systemic circulation/CV control

pop I exam 2

what is the definition of pulse pressure

difference between systolic and diastolic pressures; felt as a burst of pressure when artery is palpatated

systolic blood pressure represents what component of the cardiac cycle? what factors are important in determining SBP?

represents ventricular contraction; determined largely by ventricular contractility and compliance of large arteries

diastolic BP represents what component of the cardiac cycle? what factors are important in determining DBP?

represents ventricular relaxation; determined by systemic vascular resistance

what are three things that can increase resistance?

vessel length, blood viscosity, vessel radius (most easily changed through constriction/dilation)

what happens to arterial compliance as a vessel is stretched

compliance decreases as the artery is stretched due to volume overload

what happens to arterial compliance in hypertension and aging

heart must work harder, greater change in pressure at a given stroke volume, decreased compliance → increased BP → increased myocardial workload

what happens to stroke volume and pulse pressure as heart rate decreases

SV increases to compensate and pulse pressure goes up (to maintain a consistent MAP and CO)

what happens to MAP, SBP, DBP, and pulse pressure during exercise

SBP increases, DBP decreases, pulse pressure increases, MAP stays constant

what does an increase in SVR do to pulse pressure

decrease aortic outflow → increase aortic volume → decrease aortic compliance → increase pulse pressure

where is most of the blood in the circulatory system? what variable is reflective of this?

venous system; central venous pressure which measures preload/venous return

what does hypovolemia do to HR and what is the effect called

increases HR, decreases SV, CO, and BP; baroreceptor reflex

what does hypervolemia do to HR and what is the effect called

increases HR; bainbridge reflex

as stroke volume increases, what happens to the difference between arterial pressure and venous pressure? what factors create this difference?

the difference between arterial and venous pressure increases (build up in arterial side and drains blood from venous side); CO and compliance/resistance

increasing venous pressure has what effect on cardiac output

increases CO (increase of flow coming into heart)

increasing CO will have what effect on venous pressure

decrease venous pressure (pulling blood out of venous system so less blood=less pressure)

what is the result of the balance between venous pressure and cardiac output

net result is system achieving equilibrium to maintain CO at a given pressure

what is the effect on changing venous tone or volume on cardiac output

increase venous tone/volume → increase pressure → increase CO

decrease venous tone/volume → decrease pressure → decrease CO

changes in SVR will have the greatest effect on CO at what venous pressure

low venous pressure (hypovolemia will decrease CO)

what is the site of regulation of SVR

small arterioles going into capillaries

what three factors regulate blood flow through the capillaries?

precapillary scphincters, resistance of arterioles, resistance of venules (least important)

arteriole tone is a balance between what two hemodynamic components

maintaining BP in the system (before arteriole) and optimizing capillary blood flow (after arteriole)

what doe artiolar dilation do to SVR, capillary hydrostatic pressure, capillary blood flow, and capillary filtration

decrease SVR, increase hydrostatic pressure, increase filtration, increase blood flow

most capillaries in the body are what type

continuous → diffusion bia discontinous tight junctions

what are the other types of capillaries and where are they found

fenestrated (glomerulus), sinusoidal (liver)

what two characteristics of small venules are important to their physiologic function

leaky to allow fluid to return to the venules from interstitial space and highly compliant due to limited smooth muscle

what is the main physiologic effect of venoconstriction

increased venous return to the heart

what is the main physiologic effect of arteriolar constriction

increase SVR → increase MAP

what system serves to drain excess fluid out of the interstitial space

lymphatic system

what physiological processes allow lymphatic fluid to drain back to the heart

valves, contraction of lymph vessels, contraction of surrounding somatic muscles

what three processes occur at the capillary to deliver nutrients

diffusion, filtration, vesicular transport

what factors determine the diffusion of substances across a capillary

concentration differences, wall permeability, rate of flow

what type of substance have diffusion that is affected by blood flow

freely permeable/small, polar molecules

what types of substances have diffusion affected by diffusion rate

larger molecules

what four factors impact net filtration pressure

four starling forces: hydrostatic pressure in capillary, hydrostatic pressure in interstitial fluid, colloid osmotic pressure in capillary, colloid osmotic pressure in interstitial fluid

what direction does the four starling forces move fluid

capillary → interstitial space: capillary hydrostatic and interstitial colloid osmotic

interstitial space → capillary: interstitial hydrostatic and capillary colloid osmotic

at the beginning of the capillary, what force has the greatest impact on net filtration pressure

hydrostatic pressure in the capillary (Pc)

at the end of the capillary, which force has the greatest impact on net filtration pressure

capillary colloid osmotic pressure

which starling force is normally adjusted to effect net filtration pressure? how is it adjusted

