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OD2 Semester 1 - Applied Clinical Training > P: Drugs for Heart Failure and Dysrhythmias - Week 5 > Flashcards

P: Drugs for Heart Failure and Dysrhythmias - Week 5 Flashcards

1
Q

Name the 2 locations in the heart that have cels that can generate rhythmic activity. Which site is the principle site?

A
  1. sino-atrial Node (SA node): principle site

2. atrio-ventricular node (AV node)

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2
Q

Which site in the heart is responsible for setting the heart rate?

A

SA node

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3
Q

How does the sympathetic division of innervation affect the SA node?

A

makes the SA node fire faster, because it allows more sodium into the cells, so it’ll get to the threshold for action potential more quickly

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4
Q

How does sympathetic and parasympathetic stimulation affect contractility of the heart?

A 
parasympathetic = little to no effect
sympathetic = increased contractility due to increased calcium. The higher calcium results in a harder/stronger contraction (the muscles squeeze more forcefully)
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5
Q

List the steps on the hypertension continuum

A

hypertension – endothelial dysfunction – atherosclerosis – CAD – myocardial ischaemia – coronary thrombosis – stroke, myocardial infarction – arrhythmia and loss of muscle – remodelling – ventricular dilation – congestive heart failure – end stage hear disease

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6
Q 
For the parasympathetic division of neural control of HR and contractility, describe the following:
A: location
B: receptor and neurotransmitter used
C: mechanism
D: effect  on heart rate/contractility
A

A: SA node and AV node
B: Acetylcholine; Muscarinic (M2) receptors
C: Gi reduces cAMP, opening K+channels
D: decreases heart rate only

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7
Q 
For the sympathetic division of neural control of HR and contractility, describe the following:
A: location
B: receptor and neurotransmitter used
C: mechanism
D: effect  on heart rate/contractility
A

A: SA node, conducting tissue and myocardial cells
B: Noradrenaline; Beta-1 receptors (also circulating hormone - adrenaline)
C: Gs increases cAMP, increases Ca2+
D: increases heart rate AND contractility

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8
Q

What can over-stimulation of the sympathetic division of neural control of heart rate and contractility lead to?

A

dysrhythmia

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9
Q

Describe the SA cells

A

a group of specialised cells that have an unstable membrane potential

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10
Q

Do excitable cells tend to have higher or lower membrane potential? What does this mean?

A

Lower membrane potential (around -80 to -90mV). This means that most of the ions aren’t moving and you have ‘electrochemical stability’

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11
Q

Compare the resting membrane potentials of the SA node and Ventricle of the heart (phase 4)

A

SA node: -60mV; unstable membrane potential

Ventricle: -90mV; stable

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12
Q

Describe the depolarisation process of the SA node, including the phases

A

spontaneus depolarisation. If (I-funny) occurs and sodium and calcium come in. then:
Phase 0: depolarization, calcium in
Phase 3: repolarization, potassium out

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13
Q

Describe the depolarisation process of the ventricle, including the phases

A

Phase 0: Rapid depolarisation, Na+ and some CA2+ in
Phase 1: rapid repolarisation, K+ out
Phase 2: plateau Ca2+ in, K+ out
Phase 3: repolarization, K+ out

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14
Q

Describe the 4 major classes of drugs used to control heart rate, their molecular mechanisms and their outcomes:

A
  1. Class 1 - Na+ channel block (reduce phase 0 depolarization)
  2. Class 2 - B-adrenoceptor antagonism (slow the rate)
  3. Class 3 - K+channel blockade (extended repolarization phase)
  4. Class 4 - CA2+ channel blockade (affects refractory period)
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15
Q

Name and describe the unclassified drugs that can be used to control heart rate

A

Atropine: increase HR by blocking ACh
Adenosine: similar to parasymp stimulation
Cardiac glycosides
Electrolyte supplements

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16
Q

Why should you consider the no treatment option for arrhythmia?

A

Many arrhythmics have proarrhythmic activity and may worsen arhhythmias and cause sudden death

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17
Q

How do Na+ channel blockers target the corresponding Na+ channels

A

They selectively target the region where Na+ channels are open more frequently

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18
Q

In what state do Na+ channel blocker drugs typically bind Na+ channels?

