#nerve#impulses# have#on#heart#rate?# 11/13/13 badri@gmc 4 7 11/13/13 badri@gmc 4 8 8
Heart Rate 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 11/13/13 badri@gmc 49 Cardiac Output Effects of Heart Rate on Cardiac Output Heart Rate (Increased by Pacing) 11/13/13 badri@gmc 50 Heart Rate At high HR 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 Bowditch (Treppe) Effect 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 11/13/13 badri@gmc 51 11/13/13 badri@gmc 5 2 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 11/13/13 badri@gmc 53 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 4-Ventricles conductive system 5-Ventricle muscle No effect 6-Adrenal medulla No effect Decrease excitability (increase AV node delay) No effect Increase excitability (decrease AV node delay) Increase conduction through His bundle and purkinje cells Increase contractility Increase epinephrine secretion which enhance sympathetic stimulation on heart 7-Veins No effect Increase venous return (by vasoconstriction of veins) which increase cardiac contraction 11/13/13 badri@gmc (Frank-Starling mechanism) 54 9
Effect Of ANS on HR: Heart rate Threshold potential Parasympathetic activity Sympathetic activity (and epinephrine) Threshold potential 11/13/13 badri@gmc 55 = Inherent SA node pacemaker activity 11/13/13 = SA node pacemaker activity badri@gmc on parasympathetic stimulation 56 = SA node pacemaker activity on sympathetic stimulation 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 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) 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 Extrinsic control Sympathetic activity (and epinephrine) Intrinsic control Intrinsic control Stroke volume Strength of cardiac contraction End-diastolic volume 11/13/13 badri@gmc 57 Venous return 11/13/13 badri@gmc 58 Sympathetic stimulation can increase stroke volume and cardiac output by: A-Increase force of contraction: Resting heart without sympathetic: End-diastolic volume 135 ml -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 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 Stroke volume 70 ml End-systolic volume 65 ml 11/13/13 badri@gmc 59 11/13/13 badri@gmc 6 0 10
Sympathetic stimulation: Shift of Frank-Starling curve up and to the left by sympathetic stimulation: End-diastolic volume 135 ml Frank-Starling curve on sympathetic stimulation Stroke volume 100 ml Normal Frank-Starling curve End-systolic volume 35 ml 11/13/13 badri@gmc 61 11/13/13 badri@gmc 6 2 Effects of increased sympathetic stimulation on Cardiac output Increased venoconstriction Increased venous return Effects of increased parasympathetic stimulation on Cardiac output Increased preload Increased slope of Pace maker potential Increased force of ventricular contraction decreased slope of Pace maker potential decreased force of atrial contraction Increased heart rate Increased stroke volume decreased heart rate Decreased ventricular filling Increased cardiac output 11/13/13 badri@gmc 6 3 decreased cardiac output 11/13/13 badri@gmc 64 Parasympathetic activity Heart rate Cardiac output Extrinsic control Sympathetic activity (and epinephrine) Intrinsic control Stroke volume Intrinsic control End-diastolic volume 11/13/13 badri@gmc Venous return 65 Filling'Ime'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.% 11/13/13' badri@gmc' What#effect# will#increased# heart#rate# have#on# stroke# volume##(if# other#factors# stay#the# same)?# 66' 11
2- Hormonal (chemical) regulation $ Catecholamine: Causes increase CO (Its actions similar to sympathetic stimulation). $ Thyroxin hormone: Causes increase CO by increasing the number and sensitivity of B1 receptors to catecholamine. $ Insulin hormone: Causes increase of CO. It has +ve inotropic action (increases SV and CO). $ Glucagon hormone: Causes increase of CO. It has +ve inotropic action (increases SV and CO). $ Digitalis drug: Causes increase of CO (It has +ve inotropic action). $ Acetyl choline: Causes decrease CO (Action similar to parasympathetic stimulation). 11/13/13 badri@gmc 6 7 11/13/13 badri@gmc 68 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. 11/13/13 badri@gmc 7 0 PosiIve'inotropic'agents ' increase%contrac<lity%and% epinephrine,%norepinephrine%and%cardiac% glycosides%(e.g.,%digitalis)% What#effect#will# epinephrine#have# on#stroke#volume?# 11/13/13 badri@gmc 71 11/13/13 badri@gmc 7 2 12
