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Pathophysiology Cardiac > Modual 3 > Flashcards

Modual 3 Flashcards

1
Q

Name the cardiac layers (from heart –> pericardium)

A

Endocardium

Myocardium

Epicardium

Parietal Space = Pericardial Cavity

Parietal Pericardium

Fibrous Pericardium

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2
Q

Describe the endocardium

A

Similar to endothelial cells that line blood vessels –> smooth “frictionless” surface

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3
Q

What makes up the myocardium?

A

Cardiac Muscle CElls (contractile Tissue)

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4
Q

What is the epicardium (visceral pericardium)?

A

Connective tissue layer

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5
Q

What is contained w/in the parietal space (pericardial cavity)?

A

Pericardial fluid –> reduces friction during heart movement

**clinically –> pericardial effusion (cardiac tamponade)

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6
Q

What is the parietal pericardium?

A

Connective tissue layer insulating the heart

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7
Q

What is the fibrous pericardium?

A

Fibrous sac that “contains” the heart

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8
Q

What are muscle fibers of the myocardial cells made of?

A

Myofibrils

Single Nuclei

Mitochondira

Sarcoplasma Reticulum

Cytoplasm

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9
Q

What is the plasma membrane of myocardial cells called?

A

Sarcolemma

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10
Q

What are T-tubules?

A

Invaginations of sarcolemma into the myofibrils

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11
Q

What does the sarcolemma do?

A

Spreads action potential throughout muscle fiber

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12
Q

How does the action potential spread throughout the myofibril?

A

Lengthwise along the sarcolemma

Penetrates deep into myofibrils via T-tubules

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13
Q

What is the point of the sarcolemma/T-tubule arrangement?

A

Allows for rapid transmission of action potential

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14
Q

What are myofibrils made up of?

A

Myofilaments

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15
Q

What are myofilaments?

A

Protein filaments that provide mechanical shortening/lengthening of the muscle filament

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16
Q

How are myofilaments arranged?

A

In units called sarcomeres

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17
Q

What are sarcomeres?

A

Repeating units arranged in series (end to end) along the length of the myofibril

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18
Q

What do sarcomeres contain?

A

Myofilaments

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19
Q

What are the proteins that make up the myofilaments?

A

Actin

Myosin

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20
Q

How are myosin microfilaments arranged?

A

Chains are wrapped together each w/ protruding globular heads

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21
Q

What do the globular heads of myosin filaments do?

A

Bind to actin and swivel –> mechanical shortening of sarcomere

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22
Q

What do the globular heads of myosin contain?

A

Binding site for actin

Receptor for ATPase

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23
Q

How are actin (thin) microfilaments arranged?

A

2 chains of actin wrap together to form actin microfilaments

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24
Q

Where would you find tropomyosin on the actin microfilament?

A

“wrapped” around the length of the actin filament

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25
Q

Where would you find troponin on the actin microfilament?

A

Attached intermittently along the length of tropomyosin

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26
Q

What is the function of troponin/tropomyosin?

A

Allows exposing/covering of the binding site on actin for the myosin globular heads

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27
Q

What happens if the binding site of the globular head of myosin on actin is covered?

A

Sacromere/muscle fiber can’t contract

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28
Q

What happens if the binding site of the globular head of myosin on actin is exposed?

A

Myosin head can bind to actin –> mechanical contraction of sarcomere/muscle fiber

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29
Q

What are the subunits of troponin?

A

Troponin T

Troponin C

Troponin I

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30
Q

What does the troponin T subunit do?

A

Binds troponin to tropomyosin and actin

31
Q

What does the troponin C subunit do?

A

Contains binding site for Ca2+

**Ca2+ = on/off switch for contraction

32
Q

What does the troponin I subunit do?

A

Inhibits ATPase

**ATP is needed fuel for contraction

33
Q

What does the Z line do?

A

Anchors/connects thin filaments

**z-line to z-line = sarcomere

34
Q

Describe the cross-bridge theory of myocardial muscle contraction

A

Ca2+ binds to troponin –> exposes binding site on actin = trigger

Myosin head attaches to actin

Myosin head binds to actin –> releases ADP and Pi –> myosin head swivels

ATP binds to myosin head

ATP –> ADP + Pi –> release of myosin head from actin to relaxed position

35
Q

Describe excitiation-contraction coupling

A

Action potential travels across sarcolemma down T-tubules

Action potential reaches sarcoplasm a reticulum (stores Ca2+) –> release of Ca2+

Ca2+ diffuses into microfilaments and binds to troponin-C –> exposes myosin head binding site on actin

36
Q

Why is it important that cardiac muscle cells have a lot of mitochondria?

A

Supply ATP for contraction

37
Q

Where are the intercalated discs of cardiac muscle fibers located and what do they do?

A

Between muscle fibers

Allow action potential to travel from cell to cell

38
Q

What do desmosomes do?

A

Attach each muscle fiber to the next

39
Q

What do gap junctions do?

