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Questions and Answers
What is the relationship between stroke volume (SV) and cardiac output (CO)?
What is the relationship between stroke volume (SV) and cardiac output (CO)?
- SV is independent of CO.
- SV is unaffected by changes in CO.
- SV is directly proportional to CO. (correct)
- SV is inversely proportional to CO.
How does the Frank-Starling law affect stroke volume?
How does the Frank-Starling law affect stroke volume?
- The law states that an increase in EDV will increase stroke volume. (correct)
- The law states that an increase in EDV will increase the contractility of the heart muscle.
- The law states that an increase in EDV will lead to a decrease in heart rate.
- The law states that an increase in end-diastolic volume (EDV) will decrease stroke volume.
Which of the following factors directly affects venous return?
Which of the following factors directly affects venous return?
- Decreased contractility of the heart muscle
- Decreased heart rate
- Skeletal muscle pump (correct)
- Increased blood pressure in the aorta
Which of these factors will directly affect the cardiac output?
Which of these factors will directly affect the cardiac output?
What is the effect of increased pressure in the venous 'bag' on the cardiac function?
What is the effect of increased pressure in the venous 'bag' on the cardiac function?
Which factor does NOT directly increase contractility?
Which factor does NOT directly increase contractility?
What is the primary role of catecholamines like epinephrine in cardiac function?
What is the primary role of catecholamines like epinephrine in cardiac function?
Which component is NOT a result of catecholamines binding to b1-receptors?
Which component is NOT a result of catecholamines binding to b1-receptors?
The term 'inotropic effect' primarily refers to what aspect of cardiac physiology?
The term 'inotropic effect' primarily refers to what aspect of cardiac physiology?
How does sympathetic stimulation primarily affect heart rate?
How does sympathetic stimulation primarily affect heart rate?
Which hormone interacts with the cardiac system specifically to enhance contractility?
Which hormone interacts with the cardiac system specifically to enhance contractility?
Which component of cardiac output is influenced by the force of contraction in the ventricular myocardium?
Which component of cardiac output is influenced by the force of contraction in the ventricular myocardium?
What primarily determines heart rate during parasympathetic stimulation?
What primarily determines heart rate during parasympathetic stimulation?
What is the primary effect of venous constriction on cardiac output?
What is the primary effect of venous constriction on cardiac output?
Which mechanism enhances the contractility of the heart after the binding of norepinephrine?
Which mechanism enhances the contractility of the heart after the binding of norepinephrine?
What effect does phospholamban have on the sarcoplasmic reticulum (SR) during sympathetic stimulation?
What effect does phospholamban have on the sarcoplasmic reticulum (SR) during sympathetic stimulation?
What is the consequence of a decrease in heart rate on cardiac output (CO)?
What is the consequence of a decrease in heart rate on cardiac output (CO)?
Which of the following directly mediates the increase in heart rate due to sympathetic stimulation?
Which of the following directly mediates the increase in heart rate due to sympathetic stimulation?
How does the respiratory pump aid in venous return?
How does the respiratory pump aid in venous return?
Flashcards
Stroke Volume (SV)
Stroke Volume (SV)
The amount of blood pumped by one ventricle in one contraction, calculated as SV = EDV - ESV.
End Diastolic Volume (EDV)
End Diastolic Volume (EDV)
The volume of blood in a ventricle at the end of filling (diastole), ~135 ml.
Cardiac Output (CO)
Cardiac Output (CO)
The total amount of blood pumped by the heart per minute, CO = HR x SV.
Frank-Starling Law
Frank-Starling Law
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Venous Return
Venous Return
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Contractility
Contractility
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Catecholamines
Catecholamines
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b1-receptors
b1-receptors
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cAMP
cAMP
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Inotropic Effect
Inotropic Effect
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Voltage-gated Ca2+ channels
Voltage-gated Ca2+ channels
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Phospholamban
Phospholamban
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Sarcoplasmic reticulum (SR)
Sarcoplasmic reticulum (SR)
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Heart Rate (HR)
Heart Rate (HR)
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Autonomic Nervous System
Autonomic Nervous System
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Parasympathetic Nervous System
Parasympathetic Nervous System
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Sympathetic Nervous System
Sympathetic Nervous System
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Study Notes
Cardiac Output Regulation
- Cardiac output (CO) is the amount of blood pumped by each ventricle per minute.
- CO = Heart Rate (HR) x Stroke Volume (SV)
Factors Affecting Cardiac Output
-
Heart Rate (HR):
- Determined by the rate of depolarization in autorhythmic cells.
- Increased by sympathetic innervation and epinephrine, increasing cAMP/PKA, and increasing I(f).
- Decreased by parasympathetic innervation (M2R, Gai, ACh), lowering cAMP/PKA, and decreasing I(f).
-
Stroke Volume (SV):
- Determined by the force of contraction in the ventricular myocardium.
- Affected by contractility, end-diastolic volume (EDV), and venous return.
- Contractility: Increased by sympathetic innervation (β1R, Gas, NE/epinephrine), increasing cAMP/PKA, and affecting VGCC, SERCA, and SR Ca2+.
- EDV: Increased EDV leads to increased SV (Frank-Starling law). Stretch increases the number of crossbridges, approaching optimal sarcomere length, leading to increased force of contraction.
- Venous Return: Affected by skeletal muscle pump, respiratory pump, and sympathetic innervation. Increased venous return increases EDV, which increases SV.
End-Diastolic Volume (EDV) and Venous Return
- EDV (end-diastolic volume) is the volume of blood in the ventricles at the end of diastole.
- Venous return is the amount of blood flowing back to the heart through the veins.
- Factors affecting venous return:
- Skeletal muscle pump
- Respiratory pump
- Sympathetic innervation
End-Systolic Volume (ESV)
- ESV (end-systolic volume) is the volume of blood remaining in the ventricles after systole.
- Increased afterload can increase ESV.
- Increased inotropy can decrease ESV.
Inotropic Effect
- The effect of norepinephrine on the contractility of the heart.
- Increased norepinephrine leads to an increased slope on the ESPVR graph.
- Positive inotropic agents increase contractility, leading to a steeper ESPVR slope.
- Negative inotropic agents decrease contractility, leading to a less steep ESPVR slope.
Regulation of Cardiac Output
- Increased pressure in the venous system increases EDV, which increases SV and CO.
Mechanism of Catecholamines on Cardiac Contraction
- Catecholamines (epinephrine and norepinephrine) bind to β1-receptors on autorhythmic cells.
- This activates a cAMP second messenger system that phosphorylates proteins.
- Phosphorylated proteins increase intracellular Ca2+ entry (from ECF, SR), shortening Ca2+-troponin binding time, and increasing contractility.
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