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ESA 2 > CVS 9.1 - Drugs and the Cardiovascular System > Flashcards

CVS 9.1 - Drugs and the Cardiovascular System Flashcards

1
Q

What is arrhythmia? What can cause arrhythmia?

A
  • Abnormal heart rate or rhythm
  • Atrial flutter
  • Atrial fibrillation
  • Ventricular fibrillation
  • Tachycardia ([supra]ventricular)
  • Bradycardia
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2
Q

What can cause arrhythmias?

A
  • Ectopic pacemaker activity
  • After depolarisations
  • Re-entry loops
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3
Q

How can ectopic pacemaker activity cause arrhythmias?

A
  • Damaged myocardium becomes depolarised
  • Causes hidden pacemaker areas due to ischaemia that over power SAN
  • Activates spontaneously
  • Slower depolarisation so prolonged QRS complex
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4
Q

What does an early ectopic pacemaker activity cause?

A

Increased myocyte excitability

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5
Q

What does a late ectopic pacemaker activity cause?

A

Conduction failure

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6
Q

What is an after depolarisation?

A
  • Premature depolarisations after an action potential due to triggered activity
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7
Q

What is triggered activity?

A
  • Impulse initiation in cardiac fibres dependent on after depolarisation
  • Another action potential is caused if threshold is reached leading to arrhythmia
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8
Q

What can after depolarisations cause?

A
  • Really long action potentials/ increased QT interval
  • Increases intracellular calcium concentration
  • Increases force of contraction
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9
Q

How are re-entry loops caused?

A
  • Conduction is blocked at a damaged area

- Unidirectional block = incomplete conduction damage

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10
Q

How can re-entry loops cause arrhythmias?

A
  • Excitation spreads in wrong direction through damaged area
  • Causes a circuit looping back on itself
  • Re-excites tissue in a circle
  • Causes a circle of contractions = tachycardia
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11
Q

What can multiple re-entry loops result in?

A
  • Lots of small entry loops in atria
  • Multiple foci
  • Mitral stenosis = increased difficulty to fill
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12
Q

What are the four groups of anti-arrhythmic drugs?

A
  • Block vgNa+ channels
  • Beta-adrenoceptor antagonists
  • K+ channel blockers
  • Ca2+ channel blockers
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13
Q

What are some risk factors for arrhythmia?

A
  • Age (more common in older age)
  • Heart disease/attack
  • Leaky/narrow valves
  • High blood pressure
  • Diabetes
  • Sleep apnoea (heart doesn’t get enough O2 = stress)
  • Over-under active thyroid
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14
Q

How does bradycardia affect systemic circulation?

A
  • Decreases cardiac output

- Decreases arterial pressure

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15
Q

How does tachycardia affect systemic circulation?

A
  • Decreased stroke volume
  • Decreased cardiac output
  • Decrease preload when contraction rate is high
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16
Q

How does atrial fibrillation affect systemic circulation?

A
  • Decreases stroke volume and cardiac output during exercise

- Increased risk of thrombus formation

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17
Q

How does ventricular fibrillation affect systemic circulation?

A

Cardiac output is 0

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18
Q

How are drugs blocking Na+ channels e.g. local anaesthetics, used to treat arrhythmias?

A
  • Block vg Na+ channels when open/inactivated (use-dependent)
  • Depolarisation needs to happen first
  • Rapid dissociation means that the next normal action potential can happen
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19
Q

Why do Na+ channel blockers only affect damaged areas rather than normal tissue?

A
  • Damaged areas are depolarised
  • Na+ channels are open during depolarisation
  • Blocked by drugs as they are use dependent
  • Ensures there is no automatic firing
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20
Q

When would be an appropriate time for local anaesthetics to be used to treat arrhythmias?

A
  • Ventricular tachycardia before/after myocardial infarction

- Administered intravenously

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21
Q

How are beta adrenoreceptor antagonists used to treat arrhythmias?

