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HN220 > Chapter 13: Cardiovascular System > Flashcards

Chapter 13: Cardiovascular System Flashcards

1
Q

3 components of the cardiovascular system

A
  • the heart (the pump)
  • blood vessels/vasculature (series of tubes)
  • blood (the fluid)
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2
Q

what is the cardiovascular system?

A

a closed loop, composed of the heart that pumps blood through arteries/veins to circulate throughout the system

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3
Q

function of cardiovascular system

A

to be an efficient transport mechanism for substances:
- brings oxygen and nutrients to cells
- bring waste from cells to liver and kidneys
- bring hormone, immune cells and clotting proteins to specific target cells

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4
Q

main function of the heart in cardiovascular system

A
  • the “central pump”
  • generate the force that propels blood through the blood vessels
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5
Q

main function of blood vessels in cardiovascular system

A
  • carries blood from the heart to the organs and then back to the heart again
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6
Q

main function of blood in cardiovascular system

A
  • the fluid composed of substances (nutrients and oxygen) that is delivered to cells in the body
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7
Q

two divisions of the circulatory system

A

1) pulmonary circuit:
- moves blood between the heart and the lungs
- supplied by right side of heart
2) systemic circulation:
- moves blood between the heart and the rest of the body
- supplied by left side of heart

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8
Q

major structures of the heart

A
  • left and right atrium (upper two chambers)
  • left and right ventricles (bottom two chambers)
  • a septum separates the left and right sides (interatrial septum and interventricular septum)
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9
Q

valves of the heart

A

atrioventricular (AV) valves:
- tricuspid (right AV valve)
- bicuspid (left AV valve)

semilunar valves:
- aortic
- pulmonary valve

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10
Q

what are the steps of blood flow through the heart?

A

blood from body enters heart via venae cava –> right atrium –> tricuspid valve –> right ventricle –> pulmonary valve –> pulmonary trunk –> pulmonary arteries bring deoxygenated blood to lungs –> pulmonary veins bring oxygenated blood to heart –> left atrium –> bicuspid valve –> left ventricle –> aortic valve –> aorta –> blood leaves via systemic capillaries out of heart –>

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11
Q

anatomy of the heart

A
  • located in thoracic cavity
  • size of a fist
  • weighs 250-350g
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12
Q

3 layers of the heart wall

A
  • epicardium
  • myocardium
  • endocardium
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13
Q

pericardium

A

the membranous sac that surrounds and lubricates the heart (not a layer of the heart)

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14
Q

epicardium

A
  • outermost layer
  • connective tissue that covers and protects the heart
  • the visceral pericardium
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15
Q

myocardium

A
  • middle layer
  • muscular wall of the heart
  • concentric layers of cardiac muscle tissue
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16
Q

endocardium

A
  • innermost layer
  • composed of epithelial cells
  • acts as protection by lining the valves and heart chambers
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17
Q

why is ventricular muscle thicker than atrial muscle?

A
  • ventricles pump blood over relatively long distances through the vasulature so they must work harder to pump a given volume of blood
  • atria only pump to the next chamber
  • thicker muscle enables ventricles to develop greater pressure

ventricular muscle on the left side is greater than the right side. this is because the left side pumps to the organs whereas right side pumps to lungs

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18
Q

how does the heart “pump” blood?

A
  • rhythmic contraction and relaxation of the myocardium
  • contraction = heart wall moves inwards and squeezes the blood = increases the pressure in the chamber and forces the blood out
  • relaxation = chamber expands and fills with blood
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19
Q

how does pressure affect cardiac cycle?

A
  • the cardiac cycle depends on pressure changes that occur within the heart
  • pressure changes result in the movement of blood through different chambers of the heart and body
  • pressure within heart chambers varies with heartbeat cycle
  • the pressure difference drives blood flow (high pressure to low pressure)
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20
Q

what is the fibrous skeleton of the heart?