A

They bind Na+ channels in their activated (open) state = ‘use-dependent channel block’

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19
Q

How can we further classify Na+ channel blocker drugs?

A

Based on dissociation time of drug from channel
Class 1a: moderate Na+ channel block
Class 1b: mild
Class 1c: marked Na+ channel block (so i guess blocks it a lot)

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20
Q

How does Lignocaine act as a Na+ channel blocker?

A

provides a rapid blockade of activated and inactivated Na+ channels

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21
Q

For what purpose is lignocaine typically used?

A
  • often used in px post myocardial infarction. Is also used intravenously in emergency situations

Also used for ventricular dysrhythmias and fibrillation

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22
Q

Describe the outcome/effect of lignocaine

A
  • depresses conduction and excitability in heart (slows it down, allowing cells a chance to recover)
  • local anaesthetic actions on all excitable cells
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23
Q

List 5 adverse effects for lignocaine in order of increasing dosage that causes it

A 
4ug/ml: lip and tongue numbness
7ug/ml: visual disturbance
8ug/ml: muscular twitching
15ug/ml: coma
25ug/ml: cardiovascular depression
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24
Q

How can we more safely apply lignocaine as an anaesthetic?

A

topically. But if it gets into systemic circulation, it’ll affect cardiac exciteability and sensory + motor nerve function

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25
Q

How fast is repolarization if your heart is beating fast?

A

fast

26
Q

Describe the effect of K+ channel inhibitors (1 main point and 3 outcomes)

A

prolongs ventricular action potential

  • slowing of phase 3 repolarization
  • decrease incidence of re-entry
  • increase risk of triggered events
27
Q

For what type of arrhythmia is reducing the incidence of re-entry especially important for? Explain it

A

Especially important for the re-entrant arrhythmiaas, where the electrical activity goes to a point, reaches some damaged cells and goes and looks for healthy cells to go and pass its signal

28
Q

Why are K+ channel inhibitors considered a “double-edged sword”?

A

Because they increase the risk of triggered events

29
Q

Amiodarone is a K+ channel inhibitor. But what else does it block?

A

Also blocks Na+ (at higher concentrations), Ca2+, and B-adrenoceptors

30
Q

Name 4 side effects for amiodarone

A

`- reversible photosensitisation

  • skin discolouration
  • hypothyroidism
  • pulmonary fibrosis (with long term use)
31
Q

What is the danger in extending repolarization?

A

is that it’s re-exciteable for a longer period
- because even through there’s a refractory period, there’s a relative refractory period where it’s still excitable if a 2nd stimulus comes in

32
Q

How is bradycardia different from typical arrhythmias?

A

instead of raising heart rate, bradycardias slow heart rate

33
Q

Describe the use and mechanism for atropine in relation to the heart?

A
  • used for bradycardias

- inhibits parasympathetic activation

34
Q

How does the mechanism of adenosine for the heart compare to atropine?

A

similar. Similar effects to parasympathetic stimulation

35
Q

In relation to the heart, describe the effects of “Digoxin”

A
  • slow AV conduction, increasing vagal input to the heart (via CNS effect)
  • slows ventricular rate, improves filling
  • may cause ventricular fibrillation
36
Q

How big is the threapeutic index of digoxin?

A

low therapeutic index - therefore small window with which t can be used

37
Q

How does digoxin effect the heart rate?

A

slows heart rate. This is uesful for tachycardia (but not bradycardia)

38
Q

Describe the steps involved in the process of cardiac contraction and relaxation (9)

A
  1. The A.P enters from an adjacent cell
  2. Voltage-gated Ca2+ channels open, Ca2+ enters the cell
  3. Entry of Ca2+triggers release of Ca2+ from SR
  4. Most Ca2+ comes from SR
  5. Ca2+ ions bind the troponin to initiate contraction
  6. relaxation occurs when Ca2+ unbinds from troponin (and as Ca2+ dissociates, it fills up the SR stores)
  7. Ca2+ is pumped back into the SR for storage
  8. Ca2+ is exchanged with Na+
  9. Na+ gradient is maintained by the Na/K/ATPase
39
Q

How high is the therapeutic index of glycosides? Why?

