Atrial Fibrillation Flashcards

1
Q

Heparins and fondaparinux

MOA (NOT used in AF)

A
  • Thrombin and factor Xa are key components of the final coagulation pathway that leads to the formation of fibrin clots
  • By inhibiting these factors, prevents coagulation and propagation of blood clots
  • Unfractionated heparin (UFH) activates antithrombin that in tern inactivates clotting factor Xa and thrombin
  • LMWH (enoxaparin) only inhibit Xa
  • Fandaparinux is a synthetic compound that is similar to heparin
  • It inhibits factor Xa
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2
Q

Warfarin- MOA

A
  • Warfarin inhibits hepatic production of vitamin K-dependent coagulation factors and co-factors
  • Vitamin K must be in its reduced form for the synthesis of coagulation factors
  • It is then oxidised during the synthetic process
  • An enzyme called Vit K epoxide reductase reactivates oxidised Vit K
  • Warfarin inhibits Vit K epoxide reductase, preventing reactivation of vit K and coagulation factor synthesis
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3
Q

Warfarin

Adverse effects

A
  • Bleeding
    • A slight excess of warfarin increases the risk of bleeding from existing abnormalities such as peptic ulcers or minor trauma
    • A large excess of warfarin can trigger spontaneous haemorrhage such epistaxis (nose bleed) or retroperitoneal haemorrhage
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4
Q

Warfarin

warnings

A
  • Immediate risk of haemorrhage- trauma, requires surgery
  • Liver disease- who are less able to metabolise the drug are at risk of over-anticoagulation/bleeding
  • Pregnancy- warfarin should not be used in the first trimester as it causes fetal malformations including cardiac and cranial abnormalities
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5
Q

Warfarin

Important interactions

A
  • Low therapeutic index
  • Cytochrome P450 metabolites- e.g. fluconazole, macrolides, decrease warfarin metabolism and increase bleeding risk
  • Inducers- e.g. phenytoin, carbamazepine, rifampicin) increase warfarin metabolism and risk of clots.
    • Many antibiotics can increase anticoagulation in patients on warfarin by killing gut flora which synthesise vit k
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6
Q

Warfarin

Administration + Communication

A
  • Traditionally, warfarin is taken each day at around 6 for consistent effects on the INR taken the following morning. This may also help patients remember when to take it
  • Advise patients that warfarin treatment is a balance between benefits and risks
  • It is important for patients to understand how food, alcohol and other drugs can affect warfarin treatment
  • `Patient receives an anticoagulation book which acts as an alert to their warfarin therapy and is used to record doses, blood tests, indication and duration
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7
Q

Warfarin

Monitoring

A
  • The INR is the prothrombin time of a person on warfarin divided by that of a non-warfarin control. INR target values vary by indication for warfarin
  • In atrial fibrillation the target range is 2-3, INR is measure daily in hospital inpatients and every few days in outpatients commencing warfarin
  • Once a stable dose of warfarin has been established, INR becomes less frequent
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8
Q

dabigatran

Dose

A
  • 150mg BD
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9
Q

BB- MOA

Atenolol

A
  • Beta1-adrenoreceptors are located mainly in the heart, whereas B2-adrenoreceptors are found mostly in the smooth muscle of blood vessels and the airways
  • Via B1-receptors, BB reduces the force of contraction and speed of conduction in the heart
  • This relieves myocardial ischaemia by reducing cardiac work and oxygen demand, and increasing myocardial perfusion
  • Improves prognosis in HF by protecting the heart from teffects of chronic sympathetic stimulation
  • They slow the ventricular rate in AF mainly by prolonging the refractory period of the AV node
  • Reduce renin secretion (B1 mediated) which lowers BP
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10
Q

BB

Important adverse effects

A
  • Fatigue
  • Cold extremities
  • Headache
  • GI disturbance
  • Sleep disturbance and nightmares
  • Impotence in men
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11
Q

BB warnings

A
  • Asthma- cause life-threatening bronchospasm and should be avoided
  • This effect is mediated by blockade of B2-adrenoreceptors in the airways
  • BB is usually safe in COPD (best to use B1 selective (atenolol)) rather than non-selective
  • HF- BB should be started at a low dose and increased slowly, as they may initially impair cardiac function
  • They should be avoided in haemodynamic instability
  • Contraindicated in heart block
  • significant hepatic failure
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12
Q

BB

Interactions

A
  • BB must not be used with Non-dihydropyridine CCB (E.g. Verapamil, Diltiazem), this combination can cause HF, bradycardia and asystole
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13
Q

BB

Monitoring

A
  • The best guide to dosage adjustment is the patient’s symptoms (e.g. chest pain) and heart rate (in ischaemic heart disease)
  • Aim for Resting heart rate of 55-60 BPM
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14
Q

CCB

A
  • We can use verapamil instead of BB- look at HTN (amlodipine) for info
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15
Q

Amiodarone

Common indications

A
  • Wide range of tachyarrhythmias
    • AF
    • Atrial flutter
    • SVT
    • VT
    • VF
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16
Q

