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Cardiac, Renal, Respiratory Pathophysiololgy > Basic Cardiac Structure and Function > Flashcards

Basic Cardiac Structure and Function Flashcards

1
Q

Right-sided structures lie mostly _______ to their______ counterparts.

A

anterior………left-sided

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2
Q

Both _____ chambers located mostly to the ____ of their corresponding ________.

A

atrial…..right…..ventricles

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3
Q

What is the function of the pericardium?

A
  1. Allows heart to beat without friction

2. Allows for room to expand

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4
Q

How much fluid fills the pericardial cavity?

A

5-30 ml

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5
Q

What keeps the pericardium attached?

A
  1. Central tendon of diaphram
  2. Sternopericardial ligament
  3. Vertebropericardial ligaments
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6
Q

What are the 3 sections of the heart’s layers from outermost to innermost?

A
  1. Pericardium (heart sac)
  2. Myocardium (muscle layer)
  3. Subendocardium
  4. Endocardium (inner lining)
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7
Q

What layers make up the pericardium from outermost to innermost?

A
  1. Parietal pericardium (outermost)

2. Visceral pericardium or epicardium (innermost)

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8
Q

What is the endocardium?

A

endothelial cell layer covering trabeculae

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9
Q

What is the subendocardial layer?

A

The layer between the endocardium and myocardium

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10
Q

What structures are contained in the subendocardial layer?

A

fibroblasts, elastic & collagenous fibers, nerves, Purkinje fibers, blood vessels (Thebesian veins)

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11
Q

Describe the flow of blood through the right side of the heart.

A
  • Right atrium receives deoxygenated blood from the body (IVC & SVC) and heart (coronary sinus).
  • Right ventricle pumps deoxygenated blood through the lungs via the pulmonary artery
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12
Q

What are the structures in the right ventricle?

A
  1. Inner wall
  2. Moderator Band
  3. Papillary muscles
  4. Outflow tract
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13
Q

What covers the inner wall of the right ventricle?

A

Trabeculae canreae

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14
Q

What is the Moderator Band?

A

Large trabecula and crosses right ventricle cavity

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15
Q

Is the Moderator Band a component of a RBB or LBB?

A

RBB

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16
Q

How many papillary muscles are in the right ventricle?

A

Three on the tricuspid valve

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17
Q

What is the outflow tract called in right ventricle? How does it promote laminar flow?

A
  • Conus arteriosus

- Smooth surface

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18
Q

Describe the flow of blood through the left side of the heart.

A
  • Left atrium received oxygenated blood from the lungs via pulmonary veins.
  • Left ventricle pumps oxygenated blood to systemic circulation via the aorta
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19
Q

How does the left ventricle compare to the right ventricle?

A
  • Left ventricle has a thicker wall 9-11 mm
  • Left ventricle has 2 papillary muscles (mitral valve) when right has 3
  • Both smooth walled for laminar flow
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20
Q

What is the name of the smooth wall in left ventricle?

A

Aortic Vestibule

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21
Q

What is the origin of the RCA & LCA?

A

Just above the aortic valve cusps

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22
Q

What is the cardiac conduction system pathway?

A
  • SA node
  • Internodal bundles (RA) and Interartial bundle to LA
  • AV node
  • AV bundle of His
  • Right and Left branches of AV bundle of His
  • Subendocardial fibers (Purkinje fibers)
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23
Q

The subendocardial plexus of purkinje fibers allow what to happen?

A

-Papillary muscles to contract before ventricle wall

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24
Q

What is prevented by the papillary muscles?

A

valve regurgitation

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25
Q

What sympathetic fibers innervate the cardiac nerves and where do they terminate?

A
  • Sympathetic fibers from T1-T6

- In the heart and great vessels

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26
Q

What parasympathetic fibers innervate the heart and where?

A
  • CN X (vagus nerve)

- SA node, AV node, and Purkinje fibers

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27
Q

What occurs when the vagus nerve is stimulated?

