Cardiology Lecture 3

Front 1

What rate does the SA node fire at if there is no influence from the ANS?

Back 1

90-100 beats per minute.

Front 2

What two mechanisms can the ANS use to change the rate of the SA node?

Back 2

Front 3

What is the mechanism that increases the conduction of the SA node by the SNS (neurotransmitters and receptors)?

Back 3

When Norepi or epi bind to Beta 1 receptors (G coupled protein) second messangers transmit signal ultimately increasing influx of Na & Ca into cells causing depolarization.

Front 4

What is the mechanism that decreases the conduction of the SA node by the PNS (neurotransmitters and receptors)?

Back 4

When Acetylcholine binds to muscarinic receptors (G coupled Protein) on the pacemaker cells triggers the opening of chemically gated K+ ion channels triggering the outward flow causing the membrane to hyperpolarize.

The slope of depolarization also decreases.

Front 5

Does the SNS or PNS affect a more rapid change in HR and why?

Back 5

The PNS- The second messanger system for the PNS is shorter and faster (activates faster), and the deactivation is caused by the breakdown of acetylcholine by plasma cholinesterase. SNS requires re-uptake of norepi.

Beta receptors use cAMP which has multiple steps.

Front 6

What happens when you give atropine to a heart transplant patient?

Back 6

Nothing, the transplanted heart does not have parasympathetic innervation.

Front 7

What happens if you give atropine to a patient with a heart rate of 110 beats per minute?

Back 7

Nothing, there is no PNS stimulation when HR is above 100.

Front 8

What are the factors that can affect HR via the SA node?

Back 8

Front 9

What controls the ANS stimulation of the heart?

Back 9

The ANS receives input from the Cardiovascular Control Center (in the Medula).

Front 10

Where does the Cardiovascular Control center receive input from?

Back 10

-Nuclei of the hypothalamus(emotional, thermoregulation)

-Baroreceptors

-Atrial stretch receptors

-Other Parts of the Brain

Front 11

What is the Bainbridge Reflex?

Back 11

Atrial stretch receptors send impulse to the CV Control center with an increase in venous return stimulating an increase in the HR. (example is with respiration)

Is most apparent with slower heart rates.

Front 12

How does the Bainbridge reflex work regarding the PNS (Vagus nerve stimulation) with respiration?

Back 12

WIth inspiration (more negative chest cavity) increases venous return leads to decreased vagal activity (increased HR)

WIth expiration (more positive chest cavity) decreased venous return leads to increased vagal activity (decreased HR)

Front 13

What are the two mechanisms the heart has to increase the force of contraction ( thus SV)?

Back 13

Frank-Starling Mechanism (preload gives more stretch to line-up crossbridge sites)

Increase Contractility via Sympathetic stimulation (more Ca++ to activate crossbridges)

Front 14

What are the three determinants of stroke volume?

Back 14

Front 15

Back 15

Front 16

What determines the preload of the heart?

Back 16

The End Diastolic Volume.

Front 17

What does the Frank-Starling relationship say?

Back 17

Over a wide range of preloads the ventricles will respond to increased preload by increasing its force of contraction generating a greater SV.

Front 18

Why does the health heart never reach the descending portion of the Frank-Starling Curve (three reasons)?

Back 18

The normal heart will automatically increase SV whenever venous return increases.

Cardiac muscle is stiffer than Skeletal muscle (more resistant to overstretch)

Pericardium resists acute overfilling.

Front 19

Back 19

Increased Preload Pressure Volume Curve

Front 20

Back 20

Increased Contractility Pressure Volume Curve

Front 21

Back 21

Increased Afterload Pressure Volume Curve

Front 22

Why is contraction of the cardiac muscle not maximal when there is no sympathetic stimulation?

Back 22

Without the SNS there is not enough Ca++ to activate all the crossbridge binding sites during Excitation-Coupling Contraction (ECC).

Front 23

How does SNS stimulate stronger contractions?

Back 23

Front 24

What is protein Kinase?

Back 24

PK is an intracellular enzyme that phosphorylates one or more intracellular proteins, changing their activity.

Front 25

How do Phosphodiesterase Inhibitors (PDEs) increase contractility?

Back 25

Terminate cAMP activity preventing the activation of Protein Kinase which increases the reabsorption of Ca++ into the SR.

Front 26

How do Cardiac Glycosides increase contractility?

