Capillary Fluid Dynamics and Blood Pressure Regulation

Flashcards cover capillary filtration/reabsorption, flow and resistance, arterial vs venous pressures, MAP, venous return mechanisms, neural and hormonal BP regulation (baroreceptors, chemoreceptors, RAAS, ANP, ADH, aldosterone, EPO), and renal control of blood pressure.

What is the primary pressure causing filtration out of the capillary?

Hydrostatic pressure in the capillary.

What pressure drives reabsorption (fluid back into the capillary)?

Osmotic (oncotic) pressure due to plasma proteins in the capillary.

At the arterial end of a capillary, is net filtration or net absorption greater?

Filtration is greater; net filtration occurs.

At the venous end of a capillary, is net filtration or net absorption greater?

Absorption is greater; net reabsorption occurs.

What condition leads to net filtration across the capillary membrane?

Capillary hydrostatic pressure > capillary osmotic pressure.

What condition leads to net absorption across the capillary membrane?

Capillary hydrostatic pressure < capillary osmotic pressure.

How is blood flow related to pressure difference and resistance?

Flow = ΔP / R; larger pressure gradient increases flow, larger resistance decreases flow.

What are the three primary factors that determine total peripheral resistance (TPR)?

Blood viscosity, blood vessel length, and blood vessel diameter.

What effect does increasing blood viscosity have on resistance and flow?

Increases total peripheral resistance and decreases flow.

How does increasing vessel length affect resistance?

Longer vessels increase resistance; shorter vessels decrease resistance.

How does vessel diameter affect resistance?

Smaller diameter increases resistance; larger diameter decreases resistance (vasodilation lowers resistance).

Which vessels are pulsatile and where is pulsatility lost?

Systemic (elastic and muscular) arteries are pulsatile; arterioles lose pulsatility.

What is mean arterial pressure (MAP) and how is it calculated?

MAP is the average arterial pressure; MAP ≈ diastolic + pulse pressure/3, or MAP = diastolic + (systolic - diastolic)/3.

What is pulse pressure?

Pulse pressure = systolic pressure − diastolic pressure.

What is the normal MAP range in a healthy individual?

Approximately 70–110 mmHg.

What MAP value is commonly associated with ischemia risk when too low?

MAP less than about 60 mmHg.

Why do veins have valves?

To prevent backflow and aid venous return against gravity due to low venous pressure.

What are the three mechanisms that assist venous return?

Skeletal muscle pump, respiratory (thoracic) pump, and sympathetic venoconstriction.

Where are baroreceptors located and what do they detect?

Located in the aorta and carotid sinus; detect pressure changes in systemic arteries.

Where are chemoreceptors located and what do they detect?

In the aorta and carotid sinus; detect changes in blood O2, CO2, and pH.

What brain region contains the main BP control centers and what are they?

Medulla oblongata; includes cardioacceleratory center, cardioinhibitory center, and vasomotor center.

What are the effects of activating the cardioacceleratory center?

Increases heart rate and contractility (increases cardiac output and MAP).

What are the effects of activating the cardioinhibitory center?

Decreases heart rate (no major change to contractility) and lowers MAP.

What is the role of the vasomotor center?

Regulates sympathetic tone to the tunica media, causing vasoconstriction or vasodilation (affecting TPR).

How does a decrease in mean arterial pressure trigger the sympathetic response?

Baroreceptors fire less; cardioacceleratory and vasomotor centers activate, cardioinhibitory is inhibited; HR, contractility, and vasoconstriction increase to raise MAP.

How does an increase in mean arterial pressure affect the baroreceptor reflex?

Baroreceptors fire more; cardioacceleratory is inhibited, cardioinhibitory is activated, vasomotor is inhibited, leading to vasodilation and lower MAP.

What is the Renin-Angiotensin-Aldosterone System (RAAS) activated by?

Low blood pressure at the kidneys.

What are the steps of RAAS starting from renin release?

Renin converts angiotensinogen to angiotensin I; ACE in lungs converts to angiotensin II; Ang II causes vasoconstriction and stimulates ADH, aldosterone, and thirst; overall increases MAP.

Where is ACE located and what does it do?

ACE is in the lungs; it converts angiotensin I to angiotensin II.

What are the main effects of angiotensin II?

Systemic vasoconstriction; stimulates ADH and aldosterone; stimulates thirst; increases MAP.

What is the role of atrial natriuretic peptide (ANP) in BP regulation?

ANP promotes Na+ and water excretion, reducing blood volume and lowering MAP.

What is the role of ADH (vasopressin) in BP regulation?

ADH increases water reabsorption, increasing blood volume and MAP.

What is the role of aldosterone in BP regulation?

Aldosterone increases Na+ and water reabsorption, increasing blood volume and MAP.

What is erythropoietin (EPO) and how does it affect BP?

EPO increases red blood cell production, raising blood viscosity, which increases TP resistance and MAP.

What is direct renal regulation of MAP?

The kidneys adjust filtration rate to regulate blood volume and MAP; high renal pressure increases filtration and urine output (lowering BP), low renal pressure decreases filtration (conserving volume, stabilizing BP).

What is indirect renal regulation of MAP?

Renin–angiotensin–aldosterone pathway activation by low renal BP leads to Ang II–mediated vasoconstriction and BP increase, plus ADH/aldosterone/thirst responses.