A
  • structure of dense connective tissue that separates the atrium from the ventricles
  • provides critical support for the heart and separates the flow of electrical impulses through the heart
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21
Q

steps to the cardiac cycle

A

1) atrium contract = blood flows to ventricles
2) ventricles contract = blood flow to arteries

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22
Q

importance of valves in the heart

A
  • a one-way door keeps the blood flowing in the proper direction
  • prevents the back flow of blood (prevents the mixing of deoxygenated and oxygenated blood)
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23
Q

what does it mean for valves to open based on the pressure gradient?

A
  • heart valves open and close in response to pressure differences across them
  • when pressure is higher on one side of the valve than the other, the valve opens to allow blood to flow through
  • when pressure is higher on the opposite side, the valve closes to prevent back flow
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24
Q

role of the atrioventricular (AV) valves

A
  • allows blood to flow from the atrium to the ventricle but not in the opposite direction
  • AV valves open or close passively in response to changes in pressure that occur in every heart beat
    –> when atrial pressure > ventricular pressure = open
    –> when atrial pressure < ventricular pressure = close
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25
Q

what is prolapse?

A
  • a condition that when one or more valve cusps is pushed into the atria causing the edges of the valves to no longer seal properly
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26
Q

how is prolapse prevented?

A
  • the chordae tendinae and papillary muscles
  • the AV valve cusps are held in place by the chordae tendinae which extends from the edges of the cusps to papillary muscles protruding from the ventricular wall
  • when ventricular contraction occurs, the papillary muscles also contract, which places tension on chordae tendinae which pulls down the cusps forcing the valves shut and sealing properly
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27
Q

role of the semilunar valves

A
  • allow blood to flow into the arteries (aorta and pulmonary artery) from the ventricles without going backwards
  • when ventricular pressure > arterial pressure = open
  • when ventricular pressure < arterial pressure = close
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28
Q

what is autorhymicity?

A

the ability of the cardiac cells to generate action potentials that trigger its contractions of its own cardiac muscles on a periodic basis

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29
Q

what are cardiocytes?

A
  • the individual cells that make up the cardiac muscle.
  • cardiac muscle cells
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30
Q

2 types of cardiocytes

A

1) contractile cells
2) autorythmic cells (pacemaker cells, conduction fibers)

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31
Q

role of contractile cells

A
  • responsible for contractions that pump blood
  • account for 99% of cardiocytes
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32
Q

role of autorythmic cells

A
  • can generate and spread action potentials spontaneously

1) pacemaker cells
- initiate action potentials to establish heart rate
2) conduction fibres
- transmit and spread generated action potentials

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33
Q

characteristics of cardiac muscle

A
  • striated
  • contain sarcomeres
  • have short, wide T-tubules
  • less sarcoplasmic reticulum and no terminal cisternae
  • under control of sympathetic and parasympathetic nervous system
  • single nucleus
  • have intercalated discs that connect cells
34
Q

characteristics of contractile myocardial cells

A
  • small in size
  • bifurcated (split into two at one end)
  • have one centrally located nucleus
  • aerobic cells (high in myoglobin, mitochondria and blood supply)
  • involuntary contraction
35
Q

what is the conduction system of the heart?

A
  • specialized heart muscle cells that initiate and conduct action potentials
  • these are the pacemaker cells and conduction fibers
36
Q

role of pacemaker cells

A
  • can spontaneously generate action potentials
  • can determine the rate of heartbeat by firing action potentials on a regular basis
  • located primarily in the sinoatrial (SA) node and the atrioventricular (AV) node
37
Q

role of conduction fibers

A
  • can quickly conduct action potentials generated by pacemaker cells, triggering muscle contraction to occur
  • compose the bundle of His, internodal pathway and Purkinje fibers
38
Q

what are intercalated discs?