A

low therapeutic index, because it affects all excitable tissues

40
Q

How do glycosides affect the following tissues?
A: gut
B: CNS
C: cardiac

A

A: anorexia, nausea, diarrhoea
B: drowsiness, confusion, psychosis
C: ventricular dysrthythmias

41
Q

In what situations will glycosides have increased toxicity? (3)

A
  • low K+ (reduced competition for binding)
  • high Ca2+ (reduced gradient for Ca2+ efflux)
  • renal impairment
42
Q

How are glycosides absorbed and how long is their half life?

A

orally. around 40 hours

43
Q

Describe the volume of distribution (Vd) for glycosides and explain why

A

around 400 L. Due to high affinity binding to muscle

44
Q

How can PDE inhibitors be useful in contractility?

A

can help increase cAMP and therefor Ca2+ entry if B-receptors aren’t working or failing

45
Q

What is used to break down cAMP?

A

cAMP is broken down by PDE

46
Q

How do b-adrenoceptor agonists and PDE inhibitors work to treat heart failure?

A

Intravenous, short term support for acute heart failure, cardiogenic shock. Help with Ca2+ entry and contraction

47
Q

Name 3 b-adrenoceptor agonists for heart failure

A

noradrenaline, adrenaline: activate both alpha and beta adrenoceptors

Dobutamine: selective b1-adrenoceptor agonist

48
Q

List 3 adverse effects of B-adrenoceptor agonists

A
  • increase cardiac work
  • increase O2 demand
  • risk of dysrhythmias
49
Q

Can phosphodiesterase inhibitors treat for heart failure? How? Name one

A

(just like b-adrenoceptor agonist): used as short term support fo racute heart failure and helps Ca2+ entry and contraction

e.g. Milrinone

50
Q

Describe the effect of Inotropes on heart failure?

A
  • increase contractile force of cardiomyocytes
  • symptomatic relief: however they increase work on the heart and only provide a short term beneifit

other strategies are needed as symptoms progress

51
Q 
Define the following: 
A: preload
B: rate
C: contractility
D: afterload
A

A: The input. What comes in to be be pumped out (i.e. venous return)
B: how fast the pump runs
C: how strong is the pump
D: the amount pumped in relation to resistance. More is pumped if less resistance

52
Q

Name and describe 2 drugs that reduce preload

A
  1. Nitrate venodilators
    - used in angina
    - venous dilation greater than arterial dilation effect
    - has 1st pass metabolism and tolerance
  2. Diuretics
    - loop
    - aldosterone antagonists, K+ sparing
    - reduce mortaility in combination with ACEi, b-blockers
53
Q

Name 2 drugs that reduce afterload (and preload)

A
  1. Angiotensin inhibitors: ACE inhibitors, and AT1 receptor antagonists
  2. b-adrenoceptor antagonists
54
Q

How does angiotensin II effect cardiovascular system? (3)

A
  • vasoconstrictor (affect on afterload)
  • fluid retention due to increased aldosterone release from adrenal cortex (can effect preload, oedema)
  • ventricular hypertrophy (can effect remodelling)
55
Q

How effective are ACE inhibitors in treatment of heart failure?

A

effective at all grades of heart failure. They improve symptosm and delay progression

56
Q

Name the 3 contraindications for ACE inhibitors

A
  1. bilateral renal stenosis
  2. angioneurotic oedema
  3. pregnancy
57
Q

Name an alternative to ACE inhibitors and describe when you should use it

A

replace with AT1 receptor blockers if cough is an issue

58
Q

Name a contra-indication for b-adrenoceptor antagonists for heart failure? When is it not a contraindiction?

A

hypertension. Generally is a sort-of contra-indication unless the heart problem is sympathetic, where beta blockers can actually be helpful

59
Q

Describe the effect of b1 blockade (metoprolol) on tachycardia and cardiac work?

A

reduces them

60
Q

How does b1 blockade effect renin release and AII effects

A

inhibits renin release and subsequent AII effects.

61
Q

What does b1 blockade protect against?

A

receptor downregulation

62
Q

Describe the effects of aldosterone receptor antagonists

A
  • reduce plasma volume and preload
  • inhibit aldosterone action on cortical distal tubules that promote Na+ retention
  • improves survival with combination therapy in severe heart failure
  • require close monitoring of hyperkalaemia and renal function

OD2 Semester 1 - Applied Clinical Training (47 decks)

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