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FHB Exam 1 - Cardiovascular Physiology > Lecture 10 - Myocardial EC Coupling > Flashcards

Lecture 10 - Myocardial EC Coupling Flashcards

1
Q

Which part of the EKG shows atrial depolarization? Which shows the time from start of atrial depolarization to start of ventricular depolarization?

A

P Wave

  • P-R interval
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2
Q

Which part of EKG show ventricular depolarization? Which show ventricular depolarization, ventricular contract, and ventricular depolarization?

A

QRS

  • Q-T interval
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3
Q

What does the T wave on an EKG show? What does an inversion often indicate?

A

Ventricular depolarization

  • inversion may indicate recent MI
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4
Q

What is the ST segment show?

A

Ventricles depolarized

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5
Q

What causes the U wave?

A
  1. Hypokalemia

2. Bradycardia

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6
Q

What is the order of speed of conduction in the heart? Pacemaker?

What is the conduction pathway??

A
  1. Purkinje> Atria> Ventricles> AV Node
  2. SA Node> AV> Bundle of His/Purkinje/ventricles
  3. SA Node –> Atria –> AV NODE –> common bundle -> Bundle Branches –> Fascicles –> Purkinje fibers –> Ventricles
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7
Q

What is the function of the sarcolemma?

A

Plasma membrane of Cardiac cells

  1. propagates Action Potentials
  2. controls Ca influx by activating SLOW INWARD CALCIUM current
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8
Q

What part of the cardiac cell activates the SLOW inward calcium current?

A

depolarization of T-tubules from sarcolemma

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9
Q

What is the function of T-Tubules?

A

Transmits AP from Sarcolemma

- depolarization activates slow Ca influx

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10
Q

Where are T-tubules found?

A

Z-lines

  • connected by RyR receptors to SR
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11
Q

What is the function of the Sarcolemma?

A

intracellular Calcium storage site

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12
Q

Where are terminal cistern & longitudinal cistern found?

A

SR!!

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13
Q

What is the function of Terminal Cisternae?

A

Site in SR where Ca influx TRIGGERS opening of Calcium release channels to initiate contraction

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14
Q

What is the function of LONGITUDINAL cisternae?

A

RECYCLING

- site of Ca re-uptake to initiate RELAXATION

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15
Q

What is the function of Troponin C?

A
  • binds Calcium to initiate contraction

Calcium receptor on contractile protein (actin)

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16
Q

What is the function of Troponin I?

A

(phosphorylating it activates it)

  • prevents the binding of Calcium to Troponin C
    = causes RELAXATION when phosphorylated
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17
Q

Is the contraction mechanism (actin myosin cross bridge) the same in cardiac & skeletal muscle contraction?

A

YES

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18
Q

What is the mechanism of E-C coupling?

A
  1. AP sent down sarcolemma, enters T-tubule
  2. T-tubule depolarization activates slow inward Ca channels
  3. Ca influx binds & opens RyR receptors
  4. Increase Ca influx from SR –> binds Troponin C
  5. Tropomyosin shifts, and actin & myosin can bind
  6. CONTRACTION (CICR= calcium induced calcium release)
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19
Q

How can we maintain contraction?

A

Maintain elevated cytosolic Calcium

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20
Q

What are the mechanisms of relaxation?

A
  1. Ca re-uptake into SR by Ca-ATPase (SERCA) - 80%
  2. NA/Ca antiporter (18%)
  3. Ca out of CELL via Sarcolemma Ca pump(2%)
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21
Q

What is a mechanism for reducing CYTOSOlIC calcium?

A

SERCA

  • brings it back to SR
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22
Q

What is a mechanism for reducing CELLULAR calcium?

A

Na/Ca pump

3 Na in/1 Ca out

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23
Q

What occurs if Sodium influx is decreased via Na/Ca antiporter?

A
  • reverse action
  • less Na in
  • less Ca OUT = increase Ca in cell for CONTRACTION
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24
Q

Which cells, cardiac or skeletal, function by syncytium? How is this achieved?

A

CARDIAC

  • coordinated via gap junctions
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25
Q

How are cardiac and skeletal muscles activated?

A
  1. Cardiac = gap junctions
  2. Skeletal = NMJ –> via ACh (released into clft & binds to post-synaptic membrane causing Na influx resulting in DEPOLARIZATION
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26
Q

Contraction of skeletal muscle is dependent on what? Cardiac?

