Week 27 / Circulatory system 5 Flashcards
Question: What is Cardiac Output (CO)?
Answer: Cardiac Output (CO) is the volume of blood the heart pumps out every minute, measured in ml/min or L/min.
Question: What determines Cardiac Output (CO)?
Answer: Cardiac Output (CO) is determined by Stroke Volume (SV) and Heart Rate (HR).
Question: What is the formula for Cardiac Output (CO)?
Answer: CO = SV × HR.
Question: What is Stroke Volume (SV)?
Answer: Stroke Volume (SV) is the volume of blood ejected by the left ventricle with each heartbeat, measured in ml/beat.
Question: How is Cardiac Output regulated?
Answer: Cardiac Output can be adjusted to meet the body’s physiological and metabolic needs through changes in Stroke Volume (SV) and Heart Rate (HR).
Question: What determines Heart Rate (HR)?
Answer: Heart Rate (HR) is determined by the Autonomic Nervous System (ANS), specifically the Sympathetic Nervous System (SNS) and Parasympathetic Nervous System (PNS):
SNS increases HR.
PNS decreases HR.
Question: What is Preload in relation to Stroke Volume (SV)?
Answer: Preload is the workload imposed on the heart before contraction begins, equivalent to the end-diastolic volume or pressure (EDV/P). It represents the volume of blood or pressure in the ventricle at the end of diastole.
Question: What are the determinants of Stroke Volume (SV)?
Answer: The determinants of Stroke Volume (SV) are:
Preload
Afterload
Cardiac contractility
Question: What is the relationship between Preload and Stroke Volume (SV)?
Answer: According to the Frank-Starling Law of the Heart, Stroke Volume (SV) is directly proportional to Preload (or Venous Return). An increase in Preload leads to increased stretch of the cardiac muscle, resulting in a stronger contraction and higher SV.
Question: What does Venous Return (VR) equal in terms of Preload?
Answer: Venous Return (VR) is equal to the End-Diastolic Volume (EDV), which determines the Preload.
Question: What is Afterload in relation to Stroke Volume (SV)?
Answer: Afterload is the “load” the heart must contract against to eject blood into the aorta. It refers to the pressure the heart must generate to overcome in order to eject blood into the aorta.
Question: What determines Afterload? [2]
Answer: Afterload is determined by aortic pressure (systemic arterial blood pressure) and systemic or total peripheral resistance (TPR).
Question: What is the relationship between Afterload and Stroke Volume (SV)?
Answer: Stroke Volume (SV) is inversely proportional to Afterload (or Total Peripheral Resistance). An increase in Afterload leads to a decrease in SV.
Question: What is Contractility in relation to Stroke Volume (SV)?
Answer: Contractility is the ability of the heart to change its force of contraction without changing its resting muscle length. It reflects the strength of contraction at any given End-Diastolic Volume (EDV).
Question: What does Cardiac Contractility depend on?
Answer: Cardiac contractility depends on the availability of intracellular calcium (Ca++) to participate in the contractile process.
Question: What is the relationship between Contractility and Stroke Volume (SV)?
Answer: Stroke Volume (SV) is directly proportional to cardiac contractility. An increase in intracellular calcium concentration enhances actin-myosin cross-bridge formation, increasing contractility and thus increasing SV.
Question: How does the Sympathetic Nervous System (SNS) affect cardiac contractility?
Answer: SNS activation increases cardiac contractility, which leads to an increase in Stroke Volume (SV).
Question: What factors control Cardiac Output (CO)?
Answer: Cardiac Output is controlled by Heart Rate (HR) and Stroke Volume (SV).
Question: What are the two types of control over Cardiac Output?
Answer: Cardiac Output is controlled by both Extrinsic and Intrinsic factors.
Question: How does Parasympathetic activity affect Cardiac Output?
Answer: Parasympathetic activity decreases Heart Rate, which lowers Cardiac Output.
Question: What Extrinsic controls affect Cardiac Output? [2]
Answer: Extrinsic control involves Sympathetic activity and the action of epinephrine, which increase Heart Rate and Stroke Volume.
Question: What Intrinsic factors affect Cardiac Output? [2]
Answer: Intrinsic control includes End-Diastolic Volume (EDV) and Venous Return, which influence Stroke Volume.
Question: What is Systolic Blood Pressure (BP)?
Answer: Systolic Blood Pressure is the force exerted by blood on arterial walls during systole (when the heart contracts).
Question: What is Diastolic Blood Pressure (BP)?
Answer: Diastolic Blood Pressure is the force exerted by blood on arterial walls during diastole (when the heart is at rest between beats).
Question: What is Pulse Pressure?
Answer: Pulse Pressure is the difference between Systolic BP and Diastolic BP.
Formula: Pulse Pressure = Systolic BP - Diastolic BP.
Question: What is Mean Arterial Blood Pressure (MAP)?
Answer: Mean Arterial Pressure (MAP) is the average pressure that drives blood forward into tissues.
Question: What is the formula for
Mean Arterial BP?
Answer: Mean Arterial BP = Diastolic BP + (1/3 × Pulse Pressure).
Question: What determines Blood Pressure (BP)?
Answer: Blood Pressure (BP) is determined by Cardiac Output (CO) and Total Peripheral Resistance (TPR).
Question: What factors determine Cardiac Output (CO)?
Answer: Cardiac Output (CO) is determined by:
Heart Rate (HR) – influenced by autonomic tone and catecholamines.
Stroke Volume (SV) – influenced by cardiac contractility and venous return.
Question: What factors determine Total Peripheral Resistance (TPR)?
Answer: Total Peripheral Resistance (TPR) is determined by:
Sympathetic tone – vascular α1- and β2-adrenoceptors.
Circulating hormones – such as Angiotensin II (Ang II) and catecholamines.
Local hormones – such as Nitric Oxide (NO), Endothelins (ETs), Prostaglandins (PGs), and Adenosine.
Question: What is the formula for Blood Pressure (BP)?
Answer: BP = CO × TPR.
Question: Why is Mean Blood Pressure (BP) closely regulated?
Answer: Mean Blood Pressure (BP) is regulated to ensure two things:
BP is high enough for adequate perfusion of organs and tissues.
BP is not so high that it causes strain on the heart or damages blood vessels.
Question: What are the two mechanisms for homeostatic BP control?
Answer: The two mechanisms for homeostatic BP control are:
Short-term control via baroreceptors.
Long-term control via the kidneys.
Question: How do short-term control adjustments regulate blood pressure?
Answer: Short-term control adjustments occur within seconds and involve changes in cardiac output and total peripheral resistance. These adjustments are mediated by the autonomic nervous system’s influence on the heart, arterioles, and veins.
Question: How do long-term control adjustments regulate blood pressure?
Answer: Long-term control adjustments take minutes to days and involve renal mechanisms for maintaining normal salt and water balance. These adjustments help regulate total blood volume.
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