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CV Week 1 > Heart Physiology 3 > Flashcards

Heart Physiology 3 Flashcards

1
Q

Explain how electrical impulses lead to heart contraction.

A

1) An action potential courses through the membrane (and transverse tubules) of cardiac myocytes

2) The resultant electric field induces a conformational change in voltage-gated sodium channels, opening them to ion flow

3) The cell is depolarized as sodium rushes in and calcium-channels on the membrane open allowing calcium to rush into the cell

4) Calcium release from membrane into myoplasm further induces release of calcium resevoirs from sarcoplasmic reticulum into myoplasm, amplifying the response

5) Myoplasmic calcium (now in HUGE quantities) binds troponin C, allowing myosin and actin to interact

6) Contraction occurs as sarcomeres pulled together

7) Contraction ends as calcium concentration falls - this is due to calcium channels closing, calcium being pumped back into sarcoplasmic reticulum, calcium pumped out of cell by sodium/calcium exchanger

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2
Q

What is another name for a ryanodine receptor?

A

Calcium release channel (found on membrane of sarcoplasmic reticulum)

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3
Q

What molecules can be measured in the blood to detect myocardial damage?

A

Cardiac Troponin T (cTnT) and cardiac Troponin I (cTnI)

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4
Q

What are the contractile proteins of cardiac muscles?

A

1) Myosin and Actin

2) Troponin and Tropomyosin

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5
Q

What is the function of tropomyosin in its resting state?

A

Inhibit interaction of myosin with actin

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6
Q

What are the 3 types of troponin?

A

1) Troponin T

2) Troponin I

3) Troponin C

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7
Q

What do Troponin T, I, & C each bind to?

A

1) TnT binds tropomyosin

2) TnI binds actin

3) TnC binds Calcium

T=tropomyosin; I=inhibitory; C=calcium

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8
Q

What is dystrophin?

A

1) Rod shaped protein which attaches cytoskeletal actin (not used in contraction) to membrane-associated and ECM-associated proteins

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9
Q

What are some suggested roles of dystrophin and dystrophin-glycoprotein complex?

A

1) Membrane stability during contraction

2) Force transduction (from cell to ECM)

3) Organization of membrane specializations

4) Sarcomere and myofibril organization

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10
Q

Mutation of genes for dystrophin or dystrophin-glycoprotein complex can lead to which clinical conditions?

A

Muscular Dystrophy and Dilated Cardiomyopathy

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11
Q

Describe location and function of sodium/calcium exchanger.

A

1) Found on surface membrane

2) Pumps 1 Calcium OUT for 3 sodiums IN

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12
Q

About what percentage of calcium released into the cardiac myoplasm is from the SR or from extracellular fluid?

A

80% released from SR

20% from ECfluid

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13
Q

How does calcium concentration in myoplasm relate to contraction strength?

A

Higher calcium concentration = More forceful contraction

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14
Q

Name 2 branches of autonomic nervous system.

A

1) Sympathetic

2) Parasympathetic

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15
Q

Which branch of the autonomic nervous system has little effect on the ventricles of the heart?

A

Parasympathetic

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16
Q

What molecule does the sympathetic nerve terminal release to act on the heart?

A

Norepinephrine

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17
Q

What molecule does the parasympathetic nerve terminal release to act on the heart?

A

Acetylcholine

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18
Q

Name the 2 G-protein coupled receptors of the heart.

A

1) Beta-adrenergic

2) M2-Muscarinic

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19
Q

Which main nerve carries parasympathetic innervation to the heart?

A

Vagus nerve

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20
Q

Which neurotransmitter binds to Beta-adrenergic receptors?

A

Epinephrine and Norepinephrine

21
Q

Which neurotransmitter binds to M2-muscarinic receptors?

A

Acetylcholine

22
Q

List 8 effects of sympathetic activity on the heart (AKA activation of Beta-Adrenergic REceptors)

A

**1) Increased heart rate (positive chronotropic effect on SA node) **

2) Increased force of atrial and ventricular contraction (positive inotropic effect)

  • *3) Increased AV node action potential conduction velocity (shortened AV nodal
    delay) .**

4) Enhanced SR pump activity (due to phosphroylation of phospholamban)

5) Decreased myofilament sensitivity to Ca2+ (due to phosphorylatiion of TnI).

**6) Altered gating of the SR Ca2+ release channel (the ryanodine receptor) leading to enhanced SR release of Ca2+ **

7) Shortened action potential duration

8) Shortened duration of contraction

23
Q

Describe the G-protein pathway.

