cardiac part 2

Question 1

roles of nervous regulation of arterial pressure

Answer 1

Redistributes blood flow to different areas of the body, affects pumping activity of the heart, contributes to the rapid control of systemic arterial pressure

Acts as a nervous reflex, important in minute to minute variation in blood pressure, it is not effective for long term pressure regulation

Question 2

Baroreceptors

Answer 2

They are stretch receptors that sense BP changes from running, standing etc.

Aortic Arch Baroreceptors: afferent signals through Vagus nerve

Carotid sinus receptors: branch point of internal and external carotid arteries, they carry afferent signals through the glossopharyngeal nerves

have an increase in activity when stretched, slight changes in pressure can cause significant changes in signaling to the brain, sigmoidal bc they change firing rate in relation to small changes around normal BP

Baroreceptors act as pressure Buffers and reduce extreme changes in arterial pressure

Question 3

Response to Baroreceptor input

Answer 3

high baroreceptor activity-> decreased sympathetic activity-> decreased BP

Low baroreceptor activity-> increased sympathetic activity-> increased HR and contractility

Question 4

Basal Vasoconstrictor tone

Answer 4

Sympathetic vasoconstrictor tone normally maintains a partial state of contraction of the blood vessels (as evident by when you have total anesthesia your arterial pressure drops and when you inject Noreprinephrine it skyrockets)

Question 5

Effects of sympathetic stimulation

Answer 5

Arterioles constrict -> increased total peripheral resistance (decreased blood flow through tissues)

Veins constrict-> increased venous return (increased cardiac output)

Stimulate heart-> increased contractility and increased HR

Question 6

Effects of parasympathetic stimulation

Answer 6

Heart
Sa node: decreased heart rate
Myocardium: slight decrease in contractility

but the major way to decrease heart contractility is to remove sympathetic stimulation

Question 7

Redistribution of blood flow

Answer 7

Vasoconstrictor effect is especially powerful in kidneys, spleen, intestines and skin

The effect is less potent in skeletal muscle and brain

Question 8

Why does blood pressure increase after clamping the carotid arteries

Answer 8

Creates a large resistance at clamp, that causes pressure drop, the baroreceptors sense a low pressure, and sympathetic activation then increases BP

Question 9

Cardiac output

Answer 9

Quantitiy of blood pumped into aorta each minute by the heart

Primarily controlled by venous return to the heart, affected by peripheral circulation- Frank Starling mechanism: heart is normally able to pump whatever blood flows into the right atrium (increased stretch causes increased force of contraction

Cardiac output regulation is the sum of all local blood flow regulations, venous return is the sum of all local blood flow to individual segments (all blood thats pumped out of the heart, will come back in venous return and directly affect cardiac output)

it is synonymous with oxygen consumption (see Study guide) as oxygen consumption goes up so does cardiac output and venous return

Question 10

Cardiac output vs TPR

Answer 10

Long term cardiac out put is inversely related to total peripheral presistance as long as arterial pressure is unchanged

CO= Arterial pressure / TPR

See guide

If you increase TPR, in order to keep arterial pressure constant, you must decrease cardiac output

if you decrease TPR, in order to keep arterial pressure constant, you must increase cardiac output

Question 11

Cardiac output curves

Answer 11

Hypereffective heart: CO increased due to sympathetic stimulation and parasympathetic inhibition (which causes the heart rate to go up and the contractility to go up)
Hypertrophy -> increased contractile strength

hypoeffective heart: CO decreased could be due to increased arterial pressure (which causes an increase in afterload causing an early shut off of aortic valve), inhibition of nervous excitation of nodes, or coronary artery blockage–> cardiac hypoxia

Question 12

Cardaic output and intrapleural pressure

Answer 12

Increasing intrapleural pressure, causes an increase in RAP to allow for the same amount of Cardiac output. Cardiac Tamponade will cause a lower slope of the curve because at higher pressures it has to work harder than at lower pressures

intrapleural pressure, pressure in chest

Normal external pressure is equal to normal intrapleural pressure, but if you increase the the intrapleural pressure you need the right atrial pressure to go up to push the blood harder against the increased pressure)

Cardiac tamponade happens when theres blood leaking in the pericardial space, pushes against the hear in contraction.

