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This set of flashcards covers the mechanisms of cardiac output, blood pressure regulation, the Frank-Starling mechanism, chronotropic and inotropic control, and the short-term and long-term feedback loops involving the baroreceptor reflex and the RAAS.
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Cardiac Output (CO)
The total volume of blood pumped through the body per minute (5L/min at rest), calculated as the product of stroke volume and heart rate: CO=SV×HR.
Stroke Volume (SV)
The volume of blood ejected from a heart ventricle during each individual beat.
Mean Arterial Pressure (MAP)
The average pressure in the arteries determined by cardiac output and total peripheral resistance: MAP=CO×TPR.
Total Peripheral Resistance (TPR)
The resistance to blood flow in the systemic circulation, primarily controlled by the radius of the arterioles.
Darcy’s Law
A physical principle expressed as ΔP=F×R, where pressure difference equals flow multiplied by resistance.
Frank-Starling Mechanism
The process where increasing venous return increases ventricular filling pressure and muscle stretch, resulting in a greater contractile force and increased stroke volume.
Inotropy
The contractility of the cardiac muscle; positive inotropes like adrenaline increase the force of contraction independent of changes in venous return.
Chronotropy
Refers to the regulation of heart rate; positive chronotropes increase the rate, while negative chronotropes decrease it.
Sinoatrial (SA) Node
The heart's pacemaker located in the right atrium that generates the action potential and sets the basic rhythmicity of cardiac contraction.
Pacemaker Potential
The steadily depolarizing resting potential of the SA node that triggers an action potential once it reaches a specific threshold.
Venous Capacitance
The capacity of veins and venules to store blood, usually holding approximately 60% of the total blood volume at rest.
Baroreceptor Reflex
A rapid, short-term negative feedback mechanism that regulates MAP via sensors in the carotid sinuses and aortic arch that communicate with the medulla.
Vasoconstriction
The reduction of a blood vessel's radius, which increases resistance and pressure upstream; stimulated by noradrenaline, Angiotensin II, and Vasopressin (ADH).
Vasodilation
The increase of a blood vessel's radius, which reduces resistance; stimulated by agents such as Atrial Natriuretic Peptide (ANP) or Histamine.
Renin-Angiotensin-Aldosterone System (RAAS)
A hormonal system for the long-term regulation of blood volume and MAP via the control of sodium and water reabsorption in the kidneys.
Renin
An enzyme secreted by juxtaglomerular (JG) cells that cleaves angiotensinogen into Angiotensin I.
Angiotensin II
A potent vasoconstrictor and product of the RAAS that stimulates aldosterone secretion and increases TPR to restore MAP.
Aldosterone
A steroid hormone from the adrenal cortex that increases long-term blood pressure by increasing the expression of Na+ channels and pumps in the distal convoluted tubule (DCT).
Macula Densa
A group of specialized epithelial cells in the distal convoluted tubules of the kidney that sense changes in MAP indirectly via the delivery of Na+ in the filtrate.
Atrial Natriuretic Peptide (ANP)
A hormone stimulated by increased plasma volume that inhibits Na+ and water reabsorption in the kidney to help lower blood volume and MAP.
Glomerular Filtration Rate (GFR)
The rate at which blood is filtered in the kidney; it decreases during a drop in MAP to conserve water.
Juxtaglomerular (JG) Cells
Cells in the kidney that secrete renin in response to sympathetic drive or signals from the macula densa regarding low sodium delivery.
Resistance-Radius Relationship
The principle that resistance to flow is inversely proportional to the fourth power of the vessel radius: Resistance∝radius41.