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CARDIAC OUTPUT
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Cardiac Output Amount of blood pumped out by each ventricle per minute
In an average adult L\min. In infants & children it is low In elderly it is less than in the adult.
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Stroke Volume The amount of Blood ejected out of each ventricle per beat. In an average adult at rest = 40-60ml
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Stroke Volume X Heart Rate
Cardiac Output Stroke Volume X Heart Rate
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Cardiac Output from each ventricle should be equal
or otherwise damming of blood will take place
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Under which normal condition is CO from both ventricles not equal?
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Cardiac Output decides the rate of flow to the tissues.
Rate of flow to tissues depends on tissue needs Therefore, cardiac output is proportional to the energy requirements of the tissues.
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CO---5L\min. CO—3L\min child Adult Obese Adult 3.8L\min.Sqm
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Cardiac Index Cardiac Output per body surface area.
In an average adult it is —3.2L\min.\Sqm
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Cardiac Index Reflects the efficiency of the system
Helps to compare between 2 individuals or In the same individual in different situations
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Cardiac Index Cardiac Index (CI): Approximately 3 liters/min/m2 of body surface area. CI varies with age, peaking at around 8 years.
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Determining Factors
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Factors determining Cardiac Output
Extra Cardiac Venous Return Preload Resist. offered Afterload ? Cardiac Heart Rate Myocardial Contractility
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Venous Return
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Sympathetic Stimulation
Venomotor Tone Sympathetic Stimulation N 10 Mean circulatory Pressure 5 Volume - L
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Venomotor Tone Symp. Stimulation Symp. Inhibition Volume - L
10 Mean circulatory filling Pressure 7 5 Symp. Inhibition Volume - L
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Rt.Atrial Pressure Venous Return (L\min.)
Effect of Intra thoracic Pressure Venous Return (L\min.) 5 - 8 Rt.Atrial Pressure
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Rt. Atrial Pressure-mm Hg
10 Venous Return (L\min.) Mean filling \ Systemic filling Pressure 5 --4 Rt. Atrial Pressure-mm Hg
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Determinants of Venous Return
Mean systemic filling pressure Right Atrial Pressure Venomotor Tone Pressure change is slight. Thus, small increase in RA Pressure or a reduction in mean systemic filling pressure causes dramatic reduction in venous return.
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Cardiac Output Curve 5 L/min (CO) 7 -4 Rt. Atrial Pressure (mm Hg)
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Plateau: collapse of large veins
Working Cardiac Output 5 L/min Cardiac Output Curve VR (CO) 7 -4 Mean systemic filling pressure ~ Rt. Atrial Pressure (mm Hg)
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Gravity
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Simulates Muscle Pump water Legs immersed in water
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The filling of the ventricle is dependent on the stiffness
& therefore the Diastolic tension Stiffness dependes on Quality of muscle Thickness of the walls Dimension of the cavity Shape The angles of adj. muscle fibers
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Compliance of the Ventricle
In the aged the compliance decreases Replacement by fibrous tissue decreases the compliance. Massive hypertrophy also decreases Aneurism of Ventricles inc.
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Inc. stiffness of chamber
Normal LV End Diastolic Pressure LV End Diastolic Diameter Chamber stiffness increases as the chamber contracts because there is increase in thickness
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The Rt.Ventricle is more compliant than the Lt. because it is thinner.
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Atrial Systole increases the blood flow into the ventricles by 30% ,
Significant when the compliance of ventricles are low Atrial Booster Pump .
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LVEDP Length Pericardium Intact Constrictive Pericarditis
Pericardial Effusion W\O Pericardium LVEDP Normal Length
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Ventricular Inter dependance
Alteration of filling in one chamber will alter the pressure –vol. relation in the other. because of the resulting encroachment of Inter ventricular septum.
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Venous Return Total Blood Volume Distribution of the Blood
Body Position Intrathoracic Pressure Venomotor Tone
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Venous Return Rt.Atrial Pressure Atrial Booster Pump
Intrapericardial Pressure Ventricular Compliance
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Frank Starling’s Phenomenon
Based on length active tension relation Force of contraction & extent of shortening depends on the initial length of the muscle
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Tension (Percednt of maximum)
Skeletal Muscle Tension (Percednt of maximum) Cardiac Muscle Card. Musc. Fetus Sarcomere Length (microns)
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Cardiac muscle is more stiff.