A
  • a specialized junction between cardiac muscle cells that contain desmosomes and gap junctions
  • allow for rapid transmission of an action potential
39
Q

role of desmosomes and gap junctions

A

gap junctions and demosomes located within intercalated discs help spread AP’s

1) gap junctions
- directly connect adjacent cardiocytes so they can pass an electrical current (ions) from one cell to another
- allows for depolarization to occur between cells

2) desmosomes
- linking proteins bind adjacent cells together to maintain structural integrity that resists mechanical stress/stretching during contraction

40
Q

how does excitation spread between cells?

A

1) action potential is initiated in pacemaker cells
2) action potentials move rapidly through the conduction fibers to coordinate the spread of excitation within the heart
3) the conduction system causes a wave of excitation to move first through the atria, causing them to depolarize and then contract as a unit
4) the wave of excitation moves through the ventricles, causing them to depolarize and then contract as a unit

41
Q

steps to initiation and conduction of an impulse during a heartbeat

A

1) action potential is initiated in the SA node.
2) signals travel throughout the atrial muscle via the interatrial pathways. impulses also travel to the AV node via internodal pathways (conduction fibres in atria).
3) at the AV node, there is a delay as the AV node transmit action potentials less rapidly than other cells
4) from the AV node, the signal travels to the atrioventricular bundle (called the bundle of His)
5) the signal then splits into left and right bundle branches which transmits to both the left and right ventricles
6) from the bundle branches, impulses travel through Purkinje fibers. this spreads throughout the ventricular myocardium, from the apex upward toward the valves. from these fibers, impulses travel through the rest of the myocardial cells

42
Q

basic order of conduction through the heart

A

1) sinoatrial SA node (pacemaker)
2) atrioventricular (AV) node
3) atrioventricular bundle (bundle of His)
4) right and left bundle branches
5) purkinje fibers

43
Q

why does the AV node rarely initiate contractions of the heart?

A

1) action potentials originating in the SA node travel through the AV node on the way to the ventricles, and cells in the AV node go into a refractory period, so they cannot generate their own action potential
2) the SA node has a higher frequency of action potentials than AV node, so the AV node rarely has a chance to fire because the SA node beat it to it

44
Q

what happens if the SA node fails to fire an action potential?

A
  • the AV node will initiate an action potential if the SA node doesn’t fire, the frequency slows down or conduction between the nodes become blocked
  • an action potential initiated by the AV node will travel through the conducting system, and trigger ventricular contraction normally
  • the AV node is an emergency backup
45
Q

where are the fastest firing autorhythmic cells located?

A

SA node > AV node > bundle of His = Purkinje fibers

  • the SA node fires at 70-80 action potentials per minute
  • the AV node fires at 40-60 action potentials per minute
  • Bundle of His and Purkinje fibers fire at 20-40 AP per minute
46
Q

why does conduction slow at the AV node?

A
  • it is essential for efficient cardiac function
  • it allows the wave of excitation to spread completely throughout the atria before reaching the ventricles, ensuring that atrial contraction is complete before ventricular contraction starts
47
Q

what are the waveforms represented on an ECG?

A

P-QRS-T
- P wave = movement of depolarization (AP) through the atria, and atrial contraction
- QRS complex = ventricular depolarization and contraction
- T wave = ventricular repolarization

48
Q

what are intervals found on an ECG?

A
  • PQ interval = occurs between onset of P wave and onset of QRS complex = estimates the time of the conduction through the AV node
  • QT interval = time of onset of QRS complex to end of T wave = estimate of time ventricles are contracting (ventricular systole)
  • TQ interval = end of T wave to beginning of QRS complex = estimate of time that ventricles are relaxing (ventricular diastole)
  • RR interval = the time between the peaks of two successive QRS complexes = represents the time between heartbeats
49
Q

why are pacemaker cells different than contractile cells?

