Control Of Arterial And Peripheral Resistance

Front 1

Describe how pulse pressure is determined by SV and arterial compliance.

Back 1

Pulse pressure is defined as the difference between systolic and diastolic pressure. Pressure is related to SV and arterial compliance by the equation: compliance = change in volume/change in pressure

However, pulse pressure is calculated as the following:

Pulse P = 0.75 x SV / Compliance

The numerator reflects the assumption that arterial volume will increase by 75% of the SV during the transition from diastole to systole. The 0.75 factor also takes in account the length of the rapid ejection phase, in addition to the decrease in arterial volume attributable to flow into the arterioles (peripheral runoff)

Front 2

Describe how mean arterial pressure is determined by CO and TPR

Back 2

Remember that flow = pressure/resistance

Flow = CO
Pressure = mean arterial pressure (we neglect the contribution of the atrial pressure bc it's so small)
TPR = resistance

Thus, mean arterial pressure = CO x TPR

It can also be calculated by integrating the area under the arterial pressure vs. time curve

Front 3

Describe the factors that determine the resistance to flow in a blood vessel

Back 3

Poiseuille's Law
Resistance = 8nl/r^4

n = viscosity, mainly determined by hematocrit

l = length

r = radius

Front 4

Describe the differences between parallel and series resistance elements when applied to the vascular system.

Back 4

Parallel resistance: 1/Rtotal = 1/R1 + 1/R2 + 1/R3 + ...

You can sum the individual flows through each parallel resistance elements to calculate total flow within that parallel element (see resistance element)

Driving pressure (delta P) across a single resistance element is equivalent to the driving pressure experienced across all the parallel resistance elements

Resistance of each channel is given by the equation: R = delta P / Q

CO will increase if augmented blood flow is required. Reflexes keep the arterial pressure constant, maintaining the driving pressure across each parallel channel.

Total resistance decreases, encouraging greater blood flow. Each organ modulates its resistance to meter blood flow appropriate for its metabolic needs

Hint 4

Series resistance: Rtotal = R1 +R2 + R3 + ...

Resistances in series are additive; therefore, a change in one resistance alters the total resistance of all elements in series.

The new total blood flow is calculated using the updated total resistance in the equation: Q = delta P / R

This flow is constant across all resistance elements in series. Use the same equation to calculate the pressure change across each element.

Hypothetically, an increase in resistance in one arterial segment (ie artherosclerosed artery) causes a decrease in the blood flow to that segment and the others in series with it.

In reality, the body maintains normal tissue resistance by decreasing the resistance of the arterioles.

Arterial pressure upstream of the atherosclerosis does not increase because the normal mean arterial pressure is maintained by reflexes.

Front 5

Define the difference between local and systemic control of arteriolar resistance.

Back 5

Local Control:

Autoregulation: vascular bed is able to maintain constant blood flow even when arterial pressure changes

Metabolic regulation: depending on local cellular need of nutrients, arteriolar resistance can be increased or decreased in order to bring the right amount of nutrients. (not fully understood)

Endothelial messengers: messengers such as NO for relaxatio and endothelin for constriction are used by the endothelial cells of blood vessels to help determine the arteriolar flow/resistance needed at a specific point in time. An example would be the use of NO during injury which allows more blood flow to the area to increase an immunological response

Hint 5

Systemic Control is mediated by the ANS

SANS vs. PANS: SANS is the main controller of arteriolar resistance due to NE neuronal release stimulating G proteins that causes smooth muscle contractions. Some PANS innervation can occur, but the mechanism is unknown. Just focus on SANS innervation for systemic control

Hormonal Control: release of Epi and NE causes vasoconstriction in some vascular smooth muscle. Concurrently, Epi causes vasodilatio in some vascular beds (ie skeletal muscle)

Arterial Baroreceptors: stretch receptors in the carotid arteries and aortic arch measure BP and the CNS adjusts CO via the heart to maintain systemic BP

Front 6

Describe how autoregulation and metabolic regulation can adjust local arteriolar flow.

Back 6

see block guide for graphs

Autoregulation: when arterial pressure changes, local resistance changes to maintain constant blood flow

Mechanism: myogenic regulation --> wall stress increases Ca2+ concentration

Hint 6

Metabolic Regulation: local arteriolar resistance is controlled by local metabolic activity

increased metabolic activity --> arteriole dilation --> increased local blood flow --> More O2 and nutrients for tissue

Mechanism: metabolic substrates or waste products act as local messengers to control smooth muscle contraction (ie adenine, CO2, H+, all accumulate in active tissue and trigger relaxation

long-term metabolic regulation --> angiogenesis

Front 7

List the effects of sympathetic and parasympathetic nervous system on arteriolar resistance

Back 7

sympathetic: majority of arterioles are controlled via postganglionic nerves of the SANS. The release of NE acts on alpha-adrenoreceptors which in turn releases IP3 from the cellular membrane, causing intracellular Ca2+ to increase and contraction of smooth muscle to occur.

parasympathetic: has little importance for control of arterioles. Some mechanisms include the release of ACh and NO which cause dilation. These mechanisms are not quite understood.

Front 8

List the adrenoreceptor subtypes that control vascular resistance and heart function.

Back 8

alpha-1: vascular smooth muscle (constriction); heart (increased contraction)

alpha-2: postsynaptic adrenoreceptors (inhibits NT release)

beta-1: heart muscle (increased contraction and heart rate)

beta-2: vascular smooth muscle (vasodilation)

Front 9

Describe the location and response characteristics of the arterial baroreceptors

Back 9

see block guide for pictures:

The baroreceptors are in the aortic arch and the carotid bodies in the carotid arteries (near the bifurcation of the internal and external carotids). These stretch receptors respond to high or low pressures by activating the CNS, which respond by increasing or decreasing CO to keep blood pressure stable.

Front 10

Describe the baroreflex mechanisms that adjust CV characteristics in response to changes in arterial pressure

Back 10

If the baroreceptors sense an elevated blood pressure, then signals will be sent to the medullary control centers to decease SANS output. Thus, you will lose contractility and decrease HR. You will also induce vasodilation and increase venous capacitance. The opposite effect occurs when lower BP is detected.

Front 11

Define the role of chemoreceptors in cardiovascular control.

Back 11

Chemoreceptors are located in the same area as baroreceptors Chemoreceptors are responsible for monitoring the O2 and CO2 levels in the blood. When the receptors detect high CO2 or low O2, SANS is activated to cause VASOCONSTRICTION throughout the body. This way, the blood can be diverted to the heart and brain and can continue to receive the scarce oxygen.

This action also reduces HR (maybe bc of decrease in metabolic demand?) to decrease O2 need. But breathing rate is increased to get more O2 into the body and more CO2 out.