arrhythmia and anticoagulation Flashcards
what is the definition of arrhythmia? why do they occur?
when there is a change to the normal rhythm or rate of the heart
- due to altered impulse conduction or generation
- > changes in conduction pathway or the automaticity of pacemaker cells
what are the types of arrhythmias you can get?
- Bradycardia
- <60 bpm
- rhythm unchanged but heart rate is slow
- caused by heart block - tachycardia
- >100 bpm
- rhythm unchanged; can have super-ventricular where arrhythmias are above level of ventricles so within the atria - AF
- most common type
- rapid atrial rate and disturbance of conduction pathways increases risk of thrombus formation
what are some complications of atrial fibrillation?
- stroke
- congestive heart failure
what are risk factors for arrhythmia?
- hypertension
- CAD
- valve disease
- male
- obesity
- increasing age
- lifestyle factors
- diabetes
- pneumonia
what are symptoms of AF?
- breathlessness
- light headedness
- fatigue
- palpitations
- chest pain
how can you diagnose AF in primary care?
use a home BP monitor
it will detect pulse irregularity that can be caused by AF
what are the classifications of anti-arrhythmic drugs that are available?
- Class IA - sodium channel blocker which slows Phase 0
- Class IB - sodium channel blocker that reduces Phase 0
- Class IC - sodium channel blocker that slows Phase 0
- Class II - beta-adrenoreceptor blocker that blocks sympathetic activity and reduces rate and conduction
- Class III - K+ channel blocker that delays Phase 3 and increases AP duration
- Class iV - Ca+ channel blocker which blocks L-type calcium channels reducing rate and conduction
examples of Class I-IV drugs and other ones that might be used?
Class I -> lidocaine, quinidine, propafenone, mexiletine Class II -> atenolol, esmolol, metoprolol Class III -> amiodarone, stall, dronedarone Class IV -> dilitiazem, verapamil
- other ones are adenosine, digoxin
how to diagnose arrhythmia?
ECG
ECHO
TFTs
CXR
what are the types of AF you can get?
- paroxysmal; most often within 48 hours and can become a sustained form of AF
- persistent ; non self-terminating and longer than 7 days
- permanent; long standing AF and not terminated by cardioversion
how can you manage AF?
- control the arrhythmia
- control or treat ay underlying causes
- can do thromboprophylaxis to prevent strokes
what can be offered as a first line strategy for AF?
what are the exceptions?
offer rate control exceptions are: -> have a reversibel AF -> new-onset of AF -> have heart failure due to AF
what can be offered with the rate control strategy treatment?
beta blocker or a rate-limiting calcium channel blocker as initial mono therapy
- can consider digoxin monotherapy for people with non-paroxysmal AF
- if that doesn’t work give combination with 2 of:
- > beta blocker
- > digoxin
- > diltiazem
when should rhythm control be offered?
- when symptoms continue after heart rate has been controlled
- if rate strategy hasn’t been successful
what should be offered to patients with AF for over 48 hours?
if AF is longer than 48 hours they should be offered electrical cardioversion
- can consider giving amiodarone 4 weeks before and up to 12 months after electrical cardioversion to maintain sinus rhythm
what drug can be offered in long term rhythm control?
- standard beta blocker as first line treatment
- if unsuccessful then offer alternatives
- dronedarone is recommended and is seen to be successful
what should not be offered for rhythm control?
do not offer Class Ic antiarrhythmic drugs e.g. propafenone
if patient has frequent symptoms or has induced symptoms by things like alcohol or caffeine; offer a ‘pill-in-the-pocket’ strategy and discuss with patients
what is the effect of amiodarone?
prolongs the duration of the action potential and so the refractory period
what is the pharmacokinetics of amiodarone?
- incompletely absorbed after oral admin.
- has a prolonged half-life of several weeks
- clinical effects might not be achieved until months after initiation of treatment
what are the adverse effects of amiodarone?
it can show toxic effects common side effects can be - liver toxicity - hyper or hypothyroidism - GI tolerance - pulmonary fibrosis - neuropathy
what are the counselling points for amiodarone?
- tablet can be crushed and drank with water
- for IV injection give continuously or intermittently over 20-120 minutes
- protect your skin from sunlight and dont use sunbeds
what can rhythm abnormalities increase the risk of?
risk of blood clotting
what is CHA2DS2-VASc?
it is a stroke risk calculator
used in decision to administer antithrombotic therapy
- male patients with score of 0 and female with 1 do not need antithrombotic therapy
what is HAS-BLED?
a score to assess the risk of bleeding with patients using anticoagulants
what is an example of a Vitamin K antagonist?
warfarin
what are some anticoagulant medications that can be used in therapy?
- apixaban
- rivaroxaban
- edoxaban
- vitamin K antagonist
what are some disadvantages of oral anticoagulants?
