Dysrhythmias and AF Flashcards
What is a dysrhythmia or arrhythmia primarily caused by?
Impairment in impulse generation or conduction
Why is “dysrhythmia” a more accurate term than “arrhythmia”?
“Arrhythmia” implies absence of rhythm
What can impairment in cardiac rhythm manifest as?
Altered rate of impulse generation
What part of the heart does atrial dysrhythmia affect? What part of the heart does ventricular dysrhythmia affect?
Only the atria
Only the ventricles
Where does sinus dysrhythmia originate?
The SA node
What heart rate defines bradycardia in a sedentary adult? What heart rate range defines tachycardia in an adult? What heart rate range defines flutter? What heart rate defines fibrillation?
<60bpm
100-150bpm
150-350bpm
>350bpm
Which type of dysrhythmias respond best to drug treatments? What is the preferred treatment for persistent and symptomatic bradycardia?
Tachydysrhythmias
Pacemaker insertion
Which factors commonly disturb the heart rhythm?
Ischaemia/Hypoxia, electrolyte imbalances, trauma, inflammation, drugs
What are the 3 main areas into which the mechanisms that cause dysrhythmias may be grouped?
Inappropriate automaticity, triggered activity, re-entrant mechanisms
What is automaticity in cardiac cells? Which cells normally exhibit automaticity?
The ability to generate action potentials spontaneously
Cells of the SA node
In inappropriate automaticity, what ability do atrial or ventricular cells acquire? Which potential causes are listed as causes of inappropriate automaticity?
The ability to initiate action potentials
Ischaemia
How does ischaemia lead to inappropriate automaticity? Which electrolyte disturbance is specifically mentioned as contributing to abnormal automaticity?
Reduces the cell’s ability to control electrolyte flux
Decreased potassium
When does triggered activity occur? What causes triggered activity?
During or just after repolarisation
A depolarising oscillation of the membrane potential
When do early afterdepolarisations (EADs) occur? What condition are EADs thought to be responsible for? In what type of patients do EADs occur?
During the relative refractory period (phase 3)
Torsades de pointes
Patients with abnormally long repolarisation times
When do delayed afterdepolarisations (DADs) occur? What do DADs look like on an ECG? What happens if delayed depolarisation reaches threshold? What factors may contribute to delayed afterdepolarisations?
After the repolarisation phase is complete
Oscillating depolarising waves
It will trigger an action potential
Digoxin toxicity and excessive catecholamine stimulation
What has some genetic abnormalities in intracellular Ca2+ handling been associated with?
Triggered activity mechanisms
What is reentry thought to be a major cause of?
Most tachydysrhythmias
Which tachydysrhythmias is reentry a major cause of? When do reentry problems occur? What happens as a result of abnormally slowed electrical conduction in reentry?
Atrial and ventricular tachycardia, flutter and fibrillation
When electrical conduction is abnormally slowed
Action potential returns to nonrefractory cells
What does the return of the action potential to nonrefractory cells initiate? Which factors predispose to reentry mechanisms?
An extra, ectopic depolarisation
Myocardial ischaemia and electrolyte abnormalities
What are the 3 main categories of dysrhythmias?
Abnormal rates of sinus rhythm, abnormal site of impulse initiation, disturbances of the conduction pathways
What are the 3 types of abnormal rates of Sinus Rhythm?
Sinus tachycardia, sinus bradycardia, sinus arrest
What heart rate defines sinus tachycardia? What are the causes of sinus tachycardia? What kind of response is sinus tachycardia often?
> 100bpm
Sympathetic activation, decreased parasympathetic activity, fever, hyperthyroidism, pain, low BP, hypoxia, increased metabolism
Compensatory response
What increased demand is sinus tachycardia often a compensatory response to? What treatments are aimed at correcting the underlying cause of sinus tachycardia? When is cardiac output compromised in sinus tachycardia?
Increased demand for cardiac output or reduced stroke volume
Oxygen, bed rest and CCBs
When ventricular filling is impaired
What heart rate defines sinus bradycardia? What does sinus bradycardia result from? What are possible causes of increased parasympathetic activity that can cause sinus bradycardia?
<60bpm
Increased parasympathetic activity, drugs, increased stroke volume, acute hypertension
Pain, endotracheal suctioning etc
When should sinus bradycardia be treated?