Back 26

They decrease the activity of the Na+/K+ pump increasing Intracellular Na+ levels.

This impares the secondary active transport of Ca++ out of the cell in exchange for Na+

The extra intracellular Ca++ is then absorbed into the Sarcoplasmic Reticulum.

Front 27

Back 27

Front 28

Do Beta 1 Blockers affect contractility at rest?

Back 28

Not much, Beta 1 blockers affect on contractility is a function of how much sympathetic stimulus there is to block and at rest there is not much SNS stimulation.

Front 29

What would happen to the position of the Ventricular Function Curve (Frank-starling Curve) if a Ca++ channel blocker is given?

Back 29

At any given preload there would be a weaker contraction, SV would go down

The curve would shift down and to the right

Front 30

What happens to the VFC with sympathetic stimulation?

Back 30

Front 31

What is afterload?

Back 31

The amount of pressure the Ventricles must overcome before they can push open the semilunar valves & eject blood.

Front 32

What happens to the isometric phase of contraction as afterload increases?

Back 32

It becomes longer as well.

Front 33

Back 33

Front 34

Describe the Histology of arteries and veins.

Back 34

Front 35

What type of innervation do vascular smooth muscle (VSM) receive?

Back 35

Most receive only SNS stimulation, relatively few VSM receive dual innervation.

Front 36

What is the formula for flow?

Back 36

Front 37

What three factors affect resistance to flow and which is the most important?

Back 37

Viscosity of blood-Hematocrit

Vessel length

Radius of the vessel-Greatest effect R=1/r to the Fourth power

Front 38

What is Vascular Compliance?

Back 38

Front 39

How does SNS affect vascular compliance?

Back 39

Front 40

How is total blood volume (TBV) distributed at rest?

Back 40

Front 41

Which part of the vascular system offers the largest pressure drop?

Back 41

Arterioles, they are the main contributor to SVR.

Front 42

How does the vascular system optimize gas exchange in the capillaries?

Back 42

They have the largest cross-sectional area which causes the blood to have the slowest velocity allowing more time for gas exchange.

Front 43

What are the two primary functions of the systemic arteries?

Back 43

Provide rapid transit, low resistance passageway from the heart to the tissue

Serve as a pressure reservoirs to ensure continuous perfusion throughout the cardiac cycle.

Front 44

Back 44

Front 45

Why not just average systolic and diastolic pressures when calculating MAP instead of the formula?

MAP= DBP+1/3(SBP-DBP)

Back 45

More time is spent in diastole than systole.

Front 46

Where does the arteries branch into arterioles?

Back 46

within an organ.

Front 47

What is the function of arterioles?

Back 47

to function as a stopcock, regulating tissue blood flow and also SVR.

Front 48

What are some chemicals that affect arteriole smooth muscle?

Back 48

Norepinephrine

Epinephrine

Vasopressin

Angiotensin II

Nitric Oxide and ANP

Front 49

What controls Arteriolar smooth muscle?

Back 49

1. Local metabolic factors to match blood flow to metabolic needs (produces vasodilation)

2. Extrinsic Factors-SNS and hormones (Mostly Vasoconstriction)

3. Inflammatory/tissue damage factors (mostly Vasodilators)

Front 50

What is active Hyperemia?

Back 50

Increased blood flow related to metabolic needs.

Allows the tissue to auto-regulate blood flow according to needs

Front 51

What local metabolic ISF levels would cause vasodilation?

Back 51

Decreased Oxygen

Increased Carbon Dioxide

Increased Hydrogen ions

Increased Potassium

Increased Osmolarity

Increased Adenosine

Increased Temperature

Front 52

What is pressure/flow auto-regulation?

Back 52

With an increased perfusion pressure there is a big increase in flow (independent of metabolic changes)

Eventually flow decreases back to control value

Believed to be a myogenic response (passive stretch)

Front 53

What factors affect Extrinsic Control of arteriolar radius?

Back 53

Front 54

When local factors are conflicting with sympathetic or hormonal factors which one has a greater effect?

Back 54

Coronary and skeletal muscle vessels- local overrides extrinsic

Everywhere else-Extrinsic overrides local

Front 55

Where do the preganglionic sympathetic neurons originate from?

Back 55

Lateral horn of the spinal cord gray matter from T1-upper lumbar segments.

Inputs to the CV control center come from the cortex, thermoregulatory center of the hypothalamus, and baroreceptors.