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A&P2 > Heart Study Guide (Cards broken down) > Flashcards

Heart Study Guide (Cards broken down) Flashcards

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1
Q

What are the two major divisions of the cardiovascular system

A

The two major divisions of the cardiovascular system are the heart and blood vessels.

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2
Q

What do the two major divisions of the cardiovascular systems do?

A

The heart acts as a pump while the blood vessels act as a delivery system.

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3
Q

What is the general function of the cardiovascular system?

A

The general function of the cardiovascular system is to transport blood throughout the body to allow exchange of substances (E.g respiratory gases, nutrients, and waste products) between the blood of capillaries and the body’s cells.

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4
Q

Define perfusion.

A

delivery of blood per time per gram of tissue (in mL/min/g); it is the goal of the cardiovascular system.

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5
Q

Describe the mediastinum.

A

(medius= middle) it’s of the thoracic cavity; where the heart is located; between the lungs.

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6
Q

Define the pericardium

A

the three layers the heart is enclosed in

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7
Q

outermost covering; dense irregular ct; attaches to diaphragm and base of aorta, pulmonary trunk; anchors heart and prevents it from overfilling

A

fibrous pericardium

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8
Q

Simple squamous epithelium and areolar ct; attaches directly to heart

A

Visceral and Parietal pericardium

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9
Q

released by the 2 layers of the serous pericardium; released into the pericardial cavity; the oily mixture that lubricates the serous membranes to decrease
friction with every heart beat.

space the parietial and visceral of pericardium separated by

A

Pericardial fluid

Pericardial cavity

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10
Q

Review pulmonary and systemic circulation

A
  1. R. Atrium
  2. Tricuspid valve
  3. R. Ventricle
  4. Pulmonary valve
  5. Pulmonary trunk
  6. R., L Pulmonary arteries
  7. Capillaries (O₂ is loaded CO₂ unloaded)
  8. Pulmonary Veins (Red now)
  9. Pulmonary veins
  10. L. Atrium
  11. Bicuspid (mitral valve)
  12. L. Ventricle
  13. Aortic Valve
  14. Aorta
  15. Systemic arteries
  16. Tissue Capillaries (O₂ is unloaded, CO₂ is loaded)
  17. Systemic Veins
  18. Vena Cava
  19. R. Atrium
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11
Q

Describe the general structure of cardiac muscle.

A

The general structure of cardiac muscle is striated, short, thick, branched cells, one central nucleus surrounded by light staining mass of glycogen. Includes sarcolemma (plasma membrane), myofibrils.

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12
Q

join cardiocytes end to end with 3 features:

  • interdigitating folds
  • mechanical junctions= desmosome
  • electrical junctions= gap junctions
A

Intercalated discs

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13
Q

protein filaments that anchor into a protein plaque located on the internal surface of the sarcolemma. Acts as mechanical junctions to prevent cardiac muscle cells from pulling apart.

A

Desmosomes

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14
Q

protein pores between the sarcolemma of adjacent cardiac muscle cells. Provides a low resistance pathway for flow of ions between cardiac cells; allow action action potential to move continuously along sarcolemma of cardiac muscle cells, resulting in synchronous contraction of that chamber.

A

Gap junctions

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15
Q

Describe the metabolism of cardiac muscle.

A

The metabolism of cardiac muscle depends almost exclusively on aerobic respiration to make ATP, is rich in myoglobin and glycogen, has huge mitochondria: fills 25% of the cell.

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16
Q

Describe the metabolism of cardiac muscle.

A

The metabolism is adaptable to different types of fuels for molecules which includes fatty acids (60%); glucose (35%), ketones, lactic acid, and amino acids (5%).

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17
Q

Describe the metabolism of cardiac muscle.

A

The metabolism is more vulnerable to O₂ deficiency than lack of a specific fuel.

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18
Q

Describe the metabolism of cardiac muscle.

A

The metabolism is fatigue resistant because it makes little use of anaerobic fermentation or oxygen debt mechanisms.

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19
Q

Locate the 4 valves in the heart.

A

Right Atrioventricular (AV) valve- covers the right av opening and has 3 cusps (tricuspid valve).

Left Atrioventricular (AV) valve- has only two cusps (bicuspid, mitral)

Pulmonary Semilunar valve- located between right ventricle and pulmonary trunk

Aortic Semilunar Valve- located between left ventricle and the ascending aorta.

