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Cardiovascular System > Session 7 > Flashcards

Session 7 Flashcards

1
Q

What does initial polarisation in ventricular cells cause?

A

Voltage gated sodium channels open and depolarise the membrane rapidly

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2
Q

What occurs after immediately depolarisation of a ventricular cell?

A
  • Outward flow of potassium causes brief repolarisation
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3
Q

Why is there a delay in repolarisation of ventricular cells?

A

Voltage gated calcium channels take time to activate so the repolarisation is delayed

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4
Q

What does initial influx of calcium into a ventricular cells due to the opening of voltage gated calcium channels cause?

A
  • Further calcium is released from cellular stores in the mitochondria and SR
  • Calcium causes contraction of the ventricular cells, producing contraction
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5
Q

What repolarises ventricular cells to their resting membrane potential?

A

Potassium efflux from the cell

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6
Q

Why is the membrane potential of pacemaker cells persistently less negative than the membrane potential of ventricular muscle cells?

A

To ensure fast sodium channels remain inactivated

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7
Q

What is the funny current in pacemaker cells?

A

Spontaneous, gradual depolarisation caused by the movement of sodium ions through slow sodium channels which open during repolarisation when potential reaches its most negative values

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8
Q

What occurs in pacemaker cells when the cell reaches threshold voltage?

A

Calcium channels open to create a relatively slow depolarisation

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9
Q

How do pacemaker cells repolarise?

A

After calcium channels close, potassium efflux repolarises the cell

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10
Q

What happens to the membrane potential changes in pacemaker cells if heart rate increases?

A

Interval between contractions, and therefore depolarisations, shortens so the funny current becomes steeper

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11
Q

What effect does activating baroreceptors have on the membrane changes in pacemaker cells?

A

If stretch sensitive baroreceptors are activated (due to increased arterial blood pressure) they send signals to the medulla oblongata to increase parasympathetic innervation to the heart so the funny current becomes shallower and heart rate slows

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12
Q

What can cause cardiac arrhythmias?

A
  • Ectopic pacemaker activity
  • Abnormal depolarisations following an action potential (after-depolarisations)
  • Re-entry loop
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13
Q

What causes ectopic pacemaker activity?

A

Damaged areas of myocardium can become spontaneously active when depolarised so a latent pacemaker region is activated and dominates over the SA node causing abnormal pacemaker activity

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14
Q

What causes after-depolarisations?

A

High intracellular calcium levels

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15
Q

What causes a re-entry loop in the heart?

A

Damaged area of the myocardium prevents normal spread of excitation so there is a delay in conduction

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16
Q

What are class 1 anti-arrhythmic drugs?

A

Voltage gated sodium channel blockers: blocks sodium channels that are open or inactive and rapidly dissociates so normal firing isn’t prevented, only over-firing is prevented

17
Q

Give an example of a type 1 anti-arrhythmic drug

A

Lidocaine

18
Q

What is a class 2 anti-arrhythmic drug?

A

Beta-receptor antagonist: blocks sympathetic action by acting on beta1 receptors so funny current slope is decreased and inotrophy is decreased

19
Q

Give an example of a type 2 anti-arrhythmic drug

A

Propranolol or atenolol

20
Q

Why are type 2 anti-arrhythmic drugs used after a MI?

A

To combat increases in sympathetic activity and reduce oxygen demand of the heart

21
Q

What are type 3 anti-arrhythmic drugs?

A

Drugs which block potassium channels: prolongs the action potential and lengthens the absolute refractory period so further action potentials are delayed

22
Q

Why are type 3 anti-arrhythmic drugs not generally used?

A

They can also be pro-arrhythmic

23
Q

What are class 4 anti-arrhythmic drugs?

A

Drugs which block calcium channels: decreases the slope of the funny current at the SA node; decreases AV node conduction and decreases force of contraction of the heart. Also causes some coronary and peripheral vasodilation

24
Q

Give an example of a class 4 anti-arrhythmic drug

A

Verapamil

25
Q

What is the function of adenosine in the heart?

A
  • Produced endogenously
  • Acts on A1 receptors at the AV node to enhance potassium conductance and hyperpolarise cells
  • Acts as an anti-arrhythmic as it can act to reset the heart
26
Q

What are inotrophic drugs?

A

Drugs which affect the force of contraction of the heart

27
Q

When are negative inotrophic drugs used?

A

In circumstances where it is beneficial to reduce the workload of the heart; e.g. After a MI so oxygen requirement is reduced and further damage is limited

28
Q

Give an example of a negative inotrophic drug

A

Beta-blockers

29
Q

When are positive inotrophic drugs used?

A

In circumstances where the heart needs to beat more strongly; e.g. In cardiogenic shock or acute (but reversible) heart failure

30
Q

Give an example of a positive inotrophic drug

A

Beta receptor agonists; e.g. Doubutamine

31
Q

How are drugs used in the treatment of heart failure?

A
  • ACE-inhibitors prevent formation of vasoconstrictor angiotensin2 so vasodilation of arteries and veins is promoted and after-load and pre-load decrease
  • ACE-inhibitors also have diuretic action as angiotensin2 promotes aldosterone release which leads to sodium and water retention, therefore it causes blood volume and pre-load to decrease
32
Q

How are drugs used in angina treatment?

A

Treated with drugs that reduce the workload of the heart: beta-blockers, calcium channel blockers and organic nitrates
- Organic nitrates and calcium blockers also improve blood supply to the heart

33
Q

Describe the action of organic nitrates on the CVS

A
  • Organic nitrates in vascular smooth muscle cause NO2- to be released which is reduced to NO
  • NO acts as a powerful vasodilator by activating guanylate cyclase, increasing cGMP and lowering intracellular calcium levels to cause vascular smooth muscle to relax
  • Venous pressure lowers so pre-load lowers and force of contraction reduces
  • Can also acts on coronary arteries to improve oxygen delivery to ischaemic areas of myocardium
34
Q

How is increased risk of thrombus formation treated?

A
  • Anti-thrombotic drugs, e.g. Warfarin can be used
  • Aspirin is used following MI or in coronary artery disease to reduce the risk of platelet-rich arterial clots forming as it is an anti-platelet drug
35
Q

How can drugs be used to treat hypertension?

A

Drugs act to reduce cardiac output and/or peripheral resistance, e.g. ACE-inhibitors, diuretics, adrenoceptors blockers and calcium channel blockers

36
Q

What creates the resting membrane potential of cardiac cells?

A

Selective permeability of the cell membranes to different ions
- Mostly permeable to potassium ions

Cardiovascular System (10 decks)

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