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Questions and Answers
What happens to tropomyosin as a result of TnT movement?
What happens to tropomyosin as a result of TnT movement?
What is the optimal sarcomere length for maximum tension development in skeletal muscle?
What is the optimal sarcomere length for maximum tension development in skeletal muscle?
What is the effect of increasing sarcomere length on cardiac muscle?
What is the effect of increasing sarcomere length on cardiac muscle?
What is the primary mechanism of length dependent activation in cardiac muscle?
What is the primary mechanism of length dependent activation in cardiac muscle?
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What happens to the distance between actin and myosin as sarcomere length increases?
What happens to the distance between actin and myosin as sarcomere length increases?
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What is the optimal [Ca2+]i for maximum force development in cardiac muscle?
What is the optimal [Ca2+]i for maximum force development in cardiac muscle?
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At what sarcomere length is the force development in cardiac muscle maximally sensitive to [Ca2+]i?
At what sarcomere length is the force development in cardiac muscle maximally sensitive to [Ca2+]i?
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What is the relationship between sarcomere length and Ca2+ sensitivity in cardiac muscle?
What is the relationship between sarcomere length and Ca2+ sensitivity in cardiac muscle?
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What is the effect of titin on the thin filament?
What is the effect of titin on the thin filament?
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What determines CO at a given heart rate and contractility?
What determines CO at a given heart rate and contractility?
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What is the primary mechanism by which the heart maintains CO in the face of increased afterload?
What is the primary mechanism by which the heart maintains CO in the face of increased afterload?
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What is the term for the strength of contraction of the heart?
What is the term for the strength of contraction of the heart?
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What regulates cardiac contractility?
What regulates cardiac contractility?
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What is the effect of sympathetic stimulation on cardiac contractility?
What is the effect of sympathetic stimulation on cardiac contractility?
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What is the result of an increase in RV output?
What is the result of an increase in RV output?
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What is the consequence of an increase in CVP on LV output?
What is the consequence of an increase in CVP on LV output?
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What is the primary effect of blood loss on cardiac output (CO)?
What is the primary effect of blood loss on cardiac output (CO)?
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What happens to CVP during sustained exercise?
What happens to CVP during sustained exercise?
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What is the effect of orthostasis on blood pressure?
What is the effect of orthostasis on blood pressure?
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What percentage of blood is in the systemic veins at any given moment?
What percentage of blood is in the systemic veins at any given moment?
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What is the effect of constriction of splanchnic veins by the SNS?
What is the effect of constriction of splanchnic veins by the SNS?
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What is the approximate amount of blood mobilized into the heart by constriction of splanchnic veins?
What is the approximate amount of blood mobilized into the heart by constriction of splanchnic veins?
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What percentage of blood is in the splanchnic veins?
What percentage of blood is in the splanchnic veins?
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What is the relationship between CVP and CO?
What is the relationship between CVP and CO?
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What happens to the Frank-Starling curve in the case of heart failure?
What happens to the Frank-Starling curve in the case of heart failure?
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Which of the following is NOT a compensatory mechanism activated by heart failure?
Which of the following is NOT a compensatory mechanism activated by heart failure?
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What is the primary effect of increased sympathetic nervous system activity in response to heart failure?
What is the primary effect of increased sympathetic nervous system activity in response to heart failure?
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What does the term "EDP" refer to in the context of heart failure?
What does the term "EDP" refer to in the context of heart failure?
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Which of the following factors does NOT affect the Frank-Starling mechanism?
Which of the following factors does NOT affect the Frank-Starling mechanism?
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How does noradrenaline increase cardiac contractility?
How does noradrenaline increase cardiac contractility?
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What physiological mechanism ensures that the cardiac output of the left ventricle (COLV) remains equal to the cardiac output of the right ventricle (CORV) over time?
What physiological mechanism ensures that the cardiac output of the left ventricle (COLV) remains equal to the cardiac output of the right ventricle (CORV) over time?
