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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
T-tubules lie along the?
Z-Line and not the I-Bands (help propagate charge)
26
Sarcoplasmic Reticulum?
-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
27
SERCA2a?
Calcium reuptake pump, is inhibited by phospholamban, an integral SR protein
28
Mitochondria?
Abundant and occupy ~30% of Heart volume (because very metabolically active)
29
Cardiac Muscle has an abundance of?
Connective Tissue to prevent rupture and overstretching of Heart
30
Z-Line?
Point of attachment of thin filaments
31
Thin Filaments?
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)
32
Thick Filament?
Myosin, meromyosin and C-protein (scaffolds for thick filament), Titian. MHC has 2 isoforms: alphaMHC (faster velocity) and betaMHC
33
Titin?
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
Depolarization causes?
Calcium entry via voltage-gated Calcium Channels
35
Calcium entry triggers?
Calcium release from SR via Ryanodine receptors
36
(Calcium Homeostasis in Myocardial Cells) Increased intracellular calcium is via?
1) Release from SR (90%) via Ca-induced Ca release channels (majority) 2) Influx through voltage-gated "L-type" calcium channels (10%)
37
(Calcium Homeostasis in Myocardial Cells) Relaxation?
Intracellular Ca pumped back into SR and also out of myocyte via CaATPase pumps and Na/Ca exchanger (SERCA at 905)
38
Force generated dependent on?
Cross-Bridging cycling
39
(Excitation-Contraction Coupling) Cross-riding Cycle (ratchet mechanism)?
(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
Resting Tension (RT)?
Produced by "resting" biomechanics properties of cardiac tissue
41
Active Tension (AT)?
Produced by cross-bridge cycling
42
Total Tension (TT)?
RT plus AT
43
Lmax?
Length at which active force is maximal (increased force at particular moment)
44
Increased L?
Increased Tension
45
Force (Tension) produced with increased?
Muscle Length (Stretch)
46
Stretching the Heart increases?
Force of Contraction, but not by increasing [Ca++] or increased filament overlap
47
Frank-Starling Law of the Heart?
"Force of contraction of Heart is proportional to initial fiber length"
48
Length-dependent increase in force following stretch may be due to?
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
Increased Stretch?
Increased Tension because need more space between myosin and Z-Disk
50
Role of Titin?
-Spring in controlling distance between actin + myosin filaments -Titin binds both actin and myosin -Stretching brings the 2 filaments closer together
51
One mechanism to explain how preload influences contractile force is that increasing?
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
(Stretching increases sensitivity of cardiac muscle to calcium) Stretch sarcomere with same amount of calcium will get?
Greater larger force
53
(Stretching increases sensitivity of cardiac muscle to calcium) Will get greater force by being more sensitive to?
Calcium
54
(Heart responds to an increase in stretch) When there's an increase in venous return?
There's a greater force of contraction, resulting in a greater cardiac ejection
55
End effect?
Input = Output
56
Venous Return?
Cardiac Output ("The Heart pumps what it gets")
57
Increased Venous Return = ?
Increased Venous Return = Increased EDV = Increased Stretch = Increased Force
58
Increased Venous Return = ?
Increased Venous Return = Increased EDV = Increased Stretch = Increased Force
59
If Increase amount of blood returning to RA?
Increasing EDV
60
Sympathetic Nervous System?
("fight or flight") -Superior cervical ganglion -Middle cervical ganglion
61
Parasympathetic Nervous System?
("rest and digestion") Vagus (X) nerve
62
Sympathetic?
Increased Ca2+ release and reuptake and increased contractions
63
(Sympathetic or Parasympathetic) Epinephrine/Norepinephrine?
Sympathetic
64
Adenylyl Cyclase will produce?
cAMP
65
Beta-Adrenergic stimulation enhances?
Contraction and accelerates relaxation
66
(Gs --> Increased cAMP --> PKA which phosphorylates) a. ?
VGCC (CHPR) and increased calcium entry
67
(Gs --> Increased cAMP --> PKA which phosphorylates) b. ?
RYR, increased calcium release
68
(Gs --> Increased cAMP --> PKA which phosphorylates) c. ?
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
(Gs --> Increased cAMP --> PKA which phosphorylates) e. ?
Troponin I, makes Ca++ dissociate from myofilaments --> decreased myofilament sensitivity to Ca++ --> relaxation
70
In contrast, Vagal stimulation?
ACh --> M2 --> Gi --> Decreased cAMP (decreased amplitude Ca2+ and force and increased relaxation time)
71
Preload dependent on?
EDV, how much pressure your ventricle has sitting in it (dependent on End Diastolic Volume)
72
Preload dependent on?
EDV, how much pressure your ventricle has sitting in it (dependent on End Diastolic Volume)
73
Factors affecting EDV/ Preload?
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
Afterload?
Represents forces that Heart has to work against (all sitting in Aorta that has to go out) (ex. Systemic Aortic Pressure)
75
Increasing aortic pressure does not?
Decrease cardiac output until MAP > 160 mmHg
76
MAP?
Mean Aortic Pressure
77
Cardiac output remains constant?
Until MAP rises above 160 mmHg
78
Cardiac output remains constant?
Until MAP rises above 160 mmHg

Block 1: Physiology (10 decks)

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