If it precipitates low CO
With what should sinus bradycardia be treated if it precipitates low CO? What is sinus arrest also known as? What does sinus arrest result in?
Sympathomimetics or anticholinergics
Asystole
Flat ECG and zero CO
What are possible results from sinus arrest? What is the treatment for sinus arrest?
MI, electrical shock, electrolyte disturbances, acidosis etc
CPR etc
Which dysrhythmias are classified as Atrial Dysrhythmias? Which dysrhythmias are classified as Ventricular Dysrhythmias?
Premature Atrial Complexes and Tachycardia, Atrial Flutter and Fibrillation
Premature Ventricular Complexes, Ventricular Tachycardia, Ventricular Fibrillation
What atrial rate manifests as atrial flutter? What pattern of atrial depolarisations are seen on ECG during atrial flutter? Is the QRS complex normal in atrial flutter?
240-350bpm
Sawtooth pattern
No
What is the probable mechanism of atrial flutter? How is atrial flutter and tachycardia treated?
Reentry
By controlling ventricular rate
What drugs control the ventricular rate in the treatment of atrial flutter and tachycardia?
Digoxin, CCBs etc
What kind of atrial rhythm defines atrial fibrillation? What kind of ventricular rhythm is present in atrial fibrillation?
Disorganised and irregular
Irregular
What do atrial impulses appear as on an ECG during atrial fibrillation? Where are the majority of atrial impulses blocked during atrial fibrillation?
Small squiggly waves
At the AV node
What does atrial fibrillation cause the atria to do?
“Quiver” and not contract forcibly
What does the “quivering” of the atria during atrial fibrillation result in?
Stagnation of blood in the atria
What risk is associated with stagnation of blood in the atria during atrial fibrillation?
Thrombus formation and risk of CVA
How many consecutive ventricular complexes at a rate of more than 100/min are present in ventricular tachycardia? Is ventricular tachycardia a serious dysrhythmia? What does ventricular tachycardia usually indicate? What treatments are used for ventricular tachycardia?
3 or more
Yes
Serious cardiac disease
Antiarrhythmic drugs, CPR and cardioversion
What can compromised cardiac output due to ventricular tachycardia lead to if unmanaged?
Fatal outcome
What kind of cardiac rhythm is ventricular fibrillation? What does ventricular fibrillation result in? What do ECGs look like during ventricular fibrillation? How should ventricular fibrillation be treated?
Rapid uncoordinated
Ventricular quivering and lack of effective contraction
Rapid and erratic with no identifiable QRS complexes
CPR and defibrillation
What is the treatment followed by after CPR and defibrillation for ventricular fibrillation?
Administration of antiarrhythmic drugs
What kind of disturbances are disturbances of atrioventricular conduction? What are the types of disturbances of atrioventricular conduction listed?
Disturbances of Conduction Pathways
1st, 2nd, 3rd degree heart block
Name the 2 types of 2nd degree heart block
Name the 2 other types of disturbances of conduction pathways
Mobitz type I and Mobitz type II
Abnormal conduction pathways and Intraventricular conduction defects
What is AV block a disturbance in? What is the conduction in AV block like? Where does AV block result from? How many categories of AV block are there?
Conduction between the sinus impulse and ventricular response
Abnormally slowed or completely blocked
A functional or pathological defect in the AV node, bundle of His or bundle branches
3
How is 1st degree heart block identified? What is the rhythm like in 1st degree heart block? What is the relationship between P waves and QRS complexes in 1st degree heart block?
By a prolonged PR interval
Regular
Each P wave is associated with a QRS complex
What are the causes of 1st degree heart block? What is the management aimed at for 1st degree heart block?
Drugs, myocardial ischaemia and congenital heart defects
Alleviating cause if possible
How is 2nd degree block diagnosed? What is Mobitz type I also known as?
When some AV impulses are not conducted to the ventricles
Wenckebach
Which of the following can cause QT interval prolongation? Which antibiotic is associated with QT interval prolongation? What can prolongation of the QT interval predispose a patient to?
Amiodarone
Erythromycin
Torsades de pointes
What heart condition can be caused by sterone suppression?
Bradycardia
What does CHF stand for?
Congestive Heart Failure
Torsades de pointes is what kind of arrhythmia? What typically happens with Torsades de pointes if the underlying cause is not corrected? What can Torsades de pointes deteriorate into?
