Exam 3 - Heart Flashcards

Heart

1
Q

septum

A

muscular wall that separates the right pump (right atrium and right ventricle) from the left pump (left atrium and left ventricle)

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2
Q

fibrous skeleton of the heart

A

layer of dense, non-conductive, connective tissue between the atria and ventricles

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3
Q

myocardium

A
  • bundles of myocardial cells in the atria attach to the upper part of the fibrous skeleton to form a single unit
  • the myocardial cell bundles of the ventricles attach to the lower part of the fibrous skeleton to form a different myocardium
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4
Q

annuli fibrosi

A
  • rings formed by the connective tissue of the fibrous skeleton
  • surrounds the four heart valves
  • provides support of valve flaps
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5
Q

pulmonary arteries

A
  • carry blood that is lower in oxygen
  • blood enters the right ventricle –> pulmonary trunk and pulmonary arteries –> lungs
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6
Q

pulmonary veins

A
  • carry oxygen rich blood
  • carries blood to left atrium
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7
Q

pulmonary circulation

A

the path of the blood from the heart (right ventricle), through the lungs, and back to the heart (left atrium)

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8
Q

after oxygen-rich blood in the left atrium enters the left ventricle, where is it then pumped?

A

into the aorta (very large, elastic artery)

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9
Q

systemic circulation

A
  • from the heart (left ventricle), through the organ systems, and back to the heart (right atrium)
  • arterial branches from the aorta supply oxygen-rich blood to all of the organ systems
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10
Q

where do systemic veins empty?

A

into the superior and inferior venae cavae that then returns the oxygen-poor blood to the right atrium

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11
Q

Which circulation system presents the greatest resistance to blood flow and why?

What effect does this have on the amount of work performed by the ventricles?

A
  • the systemic circulation presents greater resistance to blood flow than the pulmonary system due to the numerous small muscular arteries and arterioles
    • despite this the rate of blood flow must match, so the left ventricle performs a greater amount of work (5-7x more) and has a thicker muscular wall (8-10 mm) to contract more strongly
    • the right ventricle wall is 2-3 mm
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12
Q

atrioventricular (AV) valves

A
  • one-way (prevent backflow of blood into the atria)
  • embedded within the fibrous skeleton
  • tricuspid valve is located between the right atrium and right ventricle and has 3 flaps
  • mitral (or bicuspid) valve is between the left atrium and left ventricles and has two flaps
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13
Q

describe when the AV valves are open and when they are closed

A
  • when the ventricles are relaxed, the venous return of blood to the atria causes the pressure in the atria to exceed that in the ventricles
    • this causes the AV valves to open and allow blood into the ventricles
  • when the ventricles contract, the intraventricular pressure rises above the pressure of the atria and pushed the AV valves closed
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14
Q

papillary muscles

A
  • papillary muscles within the ventricles contract to keep valve flaps tightly closed
  • the contraction of these muscles occurs at the same time as ventricular contraction
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15
Q

chordae tendineae

A

strong tendinous cordes that connect the papillary muscles to the AV valve flaps

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16
Q

semilunar valves

A
  • one-way
  • located at the origin of the pulmonary artery (pulmonary semilunar valve) and aorta (aortic semilunar valve)
  • not supported by chordae tendineae because they do not deal with a great amount of pressure when they are closed
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17
Q

describe when semilunar valves are open and when they close.

A
  • semilunar valves open during ventricular contraction, allowing blood to enter the pulmonary and systemic circulations
  • semilunar valves snap shut during ventricular relaxation, when the pressure in the arteris is greater than the pressure in the ventricles
    • this prevents backflow of blood into the ventricles
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18
Q

why are there no one-way valves at the inlets of the atria?