A
  • From medulla Vagus fiber is (long) preganglionic and releases Ach at nicotinic receptor in ganglia
  • Postganglionic fiber (short) releases Ach and binds to M2 receptors on nodal/muscle tissue (Purkinje fibers)
  • Effects are inhibitory
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28
Q

What are the cardiac effects of vagal stimulation?

A
  • decreased heart rate
  • increased AV node ERP (decreased conduction)
  • increased PR
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29
Q

What occurs with sympathetic stimulation in the heart?

A
  • From spinal column preganglionic fibers (short) release Ach at nicotinic receptors in ganglia
  • Postganglionic adrenergic fiber (long) releases NE at alpha/beta receptors on heart and great vessels
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30
Q

What are the cardiac effects of sympathetic stimulation?

A
  • increased heart rate
  • decreased AVN ERP (increased conduction)
  • decreased PR
  • increased contractility (SV)
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31
Q

What cardiac vessels branch of the LCA (left coronary artery)?

A
  • AIV, anterior interventricular artery (LAD)

- Circumflex artery

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32
Q

What cardiac vessels branch of the RCA (right coronary artery)?

A
  • PIV, posterior interventricular artery (PDA)

- Right marginal artery

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33
Q

Muscle fibers below endocardium in subendocardium are supplied by coronary artery terminal branch or _______?

A

-Thebesian veins (particularly in papillary muscles and left vent. wall)

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34
Q

What is a myocyte?

A
  • individual cardiac muscle cell

- 25 microns x 100 microns

35
Q

What is a myofibril?

A

a group of sacromeres

36
Q

What is a sarcomere?

A

individual contractile unit of the cell (striations)

37
Q

What is a sarcolemma?

A

an excitable cell membrane of the muscle cell

38
Q

What are the functions of intercalated discs?

A

they are gap junctions between myocytes and coordinate muscle contraction

39
Q

What is the function of the sacroplasmic reticulum?

A

Intracellular membrane network that releases Ca++ causing excitation contraction coupling

40
Q

What is a T-tubule?

A

invagination of the sarcolemma that conduct impulses from cell surface down into the cell to the sarcoplasmic reticulum

41
Q

Define action potential

A
  • reversal of electrical potential across a semipermeable membrane caused by conformational changes in selective ion channels
  • rhythmic, conducted appropriately, coupled to myocardial contraction
42
Q

What are 3 major electrically excitable cell types?

A
  1. SA and AV nodes (pacemaker cells)
  2. Purkinje fibers
  3. Cardiac myocytes
43
Q

Do pacemakers have neuromuscular junctions?

A

No, they have automaticity

44
Q

What is the resting potential of pacemaker (nodal) cells?

A

-60 mV

45
Q

What is the resting potential of myocytes?

A

-90 mV

46
Q

Where does spontaneous discharge occur in pacemaker cells?

A

SA node

47
Q

What is unique about pacemaker cells resting membrane potential?

A

-resting membrane potential -60 mV

slow voltage gate on Na+ channel cannot recover so Na+ channel remains inactivated

48
Q

What is unique about pacemaker cells ion channel?

A

allows continuous slow inflow of Na+ until threshold is reached

49
Q

Since Na+ channels are inactivated, upstroke of AP is dependent on ________?

A

Ca++ influx (slower)

50
Q

Depolarization depends on ion transport and is governed by 2 characteristics?

A
  • concentration gradients

- transmembrane potential

51
Q

How does concentration gradients govern depolarization?

A

If extracellular Na+ is 142 mEq and intracellular is 14 mEq

-Strong force drives Na+ into cell, down it conc. gradient and causes depolarization

52
Q

How does transmembrane potential govern depolarization?

A
  • the resting potential inside cell is -90 mV

- a strong electrical attraction for Na+ to enter cell.

53
Q

What type of Na+ channels do myocytes have?

A

Fast Na+ Channels

54
Q

What happens when Fast Na++ Channels are activated?

A
  • Open and close quickly

- Inactivated until membrane repolarized, providing refectory period

55
Q

Are Fast Na++ Channels active on pacemaker cells?

A

No, only on myocytes

56
Q

Why is the K+ conc. greater inside the cell?