- requires blood tests
- antidote available
- needs thorough patient counselling
what can warfarin be used for?
- pulmonary embolism
- deep vein thrombosis
- AF
- mechanical heart valves
what is the INR ?
it is a index of blood coagulability
International Normalised Ratio
a normal value of INR would be 1
how would you initiate warfarin?
- anticoagulant therapy like warfarin will change INR to 2-4
- so for AF, PE and DVT you should aim for INR to be 2-3
- must determine the base-line prothrombin time
for patients who need treatment rapidly they should get 5-10mg on first day and dosage then depends on INR and prothrombin time
should be given with heparin for at least five days and until INR is constant at 2.0 for at least two days
for patients who dont need treatment can give a loading dose over about 3-4 weeks
daily maintenance dosage is usually 3-9mg
what are NOACS?
they are non-vitamin K Antagonist oral anticoagulants
- can inhibit direct thrombin or inhibit activated factor Xa
e. g. rivaroxaban, edoxaban, apixaban
do not need INR monitoring
what is factor Xa?
it is a blood clotting factor that cleaves prothrombin to produce thrombin for the coagulation cascade
what is seen to be a good alternative to warfarin?
NOACS
they prevent strokes and systemic embolism in AF patients
as effective as warfarin but reduced risks
who should anticoagulation be offered to?
patients with a CHA2DS2-VASc score of 2 or above
- take bleeding risk into account
- dont offer aspirin monotherapy solely for stroke prevention
- patients taking VK antagonist and have stable AF should continue with current medication and regular discussions should be had about their medication treatment
what is Fondaparinux?
synthetic pentasaccharide that inhibits factor X
- used in prophylaxis of VTE and treatment of DVT and PE
- used in acute management of MI
what are LMWH? what monitoring is needed for it?
low molecular weight heparins
- contain smaller polysaccharide chains
- have an anticoagulant effect by inactivating factor Xa
- longer half life
- excreted renally so should look at renal impairment risk
- dont need to monitor APTT
what is UFH?
‘conventional heparin’
- large molecules
- immediate anticoagulant properties
- prevents fibrin production
- given IV or SC
- has a shorter half life so safer for risk of renal impairment
how can you reverse anticoagulant effects?
use idarucizumab
used in emergency surgery or urgent procedures
of an ECG graph, what is occurring at P, R and T?
P is when atrial depolarisation occurs
R is when ventricular depolarisation occurs
T is when ventricular repolarisation occurs
what is an ECG?
- measures heart electrical conduction system
- detected by electrodes attached to surface of the skin
- picks up electrical impulses from polarisation and depolarisation of cardiac tissues
- current is transformed into waveforms
why record an ECG?
allows us to see sequence of electrical events in cardiac cells
- powerful diagnostic tool to look at:
- > rhythm disturbances
- > conduction disturbances
- > MI
what are the ECG leads?
- bipolar limb leads there are four limb leads - attached to two arms and legs red = right arm yellow = left arm green = left leg black = right leg
each lead has three separate bipolar leads
what is the AVF lead?
it uses the left foot electrode as positive and both arms as the negative
what is the AVR and AVL lead?
AVR lead; the right arm electrode is positive and remaining two electrodes are negative (left foot and hand)
AVL lead; the left arm electrode is positive and the other two are negative (right arm and left foot)
how is the ‘frontal’ plane of the patients chest?
you have six leads; AVR, AVL, AVF, I, II, III
they intersecting and lie in a flat frontal plane of the patients chest
they all record form a different angle and viewpoint to provide different views of the cardiac activity ; more accurate
what kind of electrode do the leads require?
a positive electrode
where are right and left chest leads placed?
right chest leads are placed on right ventricle and left leads on left ventricle
what is the upward deflection on the ECG due to?
the depolarisation wave moving towards the positive electrode
what is the heart axis normal value? where does it usually point?
it is usually between -30 and +90 degrees
it usually points in the direction of the average electrical vector of all depolarising heart cells
what does a positive QRS complex mean in terms of the heart axis?
it means that the heart axis is going in that leads direction
QRS should be positive in lead I and II for a normal heart axis
what does ECG paper usually look like
vertically it is one large box ; represents 0.5mV
horizontally you have on small box; 0.04 secs
one large box is 0.2 secs
there are markers for every 3 seconds present
how would you do rhythm analysis?
- calculate the rate; count number of complete R to R waves in 6 sec strip then x10
- determine the regularity
- assess P waves; are there waves? do they look like the same and occur regularly?
- find the PR interval; should be 3-5 boxes (0.12-0.20 secs)
- find the QRS duration; normal is 0.04-0.12 seconds so 1-3 small boxes
what is the PR interval?
it is atrial depolarisation + delay in the AV junction (bundle of His/AV node)
why is there a delay in the AV node?
to allow the atria to contract before the ventricles contract
