Cardiovascular System

Question 1

Define the role of the cardiovascular system in overall body homeostasis.

Answer 1

Transport
Needed things to the tissues
Nutrients
Oxygen
Enzymes
Waste products away from the tissues
Hormones for signaling

Question 2

Describe the pathway of blood flow through the heart.

Answer 2

Blood is returned to the heart by the superior and interior vena cavas and enters the right atrium.Blood then passes through the right AV valve and into the right ventricle . Upon contraction blood passes through the pulmonary valve and into the pulmonary artery, where it is distributed to the lungs and oxygenated. Blood travels from the lungs to the pulmonary veins and into the left atrium . Passing through the mitral valve , blood then
enters the left ventricle .
Upon contraction blood passes through the aortic valve, into the aorta Which
distributes blood to the body.

Question 3

Contractile cells

Answer 3

receive signals from the electrical pathway of the heart or a nearby cell and immediately depolarize by opening VG Na+ channels.
Once depolarized to ~ 120mV , Na+ channels close and K+ channels open, repolarizing the cell . A plateau occurs in repolarization, however, because L-type Ca+ channels open and cause calcium entry , canceling out the potential difference of K+ exit. Ca++ do close while K+ stay open , causing repolarization back to RMP

Question 4

Autorhythmic cells

Answer 4

have an unstable RMP due to leaky Na+ channels on their membranes that remain open after repolarization. The upward slope of the RMP triggers VG t-type Ca++ channels to open , bringing the cell to threshold .This voltage changes causes
the opening of L-type Ca+ channels , depolarizing the cell . When the L-type channels close , K+ channels open and repolarize the cell.

Question 5

Compare and contrast the action potential of contractile (fast-response) and auto-rhythmic (slow-response) cardiac cells.

Answer 5

Contractile cells receive signals from the electrical pathway of the heart or a nearby cell and immediately depolarize by opening VG Na+ channels. Once depolarized to ~ 120mV , Na+ channels close and K+ channels open, repolarizing the cell . A plateau occurs in repolarization, however, because L-type Ca+ channels open and cause calcium entry , canceling out the potential difference of K+ exit. Ca++ do close while K+ stay open , causing repolarization back to RMP

Autorhythmic cells have an unstable RMP due to leaky Na+ channels on their membranes that remain open after repolarization. The upward slope of the RMP triggers VG t-type Ca++ channels to open , bringing the cell to threshold .This voltage changes causes the opening of L-type Ca+ channels , depolarizing the cell . When the L-type channels close , K+ channels open and repolarize the cell.

Question 6

Define pacemaker potential & describe basis for rhythmic electrical activity of cardiac cells.

Answer 6

pacemaker potential : the depolarization to threshold created by the SA node

the mechanism for autorhythmic cells

Question 7

Cardiac muscle

Answer 7

stimulated by AP on SA node or neighboring cell
uses gap junctions
Ca++ induced Ca++ release
Ca++ binds to troponin

Question 8

Skeletal

Answer 8

stimulated by AP from somatic motor neuron
no gap junctions (each muscle fiber has a NMJ)
depolarization triggers Ca++ release
Ca++ binds to troponin

Question 9

Compare and contrast excitation-contraction coupling in cardiac muscle to that of skeletal muscle.

Answer 9

Cardiac
- Stimulated by action potential on SA node or neighboring cell
- Uses gap junction
- Ca++ induced Ca++ released
- Ca++ binds to troponin

Skeletal
- stimulated by AP from somatic motor neuron
no gap junctions (each muscle fiber has a NMJ)
depolarization triggers Ca++ release
Ca++ binds to troponin

Question 10

Describe gap junctions and their role in cardiac excitation.

