Cardio 2 Flashcards

(28 cards)

1
Q

What is the cardiac cycle?

A

The sequence of systole (contraction) and diastole (relaxation) during one heartbeat.

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2
Q

Where does the cardiac action potential originate?

A

At the SA node in the right atrium, from the most excitable cells.

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3
Q

How does the action potential conduct through the heart?

A

SA node → atria → AV node → bundle branches → Purkinje fibres → ventricles.

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4
Q

Why is conduction faster in the atria than in the ventricles?

A

To ensure the atria contract before the ventricles.

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5
Q

What ensures unidirectional propagation of the action potential?

A

The refractory period prevents re-excitation of already stimulated cells.

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6
Q

Why is conduction slow through the AV node?

A

To give the atria time to fully contract before ventricles.

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7
Q

What is the resting membrane potential of SA node cells?

A

-60 mV, making them more excitable than other cardiac cells.

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8
Q

What is the funny current (If or Ih)?

A

A hyperpolarisation-activated sodium current that initiates SA node depolarisation.

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9
Q

What ions drive depolarisation in SA node vs. ventricular myocytes?

A

SA node: calcium; ventricular myocytes: sodium.

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10
Q

What is the process of action potential in the SA node cell

A

Resting is -60
First current is funny current as its gated by hyperpolarisation so when the potential is more negative it opens sodium channels to raise the potential again
Eventually T type calcium channels open and cause more depolarisation.

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11
Q

How does a SA node cells action potential differ from a neuronal cell action potential

A

Calcium not sodium based so can be affected by calcium channel blocker which slows heart rate

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12
Q

What is the process of an action potential in ventricular myocytes

A

Sodium channels open, sodium influx (depolarisation) - sharp uptick

At peak, potassium channels open, efflux (repolarisation)

Calcium channels also open causing calcium influx

Eventually potassium wins and the calcium channel closes and repolarisation completes

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13
Q

What causes the plateau phase in ventricular action potentials?

A

Simultaneous calcium influx and potassium efflux.

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14
Q

What drugs target the SA node to reduce heart rate?

A

Ivabradine (blocks funny current) and calcium channel blockers like verapamil.

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15
Q

How does verapamil affect ventricular myocytes?

A

Reduces calcium influx, decreasing the force of contraction.

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16
Q

How are electrical signals transmitted between heart muscle cells?

A

Through gap junctions, allowing direct ion flow between cells.

17
Q

What is an ECG and what does it measure?

A

A non-invasive recording of the heart’s electrical activity over time.

18
Q

How can electrical activity be detected on the skin?

A

Because the body is filled with conductive salt solutions.

19
Q

What do the P wave, QRS complex, and T wave represent?

A

P wave: atrial depolarisation; QRS: ventricular depolarisation; T wave: ventricular repolarisation.

20
Q

What is the PR interval?

A

Time between atrial and ventricular depolarisation.

21
Q

What does the QT interval represent?

A

Duration of ventricular depolarisation and repolarisation.

22
Q

How do beta and calcium channel blockers affect the ECG?

A

They lengthen the PR interval by slowing AV node conduction.

23
Q

Why does the SA node control heart rhythm?

A

Its cells are the most excitable and generate APs fastest.

24
Q

What role does connective tissue play in heart conduction?

A

It electrically insulates chambers, ensuring signal passes only through AV node.

25
What is the relationship between electrical and mechanical events in the heart?
Electrical signals (depolarisations) trigger contractions (systole).
26
What is the significance of the refractory period in the heart?
Prevents re-excitation, ensuring coordinated contractions.
27
Why does an electric shock restart the heart in cardiac arrest?
It depolarises all excitable cells, hoping SA node recovers first to restore rhythm.
28
What information can an ECG provide?
Heart rhythm, chamber size, conduction issues, and myocardial infarction severity.