A
  • Block sympathetic action
  • Block beta1 adrenoreceptor in the SAN
  • Decreases pacemaker potential
  • Negative chronotropy and inotropy
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22
Q

What are the overall effects of beta adrenoreceptor antagonists?

A
  • Decrease work load
  • Decrease blood volume
  • Decrease O2 demand therefore decreasing myocardial ischaemia
  • Negative chronotropy and inotropy
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23
Q

What are the effects on the heart in a beta adrenoreceptor antagonist acts on the AVN? When would this be an appropriate treatment?

A
  • Slows AVN conduction

- During atrial fibrillation to prevent supraventricular tachycardia

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24
Q

Why can’t propanolol be given to asthmatics?

A
  • Non-selective for beta1 and beta2 adrenoreceptors

- Causes bronchoconstriction as well as decreasing HR and FOC

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25
Q

Why is atenolol a more appropriate treatment for asthmatics?

A
  • Cardioselective for beta1

- Doesn’t cause bronchoconstriction

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26
Q

What is meant by a therapeutic use?

A

The use of a drug where the effects are beneficial

27
Q

What is the action of K+ channel blockers in treating arrhythmias?

A
  • Theoretically prolongs action potential therefore prolonging absolute refractory period
  • Prevents another action potential from being generated too soon
28
Q

What is the problem with using K+ channel blockers?

A
  • Actually promotes arrhythmias
  • More likely to happen during long action potentials
  • Due to after depolarisations
  • Causes another action potential if threshold is reached
29
Q

Which K+ channel blocker can actually be used to treat arrhythmias and why?

A
  • Amiodarone

- Blocks other channels too which balances out effects

30
Q

When would amiodarone be used?

A

Treatment of Wolff-Parkinson-White syndrome

31
Q

What is Wolff-Parkinson-White syndrome?

A
  • There is an extra electrical pathway between atria and ventricles
  • Causes heart to beat really fast for periods of time (supraventricular tachycardia)
32
Q

What is the action of Ca2+ channel blockers in treating arrhythmias when given intravenously?

A
  • Block Ca2+ entry into the cell
  • Decreases pacemaker potential at SAN
  • Decreases AVN conduction
  • Negative inotropy
  • Vasodilation of some coronary and peripheral vessels
33
Q

What is the significance of using dihydropyridines?

A

Only act on smooth muscle

34
Q

Why are Ca2+ channel blockers given intravenously?

A
  • Due to vasoconstrictive nature

- Could cause tissue necrosis

35
Q

When would Ca2+ channel blockers be used as treatment?

A
  • Anti-hypertensive
  • Arrhythmias
  • Heart failure
  • Angina
36
Q

What is the general action of negative inotropic drugs?

A
  • Decrease heart rate

- Decrease force of contraction

37
Q

What is the action of adenosine when given intravenously?

A
  • Enhances K+ conductance at A1 receptors on AVN
  • Hyperpolarisation of cell = further from threshold
  • Restores sinus rhythm
38
Q

What is heart failure?

A

Chronic failure of the heart to provide sufficient output to meet the requirements of the body

39
Q

What are the effects of heart failure on the heart and circulation?

A
  • Decreased force of contraction
  • Decreased cardiac output
  • Decreased perfusion
  • Oedema (peripherally if RV fails)
40
Q

Why does heart failure cause oedema?

A
  • Causes venous congestion

- Increases hydrostatic pressure

41
Q

What can be used to treat heart failure?

A
  • Positive inotropes to increase cardiac output
  • Beta adrenoreceptor AGONISTS (cardiogenic shock)
  • Cardiac glycosides (only if there’s a lot of oedema and want to increase CO)
42
Q

What is the action of cardiac glycosides?

A
  • Block Na+K+ATPase
  • Increases [Na+]in
  • Increases [Ca2+]in
  • NCX is more inefficient
  • Increases force of contraction/ positive inotropy
43
Q

Why can cardiac glycosides be used during heart failure and atrial fibrillation?

A
  • Increase in vagal activity
  • Slows AVN conduction
  • Decreases heart rate
44
Q

What are the overall effects of drugs used to treat heart failure?

