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Block 1: Physiology > Lecture 6 > Flashcards

Lecture 6 Flashcards

1
Q

Heart consists of 2 Pumps?

A

Right and Left composed of Muscular Chambers (Atria and Ventricles) separated by Valves

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2
Q

Muscular Chambers of the Heart?

A

Atria and Ventricles separated by valves

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3
Q

Muscle around Left Ventricle are?

A

Stronger because it has greater forces to work against

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4
Q

Muscle around Left Ventricle are?

A

Stronger because it has greater forces to work against

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5
Q

Movement of Heart Valves is based on?

A

Pressure differences between Atria and Ventricle

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6
Q

Open Heart Valve?

A

Ejecting blood

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7
Q

Closed Heart Valve?

A

Filling Atria/Ventricle

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8
Q

Heart valves open and close in a?

A

Coordinated way

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9
Q

(Excitation-Contraction Coupling)
Muscle contraction closely follows?

A

Wave of depolarization (excitation) throughout Heart

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10
Q

When Ventricles depolarize they?

A

Contract

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11
Q

Stroke Volume?

A

Amount of blood ejected from Heart, based on Systolic/Diastolic volume

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12
Q

Cardiac Output is?

A

Stroke Volume x Heart Rate

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13
Q

End Diastolic Volume?(EDV)

A

Amount of blood sitting there before Ventricle contracts

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14
Q

End Systolic Volume (ESV)?

A

Small amount of blood, after blood has been pushed out

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15
Q

Stroke Volume is ______ - ______?

A

SV = EDV - ESV

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16
Q

Stroke is volumetric representation of?

A

Pulse Pressure

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17
Q

Increase Pulse Pressure, Increase?

A

Stroke Volume

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18
Q

Venous Return?

A

Amount of blood returning to right atrium per minute

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19
Q

If blood not returned to right atria, Cardiac Output does?

A

Not venous return, blood accumulating in lungs or venous compartment

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20
Q

With valves closed (filling atria/ventricle), pressure develops during?

A

Myocardial Contraction (Isovolumetric Contraction)

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21
Q

When ventricular chamber pressure exceeds?

A

Aortic BP, valves open

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22
Q

Pv > Pa?

A

Open valve, ejection of blood

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23
Q

Cardiac Muscle is striated because of?

A

Thick (myosin) and Thin (actin) filaments

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24
Q

Intercalated discs between cardiac cells contain both?

A

Mechanical (Fascia Adherent and Desmosomes) and Electrical Connections (Gap Junctions) between cells (permits function as a syncytium)

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25
Q

T-tubules lie along the?

A

Z-Line and not the I-Bands (help propagate charge)

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26
Q

Sarcoplasmic Reticulum?

A

-Not as dense as in skeletal muscle
-Ca2+ mainly extracellular
-Terminal cistern about the T-tubules
-SERCA2a, calcium reuptake pump, is inhibited by phospholamban, and integral SR protein

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27
Q

SERCA2a?

A

Calcium reuptake pump, is inhibited by phospholamban, an integral SR protein

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28
Q

Mitochondria?

A

Abundant and occupy ~30% of Heart volume (because very metabolically active)

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29
Q

Cardiac Muscle has an abundance of?

A

Connective Tissue to prevent rupture and overstretching of Heart

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30
Q

Z-Line?

A

Point of attachment of thin filaments

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31
Q

Thin Filaments?

A

Actin, troponin (TNNC1, TNNI3, TNNT2), tropomyosin (TPM1), nebulin (scaffold for thin filament), alpha-actinic (anchors actin to Z-Line), tropomodulin (regulates length of thin filament)

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32
Q

Thick Filament?

A

Myosin, meromyosin and C-protein (scaffolds for thick filament), Titian. MHC has 2 isoforms: alphaMHC (faster velocity) and betaMHC

33
Q

Titin?

A

Tethers myosin to Z-Line; stretch-sensor, signal transducer, and may be involved in increasing force in response to stretch (Important for Sterling’s Law)

34
Q

Depolarization causes?

A

Calcium entry via voltage-gated Calcium Channels

35
Q

Calcium entry triggers?

A

Calcium release from SR via Ryanodine receptors

36
Q

(Calcium Homeostasis in Myocardial Cells)
Increased intracellular calcium is via?

A

1) Release from SR (90%) via Ca-induced Ca release channels
(majority)
2) Influx through voltage-gated “L-type” calcium channels (10%)

37
Q

(Calcium Homeostasis in Myocardial Cells)
Relaxation?

A

Intracellular Ca pumped back into SR and also out of myocyte via CaATPase pumps and Na/Ca exchanger (SERCA at 905)

38
Q

Force generated dependent on?

A

Cross-Bridging cycling

39
Q

(Excitation-Contraction Coupling)
Cross-riding Cycle (ratchet mechanism)?

A

(Ca2+ proportional to cross-bridge cycling)
1) Bound ATP causes conformation change in hinge region of myosin and promotes binding to actin
2) Hydrolysis of ATP causes a conformational change in hinge region of myosin, causing movement of thin filament and shortening of sarcomere
3) After movement, ADP dissociates from myosin
4) Myosin-actin remain bound with no ATP (rigor mortis state, death)
5) ATP binding to myosin
6) ATP binding causes dissociation of myosin (ATP) from actin

40
Q

Resting Tension (RT)?