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Which of the following accurately describes the concept of preload in relation to cardiac function?
Which of the following accurately describes the concept of preload in relation to cardiac function?
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How does the Frank-Starling law of the heart contribute to maintaining a constant cardiac output (CO) over a range of afterloads?
How does the Frank-Starling law of the heart contribute to maintaining a constant cardiac output (CO) over a range of afterloads?
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Which of the following factors can influence preload and affect cardiac output?
Which of the following factors can influence preload and affect cardiac output?
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How does the Anrep response differ from the Frank-Starling response in maintaining a constant cardiac output (CO) under varying afterloads?
How does the Anrep response differ from the Frank-Starling response in maintaining a constant cardiac output (CO) under varying afterloads?
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Which of the following accurately describes the relationship between end-diastolic volume (EDV) and ventricular function?
Which of the following accurately describes the relationship between end-diastolic volume (EDV) and ventricular function?
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Which of the following is NOT a factor that can affect heart rate (HR)?
Which of the following is NOT a factor that can affect heart rate (HR)?
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What is the primary mechanism by which changes in end-diastolic pressure (EDP) affect ventricular output?
What is the primary mechanism by which changes in end-diastolic pressure (EDP) affect ventricular output?
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Study Notes
Cardiac Output Control
- Cardiac output (CO) must adjust to bodily tissue metabolic needs.
- Systemic and pulmonary circulations are arranged in series; left and right ventricular outputs must be equal over time (COLV = CORV).
- Venous return matches cardiac output, allowing for transient differences in specific situations, such as standing.
Preload and Afterload
- Preload refers to the initial stretching of the cardiac muscle before contraction, influenced by end-diastolic volume (EDV).
- Afterload is the pressure against which the heart must work to eject blood during systole.
- Changes in preload and afterload significantly impact cardiac performance and output.
Frank-Starling Law
- The Frank-Starling mechanism ensures stroke volumes of both ventricles are matched, stabilizing CO despite variations in afterload or contractility.
- Increased ventricular filling leads to elevated stroke volume due to enhanced myocardial stretch linking to contractility through length-dependent activation.
Contractility and Inotropy
- Contractility is the inherent strength of heart muscle contraction, influenced by intracellular calcium levels in cardiac myocytes.
- Sympathetic stimulation increases contractility via norepinephrine acting on β1 and β2 adrenergic receptors.
- Several factors, including pH and pO2, also affect inotropic response.
Cardiac Function and EDV/EDP
- End-diastolic volume (EDV) and end-diastolic pressure (EDP) are critical in determining ventricular function and shaping cardiac function curves.
- Cellular mechanisms relating EDV/EDP to output involve actin-myosin interactions and alterations in calcium sensitivity.
Compensatory Mechanisms in Heart Failure
- Heart failure occurs when CO is inadequate for metabolic requirements or maintained only at high EDP/volume levels.
- Reduced CO activates compensatory responses, including fluid retention and increased heart rate.
- Renin-angiotensin-aldosterone system is engaged in response to low blood pressure, promoting fluid retention and venoconstriction.
Impacts of Blood Volume Changes
- Decreases in central venous pressure (CVP) affect CO, particularly during hemorrhage or prolonged exercise.
- Orthostatic changes lead to blood pooling, reducing CVP and subsequently decreasing CO and blood pressure.
Venous System Role
- Splanchnic vein constriction by the sympathetic nervous system can significantly increase CVP, mobilizing blood into the heart and arterial system efficiently without major impacts on venous return due to slow flow characteristics.
Cellular Mechanisms and Length-Dependent Activation
- Increased sarcomere length leads to enhanced actin-myosin overlap.
- Titin protein affects myosin binding protein C, modifying troponin configuration, which heightens calcium sensitivity for contraction.
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Description
This quiz covers the physiology of cardiac function, including preload, afterload, and ventricular function. It also explores the relationship between EDV/EDP and cardiac function, and drawing cardiac function curves.