Polymorphic ventricular tachycardia
It recurs
Ventricular fibrillation
What drugs are used in the emergency treatment of Torsades de pointes? Besides drugs, what other emergency treatments exist for Torsades de pointes? Name an antiarrhythmic that can cause Torsades de pointes?
Isoprenaline and magnesium
Cardiac pacing or electrical cardioversion
Sotalol
What is a major drawback to anti-arrhythmic therapy? What can limit patient acceptability of some anti-arrhythmic agents?
Limited efficacy
Adverse effects
What is a common GI side effect of anti-arrhythmic drugs? What is a cardiovascular side effect that can be caused by anti-arrhythmic drugs? Which of the following is a CNS side effect of anti-arrhythmic drugs? Which of the following is a visual disturbance associated with anti-arrhythmic drugs?
Diarrhoea
Hypotension
Tremor
Blurred vision
What is a major safety problem with many anti-arrhythmics?
They may be pro-arrhythmic (can exacerbate rhythm problem or cause new arrhythmia)
Which classes of anti-arrhythmics are particularly problematic with pro-arrhythmic effects? What is a potential consequence of anti-arrhythmic drugs? What are two specific well-recognised pro-arrhythmic problems?
Class I and III agents
Increased risk of mortality
Torsade de pointes and monomorphic VT
Why is careful consideration required regarding no therapy for some arrhythmias? What is a potential result of antiarrhythmic agents?
Due to benign nature and pro-arrhythmic agents
Polymorphic ventricular tachycardia
What are some non-drug therapies used to treat arrhythmias?
- Radiofrequency ablation
- Direct current cardioversion
- Defibrillation
- Pacemakers
- Internal cardioversion defibrillators (ICDs)
What is the overall aim of antiarrhythmic drug therapy? What is the ultimate goal of antiarrhythmic therapy?
Control frequency and severity of arrhythmias
Restore normal SR and prevent lethal arrhythmias
What effect do antiarrhythmics have on conduction velocity? What effect do antiarrhythmics have on the effective refractory period (ERP)? What effect do antiarrhythmics have on abnormal automaticity?
Decrease conduction velocity
Change the duration of ERP
Suppress abnormal automaticity
According to what two factors may antiarrhythmic drugs be grouped?
Electrophysiological effects or sites of action
What is a commonly used antiarrhythmic drug?
Adenosine
When was the Vaughan Williams Classification introduced? What does the Vaughan Williams classification predict? What is a limitation of the Vaughan Williams classification?
1970s
Drug’s therapeutic activity
Oversimplifies action of some drugs
What is the effect of Class I agents on the action potential? What do Class II agents block? What is the effect of Class III agents on the action potential?
Delay the rise in phase 0 (depolarisation)
Beta-adrenoceptors
Prolong the plateau of phase 2 (repolarisation)
What do Class IV agents block during phase 4 of the action potential?
Movement of Ca ions
Which anti-arrhythmic agent has both beta-blocking and Class III actions? Which anti-arrhythmics cannot be classified according to the Vaughan Williams system?
Sotalol
Digoxin and adenosine
How do Class I agents interfere with the action potential?
Blocking Na influx during phase 0 (depolarisation)
Disopyramide belongs to which class of antiarrhythmic agents? Lidocaine belongs to which class of antiarrhythmic agents? Flecainide belongs to which class of antiarrhythmic agents?
Class Ia
Class Ib
Class Ic
Why has the use of Class 1a agents declined?
Increased mortality with chronic use
What is the mechanism of action of Disopyramide? What effect does Disopyramide have on the refractory period of the myocardium? What is an anticholinergic effect that Disopyramide can cause?
Blocks Na and K movement across membranes
Prolongs the refractory period
Increased AV nodal conduction
What inotropic action does Disopyramide have? Which of the following is a side effect of Disopyramide? What heart condition can Disopyramide exacerbate?
Negative inotropic action
Dry mouth
HF
What proarrhythmic effect can Disopyramide cause? What enzyme do Azole antifungals inhibit in regards to Disopyramide drug interactions? Why should caution be taken when taking Disopyramide and Tricyclic antidepressants?
Torsades de pointes
Metabolising enzymes
QT interval prolongation
How is Lidocaine administered? What is the effect of Lidocaine on conduction velocity? What effect does Lidocaine have on phase 3 repolarisation?