A
  • contractile cells require a stimulus to depolarize to threshold in order to initiate an action potential
  • pacemaker cells can fire action potentials, and depolarize themselves, in an absence of an external stimulus because it doesn’t have a steady resting potential
50
Q

what are pacemaker potentials?

A
  • when a pacemaker cell spontaneously depolarizes after an AP (very slowly) until its membrane potential reaches threshold
  • causes another action potential to be generated
51
Q

steps to pacemaker cells generating an action potentials

A

1) an initial spontaneous depolarization (pacemaker potential) occurs due to the opening of Na+ “funny channels” and the closing of K+ channels
2) as a result, Na+ moves into the cell and K+ stays in the cell = becomes more positive
3) T-type calcium channels open, leading to calcium influx and further depolarization (more positive)
4) the funny channels close at -55mV, just short of threshold for an AP.
5) L-type calcium channels open, allowing a larger influx of calcium ions (some sodium) contributing to rapid depolarization and leading to the action potential occuring
6) after reaching its peak, potassium channels open and Ca2+ channels close. this allows K+ to leave the cell and and prevent Na+ flow into the cell.
7) this causes membrane become more negative and repolarize again.

52
Q

what are the channels involved with action potential?

A
  • T type: “tranisent” = (slow) depolarization
  • L type: “long lasting” = rapid depolarization
53
Q

5 phases of action potential in cardiac contractile cells

A

phase 0:
- rapid depolarization (more positive)
- Na+ channels open and increase permeability of Na+ into the cell
phase 1:
- brief repolarization (more negative)
- Na+ channels start to close and decrease permeability into the cell
- causes a small drop in membrane potential
phase 2:
- plateau occurs
- most K+ channels are closed = decreased permeability of K+ out of cell
- L type Ca2+ channels open = increased permeability to Ca2+ into the cell
phase 3:
- repolarization (more negative)
- some K+ channels are open and flow out of cell
- Ca2+ channels are closed so no flow into the cell
phase 4:
- resting membrane potential

54
Q

characteristics of action potentials in cardiac contractile cells

A
  • long duration (250-300 msec)
  • twitch summation is not possible
  • long absolute refractory period prevents tetanus from occurring = ensures rhythmic contraction of heart
  • relaxation is imperative because the heart fills with blood at rest
55
Q

what properties do cardiac contractile cells that are similar to skeletal and smooth muscles?

A

similar to skeletal:
- t-tubules
- sarcoplasmic reticulum (Ca2+)
- troponin and tropomyosin regulation

similar to smooth:
- gap junctions
- extracellular Ca2+

56
Q

steps to excitation-contraction coupling in cardiac contractile cells

A

1) the stimulus that triggers an AP comes through a gap junction to contractile cell
2) action potential spread through the plasma membrane and down into t-tubules
3) voltage sensitive Ca2+ channels on both the sarcoplasmic reticulum and plasma membrane open and release calcium into the cytosol of cell
4) the existing calcium stimuluates the Ca2+ channels to stay open longer and induces more to be released from the sarcoplasmic reticulum
5) calcium binds to troponin, shfiting tropomyosin off the myosin-binding sites on actin
6) the crossbridge cycle begins (contraction occurs)
7) in order to relax the muscle again, calcium must be removed. Ca2+ is actively transported back to the SR and ECF
8) eventually theres no calcium, so tropomyosin shifts back and blocks the myosin-binding sites. this causes the muscle fiber to relax again

57
Q

why must myocardial cells contract together?

A
  • enables the heart to contract and relax as a single unit
  • required to generate enough force to pump blood
58
Q

what is the cardiac cycle?

A

all the events associated with the flow of blood through the heart during a single, complete heartbeat

59
Q

two main periods of the cardiac cycle

A

1) systole = ventricular contraction
2) diastole = ventricular relaxation

60
Q

what are the 4 phases of cardiac cycle?

A

1) ventricular filling (diastole)
2) isovolumetric contraction (systole)
3) ventricular ejection (systole)
4) isovolumetric relaxation (diastole)

61
Q

what occurs during phase 1 of the cardiac cycle?