Length at Lmax averages 2.2 u. At 20% beyond Lmax sarcomere elongate very little but the tension falls substantially Diastolic sarcomere length is prevented from exceeding 2.3u Contraction always happens in the steep portion of the curve
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LV Pressure filling - mm Hg Tension --g 1 2 3 4 5 6
Actively Developed Tension LV Pressure filling - mm Hg Tension --g Sarcomere Length (microns)
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The active Tension developed during isometric contraction is due to the extent of overlapping
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Ca++ 5mM\l Active Tension Ca++ 2mM\l Sarcomere Lentgh
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The mechanical performance is more sensitive to changes in extracellular Ca++ at longer than at shorter muscle length---- increased contractility
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The disengagement of myofilaments cannot explain the decrement in Active Tension
Cellular damage with stretching is responsible for reduction in tension development
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The Vmax is little altered
Force Velocity relation Increasing Muscle length Velocity of shortening Load
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Stroke volume Preload
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In the intact heart the increase in preload augments the stroke volume & the velocity of wall shortening. The maximum velocity of wall shortening at zero load Vmax does not change with length (preload)
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Venous Return in Pregnancy Max.Inc. in Blood vol.—II Trimester
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SUPINE POSITION IVC Gravid Uterus LEFT LATERAL POSITION
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Immediate Post Partum. IVC Gravid Uterus
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What can increase the VR in the Fetus?
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Myocardial Contractility
Inotropy is the contractile property independent of the EDV or Preload
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The midwall fibers are circumferential-perpendicular to the long axis
The subendocardial fibers & subepicardial fibers run parallel to the long axis Major axis Minor axis The midwall fibers are circumferential-perpendicular to the long axis Isometric contraction- chamber becomes sperical
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Isotonic contraction-The fibers shorten & thicken.
During ejection- internal minor axis accounts for 85-90% of stroke volume. Ratio of Major to Minor axis becomes 1.93 from 1.49 Change in shape & the arrangement of fibers will reduce the extent of shortening.
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Inotropic agent At any given length, increases
Velocity & extent of wall shortening. Peak force developed Time to reach peak force developed decreases Increases Stroke vol. & decreases duration of contraction.
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Force Velocity relation with NE
Control +NE Velocity of shortening Load
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Adrenergic stimulation (Intrinsic)
Alpha receptors mediate inc.inotropy by inc. in Ca++ influx Beta receptors through cyclic AMP Sensitivity to Ca++ increases Enhanced pumping of Ca++ into SR Good Lusiotropic effect
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Exogenous Inotropic agents
Loss of contractile mass Physiological & Pharmacological depressants Intrinsic Myocardial depression
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Cardiac Output Curve 5 L/min (CO) 7 -4 Rt. Atrial Pressure (mm Hg)
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Cardiac Output Curve 5 L/min (CO) 7 -4 Rt. Atrial Pressure (mm Hg)
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Force Frequency Relation
A simple inc. in frequency in the Physiological range augments contractility but This effect is seen with depressed function rather than in the normal heart
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Contractile state of Myocardium
Force Frequency Relation Sympathetic & Catecholamines Exogenous Inotropic agents Contractile state of Myocardium Intrinsic depression Physio. & Pharmacologic depressants Ioss of Myocardium
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After Load Force (Tension) or stress per unit of cross sectional area, acting on the fibers after the onset of shortening.
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Peripheral Vascular Resistance
The physiological characteristics of the Arterial tree (Aorta) Blood column in the arterial system Viscosity of blood
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In diseased conditions what else can decide the After Load?
Valve size Circumferential wall stress or Tension
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After Load Force (Tension) or stress per unit of cross sectional area, acting on the fibers after the onset of shortening.
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Laplac’s Law The Circumferential Wall Stress or Tension is directly related to the Intra ventricular pressure & the Radius & indirectly so to the wall thickness. T = PR\h
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What is the afterload during the different phases of cardiac cycle?
T = PR\h During systole P increases, R decrease & h increases therefore T tends not to increase too high. Diastole-P decreases, R increases & h also dec., T –not much of a change
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Force –Velocity Relation
The extent & maximum velocity of shortening for each contraction depends on the load at any given preload
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Force Velocity relation
At a given muscle length Velocity of shortening Load
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Force Velocity relation
Vmax Normal RVH CHF Velocity of shortening Load
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In mild Hypertrophy T = PR\h h increases, P increases
therefore T remains the same or dec. However Myocardial contractility decreases.
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Wall Tension decides the Myocardial O2 consumption.
Moderate or severe Hypertrophy Hypertrophy Muscles becomes more stiff because of Ischemia -Wall Tension increases Wall Tension decides the Myocardial O2 consumption.
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Velocity of shortening
Normal Velocity of shortening Severe Hypertrophy Circumferential wall tension
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Circumferential wall tension
Normal Ejection Fraction Aortic Stenosis Circumferential wall tension
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Stroke volume Active LV Pressure
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In Pregnancy, what decides the After Load?
Why is Ejection into the Pulmonaary Artery more prolonged? What decides the After Load to the LV in the fetus?
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After Load to LV AO with MI PDA Anemia Ischemia
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Homeometric Autoregulation Anrep Effect
A positive inotropic effect follows an abrupt inc. in systolic Aortic & LV Pressure Reactive Hyperemia occurs Related to recovery from transient subendocardial Ischemia
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After load & Preload can also be influenced by the Heart under abnormal conditions
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What is the minimum CO necessary to sustain life?
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