A

because the blood is continuously flowing into both atria under low pressure

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19
Q

four essential characteristics of the atria that cause them to promote continuous blood flow

A
  1. no atrial inlet valves to interrupt blood flow during atrial systole
  2. atrial systole contractions are incomplete and do not contract to the extent that would block blood flow
  3. atrial contractions must be gentle enough so that the force of contraction does not exert significant back pressure that would impede venous flow
  4. relaxation of the atria must be timed so that they relax before the start of ventricular contraction
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20
Q

key benefit of atria

A

preventing circulatory inertia and allowing uniterrupted venous flow to the heart

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21
Q

auscultation

A
  • listening through a stethoscope
  • closing of the AV and semilunar valves produce sounds that can be heard
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22
Q

S1

A
  • first sound of heart
  • “lub”
  • produced by closing of AV valves during isovolumetric contraction of the ventricles at systole
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23
Q

S2

A
  • second sound of the heart
  • “dub”
  • produced by closing of the semilunar valves when the pressure in the ventricles falls below the pressure in the arteries (when the ventricles relax at the beginning of diastole)
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24
Q

murmurs

A
  • abnormal heart sounds produced by abnormal patterns of blood flow in the heart
  • many cause by defective heart valves
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25
Q

aortic valve stenosis

A
  • produces a mid-systolic heart murmer due to calcium deposits on the aortic side of the valve
  • stenosis = narrowing
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26
Q

rheumatic endocarditis

A
  • disease in which the heart valves become damaged by antibodies made in response to an infection cause by streptococcus bacteria
  • “rheumatic fever” is an autoimmune disease because the antibodies produced in response to the bacteria cross-react with the proteins found in the tissues of the heart valves => produces damaged valves and heart murmurs
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27
Q

mitral stenosis

A
  • when the mitral (bicuspid) valve becomes thickened and calcified
    • this impairs the blood flow from the left atrium to the left ventricle
    • an accumulation of blood in the left atrium may cause a rise in left atrial and pulmonary vein pressure, resulting in pulmonary hypertension
      • to compensate for the increased pulmonary pressure, the right ventricle grows thicker and stronger
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28
Q

chronic mitral regurgitation

A
  • when blood flows backward into the left atrium
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29
Q

mitral valve prolapse

A
  • most common cause of chronic mitral regurgitation
  • has congenital and acquired forms
    • in younger people, it is usually caused by excess valve leaflet material
  • most people lack symptoms
  • regurgitation can worsen if there is a lengthening and rupture of the chordae tendinae extending from the papillary muscles to the valve flaps
    • in those cases, the mitral valve can be repaired or replaced with a mechanical or biological (pig or cow) valve
30
Q

septal defects

A
  • holes in the septum between the right and left sides of the heart
  • can produce heart murmurs
  • usually congenital
  • may occur either in the interatrial or interventricular spetum
  • if septal defects are not accompanied by other abnormalities, blood will usually pass through the defect from the left to the right side, due to the higher pressure on the left side
    • this may lead to pulmonary hypertension and edema
31
Q

When does atrial contraction occur?

When does atrial relaxation occur?

A
  • Atrial contraction occurs toward the end of diastole, when the ventricles are relaxed
  • When the ventricles contract during diastole, the atria are relaxed
32
Q

quiescent period

A
  • relaxation phase when all four chambers of the heart are in diastole
  • the quiescent period is altered when the heart rate is changed
33
Q

How much blood fills the ventricles before the atria contracts?

Contraction of the atria adds the final % to the end-diastolic volume.

A

80%

20%

34
Q

end-diastolic volume

A

total volume of blood in the ventricles at the end of diastole

35
Q

ejection fraction

A

contraction of the ventricles in systole ejects about 2/3 of the blood they contain

36
Q

stroke volume

A

the amount of blood ejected when ventricles contract

37
Q

end-systolic volume

A

one-third of the initial amount of blood left in the ventricles

38
Q

At an average cardiac rate of 75 bpm, each cycle lasts seconds; seconds in diastole, and seconds in systole

A
  • each cycle lasts 0.8 seconds
  • 0.5 seconds spent in diastole
  • systole takes 0.3 seconds
39
Q

The right and left atria contract almost simultaneously, followed by the contraction of the left and right ventricles to seconds later

