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Pharmacology > Angina, Cardiac Arrest and Arrhythmias > Flashcards

Angina, Cardiac Arrest and Arrhythmias Flashcards

1
Q

Give 2 examples of calcium channel blockers and 2 indications for their use:

A
  • amlodipine, nifedipine, diltiazem, verapamil
  • hypertension rx - to reduce risk of stoke, MI and death
  • stable angina - symptom control
  • Supraventricular arrhythmia rx - control heart rate (diltiazem, verapamil)
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2
Q

MOA of CCBs

  • decrease Ca2+ ion entry into vascular and cardiac cells, reducing intracellular calcium concentration
  • this causes…
  • effect on inotropy and conduction?
  • overall these together reduce ___ so reduces ..
A
  • causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure
  • in heart, CCBs reduce myocardial contractility
  • they supress cardiac conduction (esp across AVN) –> slowing ventricular rate
  • together, reduces afterload so reduces myocardial O2 demand - preventing angina
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3
Q

CCBS can be

  • dihydropyridines: relatively selective for the vasculature e.g. ____ and ___
  • non-dihyropyridines: more selective for the heart, most cardioselective CCB is ___
A
  • dihydropyridines: e.g. amlodipine and nifedipine

- non-dihyropyridines: cardioselective = verapamil

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4
Q

-Amlodipine and nifedipine (CCBs): name 2 SEs caused by vasodilation and compensatory tachycardia

A
  • ankle swelling
  • flushing
  • headache
  • palpitations
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5
Q

Verapamil (CCB) commonly causes ______ less often can cause: ….. (due to effects on heart)
Therefore in who should Verapamil be used with caution, give 2 e.gs?

A
  • constipation
  • bradycardia, heart block, heart failure
  • Caution: pts with poor LV function (precipitates/worsens HF) and
  • people with AV nodal conduction delay (can provoke complete heart block)
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6
Q

-Amlodipine and nifedipine (CCBs): name 2 CIs
(one relates to the vasodilation causing a reflex in contractility and tachycardia, which increases the __ ___)
(other relates to risk of provoking collapse in pts with this pathology)

A

CI: UNSTABLE ANGINA (increases O2 demand)

SEVERE AORTIC STENOSIS

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7
Q

-Non-dihydropyrididine CCBs e.g. verapail, diltiazem, should not be prescribed with _____ except under specialist supervision as both drug classes are negatively ionotropic and chronotropic so together can cause: HF, bradycardia and asystole

A

-B-BLOCKERS

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8
Q

Rough dosages for CCBs

  • amlodipine for HT e.g. ___ mg orally daily
  • diltiazem for angina e.g. ___mg orally 12-hrly
  • verapamil for SV arrhythmias e.g. ___mg orally 8-hrly
A
  • amlodipine 5-10mg for HT
  • diltiazem 90mg for angina
  • verapamil 40-120mg for SV arrhythmias
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9
Q

Amiodarone is indicated in the treatment of several _______ such as:
(only when other therapeutic options-drugs/electrical cardioversion are ineffective)

A

-tachyarrhythmias e.g. AF. atrial flutter, SVT, VT, refractory VF

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10
Q

Amiodarone MOA:
-effect on myocardial cells is: blockade of..
-so therapeutically in the following can…
AF:
SVT AVNRT:
VT/VF:

A
  • blockades Na+, Ca2+ and K+ channels and alpha & beta adrenergic receptors
  • this reduces spontaneous depolarisation, slows conduction velocity and increases refractiveness inc. in the AVN
  • so it can reduce ventricular rate in AF/atrial flutter
  • can increase chance of conversion and maintenance of sinus rhythm
  • in SVT AVNRT can break the circuit and restore sinus rhythm
  • can treat and prevent VT and improves chance of successful defibrillation in refractory VF
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11
Q

3 Amiodarone SEs

NB: amIODarone

A
  • pneumonitis
  • bradycardia, AV block
  • hepatitis
  • photosensitivity and grey discolouration of skin
  • due to IODine content can –> thyroid abnormalities

(NB: half life is very long, months to clear)

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12
Q

Avoid amiodarone if possible in what 2 pt groups (based on MOA/SEs)

A
  • severe hypotension
  • heart block
  • active thyroid disease
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13
Q

Amiodarone interacts with very many drugs
Name 2 that in can increase the plasma concentration of which increases risk of bradycardia, AV block and heart failure…

A
  • digoxin
  • diltiazem (CCB)
  • verapamil (CCB)
  • so half the dose of these drugs if amiodarone is started
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14
Q

In ALS algorithm, immediately after the 3rd shock in cardiac arrest with VF or pulseless VT, Amiodarone is given followed by 20ml 0.9% sodium chloride or 5% glucose as a flush. What is the dose of Amiodarone given?

A

-300mg IV (bolus dose in pre-filled syringe)

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15
Q

Why in a setting outside cardiac arrest if continuous/repeated IV infusions of amiodarone are anticipated should it be given in a central line? What is the risk of peripheral IV administration?