IV
No effect
Shortens phase
What is a side effect of Lidocaine? In what patients should caution be used when prescribing Lidocaine? What can accumulation of active metabolites of Lidocaine lead to?
Dizziness
Renal and hepatic impairment
CNS toxicity
What can Flecainide aggravate? What effect does Flecainide have on Phase 0 fast depolarisation? What effect does Flecainide have on cardiac conduction?
Congestive cardiac failure
Markedly slow
Markedly slows cardiac conduction
What inotropic activity does Flecainide have? What is a common side effect of Flecainide?
Negative inotropic activity
Nausea
What have Beta Blockers been proven to convincingly reduce post-MI? What type of arrhythmias are Beta Blockers used for? What effect do Beta Blockers have on phase 0 depolarisation?
Morbidity and mortality
Sympathetic-induced arrhythmias
Diminish depolarisation
What beta blocker is ultra-short-acting and beta1 selective? Is Sotalol a selective or non-selective beta blocker? Besides beta blocking action, what other actions does Sotalol have?
Esmolol (short term control of ventricular rate)
Non-selective
Some class III actions
What effect does Sotalol have on the refractory period of the atria and ventricles? What pro-arrhythmic effects does Sotalol have?
Prolongs the refractory period
Torsades
How do Potassium channel blockers prolong the effective refractory period?
By prolonging action potential duration
What drug is classified as a Class III agent? What is it used for? And what other class activities does it have?
Amiodarone
Treatment of serious tachyarrhythmias
Class I, II and IV
What does Amiodarone decrease in the heart? What complicates Amiodarone therapy? What is a loading dose of Amiodarone?
SA node and junctional automaticity
Variable oral bioavailability and long half life
200mg TDS for 7/7, then 200mg BD for 7/7, then 200mg daily thereafter
What is a potent CYP-450 inhibitor?
Amiodarone
What is a significant adverse effect of Amiodarone? What precaution should patients on Amiodarone take? What is caused by the I2 content in Amiodarone? What is a skin condition caused by Amiodarone?
Pulmonary fibrosis
Sun precautions
Hyper/hypothyroidism
Skin pigmentations
What can Amiodarone inhibit which increases toxic effects of other drugs? Why should caution be taken when administering Amiodarone with other antiarrhythmics? What can the administration of Amiodarone with other agents that do likewise cause?
CYP2C9 and CYP2D6
Amiodarone is proarrhythmic
Bradyarrhythmias
Which antiarrhythmic drug side effect is more frequent with larger maintenance doses? What precaution must a patient with photosensitivity reactions take?
Pulmonary Fibrosis
Sun precautions
What are some potential side effects of antiarrhythmic drugs?
- Elevated transaminases and liver toxicity
- Peripheral neuropathy
- Corneal microdeposits causing issues with night vision and driving
- Skin pigmentation (Grey Man Syndrome)
- Nausea
What happens to the concentrations of drugs metabolized by CYP2C9 and CYP2D6 when taken with amiodarone? What can result from administering amiodarone with agents that also slow cardiac conduction and decrease heart rate? What effect does amiodarone have that warrants caution when administering with other antiarrhythmics?
May increase as may their toxic effects
Can cause bradyarrhythmias
Proarrhythmic
What abnormalities may lead to prolongation of QT interval and other arrhythmias? Why should caution be exercised when using amiodarone with other drugs?
Electrolyte abnormalities
Other drugs can also prolong the QT interval
When using digoxin with amiodarone, what should you watch for?
Bradyarrhythmias and ECG changes
What conditions are Non-dihydropyridines Calcium Channel Blockers used to manage? How do Non-dihydropyridines Calcium Channel Blockers work?
SVTs, AF and Atrial flutter
Slow the conductance in calcium in the current-dependent tissues
Where do Non-dihydropyridines Calcium Channel Blockers slow the conductance in calcium?
AV and SA node
What was digoxin routinely used for? When is digoxin now mainly used in CHF? Examples
Management of HF
Specific indications
Patients with both AF and CHF to control ventricular rate and patients with CHF and in sinus rhythm who still have CHF symptoms
What medications should patients already be taking before considering digoxin for CHF?
Diuretics, ACEIs, beta blockers and spironolactone
Who developed the modern use of digoxin? What plants was digoxin derived from? What condition was treated using digitalis in the 1700s?