A

0.1 to 0.2 second later

40
Q

isovolumetric contraction

A
  • phase of cardiac cycle
  • as the ventricles begin their contraction, the intraventricular pressure rises, causing the AV valves to snap shut and produce S1
    • at this time, the ventricles are neither being filled with blood (because the AV valves are closed) nor ejecting blood (because the intraventricular pressure has not risen sufficiently to open the semilunar valves)
41
Q

ejection phase

A
  • when the pressure in the left ventricle becomes greater than the pressure in the aorta, the semilunar valves open
    • the pressure in the left ventricle and aorta rises to about 120 mmHg when ejection begins and the ventricular volume decreases
42
Q

isovolumetric relaxation

A
  • as the pressure in the ventricles falls below the pressure in the arteries, the back pressure causes the semilunar valves to snap shut and produce S2
    • the pressure in the aorta falls to 80 mmHg, while pressure in the left ventricle falls to 0 mmHg
    • this phase lasts until the pressure in the ventricles falls below the pressure in the atria
  • at the beginning of diastole
43
Q

rapid filling phase

A

when the pressure in the ventricles falls below the pressure in the atria, the AV valves open and a phase of rapid filling of the ventricles occurs

44
Q

atrial contraction (atrial systole)

A

delivers the final amount of blood into the ventricles immediately prior to the next phase of isovolumetric contraction of the ventricles

45
Q

events of cardiac cycle

A
  1. isovolumetric contraction
  2. ejection
  3. isovolumetric relaxation
  4. rapid filling of ventricles
  5. atrial contraction
46
Q

maximum pressure produced at systole in the right ventricle?

what does the pressure fall to at diastole?

A

25 mmHg

8 mmHg

47
Q

when is a pulse felt?

A

when the arterial pressure rises from diastolic to systolic levels and pushes against the examiner’s finger

48
Q

dicrotic notch

A
  • di = twice and krotos = beat
  • inflection in the descending portion of the arterial pressure graph, which cannot be felt on palpation
  • produced by closing of the elastic aortic and pulmonic semilunar valves
    • the closed semilunar valves are stretched by the blood pressure dgenerated by the inward recoil of the elastic aorta and pulmonary arteries
      • this leads to a slight drop in BP
    • the elastic semilunar valves then recoil, which leads to a quick and slight upsurge in BP in the pulmonary trunk and aorta
    • the continued inward recoild of the pulmonary trunk and aorta also contributes to this slight upsurge
49
Q

myocardium

A
  • entire mass of cells interconnected by gap junctions (which function as electrical synapses)
  • a myocardium is a single functioning unit, or functional syncytium, because action potentials that originate in any cell in the mass can be transmitted to all the other cells
50
Q

automatic nature of the heartbeat is referred to as ?

A

automaticity (or intrinsic rhythmicity)

51
Q

regions that can spontaneously generate action potentials and function as pacemakers

A
  • sinoatrial (SA) node
    • the only pacemaker in the normal heart
  • AV node
    • potential, or secondary, pacemaker region
  • Purkinje fibers
    • potential, or secondary, pacemaker region
52
Q

SA node

A
  • sinoatrial node
  • located in the right atrium near the opening of the superior vena cava
  • serves as the primary (normal) pacemaker of the heart
  • do not maintain a resting membrane potential
53
Q

potential, or secondary pacemaker regions

A
  • AV node (slower than the SA node)
  • Purkinje fibers (slower than the SA node and AV node)
  • these are normally suppressed by action potentials originating in the sinoatrial node
54
Q

pacemaker potential

A
  • diastolic depolarization
  • during diastole, the SA node exhibits a slow spontaneous depolarization
  • involves ion channels in the plasma membrane and the sarcoplasmic reticulum
55
Q

HCN channels

A
  • Hyperpolarization Cyclic Nucleotide channels
  • unique to pacemaker cells
  • allow inward flow of Na+ when the channels open
    • “funny current”
  • open in response to:
    • hyperpolarization
    • cyclic AMP (produced in response to stimulation of beta-adrenergic receptors by epinephrine and norepinephrine
  • important in producing diastolic depolarization
56
Q

role of Ca2+ in diastolic depolarization

A
  • when the diastolic depolarization reaches the threshold value (about -40 mV), it causes the opening of voltage-gated Ca2+ channels in the plasma membrane (dihydropyridine receptors)
  • it is the influx of Ca2+ that causes the upward phase of the action potential in the pacemaker cells
  • while the upward phase of the action potential is occurring, the relatively small amount of Ca2+ that has entered stimulates the opening of Ca2+ release channels in the sarcoplasmic reticulum (ryanodine receptors, RyR2 type)
    • this produces a massive release of Ca2+ from the SR into the cytoplasm that causes contraction of the myocardial cells
  • repolarization is then produced by the opening of voltage-gated K+ channels that allows the outward migration of K+
57
Q

