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ELM2 - integrated cases > case 8 - palpitations > Flashcards

case 8 - palpitations Flashcards

1
Q

What type of cells make up the SA node?

A

Pacemaker cells

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2
Q

What features of pacemaker cells makes them able to generate action potentials spontaneously?

A

They have a resting membrane potential that is less negative than cardiomyocytes

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3
Q

What CNS inputs control the rate of SA node discharge?

A

Autonomic inputs - sympathetic and parasympathetic

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4
Q

Which nerve fibres slow heart rate?

A

Parasympathetic fibres, via the vagus nerve

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5
Q

Which nerve fibres increase heart rate?

A

Sympathetic fibres, via the cardiac nerves

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6
Q

How do parasympathetic inputs to the SA node slow heart rate?

A

They reduce the slope of the pacemaker potential and hyperpolarise the node, making it take longer to reach the threshold potential.

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7
Q

How do sympathetic inputs to the SA node increase heart rate?

A

They release noradrenaline which bind to B1 adrenergic receptors which increase the slope of the pacemaker potential, making it easier for pacemaker cells to reach threshold and fire.

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8
Q

What is the pathway of conduction through the heart, starting at the SA node?

A

SA node, AV node, Bundle of His, Left & Right Bundle branches, Purkinje fibres

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9
Q

What is the most common type of aryhthmia?

A

Atrial fibrillation

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10
Q

What is the nature of function of the atria during atrial fibrillation?

A

Contractions of the atria are rapid, non-functional. Multiple atrial foci discharge simultaneously causing fibrillation

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11
Q

What is fibrillation?

A

Rapid, muscular twitching involving individual fibres acting without coordination

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12
Q

Why does atrial fibrillation increase the risk of ischaemic stroke?

A

The left atrial appendage cannot empty properly when the atria are fibrillating, resulting in stasis within it, which increases the risk of thrombus formation

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13
Q

How is the regularity of the rhythm in Atrial Firllation described?

A

Irregularly irregular

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14
Q

What are the key characteristics of an irregularly irregular rhythm?

A

Irregularly spaced QRS complexes, with no temporal pattern to the complexes.

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15
Q

What are the characteristics of an ECG of atrial fibrillation?

A

Absent P waves, narrow irregularly irregular QRS complexes, tachycardia

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16
Q

Are patients in atrial fibrillation typically tachycardic or bradycardic?

A

Tachycardic

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17
Q

What are the common symptoms of atrial fibrillation?

A

Palpitations, dyspnoea, fatigue

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18
Q

Which procedure uses electrical current to re-establish sinus rhythm in patients with atrial fibrillation?

A

Cardioversion

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19
Q

What is the process of cardioversion?

A

Short acting anaesthetic given, electrodes applied to back and chest, shock coinciding with R wave on ECG

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20
Q

At which point on the ECG is a shock administered during cardioversion?

A

Coinciding with R wave

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21
Q

What is the key risk associated with cardioversion, and how is this mitigated?

A

Embolism - risk factors considered, anti-coags/anti-platelets administered.

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22
Q

What are the 3 key components to comment on when interpreting waves/complexes on an ECG?

A

rate, regularity, morphology

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23
Q

What are the 5 key classes of cardiovascular drugs?

A

ACE inhibitors, ARBS, Calcium Channel Blockers, Diuretics, Beta Blockers

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24
Q

What is the full name for ACE inhibitors?

A

Angiotensin Converting Enzyme Inhibitor

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25
Q

What do ACE inhibitors inhibit?

A

Vascular Angiotensin Converting Enzymes

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26
Q

What is the mechanism of action of ACE inhibitors?

A

They inhibit vascular ACE enzymes, which are required for the conversion of Angiotensin I to Angiotensin II. Reduced Ang II reduces systemic vascular resistance and increases vasodilation via bradykinin. Ang II action on the kidneys lowers, promoting Na+ and H2O excretion to drop plasma volume.

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27
Q

What is a commonly used ACE inhibitor in NZ?

A

Enalapril, quinapril

28
Q

What are the therapeutic indications for ACE inhibitors?

A

Hypertension, Chronic heart failure, atrial fibrillation, post-MI

29
Q

What is the key contraindication for ACE inhibitors?

A

Renal Artery Stenosis

30
Q

What is the full name of ARBs?

A

Angiotensin Receptor Blockers

31
Q

What is the mechanism of action of ARBs?

A

Selective AT1 receptor antagonists, that block the effects of Ang II, therefore causing vascular dilation, increased Na+ and H2O secretion, leading to decreased preload and a drop in blood pressure.

32
Q

What is the first line drug class used for the treatment of hypertension (unless contraindicated)?

A

ACE inhibitors

33
Q

What are the therapeutic uses of ARBs?