Answer 10

Gap junctions connect cardiac cells and electrical signals pass through them. This allows cardiac muscle to contract
as one unit

Question 11

SA Node

Answer 11

Located in right atrium
Acts as pacemaker
Leaky Na+ channels
Membrane potential goes down to ~ -55mv
When membrane potential reaches -40 mV, slow Ca++ channels open, causing action potential
After 100-150 ms, Ca++ channels close and K+ channels open more, thus returning membrane potential to -55mV

Question 12

SA Node as Pacemaker

Answer 12

Under normal conditions, SA node is the pacemaker
SA node depolarizes at rate of 70-80/min
AV node: 40-60/min
Purkinje fibers: 15-40/min

Question 13

Internodal Pathways

Answer 13

Carry signal from SA node to AV node

Question 14

AV Node

Answer 14

Transfers electrical signal from atria to ventricles
Delays impulse
This allows atria to fully contract before ventricles contract
AV Node delay: 0.09 sec
AV Bundle delay: 0.04 sec

Question 15

AV Bundle/Bundle of His

Answer 15

Transfers signal from atria to ventricles
Branches into left and right branches that carry signal down septum to apex

Question 16

Purkinje Fibers

Answer 16

Carry signal throughout ventricle walls
Rapid conduction, due to prevalence of gap junctions

Question 17

Describe the normal electrical pathway through the heart.

Answer 17

I. The SA node fires an AP after leaky Nat channels bring the membrane to threshold , opening L-type Ca++ channels (Repolarization is when Na+ channels close and K+ channels open which allows atrial contraction)
2. Intermodal Allows for fibers to carry signals from SA to AV node
3. After a slight delay , the AV node depolarizes and spreads to
4. AV bundle / Bundle of His
5. Bundle branches down septum
6. Purkinje fibers spread up ventricles, depolarizing and allowing a bottom - up contraction.

Question 18

Systole

Answer 18

contraction

Question 19

Diastole

Answer 19

relaxation

Question 20

Cardiac cycle involves changes in

Answer 20

Electrical activity (ECG)
Volume
Pressure

Question 21

Stroke Volume (SV)

Answer 21

amount of blood expelled from one ventricle during one cardiac cycle
SV = EDV-ESV mL

Question 22

Cardiac Output (CO)

Answer 22

Amount of blood pumped by one ventricle in a given time period
CO = SV X HR mL/min

Question 23

Ejection Fraction

Answer 23

the percent of blood in the ventricle that is pumped out in one beat
EF =SV/EDV

Question 24

Define stroke volume , cardiac output , and ejection fraction

Answer 24

stroke Volume is the amount of blood pumped out of one ventricle during one cardiac cycle
SV= EDV - ESV (mL)

Cardiac Output is the amount of blood pumped out of one ventricle in a given time period
CO = SV x HR (mL/min or L/min)

Ejection Fraction is the percent of blood in the ventricle that is pumped out in one beat
EF =SV/EDV

Question 25

Cardiac Force

Answer 25

Muscle tension
depends on Myosin/actin cross-bridge cycling

Question 26

Cardiac Contractility

Answer 26

Intrinsic ability of heart to generate force
Due to Ca++-troponin binding (allowing crossbridges)
Ca++ levels In SR
Entering from ECF
L-type Ca++ channel phosphorylation state
Phospholambin phosphorylation state
Increases Ca++-ATPase on SR
Sympathetic system
β1 receptors lead to increased cAMP, PKA, and phosphorylation of phospholambin

Question 27

Preload

Answer 27

Load a muscle is subjected to before contraction
Degree of myocardial stretch before contraction
Due to venous return
Frank-Starling Law

Question 28

Afterload

Answer 28

Load a muscle encounters during shortening
Due to arterial pressure

Question 29

Define force/tension, contractility, preload and afterload; give the affects of preload and afterload on tension development, shortening capabilities, contractility, stroke volume, and the pressure-volume relationship.