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20
Q

What is the function of valves? How do they open and close?

A
  • When open, cusps of valves extend into ventricles which allows blood to move from atrium to move into ventricles.
  • When ventricles are contracting, blood is forced superiorly which causes AV valves to close.
  • Semilunar valves open when ventricles contract and the force of blood pushes the semilunar valves open and blood enters the arterial trunks.
  • the semilunar valves close when the ventricles relax and the pressure in the ventricle becomes less than the pressure in an arterial trunk; closure of semilunar valves prevents blood flow back into the ventricle.

*When AV valves are open, SL are closed (Diastole), When SL are open, AV valves are closed (Systole)

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21
Q

framework of collagenous and elastic fibers

A

Fibrous Skeleton of heart

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22
Q

The fibrous skeleton provides:

A

Structural support, attachment for cardiac muscles, anchors valve tissue, *electrical insulation between atria and ventricles; important in timing and coordination of contractile activity.

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23
Q

Do the coronary arteries fill with blood when the heart is contracting or relaxing?

A

Coronary arteries fill with blood when the heart is relaxing. (Doesn’t flow when the heart is contracting because the vessels are compressed.)

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24
Q

Describe the conduction system in the heart:

A
  1. SA node fires
  2. Excitation spreads through atrial myocardium
  3. AV node fires
  4. Excitation spreads down AV bundle
  5. Purkinje fibers distribute excitation through ventricular myocardium.
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25
Briefly describe the cardiac center
houses both the cardioinhibitory and cardioaccelerator centers. - modifies cardiac activity including both heart rate and its force of contraction. - The cardioinhibitory center is parasympathetic - the cardioacceleratory center is sympathetic
26
Briefly describe autonomic nerve supply to heart
controls rate and force; adjusts SA node Vagus is parasympathetic Parasympathetic shows your heart rate Sympathetic innervates muscle and force of contraction.
27
What physiologic processes are involved in heart contraction?
The conduction system and cardiac muscle cells are involved in heart contraction. Conduction- Initiation- SA node initiates action potential. Spread of Action Potential- an action potential is propagated throughout the atria and the conduction system Cardiac Muscle Cells- The action potential- the action potential is propagated across the sarcolemma of cardiac muscle cells. Muscle contraction- thin filaments slide past thick filaments and sarcomeres shorten within cardiac muscle cells.
28
Why does the SA node spontaneously fire at regular intervals?
Nodal cells have an unstable resting membrane of -60mV. | Reference off of the ECG and understand the process.
29
leaky channels, more negative
Resting potential
30
cardiocytes (cardiac nodal cells) are self-excitatory; they require no nerve stimulus for contraction
Autorhythmic
31
Slow voltage-gated Na+ channels open. Inflow of Na+ changes membrane potential from -60 mV to -40 mV.
SA node Reaching threshold
32
Fast voltage-gated Ca+ channels open. Inflow of Ca2+ channels open. Inflow of Ca2+changes membrane potential from -40 mV to just above 0 mV.
Depolarization of SA node-
33
Fast voltage-gated Ca2+ channels close. Voltage-gated K+ channels open allowing K+ outflow. Membrane potential returns to RMP -60 mV, and K+ channels close. Reference off of the pacemaker physiology.
Repolarization
34
the normal resting heart rate of 75 beats per minute is due to continuous parasympathetic stimulation of the SA node by the vagus nerve; slowing of heart rate.
Vagal tone
35
Describe the spread of the action potential through the heart’s conduction system.
An action potential is generated at the SA node. It spreads via gap junctions between cardiac muscle cells throughout the atria to AV node. The action potential is delayed at the AV node before it passes to the AV bundle within the interventricular septum. The Av bundle conducts the action potential to the left and right bundle branches and then to the Purkinje fibers. The action potential is spread via gap junctions between cardiac muscle cells throughout ventricles.
36
What 2 events occur within cardiac muscle cells after stimulation by the conduction system?
Propagation of action potential at sarcolemma and contraction of sarcomeres within cardiac muscle cells.
37
Describe the feature of the sarcolemma of cardiac muscle cells.
In cardiac muscle, sodium channels are fast channels, Ca channels are slow, K is normal; resting membrane potential is -90 mV.