A

phase 1: ventricular filling
- blood returning to the heart from systemic and pulmonary veins into relaxed atria (called venous return)
- blood passes through the AV valves and into the ventricles
- semilunar valves are closed (ventricular pressure is lower than arterial pressure) so no blood leaving the ventricles
- at the end, the atria contract and drive even more blood into the ventricles. eventually the atria relax.

62
Q

what occurs during phase 2 of the cardiac cycle?

A
  • the ventricles begin to contract, therefore raising the pressure within them
  • when ventricular pressure exceeds atrial pressure, the AV valves close (and the semilunar valves too)
  • no blood is flowing into or out of the ventricles at this point, and volume remains constant
  • phase 2 ends when ventricular pressure is great enough to force open semilunar valves
63
Q

what occurs during phase 3 of the cardiac cycle?

A
  • blood is expelled from the ventricle into the aorta and pulmonary arteries through the open semilunar valves
  • the pressure reaches a peak within the ventricles as contraction and blood efflux continue
  • ventricular volume decreases as blood leaves the chamber
  • blood is ejected from the ventricle until the semilunar valves close. this is when pressure in ventricle is less than the arterial pressure.
64
Q

what occurs during phase 4 of the cardiac cycle?

A
  • the heart is resting
  • there is still some blood present in the ventricles, but the volume is constant as the valves are all closed
  • there is still some pressure within the ventricles, as it takes time for tension to decrease
  • ventricles eventually relax
65
Q

are duration of systole and diastole equal?

A

NO
- most of the cardiac cycle is spent in diastole (relaxation)
- this is to provide the heart adequate time to fill with blood
- also provide more time to relax, decreasing fatigue for efficient pumping

66
Q

how does aortic pressure affect blood pressure?

A

during diastole:
- aortic valve closes
- blood is still leaving the aorta, so volume decreases within the artery = slow decline in aortic pressure
- pressure reaches a minimum = diastolic pressure

during systole:
- aortic valve opens and blood rushes through it (phase 3)
- pressure rapidly increases within the aorta (because blood is flowing into the aorta faster than it can flow out)
- pressure reaches a maximum = systolic pressure

67
Q

how do the aorta and large arteries contribute to the maintenance of continuous blood flow during the cardiac cycle?

A
  • they act as elastic pressure reservoirs
  • they can store energy during systole (contraction) as their walls expand. this stored energy is released during diastole as the walls recoil inward
  • this released energy propels blood flow through downstream vessels during diastole, facilitating continuous circulation throughout the cardiac cycle.
  • by efficiently storing and releasing energy, it takes some energy off the heart
68
Q

what is mean arterial pressure?

A

average aortic pressure occurring during the cardiac cycle

69
Q

what is cardiac output?

A
  • the volume of blood pumped by each ventricle per minute
  • cardiac output (CO) = heart rate (HR) x stroke volume (SV)
70
Q

what role does CNS play in cardiac output?

A
  • even though autorhythmic cells can initiate action potentials within the heart, the central nervous system regulates the rate and force of heart muscle contraction via intrinsic and extrinsic regulation
71
Q

extrinsic and intrinsic control of cardiac output

A
  • intrinsic control = regulated by factors originating from within the heart (auto regulation)
  • extrinsic control = by neural input, circulating hormones, or any other factor originating from outside the heart
72
Q

4 types of ventricular volumes

A
  • EDV (end diastolic volume) = volume of blood in ventricle at end of each diastole
  • ESV (end systolic volume) = volume of blood in ventricle at end of systole
  • SV (stroke volume) = volume of blood ejected from ventricle each cycle: SV = EDV - ESV
  • EF (ejection frtaction) = fraction of end diastolic volume ejected during a heartbeat: EF = stroke volume / end diastolic volume
73
Q

autonomic input to the heart

A
  • neural control of the heart is carried about by the autonomic nervous system
  • fibers of the ANS (parasympathetic and sympathetic) project to nearly every region of the heart which regulates heart rate and stroke volume
  • the ventricular myocardium is regulated mostly by the sympathetic nervous system
74
Q

what determines heart rate?

