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Year 1 Summative 1 > BMS10-1025 Cardiac Function 2 > Flashcards

BMS10-1025 Cardiac Function 2 Flashcards

1
Q

Why don’t we want tetany of the heart?

A

The heart would remain contracted so no matter how many stimulants there are there is only 1 response

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2
Q

What develops tension in the heart?

A

Entry of calcium into cardiac muscle

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3
Q

How do we prevent tetany?

A

Have a long refractory period so a new action potential cant be initiated until the last one is over

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4
Q

Why does the SAN demonstrate spontaneous electrical activity?

A

It has an unstable resting membrane potential

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5
Q

How do the action potentials of the heart differ?

A

SAN doesn’t start from -90 like the others

The purkinje fibres, ventricles and atria also all have differing curves

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6
Q

Why does the SAN have a more positive resting membrane potential?

A

It has fewer potassium ions

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7
Q

Describe the differences between the SAN and ventricular action potentials? (3)

A

Varying resting potentials
Increases faster
Ventricular lasts longer

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8
Q

Describe SAN ions in the action potential

A

Na doesn’t really have any channels in the SAN
Ca channels are long acting so make a slow rising action potential
Ka channels allow for repolarisation

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9
Q

What blocks SAN K channels?

A

Barium

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10
Q

What blocks SAN Ca channels?

A

Verapamil

Nifedipine

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11
Q

What blocks SAN Na channels?

A

Ivobrodine

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12
Q

What is a long acting Ca channel?

A

Stay open for a long time but let fewer in at a time

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13
Q

What is a transient Ca channel?

A

Doesn’t stay open for long but let loads in at a time

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14
Q

What is the pacemaker potential?

A

The gradual depolarisation after the last action potential has finished, giving it its resting potential, this time decides heart rate (decay)

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15
Q

Chronotrophic

A

Something affecting heart rate

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16
Q

Give examples of chronotrophic agents

A

Noradrenaline

Acetylcholine release

17
Q

What NS releases noradrenaline?

A

SNS

18
Q

What does noradrenaline do?

A

Increase ion conductance

19
Q

How are myocytes coupled?

A

Intercalated disc with desmosome, connexion and hen a gap junction

20
Q

What does rate of conductance depend on? (2)

A

Resistance of gap junctions and membrane capacitance

21
Q

Terminal cisterns

A

Enlarged areas of the sarcoplasmic reticulum surrounding the t tubules, storing calcium

22
Q

Dyad

A

At the Z-line it is a t-tubule paired with a terminal cisterna of the sarcoplasmic reticulum. The diad plays an important role in excitation-contraction coupling by juxtaposing an inlet for the action potential near a source of Ca 2+ ions

23
Q

What is the Treppe effect?

A

Increase in heart rate increases tension as there is a high amount of Ca present so there’s less time to remove it so contraction force increases

24
Q

How do we get rid of Ca during repolarisation?

A

Put them back into stores

25
Q

Where do you place the electrodes?

A

Red and black on clavicles and green on left rib

26
Q

What controls CO and peripheral resistance? (2)

A

Neural and endocrine mechanisms

27
Q

Mean arterial blood pressure =

A

Diastolic blood pressure + (systolic blood pressure-diastolic blood pressure)/3

28
Q

How do you calculate pulse pressure?

A

SBP-DBP

29
Q

CO=

A

SV x TPR

30
Q

Inotropic agents

A

Alter heart contractility

31
Q

3 positive inotrophic agents

A

Noradrenaline form the SNS
Increase Ca
B agonists

32
Q

Negative inotrophic agents

A

Acidity

33
Q

Positive chronotrophic agents

A

Noradrenaline from the SNS

34
Q

4 negative chronotrophic agents

A

Acetylcholine from the PNS
B/B1 blockers
Glycosides increase vagus activity Activate K channels

35
Q

How do we get the ECG shape?

A

It goes up or down depending on whether the muscle impulse is going towards or away from the electrode
The size of the line indicates how far the impulse travels

36
Q

How is tension related to action potential?

A

No matter how much tension the same size action potential is always generated

Year 1 Summative 1 (56 decks)

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