sinoatrial conduction pathways

A
  • the SA node consists of different pacemaker regions that are electrically separated from each other and from the surrounding myocardial cells of the right atrium
    • these regions communicate electrically through these pathways
  • action potentials spread through these pathways to depolarize both atria
58
Q

ectopic pacemaker

A
  • ectopic focus
  • a region that serves as an abnormal pacemaker when the SA node is blocked
    • AV node, purkinje fibers
  • rate set by an ectopic pacemaker would be slower than the normal sinus rhythm
59
Q

resting membrane potential of myocardial cells

A

-85 mV

60
Q

myocardial action potential steps

A
  • step 1: upshoot phase of the action potential of nonpacemaker cells is due to the rapid inward diffusion of Na+ through fast Na+ channels
    • membrane potential quickly declines to about -15 mV (maintained for about 200-300 msec before repolarization; this is the plateau phase)
  • step 2: plateau phase (absolute refractory period) that results from slow inward diffusion of Ca2+ through slow Ca2+ channels (dihydropyridine receptors) which balances a slow outward diffusion of K+)
    • begins excitation-contraction coupling
  • step 3: rapid repolarization by opening of voltage-gated K+ channels and rapid outward diffusion
61
Q

conducting tissues of the heart

A
  • action potentials spread from SA node, through the atria, and into the atrioventricular node (AV node)
    • located on the inferior portion of the interatrial septum
  • action potentials continue through the atrioventricular bundle (or bundle of His)
    • at top of interventricular septum
    • spreads into right and left bundle branches that are continuous with the purkinje fibers within ventricular walls
62
Q

conduction of impulse

A
  • SA node
    • rate of 0.8 to 1.0 m/sec
  • then conduction rate slows considerably as the impulse passes into the AV node
    • 0.03 to 0.05 m/sec (accounts for over half of time delay between excitation of atria and ventricles)
  • conduction rate increases in the atrioventricular bundles and reaches 5 m/sec in the purkinje fibers
63
Q

signaling complexes

A
  • regions where the sarcolemma come in close proximity to the sarcoplasmic reticulum
  • ~20,000 in a myocardial cell
    • all activated at the same time by depolarization
64
Q

ways to reduce sarcoplasmic Ca2+

A
  • the concentration of Ca2+ must be sufficiently lowered to allow myocardial relaxation
  • 1) sarcoplasmic reticulum Ca2+ ATPase, or SERCA pump
    • actively transports Ca2+ into the lumen of the SR
  • 2) Na+/Ca2+ exchanger (NCX)
    • secondary active transport
    • downhill movement of Na+ into the cell powers the uphill extrusion of Ca2+ (across sarcolemma into the extracellular fluid)
  • 3) Ca2+ ATPase pump
    • primary active transport (transports across sarcolemma into the extracellular fluid)
65
Q

functional synctium

A
  • functional syncytium of the atria and functional synctium of the ventricles is stimulated as a single unit and contracts as a unit
66
Q

QRS wave

A
  • spread of depolarization through the ventricles (contraction)
    • corresponds to the action potential
  • seen at the beginning of systole
  • stimulation of contraction by promoting diffusion of Ca2+ into the regions of the sarcomeres
67
Q

P wave

A
  • spread of atrial depolarization
  • when about half the mass of the atria is depolarized, the upward defelection reaches a maximum value because the potential difference between the depolarized and unstimulated portions of the atria is at a maximum
  • when the entire mass of the atria is depolarized, the ECG returns to baseline because all regions of the atria have the same polarity
68
Q

S-T segment

A

plateau phase of cardiac action potential

69
Q

T wave

A

repolarization of the ventricles

70
Q

direction of depolarization and repolarization of ventricles

A
  • depolarization of the ventricles occurs from the endocardium to the epicardium
  • repolarization occurs from the epicardium to the endocardium
71
Q

S1 and S2 in relationship to ECG

A
  • S1 is produced immediately after the QRS wave
  • S2 is produced shortly after the T wave begins