A

Hypertension, Heart Failure

34
Q

What are the contraindications for ARBs?

A

Renal Artery stenosis

35
Q

What is the mechanism of action of calcium channel blockers?

A

The antagonise L-type Calcium channels, to prevent Ca2+ entry to vascular smooth muscle, cardiac muscle, and SA/AV nodal tissues, resulting in vasodilation, reduced force & rate of contraction and reduced conduction velocity to the ventricles.

36
Q

What are the 3 key -tropic effects of calcium channel blockers on the heart?

A

Negative inotropic (reduced force of contraction)
Negative chronotropic (reduced rate of contraction)
Negative dromotropic (reduced conduction velocity to the ventricles)

37
Q

What are the 2 types of selectivity of calcium channel blockers?

A

Vasoselective, cardioselective

38
Q

What selectivity of calcium channel blocker is used to treat hypertension?

A

Vasoselective

39
Q

What selectivity of calcium channel blocker is used to treat arrhythmias?

A

cardioselective

40
Q

What selectivity of calcium channel blocker is used to treat angina?

A

Cardioselective

41
Q

Which calcium channel blocker is the first line treatment for arrhythmia?

A

Diltiazem

42
Q

What are the therapeutic uses of calcium channel blockers?

A

Hypertension, arrhythmia, angina

43
Q

What is a key example of a vasoselective calcium channel blocker, used to treat hypertension?

A

Amlodipine

44
Q

What is the general mechanism of action of diuretics?

A

They decrease Na+ and H2O reabsorption in the tubules, with different classes acting on different parts of the Loop of Henle

45
Q

What are the key types of diuretic?

A

Osmotic, Loop, Thiazide, Thiazide-like, potassium sparing.

46
Q

What is a key example of an osmotic diuretic?

A

mannitol

47
Q

What is a key example of a loop diuretic?

A

Frusemide

48
Q

What is the mechanism of action of loop diruetics?

A

They bind reversibly to carreir proteins in the loop of Henle, reducing Na+ reabsorption, and therefore reducing H2O reabsorption.

49
Q

What are the therapeutic uses for diuretics?

A

Emergency reduction of intercranial pressure, hypertension, oedema.

50
Q

What is the key contraindication for diuretics?

A

Gout

51
Q

What is the mechanism of action of beta blockers?

A

Reversibly antagonise binding of adrenaline and noradrenaline to Beta receptors (B1 (+ B2)), to reduce cardiac output and blood pressure.

52
Q

What are the two forms of selectivity of beta blockers?

A

Selective (for B1 receptors), Non-selective (for B1, B2 and a1 receptors)

53
Q

What is the most commonly used selective Beta Blocker?

A

Metoprolol

54
Q

What is a commonly used non-selective Beta Blocker?

A

Carvedilol

55
Q

What are the therapeutic uses of beta blockers?

A

Cardiac rate control/arryhthmia, angina, heart failure, hypertension (occasionally)

56
Q

What are the contraindications for Beta Blockers?

A

Asthma, peripheral vascular disease, heart block

57
Q

What are the 3 key components of atrial fibrillation treatment?

A

Rate control, sinus rhythm maintenance, stroke prevention

58
Q

What are the pharmacological treatments for rate control in AF?

A

Beta-Blockers, Calcium Channel Blockers, Digoxin

59
Q

What are the non-pharmacological treatments for rate control in AF?

A

Ablation, pacemaker

60
Q

What are the pharmacological treatments for sinus rhythm maintenance in AF?

A

Antiarhythmics - sodium channel antagonists, beta blockers, amiodarone

61
Q

What are the non-pharmacological treatments for sinus rhythm maintenance in AF?

A

Catheter ablation, cardioversion, pacemaker, surgery

62
Q

What are the pharmacological treatments for stroke prevention in AF?

A

Vitamin K antagonists (e.g. warfarin),
direction thrombin inhibitors (e.g. dabigatran)

63
Q

What are the non-pharmacological treatments for stroke prevention in AF?

A

Surgical isolation of the left atrium

64
Q

Why is warfarin used in treatment of atrial fibrillation?

A

It is an anti-coagulant, so reduces the risk of thrombus formation in the atrial appendages, and therefore lessens the likelihood of iscahemic stroke.

65
Q

What is the mechanism of action of warfarin?

A

Inhibits the synthesis of Vitamin K, which is required for the activation of the clotting factors X, IX, VII and II (thrombin) and Protein C and S via gamma-carboxylation. It therefore interrupts clotting via the intrinsic pathway.

66
Q

How can warfarin therapy be reversed?

A

Vitamin K injection, or if severe, infusion of the depleted factors.

ELM2 - integrated cases (9 decks)

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