A

Produced by “resting” biomechanics properties of cardiac tissue

41
Q

Active Tension (AT)?

A

Produced by cross-bridge cycling

42
Q

Total Tension (TT)?

A

RT plus AT

43
Q

Lmax?

A

Length at which active force is maximal (increased force at particular moment)

44
Q

Increased L?

A

Increased Tension

45
Q

Force (Tension) produced with increased?

A

Muscle Length (Stretch)

46
Q

Stretching the Heart increases?

A

Force of Contraction, but not by increasing [Ca++] or increased filament overlap

47
Q

Frank-Starling Law of the Heart?

A

“Force of contraction of Heart is proportional to initial fiber length”

48
Q

Length-dependent increase in force following stretch may be due to?

A

1) Decreased interfilament spacing (decreased space between actin + myosin) between actin and myosin, brought about by Titin, which binds both of filaments
2) Increase in sensitivity to calcium of actin-myosin complex

49
Q

Increased Stretch?

A

Increased Tension because need more space between myosin and Z-Disk

50
Q

Role of Titin?

A

-Spring in controlling distance between actin + myosin filaments
-Titin binds both actin and myosin
-Stretching brings the 2 filaments closer together

51
Q

One mechanism to explain how preload influences contractile force is that increasing?

A

Sarcomere length increases troponin C calcium sensitivity, which increases rate of cross-bridge attachment and detachment, and amount of tension developed by muscle fiber

52
Q

(Stretching increases sensitivity of cardiac muscle to calcium)
Stretch sarcomere with same amount of calcium will get?

A

Greater larger force

53
Q

(Stretching increases sensitivity of cardiac muscle to calcium)
Will get greater force by being more sensitive to?

A

Calcium

54
Q

(Heart responds to an increase in stretch)
When there’s an increase in venous return?

A

There’s a greater force of contraction, resulting in a greater cardiac ejection

55
Q

End effect?

A

Input = Output

56
Q

Venous Return?

A

Cardiac Output
(“The Heart pumps what it gets”)

57
Q

Increased Venous Return = ?

A

Increased Venous Return = Increased EDV = Increased Stretch = Increased Force

58
Q

Increased Venous Return = ?

A

Increased Venous Return = Increased EDV = Increased Stretch = Increased Force

59
Q

If Increase amount of blood returning to RA?

A

Increasing EDV

60
Q

Sympathetic Nervous System?

A

(“fight or flight”)
-Superior cervical ganglion
-Middle cervical ganglion

61
Q

Parasympathetic Nervous System?

A

(“rest and digestion”)
Vagus (X) nerve

62
Q

Sympathetic?

A

Increased Ca2+ release and reuptake and increased contractions

63
Q

(Sympathetic or Parasympathetic)
Epinephrine/Norepinephrine?

A

Sympathetic

64
Q

Adenylyl Cyclase will produce?

A

cAMP

65
Q

Beta-Adrenergic stimulation enhances?

A

Contraction and accelerates relaxation

66
Q

(Gs –> Increased cAMP –> PKA which phosphorylates)
a. ?

A

VGCC (CHPR) and increased calcium entry

67
Q

(Gs –> Increased cAMP –> PKA which phosphorylates)
b. ?

A

RYR, increased calcium release

68
Q

(Gs –> Increased cAMP –> PKA which phosphorylates)
c. ?

A

Phospholamban, removing its inhibition of CaATPase, thus increased uptake of Ca++ by CaATPase –> shortened contraction and increased rate of relaxation (lusitropic effect) due to rapid accumulation of calcium, which also increased Ca++ stores for next contraction

69
Q

(Gs –> Increased cAMP –> PKA which phosphorylates)
e. ?

A

Troponin I, makes Ca++ dissociate from myofilaments –> decreased myofilament sensitivity to Ca++ –> relaxation

70
Q

In contrast, Vagal stimulation?

A

ACh –> M2 –> Gi –> Decreased cAMP (decreased amplitude Ca2+ and force and increased relaxation time)

71
Q

Preload dependent on?

A

EDV, how much pressure your ventricle has sitting in it (dependent on End Diastolic Volume)

72
Q

Preload dependent on?

A

EDV, how much pressure your ventricle has sitting in it (dependent on End Diastolic Volume)

73
Q

Factors affecting EDV/ Preload?

A

1) Ventricular compliance (stretch/stiffness)
2) Filling time (Heart Rate) (increased time = increased preload = increased EDV)
3) Venous Return (increased return = increased preload = increased EDV)

74
Q

Afterload?

A

Represents forces that Heart has to work against (all sitting in Aorta that has to go out)
(ex. Systemic Aortic Pressure)

75
Q

Increasing aortic pressure does not?

A

Decrease cardiac output until MAP > 160 mmHg

76
Q

MAP?

A

Mean Aortic Pressure

77
Q

Cardiac output remains constant?

A

Until MAP rises above 160 mmHg

78
Q

Cardiac output remains constant?

A

Until MAP rises above 160 mmHg

Block 1: Physiology (10 decks)

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