Cardiac Excitation And Contraction Flashcards

1
Q

Cardiac output split between atria and ventricles (CO)

A

Atria/ventricles = 10/90

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2
Q

P-wave (EKG)

A

The first ‘bump’ on the EKG

Represents the wave of depolarization across the atria

Signal starts at SAN —> hits all parts of the atria and converges at the AVN

Fibrous ring keeps the conduction from traveling to the ventricles…and only to the AVN

I.e. the signal conduction can only get to the ventricles through the AVN

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3
Q

Role of AVN

A

Slows down conduction

‘Electrical filter’ to protect the ventricles

Structurally it can do this because…

  1. Fewer gap junctions
  2. Low expression levels of Na+ channels

THEREFORE Ca2+ is the dominant current, which has a smaller amplitude

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4
Q

Flat line immediately after P-wave

A

Signal is limited to the small area of the AVN…

So small that cannot detect electric potential on machine

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5
Q

QRS interval

A

Time taken for ventricular depolarization

AVN —> bundle of His (Purkinje Fibers)

Very very fast

Flow of conductance: endocardium —> epicardium

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6
Q

Gap junctions / intercalated discs in muscle cells

A

Highly permeable

Protein = connexons

Open condition = low [Ca2+] and normal pH

Closed = high [Ca2+] and low pH

—> mechanism to protect neighboring cells…so dangerous environment conditions don’t spread uncontrollably

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7
Q

Relationship between ATP levels and gap junction conformation

A

Low ATP —> increase [Ca2+] —> lower pH —> closed channels

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8
Q

T-wave

A

After QRS interval

Repolarization of ventricles

Flow: epicardium —> endocardium (reverse of depolarization)

—> due to the fact that APs have a shorter duration in the epicardium

Why T-wave is upright

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9
Q

What does a large P-wave indicate (amplitude)

A

Large Atria

= congestive heart failure

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10
Q

Abnormally wide QRS interval =

A

LV hypertrophy

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11
Q

If T-wave too high

A

Hyperkalcemia

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12
Q

If QT (ventricular repolarization) is too prolonged…

A

Rish for death!!! AAAHHHHHH

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13
Q

Regional differences in AP duration

A

Purkinje > ventricular&raquo_space;> atrial

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14
Q

Regional differences in phase 1 notch

A

Epicardial&raquo_space; endocardial

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15
Q

Regional differences in unstable diastolic potential

A

SAN > AVN > purkinje

They have to ability to spontaneous depolarized

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16
Q

Ionic basis of cardiac action potential

A
  1. K+ outflow (I-k1)
  2. Na+ influx (I-Na)

(Then most Na+ channel close)

  1. Some transient outflow of K+ (I-to)

(Then Ca2+ channels start to open)

  1. Ca2+ influx

(Ca2+ influx (+) K+ outlfow —> ‘plateau’ in graph ‘#2’)

  1. I-k activates outflow —> rapid repolarization
17
Q

Relationship between conduction velocity and Na+ current

A

Direct relationship

18
Q

Steps 0 —> 4 of cardiac AP

And their corresponding responsible current

A

0 = I-Na+ (influx)

1 = ‘notch’ = I-to (outflow)

2 = I-Ca2+ (influx)

3 = I-K (outflow)

4 = RP = I-K1 (@ E-k)

19
Q

Effects of voltage and time on Na+ availablity

A

At -40mV = all channels inactivated

Cannot initiated AP until atleast 50% of channels are rested (RRP) - not ideal thou