A

-Can cause significant phlebitis peripherally

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16
Q

2 indications for Digoxin prescription:

A
  • AF and atrial flutter to reduce the ventricular rate (but a B-blocker or non-dihydropyridine CCB is often more effective)
  • in severe HF: for pts already taking an ACEi, B-blocker, and an Aldosterone antagonist/ARB
17
Q

Digoxin MOA

-effect on HR and contractility? How is is useful in AF and how does it help in HF - different aspects

A
  • negatively chronotropic
  • positively ionotropic
  • increases vagal parasympathetic tone , reduces conduction at AVN, reducing ventricular rate in AF/AFlutter
  • in HF: inhibits Na+/K+ ATPase so Na+ accumulates in cell, as cell extrusion of Ca2+ requires low intracellular Na+ concs, elevated Na+ conc causes calcium to accumulate in cell so increases contractile force.
18
Q

3 adverse effects of Digoxin therapy:

A
  • bradycardia
  • GI disturbance
  • rash
  • diziness
  • visual disturbances (blurred or yellow vision)
  • pro-arrhythmic in digoxin toxicity (!)
19
Q

2 Contraindications for use of Digoxin and 2 cautions for its use:

A

-CI: 2ND DEGREE HEART BLOCK
-CI: INTERMITTENT COMPLETE HEART BLOCK
-CI: PTS W/AT RISK OF VENTRICULAR ARRYTHMIAS
Caution: reduce dose in renal failure (is eliminated renally)
Caution: hypoK+, hypoMg2+ and hyperCa2+ increase the risk of digoxin toxicity

20
Q

By what mechanism do some diuretics increase the risk of digoxin toxicity? Name 1 other drug that increases plasma conc of digoxin so increases risk of toxicity?

A
  • loop and thiazides can cause hypokalaemia, as result when K+ is low, competition with K+ to bind to Na/K+ ATPase is low so effects of Digoxin are enhanced
  • Amiodarone, CCBs, Spironolactone and Quinine can increase plasma conc of Digoxin
21
Q

What ECG change may be seen with therapeutic levels of Digoxin therapy?

A

-ST-segment depression, reverse tick sign on ECG

expected effect, doesn’t signify toxicity

22
Q

-Atropine, hyoscine butylbromide (buscopan) and glycopyrronium are all medications belonging to the class “______ “
give 1 cardio and 1 GI indication for their use.

A

Anti-muscarinics

  • bradycardia
  • IBS (anti-spasmodic)
  • in care of dying patients to reduce copious respiratory secretions
23
Q

Anti-muscarinics antagonise the rest and digest effects therefore name 3 SEs associated with their use?

A
  • tachycardia, dry mouth, constipation
  • reduce detrusor activity so –> urinary retention in BPH pts
  • blurred vision
  • drowsiness and confusion
24
Q

Pts susceptible to ___-__ ___ should not have anti-muscarinics as they can precipitate a rise in ___. And avoid in pts at risk of ____

A
  • acute-angle glaucoma
  • rise in ICP
  • arrhythmias
25
Q

Atropine dose for bradycardia. give incremental doses by __, can start from ___micrograms and give up to ___mg

A
  • IV in incremental doses

e. g. 500micrograms every 1-2mins until an acceptable HR is reached, up to maximum of 3mg.

26
Q

Lidocaine is indicated for what? (2)

A
  • local anaesthetic e.g. in urinary catheterisation and minor procedures
  • VT and VF rx refractory to electrical cardioversion but amiodarone is preferred
27
Q

Lidocaine MOA

  • enters cell
  • accepts a …. –> —
  • from inside cell it enters then blocks ….
  • this prevents …
  • in heart …
A
  • enters cell
  • accepts a proton to become + charged
  • from inside cell it enters then blocks VGNa+Channels on surface membrane
  • this prevents initiation and propagation of APs in nerves and muscle
  • in heart reduced duration of APs slows conduction velocity and increases refractory period
28
Q

SEs of Lidocaine administration

A
  • stinging
  • rarely systemic effects: drowsiness, restlessness, tremor, fits
  • OD can cause hypotension/arrhythmias
29
Q

-as lidocaine depends heavily on hepatic blood flow for its elimination, lower doses should be used in states of reduced ____ ____

A

-cardiac output

30
Q

What is the first line drug in the treatment of supraventricular tachycarida (SVT)?

A

-Adenosine

31
Q

What is the ECG appearance of SVT (NB: adenosine is the 1st line treatment)

A

-regular narrow complex tachycardia

32
Q

Adenosine binds to adenosine receptors on cell surfaces in the heart, it activates these GPCRs leading to what effects
(treats SVT)

A
  • overall = increases AV node refractoriness
  • reduces frequency of spontaneous depolarisations
  • increases resistance to depolarisation
  • so transiently slows the sinus rate and conduction velocity
33
Q

What is the approximate half life of adenosine in plasma ?

A

-10seconds

34
Q

adenosine can break the re-entry circuit of a SVT taking place in the AVN by increasing the refractoriness, this allows SAN to resume control of heart rate = “cardioversion”. Why can it not induce cardioversion in atrial flutter, and why is it still given in atrial flutter then?

A
  • in atrial flutter the circuit does not involve the AVN so it won’t induce cardioversion
  • but it blocks conduction to the ventricles so allows closer inspection of the atrial rhythm on ECG by slowing the HR so may help reveal the diagnosis
35
Q

As adenosine interferes with SAN and AVN functions adenosine can induce what v adverse effects during it’s brief action? What do pts report?

A
  • induce bradycardia and even asystole

- pts feel sinking in chest, with breathlessness and sense of impending doom

36
Q

3 CI to adenosine use relate to pts that wouldn’t tolerate it’s bradycardic effects, suggest 2:

A
  • CI: HYPOTENSION
  • CI: CORONARY ISCHAEMIA
  • CI: DECOMPENSATED HEART FAILURE
37
Q

Adenosine should be avoided in pts with asthma/COPD due to the risk of it inducing what?

A

-Bronchospasm

38
Q

Dipyridamole (an antiplatelet agent) has what effect on cellular uptake of adenosine, (____ the half-life) therefore what should you do if co-prescribed?

A
  • dipyradamole blocks adenosine cellular uptake
  • so prolongs half life/potentiates effect
  • so halve the dose of adenosine
39
Q

the initial dose of adenosine is usually 6mg, by what route is it given?

A

IV

Pharmacology (14 decks)

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