capillary hydrostatic pressure; adjusted by arteriole constriction/dilation

what effect would an arteriole dilator have in the capillary

increased flow and increased capillary hydrostatic pressure → increase in net filtration and edema

what would happen if there was an increase in capillary permeability

increase in net filtration and edema

what would happen if there was a decrease in plasma proteins that decrease plasma oncotic pressure

increase net filtration pressure along the entire capillary and lead to edema

what would happen in the capillary if there was fluid overload or a decrease in cardiac output causing fluid to back up into the venules

increase in venous pressure → increase capillary hydrostatic pressure → increase in net filtration and edema

what other factors can cause edema

low plasma protein concentration, arteriolar dilation, venous obstruction, lymphatic obstruction

what is the effect of a sudden increase in pressure at the arteriolar level

increase in calcium via stretch-gated Ca2+ channels → increase vasoconstriction (myogenic response that prevents excess flow with sudden increases in pressure)

what key factors can increase capillary blood flow by decreasing arteriolar constriction

high CO2/H+/adenosine levels, NO, low O2 levels, increased tissue metabolism (hyperemia), decreased organ perfusion (ischemia)

what three organs can autoregulate flow over a range of blood pressures

brain, heart, and kidneys

what happens in brain/heart/kidneys when there is a sudden decrease in pressure? how does this compare to other vascular beds?

arteriole dilation to protect the organs and maintain flow at a consistent rate; other vascular beds are constricting to raise SVR and BP

what is the mechanism of fast/short term regulation of blood pressure

ANS regulates HR and contractility, venous tone, and arterial resistance, and maintains pressure by changing HR, contractility, and peripheral resistance

what is the mechanism of slow/long term regulation of BP

renin-angiotensin-aldosterone regulates water balance, increased sympathetic tone increases renin (beta 1 receptors in kidneys)

what are some ways to sympathetically control BP

constrict/dilate arterioles, constrict/dilate venules, increase/decrease HR and contractility

sympathetic activation has what effect on heart, arterioles, and kidneys

increases HR and contractility, arterial diameter changes, venoconstriction, increase renin release (water retention)

how does epi and norepi differ in their physiological effect

norepi → vasoconstriction (alpha 1)

epi → vasodilation in large muscle groups (beta), predominates in lower doses to decrease SVR

what areas of the brain regulate blood pressure

medulla oblongata (brain stem), nucleus amiguous, rostral ventrolateral nucleus

where are the baroreceptors located that sense changes in pressure?

arterial baroreceptors are located in the aortic arch and carotid bodies

what happens when arterial baroreceptors are activated (stretched)

activate nucleus ambiguous → decrease sympathetic outflow → increase parasympathetic outflow

where are the baroreceptors that sense change in volume located

cardiopulmonary receptors are located in the atria and pulmonary vessels

what happens when there is low stretch for cardiopulmonary baroreceptors

water and sodium retention in the kidneys (holding on to water/salt increases volume!)

what is the result of stimulation of low blood pressure receptors

vasoconstriction and increased cardiac output

what happens to high pressure baroreceptors after several days

receptors become desensitized to higher pressures → can no longer regulate long-term BP, just short-term BP

what causes atrial baroreceptors to be activated and what is the result

type B: fire during atrial filling (causes renal vasodilation/water loss, bainbridge reflex, increased HR), release ANP which causes water/sodium loss

**makes sense bc fire during filling → volume overload → get rid of some volume by losing water and sodium

what are the three chemoreceptors located in the carotid bodies and aorta

high CO2, high H+, low O2 → causes sympathetic stimulation

what is the purpose of proprioceptors

anticipate increased demand and increase HR/CO prior to the actual need (feed forward control)

what happens in a patient with a sudden decrease in cerebral blood flow

cerebral ischemic response → activate vasomotor center → powerful sympathetic response

how do physiological levels of norepi compare to epi in regards to their effects

epi (vasodilation): increase CO, decrease SVR, increase systolic, decrease diastolic, MAP stays the same

norepi (vasoconstriction): CO stays the same, increase SVR/MAP/systolic/diastolic

what is the hemodynamic effect of standing and what is the physiologic response

venous pooling and decreased venous return (orthostatic hypotension); activates SNS and deactivates PNS, activates RAAS to promote sodium and water retention

what is the main purpose of hormonal blood pressure regulation

adjusting sodium and water balance

what hormones are involved and what do they do (hormonal BP regulation)

renin-angiotensin-aldosterone: sodium/water retention

atrial natriuretic peptide (ANP): sodium/water loss

B-type natriuretic peptide: sodium/water loss

epoetin: RBC production

what does an acute increase in BP do to fluid excretion in the kidneys

increased filtration and water loss (pressure diuresis)

artery non-linear compliance

compliance decreases as artery is stretched at high volume/pressure