A
  1. AP via NMJ!

NOT CICR –> Voltage Sensor of Calcium (DHPR) that allows Calcium to enter cell via RyR receptors

  1. Calcium induced Calcium release
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27
Q

How is contraction increased in cardiac cells? Skeletal?

A
  1. INCREASE CALCIUM influx via SLOW CALCIUM CURRENT & SR Ca Content!
  2. increase in AP frequency increases amplitude of contraction (& recruitment of muscle fibers)
28
Q

Which cells, cardiac or skeletal, experiences tetany or summation?

A

Skeletal (summation of AP & muscle fiber recruitment)

29
Q

True or false: Cardiac cells utilize primarily anaerobic metabolism

A

FALSE!

  • use Aerobic, have a lot of mitochondria & use a lot of ATP
  • skeletal is primarily via Glycolysis
30
Q

Relaxation is occurred when what is reduced?

A

CYTOSOLIC CALCIUM

31
Q

What is the TRIGGER for Calcium Induced Calcium release?

A

Calcium influx from SLOW channels (L-Type)

32
Q

Contraction strength depends on what?

A
  1. Amount of calcium in SR
  2. Calcium influx
  • can increase by Autonomics (NE –> ATP to cAMP via AC–> PKA –> phosphorylate calcium channels to increase calcium influx)
33
Q

Most calcium channels are found where? Why?

A
  1. Along T- tubules
  2. short distance from RyR (on SR) to T-Tubule
  • sarcolemma does not have a lot of Ca channels
34
Q

What part of the SR releases calcium?What re-uptakes?

A

TERMINAL CISTERNAE

LONGITUDINAL cisternae

35
Q

What removes calcium from cytosol?

A

SERCA

- brings calcium back via longitudinal cistern to SR = relaxation

36
Q

Congestive Heart failure causes irregular Cardiac Output for what reason?

A

ABNORMAL calcium handling

  1. release
  2. influx
  3. re-uptake
37
Q

What are the differences between NE andE?

A

NE = neurotransmitter

Epinephrine = hormone

38
Q

What is a positive inotropic affect? What are two ways to achieve this?

A

Increase in CONTRACTILITY

  1. Catecholamines (NE)
  2. Cardiac Glycosides (Digitalis)
39
Q

What is the mechanism of Catecholamine stimulation?

A
  1. B1 receptors on the heart bind Catecholamine
  2. acts via Gs to stimulate Adenylate cyclase to convert ATP to cAMP
  3. cAMP activates PKA (cAMP dependent protein kinase A)
  4. PKA phosphorylates
    - Ca channels to increase influx
    - Phospholambin to enhance relaxation

BOTH INCREASE CICR
- decreases time course f relaxation

40
Q

What is the result of phosphorylating Ca channels & phospholamban?

A
  1. causes more Ca channels to open
  2. inhibits a Ca-ATP ase inhibitor and thus enhances relaxation

(SERCA is able to re-uptake Ca once phospholamban is phosphorylated= speeds uptake of Calcium into SR) –> increasing Ca stores in SR –> and reducing in cytosol causes relaxation

41
Q

What is the affect of phosphorylating Troponin I?

A

Able to inhibit Troponin C from binding to calcium (so tropomyosin goes back to blocking the myosin binding site)

= ENHANCE RELAXATION

42
Q

Why is enhanced relaxation important in the heart?

A

If relaxation is enhanced, filling is quicker and the whole cycle is shortened (quicker)

  • filing & pumping is quicker
43
Q

Catecholamines cause relaxation of the heart and yet an increase in contraction. True or False?

A

TRUE!

Relaxation just as important as contraction

44
Q

What is diastolic heart failure?

A

Heart cannot relax enough to allow filling

  • systolic = heart cannot generate enough force to pump
45
Q

What is a critical component of relaxation in cardiac cell?

A

SERCA

  • SR Ca-uptake (relaxation)
  • increases Ca storage = greater contraction upon next AP
46
Q

What are 2 ways to induce relaxation?

A
  1. Reduce Calcium binding to Troponin C

2. Increase Reuptake of Calcium from SR

47
Q

If RyR is inhibited, what occurs in cardiac cell?

A

NO CONTRACTION

  • initial slow Ca influx is too small to initiate contractionn
48
Q

A DAD occurs if what is inappropriate?

A

CALCIUM RELEASE

49
Q

What is the 5 step mechanism of function of Cardiac Glycosides?