A

Sodium-potassium pump

3 Na+ out
2 K+ in

57
Q

What is the function of the inward rectifier channels?

A
  • open in resting state allowing some K+ to flow out of cell

- overall negative interior charge slows K+ outflow

58
Q

What is the K+ equilibrium potential?

A

-91 mV (zero net movement)

59
Q

What is phase 4 of cardiac muscle AP?

A
  • Resting state before depolarization

- rectifier channels leak K+ out to keep TMP at -90 mV

60
Q

What is phase 0 of cardiac muscle AP?

A

-Rapid influx of Na+ through Fast Na+

61
Q

What is phase 1 of cardiac muscle AP?

A

-transient K+ channels open and K+ efflux returns TMP to 0 mV

62
Q

What is phase 2 of cardiac muscle AP?

A
  • influx of Ca++ through L-type Ca++ channels

- electrically balanced through delayed rectifier K+ channels

63
Q

What is phase 3 of cardiac muscle AP?

A
  • Ca++ channels close

- delayed rectifier K+ channels remain open until TMP returns to -90mV

64
Q

What is the “Fibrous Skeleton” of the heart?

A
  • fibrous connective tissue surrounding AV valves

- serves as electrical insulator, isolates atria & ventricles

65
Q

What is the only electrical conductor to the ventricles?

A

AV node

66
Q

Why is there a delay at the AV node?

A

allows atria time to contract before ventricles

67
Q

What is known as the “electrical gatekeeper”? Why?

A

AV node and limits ventricular stimulation during abnormal rapid atrial rhythms

68
Q

What is excitation-coupling contraction?

A

electrical AP leads to physical contraction

69
Q

What is regularly spaced on actin and has 3 subunits?

A

Troponin

70
Q

What is the double helix that lies between actin filaments and blocks actin and myosin interactions?

A

Tropomysin

71
Q

Thin filaments, a-helix?

A

actin

72
Q

What is myosin?

A
  • protein arranged in thick filaments

- globular heads contain myosin ATPase

73
Q

What are contractile proteins in muscles contractions?

A
  • myosin

- Actin

74
Q

What are regulatory proteins in muscle contractions?

A
  • Tropomyosin

- Troponin

75
Q

Describe the process of calcium induced calcium release.

A
  • L-Type Ca++ channels open during phase 2 of AP
  • Ca++ enters cell via T tubule
  • Ca++ triggers ryanodine receptorts on SR
  • SR dumps its stores of Ca++
76
Q

What is the MOA of Ca++ channel blockers?

A
  • bind to L-type Ca++ channels

- once bound, causes reduction in the transmembrane Ca++ current

77
Q

What are the effects of Ca++ channel blockers?

A
  • decrease SA node rate
  • decrease AV node rate
  • decrease contractility
  • increase vasodilation
78
Q

What are the three classifications of Ca++ channel blockers?

A
  1. benzothiazepines (diltiazem)
  2. phenylalkylamines (verapamil)
  3. dihydropyridines (nicardipine, amlodipine, nifedipine)
79
Q

Similarities between Diltiazem and Verapamil?

A
  • both exert the most negative inotropic effects

- both possess local anesthetic activity (increased toxicity during regional anesthesia)

80
Q

What adverse effects can Verapamil have on conduction?

A
  • Augment conduction of cardiac impulse over accessory tract through reflex sympathetic activity
  • resulting in increased ventricular response (WPW)
81
Q

Which Ca++ channel blocker has the greatest degree of vasodilation?

A

-Nicardipine

coronary antispasmoditc/vasodilatory effects are GREATER than its systemic arterial vasodilatory effects

82
Q

Adrenergic signaling

A
  • beta-adrenergic stimulation enhances Ca++ fluxes
  • NE binds to beta receptors
  • STIMULATES adenylate cyclase production; increases force of contraction
83
Q

Cholinergic signaling

A
  • Ach from parasympathetic nerve terminals bind to M2 receptors
  • INHIBITS adenylate cyclase; reduces HR

Cardiac, Renal, Respiratory Pathophysiololgy (2 decks)

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