A
  • Decrease work load of the heart
  • Decrease afterload and therefore TPR
  • Decrease preload (venous return)
45
Q

What is the general action of ACE inhibitors?

A

Inhibit the angiotensin converting enzyme

46
Q

What is the renin-angiotensin-aldosterone system?

A

Hormonal regulation of blood pressure and fluid balance. It is up-regulated during heart failure

47
Q

What is the first step of the renin-angiotensin-aldosterone system?

A
  • Liver releases angiotensin (hormone)
  • Kidney releases renin (enzyme)
  • Renin cleaves angiotensin to form angiotensin 1
48
Q

What stimulates the release of renin?

A
  • Decrease in Na+ delivery to distal tubules
  • Renal artery hypotension
  • Beta1 agonism by the SNS
49
Q

What is the second step of the renin-angiotensin-aldosterone system?

A
  • Vascular endothelium in the lungs releases ACE (converting enzyme)
  • ACE + Angiotensin 1 = angiotensin 2 forms
  • Causes heart to work harder
50
Q

What is the effect of angiotensin 2 in the zona glomerulosa of the adrenal glands?

A
  • Stimulates aldosterone secretion
  • Increases Na+ absorption
  • Increases fluid which increases blood pressure
  • Decreases K+ absorption
51
Q

What is the effect of angiotensin 2 in the kidneys?

A
  • Vasoconstriction in arterioles
  • AT1 receptors are coupled to G-alphaQ proteins
  • Follows IP3 pathway
  • Increases blood pressure due to increased resistance
52
Q

What is the action of ACE inhibitors?

A
  • Prevent angiotensin 2 from forming
  • Vasodilates arterioles in kidneys
  • Venous dilation = decreased afterload (↓ vasomotor tone and ↓ blood pressure) and ↓preload (↓ fluid retention = ↓blood volume)
  • ↓blood volume by ↓Na+ absorption in zona glomerulosa = ↓ preload (antihypertensive treatment)
53
Q

Which three groups of drugs decrease the work load of the heart?

A
  • ACE inhibitors
  • Beta adrenoreceptor antagonists
  • Diuretics
54
Q

What is angina?

A
  • Severe chest pain that spreads due to an inadequate coronary blood supply that is caused by atheromatous arteries
  • Is transient and has no cell death (just ischaemia)
55
Q

How can angina be treated?

A
  • ↓ work load
  • Beta adrenoreceptor blockers
  • Ca2+ channel antagonists (improves blood supply)
  • Organic nitrates (improves blood supply a little)
56
Q

What is the action of organic nitrates?

A
  • React with smooth muscle
  • Releases NO2-
  • NO2- is reduced to NO (produced by endothelium anyway)
  • Causes vasodilation
57
Q

How does NO cause relaxation of cardiac smooth muscle?

A
  • Activates guanylate cyclase = ↑cGMP = ↓[Ca2+]in = activates protein kinase G = ↑[Ca2+] in SR
  • Activates K+ channels = hyperpolarises the cell
  • Stimulates a protein kinase for activation of MLCP = myosin light chain is dephosphorylated
58
Q

What is the result of vasodilation of veins when organic nitrates are pharmalogically administered?

A
  • ↓ preload = ↓ filling = ↓ work load

- ↓ O2 demand

59
Q

What can happen in the heart to increase the risk of thrombus formation?

A
  • Atrial fibrillation
  • Acute myocardial infarction
  • Prosthetic heart valves
60
Q

What is the action of anticoagulants and antiplatelets?

A
  • Anticoagulations = thrombin/vitamin K inhibition

- Antiplatelets = ↓ platelets

61
Q

What are the effects of hypertension on circulation?

A
  • ↑ arterial blood pressure
  • ↑ total peripheral resistance
  • ↑ Na+ and water uptake
62
Q

What is the equation for pressure?

A

Pressure = Flow x Resistance

63
Q

What is the equation for blood pressure?

A

Blood pressure = Cardiac output x Total Peripheral Resistance

ESA 2 (63 decks)

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