A
  1. Inhibit Na/k pump
  2. More Na in –> Na gradient reduced
  3. Na/Ca antiporter reduced–> Ca pumped out is reduced! - more in cytosol
  4. increase intracellular Ca
  5. increase in SR Calcium leads to greater SR Ca release & contraction
50
Q

Contraction of skeletal muscle is dependent on calcium INFLUX. True or False?

A

FALSE!

  • dependant on Ca voltage sensors (DHPR) that activate RyR
51
Q

Contractility is specifically in regards to what?

A

cellular Calcium changes

52
Q

How can Supraventricular Tachycardia be blocked?

A

Stimulate VAGUS

  1. Valsalva
  2. Carotid Sinus Massage
  3. Cold compress
  • WPW (re-entry)–> if increase refractory period of AV node–> can better filter conduction since it is SLOWED
53
Q

What are Ca channel blockers clinical used as?

A

Vasodilators –> relax smooth muscles

54
Q

What is the mechanism of Ca channel blockers?

A
  1. blocks slow Ca influx

2. decreases in SR Calcium release and SR calcium content which leads to less contraction in VASCULAR SMOOTH MUSCLE

55
Q

What side affect does Ca Channel blocking induce?

A

Negative Inotropic effects on heart (decrease contractility)

56
Q

How are cardiac anti- arrhythmic effects induced by Ca channel blockers?

A

Reduce SLOW Ca influx current which inhibits AV Nodal conduction of AP’s

  • blocks Supraventricular Tachycardia by increasing refractory period of AV Node –> better filter
57
Q

The beating rate & rhythm of the heart (cycle length) influences cardiac contraction amplitude by altering CONTRACTILITY. This describes what?

A

Force- Frequency relationship

  • alter TIME for Ca HANDLING = alter CONTRACTILITY
58
Q

Changing the time for Ca handling changes what?

A

Contractility!

59
Q

What is the POSITIVE staircase? How is it achieved?

A

As HR increases, strength of contraction increases

  1. increase Ca release per unit time, & less time for Ca efflux via Na/Ca
  2. increased SR content and SR calcium release = larger contraction
60
Q

What is the NEGATIVE staircase? How is it achieved?

A

As HR decreases, strength of contraction decreases (amplitude)

  1. less time for Ca influx, more time for Ca efflux via Na/Ca
  2. less SR content & less Sr Calcium release (CICR) = smaller contraction strength
61
Q

What is a smaller than normal contraction?

A

Premature beat

62
Q

The following is a mechanism for a premature beat or PESP?

  1. Less time for recovery of slow Ca influx channels
  2. LESS time for recovery of SR Ca release channels (RyR)
  3. LESS time for re-distribution of Ca in TERMINAL CISTERNAE

Will this cause a smaller or larger CICR and contraction strength?

A

PREMATURE BEAT!!!

  • smaller Calcium induced calcium release = decreased contraction strength
63
Q

The following is a mechanism for a premature beat or PESP?

  1. MORE time for recovery of slow Ca influx channels
  2. MORE time for recovery of SR Ca release channels (RyR)
  3. MORE time for re-distribution of Ca in TERMINAL CISTERNAE

Will this cause a smaller or larger CICR and contraction strength?

A

PESP!!

  • larger Calcium induced Calcium release = larger contraction strength
64
Q

What is a PESP? Does it result in smaller or larger contraction?

A

Post-extrasystolic potentiation

  • occurs after premature beat and results in larger than normal contraction!
65
Q

A positive staircase occurs following what? A negative staircase?

A
  1. Premature beat
    - pause occurs
  2. PESP –> thinks contraction is still at same amplitude and fires higher, begins to slowly decline back to base level
66
Q

Force is dependent on what?

A

INTERVAL BETWEEN BEATS

  • if interval is irregularly irregular force is affected

–> ATRIAL FIBRILLATION

67
Q

What is it said that a beat is “skipped” after PVC?

A

PVC is lower amplitude since premature beat introduced
- calcium handling is cut short (less time for cycle) = CONTRACTILITY REDUCED
-
contraction is so small that aortic valve not opening (not enough force)

  • SKIP A BEAT (thumping)
    earlier Premature beat comes, less likely valve will open
    (felt when taking radial pulse –> seems as though a beat is SKIPPED)

FHB Exam 1 - Cardiovascular Physiology (26 decks)

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