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?

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
Where do you place the electrodes?
Red and black on clavicles and green on left rib
26
What controls CO and peripheral resistance? (2)
Neural and endocrine mechanisms
27
Mean arterial blood pressure =
Diastolic blood pressure + (systolic blood pressure-diastolic blood pressure)/3
28
How do you calculate pulse pressure?
SBP-DBP
29
CO=
SV x TPR
30
Inotropic agents
Alter heart contractility
31
3 positive inotrophic agents
Noradrenaline form the SNS Increase Ca B agonists
32
Negative inotrophic agents
Acidity
33
Positive chronotrophic agents
Noradrenaline from the SNS
34
4 negative chronotrophic agents
Acetylcholine from the PNS B/B1 blockers Glycosides increase vagus activity Activate K channels
35
How do we get the ECG shape?
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
How is tension related to action potential?
No matter how much tension the same size action potential is always generated