A

1) Ligand-bound receptor activates G-protein

2) G-protein activates adenyly cyclase

3) Adenyly cyclase creates cAMP from ATP

4) cAMP activates PKA

5) PKA phosphorylates ionic channels (or orther targets)

6) Ion flux is altered

24
Q

What process allows cAMP levels to quickly drop after Beta-adrenergic receptors are no longer stimulated?

A

cAMP Phosphodiesterase destruction of cAMP

25
Q

Name 4 ionic channels phosphorylated by G-protein pathway.

A

1) L-type Calcium channel

2) Pacemaker channel

3) Delayed-rectifier potassium channel

4) cAMP-dependent chloride channel

26
Q

What 4 parts of the heart does the sympathetic system innervate?

A

1) Atria

2) Ventricles

3) SA node

4) AV node

27
Q

What 3 parts of the heart does the parasympathetic system innervate?

A

1) SA node

2) AV node

3) Atria

28
Q

List 3 effects of parasympathetic activity on the heart.

A

1) decreased heart rate (effect on SA node)

2) decreased action potential conduction velocity at the AV node

3) decreased force of contraction of the atria only.

29
Q

What does channel facilitation mean?

A

More easily and frequently opened

30
Q

How can you phyiologically explain an increased heart rate?

A

Rate of SA node action potential firing increases (pacemaker picks up speed) because of calcium channel and pacemaker channel facilitation

31
Q

How can you phyiologically explain increased conduction velocity at AV node?

A

Facilitated calcium channels at AV node

32
Q

How can you phyiologically explain increased force of contraction?

A

Facilitated calcium channels allows more calcium to enter myoplasm and elicit more cardiac cell contraction

33
Q

Why are contractions more forceful but of shorter duration in the heart after sympathetic response?

A

1) Phosphorylated Troponin I decreases myofibirl sensitivity to calcium (not as major effect)

2) Phospholambdin phosphorylation amps up calcium sarcoplasmic reticulum pump so that calcium is quickly absorbed back into SR (this also leads to greater contraction force because greater resivoir release)

34
Q

How can you phyiologically explain shortened action potentials?

A

Faciliate rectifying postassium channels which can end action potential faster

35
Q

How do muscarinic receptors affect the G-protein pathway?

A

Acetylcholine activates a certain G-protein which inhibits adenyly cyclase activity

36
Q

How can you phyiologically explain slowing of SA node (heart rate)?

A

**1) Calcium and pacemaker channels no longer facilitated (because of no cAMP production) and probably inhibited **

2) Special potassium channels are activated to keep resting membrane low and slow depolarization at SA node

37
Q

How can you phyiologically explain a weakened heart contraction?

A

Calcium channels inhibited so not as many myofibrils contract as normal.

38
Q

What is the function of inotropic drugs?

A

Increase heart contraction

39
Q

Name 3 classes of inotropic drugs

A

1) Cardiac Glycosides

2) Sympathomimetic amines

3) Phosphodiesterase inhibitors

40
Q

What is the final physiological effect of inotropic drugs?

A

Increase myoplasmic Calcium concentration

41
Q

What is another name for digitalis drugs?

A

Cardiac Glycosides

42
Q

How does Digitalis work?

A

1) Inhibition of Sodium/Potassium pump

2) This creates influx of sodium inside cell

3) This decreases calcium efflux (decreased ability of sodium/calcium exchanger to remove calcium from cell)

4) Increased concentration of Calcium in myoplasm mopped up by SR Calcium ATPase pump

5) More calcium released during burst of SR calcium resevoir leading to increased contraction of myofibrils

43
Q

What is a desired side effect of Digitalis aside from forceful heart contraction?

A

Inhibition of Sodium/Potassium pump also increases parasympathetic response, decreased sympathetic response, and slows AV node to help ventricular contraction in patients with A-fib

44
Q

What are 3 common names of Digitalis drugs?

A

Digoxin, Digitoxin, Ouabain

45
Q

How do Sympathomimetic amines work?

A

Stimulate beta-adrenergic receptors just like natural sympathetic nervous system (increased cAMP)

46
Q

Name 5 molecules which can stimulate Beta1-Adrenergic receptors

A

1) Epinephrine

2) Norepinephrine

3) Dopamine

4) Dobutamine

5) Isoproterenol

47
Q

How do phosphodiesterase inhibitors work?

A

**By inhibiting phosphodiesterase (which keeps cAMP levels high and thus facilitated phosphorylated calcium channels and thus myoplasmic influx of calcium **

48
Q

Provide 2 names of common phosphodiesterase inhibitors.

A

1) Amirinone

2) Milrinone

CV Week 1 (6 decks)

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