A
  • heart rate is determined by the frequency of action potentials generated by pacemaker cells in the SA node of the heart
    –> when pacemaker cells depolarize more frequently = more action potentials = more contraction = the heart rate increases
    –> when pacemaker cells depolarize less frequently = less action potentials = less contraction = the heart rate decreases
75
Q

what variables affect cardiac output?

A

affect heart rate:
- sympathetic and parasympathetic nervous activity
- circulating epinephrine

affect stroke volume:
- afterload
- end diastolic volume
- ventricular contractility

76
Q

how does sympathetic and parasympathetic nervous system affect HR?

A
  • pacemaker cells receive direct input from the autonomic nervous system which can alter the frequency of action potentials generated by cells receiving the input
    –> increased activity by sympathetic neurons to SA node increases the frequency of action potentials by the release of norepinephrine
    –> increases activity by the parasympathetic neurons to the SA node decreases the frequency of action potentials by the release of acetylcholine
77
Q

how do hormones affect HR?

A
  • epinephrine is secreted by the adrenal medulla in response to increases sympathetic activity
  • epinephrine increases action potential frequency at the SA node and increase heart rate
  • epinephrine also increases the velocity of action potential conduction through cardiac muscle fibers, which speeds up the spread of electrical impulses through the heart, leading to more efficient contractions
78
Q

how does ventricular contractility affect stroke volume?

A
  • a more forceful contraction will expel more blood
  • the sympathetic nervous system regulates ventricular contractility
  • the neurons project to the atria and influence the force of atrial contraction. so increased SNS activity causes the atria to contract with more force, raising atrial pressure and increases the volume of the blood the atria pumps into the ventricles
  • SNS neurons also project to ventricular myocardium, so when sympathetic activity increases = the strength and rate of ventricular contractile cells increases = ventricular contractility increases and raises cardiac output
  • hormones, such as epinephrine, increases myocardial contractility = stroke volume and cardiac output
79
Q

how does end-diastolic volume (EDV) affect stroke volume?

A
  • more blood in the heart at the end of diastole increases stroke volume
  • depends on Starlings law: increased stretching of the muscle fibers results in a stronger contraction
  • this means that increased EDV (blood in the ventricles) stretches muscle fibers closer to their optimal length causing a stronger muscle contraction and higher stroke volume

–> an increase in venous return = increase in end-diastolic volume = stretching of ventricular muscle fibers = stronger contraction of the heart = contraction increases stroke volume = enhancing cardiac output

80
Q

what is the Frank - Starling law of the heart?

A
  • describes the heart’s intrinsic ability to adjust its output (stroke volume) in response to changes in the rate of blood flow into the heart from the veins (venous return)
  • ensures that the heart pumps out the same volume of blood it receives, maintaining equilibrium in the cardiovascular system.
  • the heart can adapt to changes in venous return by adjusting the force of contraction, thereby regulating stroke volume.
    –> an increase in the volume of blood in the heart’s ventricles at the end of diastole (EDV) leads to a stronger contraction of the heart muscle fibers, resulting in an increased stroke volume (SV) and VICE VERSA
81
Q

how does afterload affect stroke volume?

A
  • afterload refers to the resistance that the heart must overcome to eject blood from the left ventricle into aorta for systemic circulation
  • when the heart ejects blood, the ventricular muscle must work against the arterial pressure in the aorta
  • as mean arterial pressure (MAP) decreases = resistance (afterload) that the ventricular muscle must overcome also decreases = heart can more effectively eject blood into the aorta during systole = increased stroke volume

HN220 (12 decks)

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