NegaIve'inotropic'agents ' decrease%contrac<lity%and% include%calcium%channel%blockers%(e.g.,% verapamil).% What#effect#will# blocking#calcium# channels#have#on# stroke#volume?# 11/13/13 badri@gmc 73 11/13/13 badri@gmc 74 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). 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 11/13/13 badri@gmc 7 5 11/13/13 badri@gmc 76 Factors Regulating Inotropy (-) Parasympathetic Activation (+) Afterload (Anrep) (+) Sympathetic Activation Inotropic State (Contractility) (-) Systolic Failure (+) Catecholamines (+) Heart Rate (Treppe) Ancillary Factors 11/13/13 badri@gmc 77 13
Ancillary Factors Affect the Venous System and Cardiac Output Gravity Venous pooling may significantly reduce CO Muscular Activity and Venous Valves Respiratory Activity 11/13/13 badri@gmc 79 11/13/13 badri@gmc 80 Venous'return' depends%on%how% much%blood% returns%to%the% heart,%which%is % affected%by:% blood%volume,% venous%pressure% and%% intrathoracic% pressure% What#effect#will#increased# venous#return#have#on#edv?# 11/13/13' badri@gmc' 81' Gravity " Gravity acts on vascular volume # Mostly venous due to high compliance # Preload decreases # CO and arterial pressure fall # Baroreceptor reflex " HR increases " Vasoconstriction 11/13/13 badri@gmc 82 Effects of Gravity on the Venous System and Cardiac Output Effect Of Gravity on Venous Pressure Gravity Venous pooling may significantly reduce CO 11/13/13 badri@gmc 83 11/13/13 badri@gmc 84 14
11/13/13 badri@gmc 85 11/13/13 badri@gmc 86 Skeletal Muscle Pump (Increase Venous Return) Muscular Activity and Venous Valves 11/13/13 badri@gmc 87 11/13/13 badri@gmc 8 8 Effect of Venous Valves Effects of Respiration Spontaneous respiration Decreased intra-thoracic pressure results in a decreased right atrial pressure which enhances venous return Mechanical ventilation Increased intra-thoracic pressure during positive-pressure lung inflation causes increased right atrial pressure which decreases venous return Valsalva Maneuver Causes a large increase in intra-thoracic pressure which impedes venous return to the right atrium 11/13/13 badri@gmc 89 11/13/13 badri@gmc 9 0 15
Increase Pleural Negative Pressure (Increase Venous Return) 15 IPP = INTRAPLEURAL PRESSURE CARDIAC OUTPUT (L/min) 10 5 IPP= -5.5mmHg IPP= -4mmHg IPP= -2mmHg IPP= 2mmHg CARDIAC TAMPONADE 11/13/13 badri@gmc 91 0-4 0 4 8 12 RIGHT ATRIAL PRESSURE (mmhg) 11/13/13 badri@gmc 92 Intrathoracic' pressure'(which% decreases% during% inspira<on%and% increases%during% expira<on)% inversely%affects% venous%return.% What#effect#will#inhaling#more# deeply#have#on#venous#return?# 11/13/13' badri@gmc' 93' Blood'volume' and%venous'' pressure'(which% increases%during% venoconstric<on% [constric<on%of% the%veins])% directly%affect% venous%return.% What#effect#will#blood#loss#have# on#edv?# 11/13/13' badri@gmc' 94' Factors that Facilitate Venous Return 11/13/13 badri@gmc 95 11/13/13 badri@gmc 96 16
11/13/13 badri@gmc 97 11/13/13 badri@gmc 98 11/13/13 badri@gmc 99 11/13/13 badri@gmc 100 11/13/13 badri@gmc 101 11/13/13 badri@gmc 102 17
The Cardiac Output Curve CARDIAC OUTPUT CURVES 25 HYPEREFFECTIVE Plateau of CO curve determined by heart strength (contractility + HR)" Sympathetics plateau Parasympathetics (HR ) (? plateau)" Plateau Heart hypertrophy s plateau Myocardial infarction (? plateau) Plateau 11/13/13 badri@gmc 103 CARDIAC OUTPUT (L/min) 20 15 NORMAL 10 HYPOEFFECTIVE 5 0-4 0 +4 +8 RIGHT ATRIAL PRESSURE (mmhg) 11/13/13 badri@gmc 104 The Cardiac Output Curve (cont d) Valvular disease plateau (stenosis or regurgitation) Myocarditis plateau Cardiac tamponade (? plateau) Plateau Metabolic damage plateau 11/13/13 badri@gmc 105 11/13/13 badri@gmc 106 Cardiac and Vascular function curves " Point of equilibrium % predicts cardiac output and central venous pressure " Steady state of this particular system 11/13/13 badri@gmc 107 11/13/13 badri@gmc 108 18
CARDIAC OUTPUT AND VENOUS RETURN (L/min/m) 25 20 15 10 5 0 MAX SPINAL VR CURVE NORMAL ANESTHESIA MAXIMAL SYMPATHETIC STIMULATION NORMAL CARDIAC SPINAL ANESTHESIA SYMPATHETIC STIMULATION -4 0 4 8 12 16 RIGHT ATRIAL PRESSURE (mmhg) 11/13/13 badri@gmc 109 Copyright 2006 by Elsevier, Inc.! Changes in contractility " Digoxin: # inhibits Na-K ATPase # Ca ++ builds up Ejection fraction is an indicator of contractility EF= SV/EDV 11/13/13 badri@gmc 110 11/13/13 badri@gmc 111 11/13/13 badri@gmc 112 Changes in volume: mean systemic pressure " Decreased blood volume " Decreased venous compliance 11/13/13 badri@gmc 113 11/13/13 badri@gmc 114 19
