3-1: 8/23: Regulation And Control Of Arterial Pressure

Front 1

Pressure in elastic or conducting arteries must be held at _______.

Back 1

100mmHg

Front 2

Local control of pressure at tissue/organs occurs at the level of this blood vessel.

Back 2

Arteriole

Front 3

Formula for arterial pressure

Back 3

Arterial Pressure = Cardiac Output x Total Peripheral Resistance

(TPR)

Front 4

What mechanisms for maintaining arterial blood pressure kick in first after a sudden change in pressure?

Back 4

Those under neural control (baroreceptors, ischemic receptors, chemoreceptors)

(NEURAL CONTROL = AUTONOMIC NERVOUS SYSTEM)

Front 5

What neural mechanisms are most effective at responding to changes in blood pressure?

Back 5

CNS Ischemic>Baroreceptors>Chemoreceptors

Front 6

Through what effects does the autonomic nervous system maintain arterial blood pressure?

Back 6

Heart rate, contractility (cardiac output), vasomotor tone, venous compliance (TPR)

Front 7

How do the hormonal reponses to change in blood pressure compare to neural controls in terms of time? In terms of effect?

What is the main hormonal control?

Back 7

Hormonal control is much slower than neural response, takes hours to days

Effect is HUGE!!! bc there is modification of blood volume

Main control is Renin-Ag-Aldosterone system

Front 8

What does the Frank-Starling relatinoship state?

Back 8

Cardiac Output = Venous Return

Front 9

How does the length-tension relationship of cardiac muscle relate to the Frank-Starling relationship?

Back 9

The more stretch to cardiac muscle, the more forcefully it will contract. So if you increase cardiac output, heart will contract more forcefully (increased volume = increased stretch)

Front 10

There is a strong correlation between Ventricular End Diastolic Volume and _____________.

Back 10

Right Atrial Pressure
Venous Return

Front 11

As you increase pre-load, you increase _______.

Back 11

Stroke Volume

Front 12

As right atrial pressure increases, cardiac output ______.

Back 12

Increases (Frank-Starling relationship)

Front 13

What is average venous pressure?

Back 13

5-10 mmHg

Front 14

As right atrial pressure increases, venous return ______.

Back 14

Decreases

Front 15

As right atrial pressure decreases, venous return ______.

Back 15

Increases UNTIL negative pressure is reached because that's when veins collapse.

Front 16

Cardiac function curve vs Vascular function curve:
Axis Labeling
Point of Intersection


Why would changing either curve affect cardiac output?

Back 16

Cardiac Function:
Cardiac Output vs Right Atrial Pressure

Vascular Function:
Venous Return vs Right Atrial Pressure

Where the two intersect is the steady-state operating point

Changing either curve will change the point of intersection and thus change cardiac output

Front 17

What is a positive inotropic effect and how is it achieved? How would the Frank-Starling Curve appear?

Back 17

Positive ionotropic effect:
Increased contractility results in increased cardiac output (heart beats more forcefully)

So at a given atrial pressure, cardiac output is greater

Would cause Frank-Starling curve to move up and to the left

Front 18

How can contractility be increased?

Back 18

Sympathetic Stimulation
Sympathomimetic Drugs
Antimuscarinic Drugs (block Parasymp NS by blocking muscarinic receptors where ACh binds)

Front 19

What is a negative inotropic effect and how is it achieved? How would the Frank-Starling Curve appear?

Back 19

Negative inotropic effect:
Decreased contractility results in decreased cardiac output for a given Right Atrial Pressure

Curve would be lower and to the right

Front 20

How can contractility be decreased?

Back 20

Parasymp Stim
Parasympathomimetic Drugs
Sympatholytic Drugs (alpha, beta blockers to block Symp NS)

Front 21

Unstressed volume is blood volume in ______

Back 21

Veins

Front 22

Stressed volume is blood volume in ________

Back 22

Arteries

Front 23

What is the effect of increased blood volume on the venous return curve?

How could this be achieved?

Back 23

Increasing blood volume will increase venous return at lower Right Atrial pressures

Achieved by blood infusion

Front 24

What is the effect of decreased blood volume on the venous return curve?

How could this be achieved?

Back 24

Decreased cardiac output/venous return at given right atrial pressures

Achieved by hemorrhage

Front 25

Through what mechanism are stressed and unstressed volumes redistributed (from one to the other)?