Answer 29

Cardiac force is the tension of cardiac muscle due to crossbridge cycling.
Contractility is the ability of the heart to generate force
Preload is the load a muscle is subjected to before contraction the degree of stretch before a contraction , due to venous return
Afterload is the load a muscle is subjected to during contraction
↳ due to arterial pressure

Question 30

Explain the length tension relationship in cardiac muscle

Answer 30

As length decreases , tension development increases until no more crossbridges can form
As length increases , tension development decreases until no more crossbridges can form

Question 31

Frank-Starling Law

Answer 31

Increased EDV causes increased SV (all other factors remaining unchanged)
Increased EDV
Venous return
Sympathetic innervation of veins
Respiratory pump
Skeletal muscle pump
Heart will pump all blood that comes into it
Extra blood into it creates extra stretch
Extra stretch results in more force

Question 32

State & explain the importance of the relationship between ventricular filling and cardiac output (Starling’s Law).

Answer 32

An increased EDV causes increased SV , which increases CO due to the “extra” blood in the heart. The heart will have increased
stretch , resulting in more force until all of the extra blood is pumped out.
Due to increased Venous return
↳ caused by
① sympathetic vasoconstriction : causes venous blood to travel to heart
② respiratory pressures : a increase in thoracic pressure encourages venous return
③the skeletal muscle pump : muscle squeezes blood up vein , which cannot go back down due to valves

Question 33

Venous return depends on

Answer 33

Sympathetic innervation of veins - causes venous blood to travel to heart
Respiratory pump- a increase in thoracic pressure encourages venous return
Skeletal muscle pump- muscle squeezes blood up vein , which cannot go back down due to valves

Question 34

What would happen to SV if you increase contractility?

Answer 34

Increase due to decrease in ESV

Question 35

What would happen to SV if you increase pre-load?

Answer 35

Increase due to increase in EDV

Question 36

What would happen to SV if you increase afterload?

Answer 36

Decrease due to increase in ESV

Question 37

Explain the differences between pressures in left and right
ventricles

Answer 37

The right ventricle distributes blood to the lungs and the left ventricles distributes blood to the body . The volume in the
ventricles is the same , but the left ventricle undergoes more pressure due to the size of distribution.

Question 38

Parasympathetic

Answer 38

Vagal nerve releases Ach at SA node
Ach binds to M2 muscarinic receptor
GPCR (Gi)
Causes hyperpolarization
Increased K+ permeability
Decreased transmission of impulses (conduction)
Decreases HR
And therefore CO
Not much effect on contractility

Question 39

Sympathetic

Answer 39

Releases NE at SA node and throughout heart
β1 receptors at SA node
GPCR (Gs)
Causes depolarization
Increases rate of conduction of impulse
β1 receptors throughout
Increases force of contraction
HR up to 180-200bpm
Increases SV
Through increased contractility
CO up to 15-20L/min

Question 40

Identify the distribution of sympathetic & parasympathetic nerves in the heart and list the effects of these nerves on cardiac function.

Answer 40

Sympathetic postganglionic neurons have cell bodies in the spinal cord . Their axons innervate both autorhythmic and contractile cells throughout the heart. These axons release NE onto bl adrenergic receptors throughout the heart. This activates the Gas GPCR to activate the CAMP 2nd messenger pathway . CAMP increases the cardiac cell’s permeability to Nat an*dbKt , leading to a faster depolarization. CAMP will also lead to the phosphorylation of L type and T type ca” channels, la” ATPase , RYRS ,and MLCK which all contribute to a faster signalman and strength of contraction. Sympathetic innervation of the heart ultimately increases venous return , HR , SV , which96.

The vagus nerve (CN #10) is the main component of the parasympathies nervous system .Its axons innervate the SA node and other autorytnmil
cardiac cells .These axons release Ach onto M2 muscarinic receptors which activate the Gai GPCR which inhibit CAMP. This causes an increased permeability to K+ , causing hyperpolarization of the autorythmic cells, slowing the signal transmission down the heart’s electrical pathway . Ultimately , parasympathetic innervation leads to a decrease in HR , W, and BP. It does not affect SV