Changes in Total Peripheral Resistance " Constrict arterioles # Increased afterload # Decreased venous return 11/13/13 badri@gmc 115 11/13/13 badri@gmc 116 11/13/13 badri@gmc 117 11/13/13 badri@gmc 118 Pressure-Volume Loop " Preload " Afterload " Contractility Pressure-Volume Loop " Preload " Afterload " Contractility 11/13/13 badri@gmc 119 11/13/13 badri@gmc 120 20
Pressure-Volume Loop " Preload " Afterload " Contractility Pressure-Volume Loop " Preload " Afterload " Contractility 11/13/13 badri@gmc 121 11/13/13 badri@gmc 122 Sympathetic and parasympathetic control Stroke Volume = EDV-ESV " Sympathetic # Stimulate: increase HR and increase vasoconstriction # Inhibit: decrease HR and decrease vasoconstriction " Parasympathetic (vagus) # Stimulate: decreases HR and causes vasodilation Preload End Diastolic Volume End Systolic Volume Contractility Afterload 11/13/13 badri@gmc 123 11/13/13 badri@gmc 124 Summary of Factors That Influence Cardiac Output and Mean Arterial Pressure 11/13/13 badri@gmc 126 21
Control of Cardiac Output Factors that affect the Cardiac Output 11/13/13 badri@gmc 127 11/13/13 badri@gmc 128 Cardiac%Output%Concept%Map% 11/13/13' badri@gmc' 129' 11/13/13' badri@gmc' 130' Myocardial Oxygen Consumption Myocardial Oxygen Consumption Oxygen consumption is defined as the volume of oxygen consumed per minute (usually expressed per 100 grams of tissue weight) 11/13/13 badri@gmc 132 22
Myocardial Oxygen Demand is Related to Wall Stress LaPlace s Law Wall Stress σ Pr h h Wall Stress P r Factors Increasing Myocardial Oxygen Consumption Increased Heart Rate Increased Inotropy (Contractility) Increased Afterload Increased Preload Changes in preload affect myocardial oxygen consumption less than do changes in the other factors 11/13/13 badri@gmc 133 11/13/13 badri@gmc 134 Magnitude & Distribution of CO at Rest & During Moderate Exercise In%Summary % Heart%rate%and%stroke%volume%are%the%two% factors%that%determine%cardiac%output.% Each%of%these%is%affected%by%many%factors.% Chronotropic%agents%affect%heart%rate%while% inotropic%agents%affect%contrac<lity,%which% affects%stroke%volume.% Some%factors%(e.g.,%epinephrine%and% norepinephrine)%affect%both.% 11/13/13 badri@gmc 135 11/13/13' badri@gmc' 136' Normal stroke volume Decrease in stroke volume Stroke volume with uncompensated heart failure Shift to the right and downwards of the (Frank-Starling )curve by heart failure Normal end-diastolic volume Normal heart Failing heart 11/13/13' badri@gmc' 137' Answers%to%Ques<ons% If#HR#increases,#what#will#happen#to#cardiac#output# TCardiac%output%increases.% If#SV#decreases,#what#will#happen#to#cardiac# output?# 9Cardiac%output%is%expected%to%decrease%(note%that% heart%rate%can%be%increased%to%compensate).% What#effect#will#sympathe>c#nerve#impulses#have# on#heart#rate?# TThe%norepinephrine%released%will%increase%heart%rate.% What#effect#will#parasympathe>c#nerve#impulses# have#on#heart#rate?## GThe%ACh%released%will%decrease%heart%rate.% 11/13/13' badri@gmc' 138' 23
Answers%to%Ques<ons% What#effect#will#increased#heart#rate#have#on#stroke# volume#(if#other#factors#stay#the#same)?# #Stroke%volume%will%increase%to%some%extend%and%if%further% increases%will%lead%to%reduced%filling%<me%and%sv%will%decrease% (note%that%sv%may%be%maintained%if%the%cause%of%the%increased% heart%rate%also%increases%contrac<lity).## What#effect#will#increased#venous#return#have#on#EDV?# EDV%will%increase.# What#effect#will#blood#loss#have#on#EDV?# #EDV%%will%decrease%(note%that%the%body%has%compensatory% mechanisms%to%ini<ally%maintain%sv%when%blood%is%lost).% Answers%to%Ques<ons% What#effect#will#inhaling#more#deeply#have#on# venous#return?# %Venous%return%will%increase%because%deeper%inhala<on% lowers%thoracic%pressure%more%than%normal.% What#effect#will#epinephrine#have#on#stroke# volume?# Stroke%volume%will%increase%due%to%the%increased% contrac<lity.% 11/13/13' badri@gmc' 139' 11/13/13' badri@gmc' 140' Answers%to%Ques<ons% What#effect#will#blocking#calcium#channels#have#on# stroke#volume?# ##Stroke%volume%will%decrease.% What#effect#will#hypertension#have#on#aGerload?## #AVerload%will%increase.## What#effect#will#hypertension#have#on#stroke# volume?## Stroke#volume#will#decrease#(and#the#heart#will#have#to# work#harder#to#eject#blood).# 11/13/13' badri@gmc' 141' The End 24