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
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
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
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
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
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
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
8
Q
dabigatran
Dose
A
- 150mg BD
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
10
Q
BB
Important adverse effects
A
- Fatigue
- Cold extremities
- Headache
- GI disturbance
- Sleep disturbance and nightmares
- Impotence in men
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
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
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
14
Q
CCB
A
- We can use verapamil instead of BB- look at HTN (amlodipine) for info
15
Q
Amiodarone
Common indications
A
- Wide range of tachyarrhythmias
- AF
- Atrial flutter
- SVT
- VT
- VF
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
- Rapid reversion to sinus rythm in SVT
- Used to diagnose SVT
- 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
