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15 Cards in this Set

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Cardiac Output:
Definition
Regulation
The volume of blood ejected from the left ventricle per minute is the cardiac output (CO). Regulation of the CO involves a complex set of responses from control centers in the CNS and a variety of sensor-effector networks, which influence the pumping function of the heart and the resistance in the different vascular beds.
Equations:
Cardiac Output (L/min)
Ejection Fraction
Cardiac Output: Q(CO) = Fc(HR) x SV
SV = EDV – ESV (end diastolic vol – end systolic vol)
Ejection Fraction: EF = (EDV – ESV)/EDV x 100
EF = (110mL – 50mL)/110mL x 100 = 55%
What affects the Cardiac Output Q?
CO is affected by the balance of sympathetic and parasympathetic nerve stimuli which affects the sinus node and cardiac contractility. The HR is also sensitive to other factors like circulating hormones such as epinephrine.
What does the Stroke Volume (SV) depend on?
SV depends on the size of the heart (a larger person has a larger heart which has a larger volume capacity) and strength of heart muscle (a stronger heart has a greater capacity to contract). Normally at rest, the CO is ~5 L/min for an avg size person. During exercise the CO increases up to 20+ L/min, due to the metabolic and nutritional demands of the tissues.
Factors Affecting End Diastolic Volume (EDV): Venous Return
The amount of blood coming back to the heart, which affects the filling pressure of the left ventricle. The venous return is also known as the preload, which may be affected by ventricular compliance.
Factors Affecting End Diastolic Volume (EDV): Ventricular Compliance
Compliance (DV/DP) is a measure of the ease with which the ventricular wall can be stretched to accept blood. For example, for the same filling pressure, a reduction in ventricular compliance (due to scarring from injury, for instance) reduces the filling of the ventricle.
Factors Affecting End Diastolic Volume (EDV): Heart Rate (Diastolic Interval)
Increases in HR usually occur at the expense of the diastolic time with the time of systole remaining relatively fixed. Usually the diastolic interval is adequate for the ventricle to fill appropriately, provided that the venous return is not reduced. At very high HR’s, the diastolic time is so short that the ventricle may not be filled adequately, and during these periods, atrial contraction becomes more important to maintain cardiac filling.
Factors Affecting End Systolic Volume: Contractility
At a given fiber length, it is possible to change the force of contraction. Positive Ionotropic Agents (NE, E, Isoproterenol, increased [Ca2+]) enhance the contraction force and negative ionotropic agents (ACh, Increased [K+], Decreased [Ca2+]) diminish the force of contraction. The principal ionotropic agent is NE released from sympathetic nerves to increase contractile force at any length. Overall, the primary mechanism to adjust the force of contraction of the cardiac muscle is a change in the force-velocity response, mediated by changes in sympathetic nerve activity.
Factors Affecting End Systolic Volume: Frank-Starling Mechanism (length-tension curve)
This states that the contraction force increases as the initial sarcomere length of the muscle increases (thus more crossbridges are formed), within the normal physiological range, beyond which the contractile tension declines. When the venous filling pressure increases during diastole, EDV is increased, and this increases the initial fiber length, which increases the contraction force and the CO. The Starling mechanism operates in the normal heart to balance the output of the right and left sides of the heart.
Factors Affecting End Systolic Volume: Aortic Pressure (Afterload)
Depends on stroke volume (SV), aortic compliance, and total peripheral resistance (TPR).
During ea. ventricular systole the heart ejects a volume of blood into the aorta which is already filled with blood at diastolic pressure. The aortic compliance determines how much the pressure will rise with the ejection of this volume of blood. During diastole, how much blood flows into the aorta varies inversely with the resistance of each vascular bed. The total quantity of blood leaving the aorta is determined by the sum of all these resistances, and this is termed the TPR.
What does an ejection fraction (EF) of <40% indicate?
Heart failure may be present or one might have valvular disease, as the ventricle is not able to squeeze out enough blood. Also the ventricle may be scarred from a heart attack.
What happens to the ejection fraction (EF) when one exercises?
The EF increases to 65-75%.
1) Skeletal muscle squeezes the veins. The peripheral blood is squeezed back towards the heart due to the presence of venous valves. If EDV increases, ESV will decrease (Frank-Starling Mechanism)
2) SNS activation will increase contractility and therefore decrease ESV.
What are the 2 major factors that affect the ejection fraction (EF)?
1) Intrinsic Control (Frank-Starling mechanism): SV increases as fiber length increases: more CB’s = more force. However, if EDV is too large and the muscle stretched too far, stroke volume decreases. This occurs in heart failure. Surgery can remove a portion of the ventricle to allow more appropriate fiber lengths to be achieved.
2) Extrinsic Control (Increased contractility due to SNS activation): max velocity depends on ATPase activity; the load depends on the # of CB’s. Sympathetic stimulation allows for greater velocity at a given force as more Ca2+ is available, and thus the contractility is increased. An increased Ca2+ entry also allows for the shifting of the curve to the right with SNS activation.
Autonomic Regulation of Cardiac Contraction
Most of the effects of catecholamines in the cardiac muscle are mediated by cAMP-dependent protein kinase. In their phosphorylated state, Ca2+ channels are more likely to be open than in the dephos state, resulting in increased Ca2+ influx during an AP. More CB’s are formed by increasing Ca2+ influx. This also affects ATPase activity, and thus the CB’s form and break at a faster rate.
The Fick Principle
This states that the amt of substance taken up by an organ (or the whole body) per unit time is equal to the arterial level of the substance minus the venous level (the a-v difference) times the blood flow.
Accumulation = Input – Output, or
VdotO2 = Qdot (CAO2 – CVO2) = Qdot(O2 Extraction), where VdotO2 is the rate of volume of O2 consumption and CAO2 is the arterial O2 content and CVO2 is the venous O2 content. This can be used to calculate the CO. Thus, O2 deliveryt to tissues depends on O2 content and blood flow.