Amiodarone

MOA

A
  • Amiodarone has many effects on myocardial cells, including the blockade of sodium, calcium and potassium channels and antagonism of alpha and beta-adrenergic receptors
  • These effects reduce spontaneous depolarization (automatically), slow conductance velocity and increase resistance to depolarisation (refractoriness) including the AV node
  • By interfering with Av node conduction, amiodarone reduces the ventricular rate in AF and atrial flutter
  • Through its other effects, it may also increase the chance of conversion to and maintenance of sinus rhythm
  • Amiodarone’s effects in suppressing spontaneous depolarisations make it an option for both treatment and prevention of VT
  • The same rationale underlies it’s use in refractory VF, although there is little evidence from clinical trials to support this
17
Q

Amiodarone

Adverse effects

A
  • Hypotension during IV infusion
  • Pneumonitis
  • Bradycardia and AV block
  • Hepatitis
  • Photosensitivity and grey discolouration of skin
  • Thyroid abnormalities- due to its iodine content- can be hypo and hyper
18
Q

Amiodarone

Warnings

A
  • Amiodarone is a dangerous drug
  • Avoid in
    • Severe hypotension
    • Heart block
    • Active thyroid
19
Q

Amiodarone

Interactions

A
  • Amiodarone interacts with many drugs- too many to list here
  • increases plasma concentrations of: Digoxin, diltiazem, verapamil
  • This may increase the risk of bradycardia, AV block and HF
  • The dose of these drugs should be halved if amiodarone is started
20
Q

Amiodarone

Communication

A
  • As appropriate advise treatment aimed at correcting their fast or irregular heart rhythm
  • Explain that it has a number of important and potentially serious side effects, and it is being used only because their condition is serious and no other treatments are suitable
  • In long-term use, ask the patient to report any symptoms: breathlessness, persistent cough, jaundice, weight loss or gain
  • Advise the patient not to drink grapefruit juice
21
Q

Amiodarone

Monitoring

A
  • The efficacy is best judged by HR and rhythm
  • For safety, baseline tests should be renal, liver and thyroid profiles and a chest X-rays
  • The liver and thyroid profiles should be repeated 6 monthly
22
Q

Digoxin

Common indications

A
  • AF and atrial flutter, digoxin is used to reduce the ventricular rate
  • Severe HF- digoxin is used as a third-line treatment in patients who are already taking an ACEI and BB and either aldosterone antagonist or ARB
  • It is used at an earlier stage in patients with co-existing AF
23
Q

Digoxin

MOA

A
  • Digoxin is negatively chronotropic (it reduces the heart rate) and positively inotropic (Increases contraction of the heart contraction)
  • In AF/flutter, it’s therapeutic effect arises mainly via an indirect pathway involving a vagal tone
  • This reduces conduction at the atrioventricular node, preventing some impulses from being transmitted to the ventricles, thereby reducing the ventricular
  • In HF it has a direct effect on myocytes through inhibition of Na/K/ATPase pumps, causing Na to accumulate in the cells
  • As cellular extrusion of Ca requires low intracellular Na concentrations, the elevation of intracellular Na and Ca to accumulate in the cell, increasing contractile force
24
Q

Digoxin

Adverse effects

A
  • Bradycardia, GI disturbance, rash, dizzieness and visual disturbance
  • Digoxin is proarrhythmic and has a low therapeutic index- Low TI
  • Digoxin toxicity and these may be life-threatening
25
Q

Digoxin

Warnings

A
  • Digoxin is contraindicated
    • Second-degree heart block
    • Intermittent complete heart block
    • Ventricular arrhythmias
  • Should be reduced in renal failure- digoxin is eliminated by the kidneys
  • Certain electrolyte abnormalities increase the risk of digoxin toxicity: Hypokalaemia, magnesaemia and calcaemia
    *
26
Q

Digoxin

Interactions

A
  • Loop and thiazide diuretics can increase the risk of digoxin toxicity by causing hypokalaemia
  • Amiodarone, CCB, Spironolactone and quinine can all increase the serum concentration and therefore lead to toxicity
27
Q

Digoxin

Monitoring

A
  • The best guide to the effectiveness of digoxin is the patients symptoms and heart rate
  • Check their ECG electrolytes and renal function periodically and particularly when these changes (during illness or after medication change)
  • Digoxin can cause ST-segment depression on ECG
    *
28
Q

Adenosine

Indications

A
  1. Rapid reversion to sinus rythm in SVT
  2. Used to diagnose SVT
  3. Can be used in heart transplant
29
Q

Adenosine

MOA

A
  • Purine nucleoside which is negative dromotropic (slows conduction speed) and acts on the AV node
  • It also has a peripheral vasodilatory effect
30
Q

Adenosine

Adverse effects

A
  • Generally mild and short duration of action and generally well tolerated by patients
  • Hypotension
  • Anaphylaxis
  • AV block
  • Dyspnea
31
Q

Adenosine

Warnings

A
  • Contraindicated in: AV block, COPD/Asthma, QT prolongation, hypotension and decompensated HF
  • Cautions
    • Arterial stenosis
    • Severe HF
    • Recent MI
32
Q

Adenosine

Interactions

A
  • Dipyridamole- inhibits uptake and metabolism and also potentiates the effect of adenosine
  • Aminophylline/theophylline- Xanthines are competitive adenosine antagonists and should be avoided up to 24hrs after
  • Food and drinks containing Xanthines (tea, coffee, coke, chocolate)
  • QT prolonging drugs
33
Q

Adenosine

Monitoring

A
  • BP
  • ECG
  • HR