38
List the electrical events of an action potential that occur at the sarcolemma.
Depolarization- fast voltage -gated Na+ channels open and Na+ rapidly enters the cell, reversing the polarity from negative to positive (-90 mV to +30 mV). These channels then close. Plateau- Voltage-gated K+ channels open and K+ flows out of the cardiac cells. Slow voltage-gated Ca2+ channels open and Ca2+ enters the cell, with no electrical damage and the depolarized state is maintained. Repolarization- Voltage gated Ca2+channels close, voltage gated K+ channels remain open, and K+ moves out of the cardiac muscle cell, and polarity is reversed from positive to negative(+30 mV to 90mV).
39
Describe the mechanical events of cardiac muscle cell contraction.
Ca2+ enters sarcoplasm from interstitial fluid and SR leading to contraction. As in skeletal muscle, it binds to troponin and initiates crossbridge cycling Ca2+ levels decrease leading to relaxation; channels close and move pumps it into SR and out of cell.
40
How do cardiac muscle cells differ from skeletal muscle cells?
Cardiac muscle cells- cannot exhibit tetany, have a long refractory period. - cell cannot fire a new impulse during refractory period - cardiac muscle cell’s plateau phase leads to refractory period of 250 ms - the heart cell contracts and relaxes before it can be stimulated again - makes sustained (tetanic) contraction impossible Skeletal muscle cells- can exhibit tetany; have a short refractory period; doesn’t have enough time to relax.
41
non-responsive
Refractory period
42
contraction and relaxation associated with sarcomeres within skeletal muscle fibers occurs over approximately 100 milliseconds. Repolarization at the sarcolemma occurs immediately following depolarization, which results in a refractory period that is relatively short (about 1-2 milliseconds). While sarcomeres are still contracting within skeletal muscle fibers, sarcolemma has already been repolarized for new stimulation. skeletal muscle cells can be restimulated at a frequency that does not allow the skeletal muscle sufficient time to relax completely. Skeletal muscle can be stimulated at a rate that the muscle remains contracted (without any relaxation). Tetany.
Skeletal muscle single stimulation and Skeletal muscle frequent stimulation
43
muscle contraction and relaxation associated with sarcomeres within cardiac muscle cells are over 250 milliseconds (a longer period than in skeletal muscle). Repolarization at sarcolemma does not occur immediately following depolarization, which results in a refractory period that is relatively long (almost 250 milliseconds). Long refractory period is due to a plateau event at sarcolemma which delays repolarization. Sarcolemma has not been repolarized to allow for new stimulation. delay in stimulation allows time for sarcomeres of cardiac muscle cells within the heart chamber wall to fully contract and relax before being stimulated again. Cardiac muscle cells continue to both contract and relax following each stimulation.
Cardiac muscle single stimulation and Cardiac muscle frequent stimulation
44
What causes the plateau
Voltage-gated K+ channels open and K+ flows out of cardiac muscle cells. Slow voltage-gated Ca2+ channels open and Ca2+ enters the cells, with no electrical change and the depolarized state is maintained.
45
significance of plateau
Plateau phase lasts 200 to 250 ms, sustains contraction for the expulsion of blood from the heart.
46
the collection chart of the electrical signals from the heart
ECG (electrocardiogram)
47
ECG measures
measures the electrical activity of the heart.
48
Draw a typical wave and label these waves; P, QRS, T.
Use ECG drawing from lab.
49
What is happening in the heart at each wave?
P- wave- atrial depolarization (causes systole) QRS complex- ventricular repolarization (Causes systole; electrical activity of ventricular depolraization masks atria repolarization) T-wave- ventricular repolarization
50
electrical changes with depolarization and repolarization.
wave
51
(on line, isolelectric) between waves.
segment
52
What happens during the PQ and ST segments?
PQ segment- time of impulse conduction from the AV node to ventricular myocardium. ST segment- period of time representing the early part of ventricular repolarization during which ventricles are more or less uniformly excited.
53
What are the P-R interval and the Q-T interval?
PR interval- time from onset of atrial depolarization to onset of ventricular depolarization. QT interval- time from onset of ventricular depolarization to the end of ventricular polarization; represents refractory period of ventricles.
54
all events in heart from the start of one heartbeat to the start of the next.
Cardiac cycle
55
Define systole and diastole.
Systole- contraction | Diastole-relaxation
56
What 2 processes within the heart occur due to pressure changes?