Question 13

Venous Return

Answer 13

Psf-RAP= VR (venous return) x RVR (RVresistance)

Systemic Filling Pressure: Psf is the pressure in the veins that is pushing blood in the RA (RAP)

When Psf=RAP there is no blood flow (there is no venous return)

As RAP decreases there is a larger difference in the pressure gradient between RAP and Psf and causes an increase in the blood flow (more blood goes from a high pressure to low pressure system)

At very low RAPs, the veins collapse to a certain point where there is no Venous Return

Question 14

Effects on Venous Return

Answer 14

Systemic Filling pressure (Psf) increases with:

• Increased blood volume (stretches the walls of the vasculature)
• Sympathetic stimulation (capacity of system decreases so the filing pressure increases)

Question 15

Things that Change cardiac output/venous return

Answer 15

Cardiac contractility: changes only the slope of the CO curve, leads to more VR if contractility goes up

Arterial resistance changes both slope of VR and CO

Venous comliance and blood volume change the Mean systemic volume

Question 16

Fick principle for determining cardiac output

Answer 16

CO= O2 consumption/ (o2 in arterial blood- o2 in venous blood)

CO= Stroke volume x Heart rate

Question 17

AV fistula effects on venous return and cardiac output

Answer 17

1. Decrease resistance to venous return leads to an increase in venous return, increase CO (due to decrease in after load)
2. Baroreceptors sense a decrease in Arterial pressure, so sympathetic constriction of veins and arteries which increases Psf/ MSV, sympathetic stimulation of heart causes increase in CO
3. Long term, kidneys cause salt and water retention due to decrease in arterial pressure and increased sympathetic activity, hypertrophy of heart causes a larger increase in CO

Question 18

Effect of infusion on CO and Arterial Pressure

Answer 18

Infusion of Blood increases arterial pressure, resulting in an increase in urinary output to decrease arterial pressure

Question 19

Feedback mechanism of kidney on arterial pressure

Answer 19

as arterial pressure is increased, renal output of water and salt are also increased to reduce the amount of fluid in the CV system

Increase in extracellular fluid volume -> increase in blood -> increase in mean circulatory filling pressure-> increase in venous return of blood to the heart -> increased cardiac output-> increase in TPR (arterioles constrict to reduce unneccary perfusion ie autoregulation) -> increased urine out put

Question 20

Renin-Angiotensin System

Answer 20

When theres a decrease in arterial pressure, Renin (enzyme) is released that aids in the conversion of Angiotensin 1 (inactive)–> Angiotensin 2 (active)

ACE (angiotensin converting enzyme) is a catalyst in the lung that converts ANG1–> ANG2

Angiotensin 2: stimulates and secretes aldosterone (Na reabsorption, to increase Na and Water retention), increases thirst, causes extreme vasoconstrictions of the arterioles, increasing TPR and arterial pressure

Question 21

Regulation with increased Salt intake

Answer 21

Increase salt intake-> increased extracellular volume-> increase in arterial pressure-> decreases renin and angiotensin system-> decreased renal retention of salt and water-> return of extracellular volume to nomal -> return to normal arterial pressure

Question 22

One kidney Goldblatt hypertension

Answer 22

Kidney senses low blood pressure, and secretes large quatities of renin, immediate increase in pressure due to Ang2 vasoconstriction, long term increase due to retention of salt and water

Question 23

Volume loading hypertension

Answer 23

Decrease renal mass (chop out parts of kidney)

Increase salt and water intake

Acute response: increase in extracellular volume, increased blood Volume, increased CO

Acute responses will go down to normal after a while

Initially, there is a decrease in total peripheral resistance due to baroreceptors, baroreceptors will adapt after 2 days and arterial pressure will begin to rise more slowly (due to increased cardiac output)

Prolonged changed: increase in TPR and decreased cardiac output (autoregulation)