Hemodynamics

Question 1

What happens to pressure as we move through circulation?

Answer 1

It decreases. Biggest drop occurs in arterioles.

Question 2

How do flow, pressure and resistance relate?

Answer 2

Flow = change in hydrostatic pressure / Resistance Q=P/R

Question 3

How does velocity relate to flow and vessel area?

Answer 3

Flow = velocity X cross sectional area

Question 4

Poiseuille’s Equation for Vascular Resistance

Answer 4

Question 5

Blood viscosity increases with…

Answer 5

Increased hematocrit! More force needed to move fluid.

Question 6

Vessel compliance

Answer 6

Compliance = Volume/Pressure

Low compliance: stiff, difficult to fill

High Compliance: loose, easy to fill (veins)

Compliance is like capacitance, the ability for a vessel to store fluid.

Question 7

Flow in series

Answer 7

Q1=Q2=Q3

Flow through aorta = flow through all capillaries = flow through all veins

Question 8

Flow in parallel

Answer 8

Q total = Q1 + Q2 + Q3

Question 9

Resistance in series

Answer 9

R total = R1 + R2 + R3

If one resistance is much greater than other two, the total resistance is effectively that number.

Question 10

Resistance in series

Answer 10

1/Rtotal = 1/R1 + 1/R2 + 1/R3

Overall resistance is less than each individual resistance.

Question 11

Why do capillaries have such low resistance if they have such tiny radii?

Answer 11

Because there are 3 billion of them wired in parallel. The total resistance is less than each individual resistance.

Question 12

Which vascular section presents the greatest resistance?

Answer 12

Arterioles! Greatest pressure drop equals greatest resistance because flow doesn’t change.

Question 13

Is blood flow through capillaries slow or fast?

Answer 13

Because v=Q/A, we’d suspect that the flow would be fast, but not so. It’s very slow. Why? Because need to consider total area, or need to divide flow by three billion.

Question 14

How does the body control blood flow to different organs?

Answer 14

By increasing the resistance in some regions, diverting flow to others. Organs are wired in parallel, so increased resistance at one means reduced resistance at the other!

Question 15

Why do arterioles have such high resistance?

Answer 15

Not due to the presence of smooth muscles, more due to the fact that they’re not much bigger than capillaries, and there aren’t nearly as many.

Question 16

MAP

Answer 16

Mean arterial pressure = Cardiac output x Total peripheral resistance.

This is a causal relationship. Changes in cardiac output and total peripheral resistance cause changes in MAP.

Question 17

MAP relationship to diastolic and systolic BP

Answer 17

MAP = 2/3 DP + 1/3 SP

Because diastole is longer than systole.

Question 18

Baroreceptors

Answer 18

Located in carotid sinus and aortic arch. When they stretch, they send more impulses to the medulla to regulate BP.

Question 19

Three phases of the baroreceptor response

Answer 19

Direct response that changes MAP. The reflex response, which attempts to return MAP to where it was initially. A new steady state is achieved.

Question 20

Direct Response After Hemorrhage

Answer 20

Decreased blood volume leads to reduced ventricular filling. Reduced ventricular filling leads to reduced stroke volume. Reduced stroke volume causes decreased cardiac output, which decreases MAP.

Question 21

Cardiac Output = ?

Answer 21

CO = HR X Stroke Volume

Question 22

The Reflex Response after hemorrhage

Answer 22

Decreased MAP due to decreased cardiac output causes reduced baroreceptor firing to medulla. This causes increased sympathetic output to SA node, ventricles, arterioles, veins, and decreased parasympathetic output to SA node.

Increased sympathetic output to SA node increases HR, to ventricles increases contractility,

Question 23

How does increased sympathetic output and decreased parasympathetic output affect hr on a molecular level?

Answer 23

Increased Symp: Beta adrenergic activation of cAMP which increases If.

Decreased Para: Decreased activation of Ik,Ach by BG subunit of mAChR.

Question 24

How does increased sympathetic output to ventricles increase contractility on a molecular level?

Answer 24

Increased B adrenergic activation causes PKA activation, which P’s phospholamban to increase amount of Ca in SR and which P’s L type Ca channels to increase amount of Ca in cell.

Question 25

How does increased sympathetic output to arterioles increase total peripheral resistance on a molecular level?

Answer 25

Activation of alpha 1 receptors by NE causes the production of IP3, which causes SR Ca2+ release and smooth muscle contraction. This occurs slowly.

Question 26

Venoconstriction

Answer 26

Reduces venous compliance, which increases ventricular filling (preload).

Question 27

Atrial Stretch Receptors

Answer 27

As blood volume increases in atria, they stretch and ANP is released into bloodstream.

Question 28

ANP

Answer 28

Atrial Natriuretic Peptide, which dilates blood vessels to decrease TPR and MAP. Also blocks renal sodium reabsorption to cause increased Na secretion, which will decrease blood volume.

Question 29

Where are central chemoreceptors located? What do they do?

Answer 29

Located in the carotid body and the aortic arch. Respond to decreases in O2. Causes vasoconstriction and increased breathing.

Question 30

Long term regulation of blood pressure

Answer 30

Accomplished by the renin-angiotensin-aldosterone system.

Question 31

RAAS

Answer 31

Decreased pressure in kidneys causes release of renin. Renin cleaves angiotensinogen to angiotensin I, which is cleaved by angiotensin converting enzyme (ACE) to angiotensin II, which causes 1) increased aldosterone, and 2) vasoconstriction.

Increased aldosterone causes Na reabsorption in kidney and increases blood volume.

Question 32

How does AngII cause vaso constriction?

Answer 32

By activating the release of Ca through an IP3 Gq pathway.

Question 33

What are the long term effects of angiotensin II

Answer 33

Can reset baroreceptors. When AngII is present, higher heart rate and higher pressure.