Unidirectional movement of blood through the heart chambers, as blood moves along a pressure gradient (i.e, from an area of greater pressure to an area of lesser pressure) Opening and closing of the heart valves to ensure that blood continues to move in a “toward” direction without backflow.
57
What 2 forces move blood through the heart and open and close valves?
Ventricular contraction and Ventricular relaxation
58
Describe the events of ventricular contraction and relaxation.
Ventricular contraction- raises ventricular pressure - AV valves pushes closed - Semilunar valves pushed open and blood ejected to artery. Ventricular relaxation- lowers ventricular pressure - semilunar valves close; no pressure from below keeping them open. - AV valves open; no pressure pushing them closed.
59
Describe the 5 events of the cardiac cycle. Use Figure 19.21 to help you.
Atrial contraction and Ventricular filling Isometric contraction Ventricular ejection Isovolumetric relaxation Atrial relaxation and ventricular filling.
60
Describe what occurs during the 5 phases of the cardiac cycle.
Atrial contraction and Ventricular filling- more pressure to lower pressure Isovolumetric contraction- no blood is moving, all valves are closed. Ventricular ejection- ventricular pressure exceeds pulmonary and aortic Atrial relaxation and ventricular filling- Isovolumetric relaxation (no blood is moving, both chambers are relaxed.)
61
- equal amounts of blood are pumped by left and right sides of the heart - left heart pumps blood farther and so must be stronger (thicker) - ejected blood volumes must be the same or else edema (swelling) may occur - Congestive heart failure (CHF) results from the failure of either ventricle to eject blood effectively. - due to heart weakened by myocardial infarction, chronic hypertension, valve insufficiency, or congenital defects in heart structure.
Ventricular balance-
62
amount of blood ejected by each ventricle in 1 minute. | heart rate x stroke volume
Cardiac output
63
of beats per minute
Heart rate
64
the volume of blood ejected during one beat and is expressed as millimeters per beat.
Stroke volume (SV)-
65
How is resting cardiac output maintained?
Cardiac output is a function of both heart rate and stroke volume, and the value of one influences the value of the other. Cardiac output must meet tissue needs: Individuals with smaller hearts have smaller stroke volume, so must have higher heart rate (e.g women, children.) Individuals with larger hearts have greater volume and slower heart rate (e.g endurance athletes have larger and stronger hearts)
66
- capacity to increase cardiac output above rest level - subtract cardiac output at rest from input with exercise - HR accelerates and stroke volume increases during exercise - Gives measure of level exercise an individual can pursue (e.g Cardiac output can increase four-fold in healthy nonathlete and up to seven fold in athlete)
Cardiac reserve-
67
change heart rate.
Chronotropic agents
68
Define chronotropic agents, both positive and negative.
Chronotropic agents change heart rate. Positive chronotropic agents- increase heart rate Negative chronotropic agents- decrease heart rate LOOK ON SLIDE 41 to see positive and negative agents in depth.
69
protects the heart from overfilling - increased venous return causes increased right atrial pressure - baroreceptors set up reflex and increase heart rate and stimulates atrial receptors
Atrial (Bainbridge)
70
List 3 variables that influence stroke volume.
Stroke volume- how well muscle contracts Venous return- contractility is affected Inotropic agents- how well muscle can contract Afterload- what’s already in arteries.
71
blood that enters the heart at the end of heart relaxation
EDV(End-diastolic volume)
72
the blood remaining in a ventricle at the end of ventricular contraction
ESV(End-systolic volume)-
73
How do EDV/ESV affect SV?
They affect the SV by venous return ,inotropic agents, and afterload.
74
volume of blood returned to to the heart
Venous return
75
volume of blood in ventricles at the end of diastole (end diastolic pressure).
Preload (venous return)
76
venous return increases during exercise and with a slower heart rate (e.g in high-caliber athletes with strong hearts).
Starling’s law
77
What are inotropic agents, both positive and negative.
Inotropic agents- change stroke volume; alter contractility (force of contraction); generally due to a changes in Ca2+available in sarcoplasm; Ca2+levels directly to the number of cross bridges formed. Positive inotropic agents increase available Ca2+ Negative inotropic agents decrease available Ca2+ Look at slide 47 for in depth examples of Positive and negative inotropic agents.
78
pressure that must be exceeded before blood ejected; hypertension; atherosclerosis (plaque in vessel linings) increases afterload.
Afterload

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