Back 25

Via changes in venous compliance

Front 26

What is circulatory shock?

Back 26

Insufficient perfusion of tissues (inadequate tissue levels of O2)

Front 27

Causes of hypovolemic circulatory shock.

Back 27

Bleeding
Burns

Front 28

Causes of distributive circulatory shock.

Back 28

Septic, anaphylactic (plasma spilled into extra cellular space), neurogenic shock (lose vasomotor tone, veins hold more of blood volume)

Front 29

Causes of obstructive circulatory shock.

Back 29

Tamponade (fluid accumulates in pericardium)
Tension pneumo (air pushign on heart, not allowing it to fill with blod)
Pulmonary embolism

Front 30

Causes of cardiogenic circulatory shock.

Back 30

MI
Arrythmia
CHF

Front 31

What is the effect of increasing total peripheral resistance on cardiac function and venous return curves?

What effect would this have on afterload?

Back 31

Increased TPR:
Cardiac function:
Decreased cardiac output at given atrial pressure

Venous return:
Decreased venous return at given pressure

Inc'd TPR-->Inc BP, Inc Afterload (harder for heart to push), Dec Cardiac Output

Front 32

What is the effect of decreasing total peripheral resistance on cardiac function and venous return curves?

Back 32

Decreased TPR:
Cardiac Function:
Increased cardiac output at given R atrial Pressure

Venous Return:
Increased venous return at given R atrial pressure

Dec'd TPR-->Dec BP, Dec Afterload (easier for heart to push), Inc Cardiac Output

Front 33

What do baroreceptors detect? Where are they located?

Describe events of baroreceptor reflex. List neurotransmitters and receptors involved.

Back 33

Detect stress (more stress-->higher pressure-->more signals fired to medulla)

Located in Carotid Sinus and Aorta

Carotid Sinus-->CN IX (Glossopharyngeal)-->Nucleus Solitarius of Medulla

Aortic Arch-->CN X (Vagus)-->Nucleus Solitarius of Vagus

Medulla-->
Parasymp (Cardiac decelerator)--Cholinergic (ACh)
-->SA Node (Muscarinic receptors--slow down heart rate)

Medulla-->
Symp: Cardiac Accelerator, Adrenergic (NE, Epi)
-->SA node (increase heart rate at adrenoreceptors)
-->Contractility (at level of myocardium; increased via adrenoreceptors)


Symp: Vasoconstrictor, Adrenergic (NE, Epi)
-->Arterioles, Veins (increase tone via adrenoreceptors)

IMPORTANT: There is interaction between symp and psymp NS's via RECIPROCAL INHIBITION

Front 34

Where are O2 receptors located? What do they respond to?

Back 34

In Carotid Body, aortic arch

Control breathing in reasponse to low CO2 (high CO2, low pH), blood flor redirected to lungs via aterial vasoconstriction

Front 35

What is the CNS ischemic response?

Back 35

Chemoreceptors in medulla detect increased CO2, dec'd pH causes intense vasoconstriction in non-brain vascular beds to redirect blood to head

Front 36

Where are cardiopulmonary baroreceptors located? Response?

Back 36

In low pressure systems (veins, atria, pulmonary arteries); inc'd BP (volume) activates mechanism to reduce BP

Front 37

Which neural response involves the release of atrial natriuretic peptide?

Back 37

Cardiopulmonarhy baroreceptors (increases Na+ and H2O excretion from kidney)

Front 38

___________ is due mainly to passive properties of blood vessel structure.

Back 38

Stress relaxation and capillary fluid shift

Front 39

Describe hormonal control by the reinin-Ag system.

Back 39

Dec'd BP detected by mechanoreceptors in afferent arterioles of kidney

Prorenin-->Renin in Kidney

Renin released into blood

Renin: Angiotensinogen-->AgI

In lungs and kidneys: Ag1-->Ag2 via ACE

AgII acts on hthal, adrenal cortex, vasc smooth muscle, and kidneys to
increase thirst and secretion of ADH (hthal)
release aldosterone (adrenal cortex)
contract smooth muscle in arterioles to increase TPR (vasc smooth muscle)
Increase Na resorption and H2O resorption (water follows--occurs in kidneys)