A

Allows electrical action potential to spread through intercalated disc from one muscle fiber to the next

40
Q

What is the frank starling law of the heart?

A

The length-tension relationship between the length of myocardial muscle and force generation

41
Q

What is the length-tension relationship of healthy cardiac muscle?

A

Length of cardiac muscle fiber (sarcomere) is DIRECTLY related to the force generated by the muscle fiber

42
Q

What is the end-diastolic volume?

A

The volume that fills the ventricles

43
Q

What does the end-diastolic volume do?

A

Determines amount of “stretch” on the cardiac muscle fibers, which means:

Increase end-diastolic volumes = increase contractility

Increase contractility = increase stroke volume/cardiac output

44
Q

What happens to unhealthy cardiac muscle (heart failure)?

A

Has been dilated/damaged

Sarcomeres have been lengthened too far –> Frank Starling Law no longer applies

45
Q

What is LaPlace’s Law?

A

Wall tension (contraction force) is DIRECTLY related to the product of intraventricular pressure x internal radius (ventricular volume)

Wall tension (contraction force) is INDIRECTLY related to wall thickness

46
Q

What does LaPlace’s Law mean for a dilated thin walled ventricle full of blood?

A

It requires more time to generate a contraction force (wall tension) strong enough to generate intraventricular pressure needed to eject blood from the heart

**poor cardiac output/performance

47
Q

What is left ventricular preload?

A

Pressure generated in the L ventricle @ the end of diastole (ventricular filling)

**Preload = Left end-diastolic pressure

48
Q

What determines preload in a healthy heart?

A

L end-diastolic volume (Starling’s law of the heart)

49
Q

What happens if you increase left end-diastolic volume?

A

Increase Preload

Increase stroke volume/cardiac output

50
Q

What happens to preload in a pt w/ ventricular hypertrophy?

A

Increases preload

BUT less ventricular filling (decreased end diastolic volume) –> output will be reduced

51
Q

What will excessive left end-diastolic filling pressures cause?

A

Congestive back-up in pulmonary circulation

52
Q

What is afterload?

A

The voce the left ventricle must generate during systole to overcome aortic pressure to open the aortic valve

53
Q

What happens if there is increased afterload?

A

Ventricle has to work harder to eject blood:

Takes longer contraction time to generate necessary force

Increased afterload + insufficient contraction time = reduced stroke volume

54
Q

What could happen clinically with increased afterload?

A

Elevated systemic BP

Aortic Stenosis

Dilated ventricle

Decreased stroke volume (increased end systolic volume)

Hypertrophy to compensate

55
Q

Where are the cardiovascular control centers located in the brain?

A

Medulla

56
Q

What does the sympathetic nervous system do to the heart?

A

Increase HR

Increase Contractility

57
Q

What does the parasympathetic nervous system do to the heart?

A

Decrease HR

Decrease Contractility

58
Q

Which part of the autonomic nervous system dominates during rest?

A

Parasympathetic @ SA node

59
Q

What happens to the autonomic nervous system early during exercise?

A

Removal of parasympathetic influence @ SA node

60
Q

Which part of the autonomic nervous system dominates during intensive exercise?

A

Sympathetic @ SA node

61
Q

Where are arterial baroreceptors located?

A

Aortic Arch

Carotid Sinus

**systemic “stretch” receptors

62
Q

What will increased pressure cause the baroreceptors to do?

A

Increase parasympathetic nervous system
stimulation

Decrease sympathetic nervous system stimulation

Net Effect = ↓ HR, ↑ vasodilation which ↓ BP

63
Q

What will decreased pressure cause the baroreceptors to do?

A

Increase sympathetic nervous system
stimulation

Decrease parasympathetic nervous system stimulation

Net Effect = ↑ HR, ↑ vasoconstriction which
↑ BP

64
Q

Where are atrial stretch receptors located?

A

R and L atria

65
Q

What do atrial stretch receptors control?

A

Blood Volume

66
Q

What will stimulation of atrial receptors result in?

A

Stimulate the release of ANP from atria

67
Q

What does ANP do?

A

Stimulate kidneys to excrete urine and sodium

**end result = reduced blood volume

68
Q

What does the stimulation of atrial receptors result in (in terms of HR)?

A

Increase HR

**arterial baroreceptors have dominant role in maintaining HR compared to atrial receptors

69
Q

What stretch receptors are involved in the bainbridge reflex?

A

Stretch receptors in atria

70
Q

What is the bainbridge reflex do?

A

↑ HR after IV infusion (increase blood volume)

71
Q

What are the 2 factors that determine contractility?

A

Sympathetic nervous input

Increased stretch of ventricle (healthy heart)
Starling’s Law of the Heart –> ↑ preload =
↑ contractility

72
Q

What are the factors that determine cardiac output?

A

CO = HR x SV

73
Q

What happens with increased stroke volume?

A

↑ venous return –> ↑ blood volume/↑ sympathetic activity on veins

↑ end-diastolic volume

↑ preload

Pathophysiology Cardiac (4 decks)

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