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Physiology And Pharmacology Of Systems > Initiation of the Heartbeat > Flashcards

Initiation of the Heartbeat Flashcards

1
Q

Definition of absolute refractory period

A

No action potentials possible here whilst depolarization and depolarization is happening

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2
Q

Definition of relative refractory period

A

Action potentials possible here but stimulus must be greater

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3
Q

Definition of funny current

A

Inward current activated when membrane potential hyperpolarises

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4
Q

Definition of anisotropic

A

Property of being directionally dependent which implies different properties in different directions

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5
Q

Definition of isotropy

A

Uniformity in all orientations, same properties in all directions

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6
Q

Definition of isoelectric line

A

Straight horizontal line on ECG, no +ve or -ve changes of electricity to create deflections

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7
Q

Definition of electric dipole

A

Wave of +veness followed by a wave of -veness

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8
Q

Definition of chronotropy

A

Anything that affects heart rate

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9
Q

Definition of inotropy

A

Anything that affects strength of contraction

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10
Q

Definition of lusitropy

A

Anything that affects rate of relaxation

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11
Q

How long is the neuronal action potential duration

A

AP duration = 500us, v short

Absolute refractory period is v short

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12
Q

How long is the cardiac action potential duration and how does this compare to the neuronal AP

A

AP duration = 200-400ms, v long

Longer than neurons but can vary with HR

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13
Q

Describe the ionic changes that occur in a cardiac action potential in cardiac contractile cells

A

1, Na influx
2, Ca influx and K efflux
3, More K efflux
4, NaKATPase, NaCa exchange to maintain resting potential

Have a stable resting membrane potential so do not contract spontaneously

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14
Q

How does the heart rate affect the action potential duration
What is the average AP duration at rest

A

As HR increases, AP duration decreases
As HR decreases, AP duration increases

APD roughly equal to QT interval on ECG

350-380ms

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15
Q

Why is the cardiac action potential long

A

Prevents tetany unlike skeletal muscle
Protects against reentrant arrhythmias
Long AP = long ARP, needed to allow for contraction and relaxation for cardiac output

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16
Q

Describe the shape of the electrical impulse in the cardiac conducting cells
Why is this important

A

All have diastolic depolarisation, don’t have stable resting potential
Results in pacemaker function
Diastolic depolarisation sets tempo for HR

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17
Q

What are the relative intrinsic rates of conduction

What happens if the SAN is out of control

A

SAN (fastest intrinsic rate)
AVN
His Bundle
Purkinje Fibres (slowest intrinsic rate)

If SAN goes wrong, other structures can take over pacemaker function but at a slower rate

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18
Q

Describe the cells in the SAN and their structure

What is the function of the SAN

A

Embryologically derived from muscle

  • Poorly differentiated
  • Empty membrane bags with no cytoplasm
  • Numerous cavaeolae
  • Lots of membrane for AP generation
  • Many pseudopodia, coupling between adjacent cells

Designed for AP generation, not contraction

19
Q

What are the 2 clocks that generate pulse

A

Membrane clock

Calcium clock

20
Q

Describe the membrane clock

A

Cyclic changes in ionic currents driven by NaK help the membrane potential exceed the threshold

When the membrane potential hyperpolarises, funny current activated

Stimulated by NA/A
Inhibited by Ach, both alter funny current

21
Q

Describe the calcium clock

A

Cyclical Ca release from intracellular stores drives membrane potential to threshold

22
Q

Describe the steps in cardiac conduction

A

SLOW conduction from SAN=>AVN via atrial muscles

SLOW conduction through AV (AV pause)

  • Ventricles given time to fill
  • Prevents high transmission rates from atria

FAST conduction through Bundle of His to apex

Conduction spreads through ventricle via muscle cells from apex => base

23
Q

How are electrical impulses spread throughout cardiac contractile cells

A

100um long

Intercalated discs with connexons allows diffusion of ions, small molecules from cell to cell

24
Q

Describe anisotropic conduction and why its is found in the ventricular myocytes

A

Electrical impulses travel faster along fibres connected via more connexons.

Many connexons at the ends of myocytes than the sides
Main direction of conductance is along the fibre

25
Q

How does fibre orientation affect conduction

A

Fibre orientation dictates impulse direction

Fibre orientation depends on whether its epicardium, myocardium or endocardium

26
Q

Where are the electrodes placed for an ECG

A

Reference electrode on right shoulder

Recording electrode on left leg

27
Q

Describe the causes of each section of the ECG wave

A

P, atrial depolarization
Q, Septum depolarization towards atria
R, ventricular depolarization towards apex (spread by PF)
S, ventricular depolarization towards atria (endocardium => epicardium)
T, depolarization of ventricles (epicardium => endocardium)

28
Q

What do the upward lines on the ECG mean

A

Net depolarisation (increased positivity) towards measuring electrode

29
Q

What do the downwards lines on the ECG mean

A

Net repolarisation (increased negativity) towards measuring electrode

30
Q

What is happening during the PQ section

What could be occurring if this section cannot be seen?

A

Atrial conduction
AVN delay

AV block

31
Q

What is happening during the QRS section

What could be occurring if this section cannot be seen

A

Ventricular conduction velocity

Bundle branch block

32
Q

What is happening during the ST plateau section

What could be occurring if this section cannot be seen

A

All of ventricle depolarised

MI

33
Q

What is happening during the QT section

What could be occurring if this section cannot be seen

A

Ventricular AP duration

Long QT syndrome

34
Q

How much does the intracellular [Ca] increase by during excitation contraction coupling

A

200nM -> 1uM

35
Q

How does cardiac muscle contract

A

Calcium induced calcium release

Depolarization of T tubule causes L type channels to open, Ca enters
Increase in intracellular Ca triggers ryanodine receptors
Ryr open and release more Ca which diffuses to myofilaments

36
Q

How does cardiac muscle relax

A

SERCA uses ATP to reabsorb Ca back into SE
SERCA activity regulated by PLB

Some Ca removed via NaCa exchanger

37
Q

What is chronotropy and causes positive and negative chronotropic events

A

Affects HR and SAN

Sympathetics (NA/A)

  • increase funny current
  • increase rate of diastolic depolarisation
  • increase HR

Parasympathetics (Ach)

  • decrease funny current
  • Opens Kach channels
  • Decreases rate of diastolic depolarization
  • decreases HR
38
Q

What is inotropy and lusitropy and how are they stimulated?

A

B1 receptor stimulation (PKA and Gs) (NA/A)

Results in accelerated rate of contraction in inotropy
Higher rate of Ca removal in lusitropy

39
Q

What happens when L type Ca channels are phosphorylated by PKA

A

Increased channel opening
+ve chronotropy
+ve ionotropy

40
Q

What happens when ryanodine receptors are phosphorylated by PKA

A

Increased SR ca release

+ve ionotropy

41
Q

What happens when the myofilaments are phosphorylated by PKA

A

Troponin I and myosin binding protein C
Increases rate of cross bridge cycling
+ve ionotropy
+ve lusitropy

42
Q

What happens when the pacemakers are phosphorylated by PKA and cAMP

A

Activates membrane and Ca clocks

+ve chronotropy

43
Q

What happens when ATPases are phosphorylated

A

PLB (for SERCA), PLM (for NaKATPase) phosphoryated to increase Ca uptake
+ve lusitropy

Physiology And Pharmacology Of Systems (22 decks)

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