William Withering
Digitalis purpurea and Digitalis lanata (Foxglove)
Dropsy (accumulation of fluid)
What type of drug is Digoxin? What are the main effects of digoxin on the heart?
Cardiac glycoside (another used in the past was Digitoxin and Ouabain)
Increased contractile force (positive inotrope), decreased conduction through the AV node (negative dromotrope) and decreased heart rate (negative chronotrope)
What is a potential side effect of digoxin on the heart? What does Digoxin bind to? What is the function of this?
Disturbance of cardiac rhythm
Na+-K+-ATPase
Hydrolyses ATP to give energy for the Na+−K+ pump
What ions does the Na+-K+ pump expel and transport? When does the pump do this action into the cardiac cell?
Expels Na+ and transports K+
During repolarisation
What accumulates inside the cell when digoxin binds to Na+−K+−ATPase? What does the accumulation of intracellular Na+ inhibit? Where is more Ca2+ taken up when intracellular Na+ accumulates?
Intracellular Na+
The extrusion of Ca2+ ions
The sarcoplasmic reticulum
What is essential for linking electrical excitation of the cell membrane to the mechanical contraction of the myocardial cell? What is excitation-contraction coupling?
Free Ca2+ ions
Linking electrical excitation of the cell membrane to the mechanical contraction
What happens when the availability of Ca2+ ions released from the sarcoplasmic reticulum increases? What does this result in?
Increasing the coupling of actin and myosin
A more forceful contraction and increase in CO
How can cardiac glycosides increase the force of myocardial contraction without increasing myocardial oxygen consumption? How does digoxin inhibit the action of Na+-K+-ATPase?
Through excitation-contraction coupling
By inhibiting active transport of Na+ and K+
What effects are digoxin’s negative chronotropic and dromotropic effects due to?
Ability to alter the electrophysical properties of the cardiac tissues
What is automaticity? What does digoxin do to automaticity and the resting potential of atrial tissue and the AV node at therapeutic doses? What results from the augmentation of vagal activity?
The inherent ability of cardiac tissue to initiate and propagate an impulse
Decreases automaticity and increases the resting potential
Decreases HR
What can result from increasing plasma digoxin concentrations? What can result from toxic digoxin concentrations? What does toxic digoxin concentrations do to the rate of spontaneous depolarisations and the development of arrhythmias?
Severe bradycardia and heart block
Increase sympathetic NS activity and increase automaticity
Increases
What effect does digoxin have on conduction velocity at all plasma concentrations? What slows AV conduction velocity, besides the direct action of digoxin? What does an ECG show when taking digoxin?
Can decrease conduction velocity
Increased vagal action
Prolonged PR interval
What is the bioavailability of digoxin from tablets? What is the bioavailability of digoxin from liquid? What delays digoxin absorption?
60-80%
70-85%
Food
What is the half-life of digoxin in patients with normal renal function? What happens to the half life of digoxin in patients with renal impairment? Does digoxin have a narrow or wide therapeutic index? When can digoxin display toxic effects?
20-50 hours
Much longer
Very narrow
When in the normal range
What conditions require precaution when administering digoxin and why?
- Renal impairment (decreased elimination)
- Hypothyroidism (increased sensitivity)
- Hyperthyroidism (digoxin resistance)
- Electrolyte abnormalities (hypokalaemia, hypomagnesaemia or hypercalcaemia)
What patient demographic requires precaution when administering digoxin? What adjustment is needed? Are adverse effects of digoxin related to plasma concentrations? What plasma concentration of digoxin is adverse effects rare at?
Elderly (age-related renal and hepatic impairment and reduced volume of distribution)
Lower dosing
Yes
<0.8mcg/L
What ECG change is a sign of digoxin toxicity? What ECG change can be seen when taking digoxin?
Prolonged PR interval
ST depression or T wave inversion
What are common adverse effects of digoxin?
- Anorexia
- Nausea
- Vomiting
- Diarrhoea
- Blurred vision
- Visual disturbances
What are less common adverse effects of digoxin?
- Acute psychosis
- Delirium
- Amnesia
- Shortened QRS complex
- Arrhythmias
- Rash
- Thrombocytopenia
- Seizures
- Xanthopsia (yellow vision)
What is the therapeutic range for digoxin? At what plasma concentration of digoxin does anorexia occur? At what plasma concentration of digoxin does nausea occur? At what plasma concentration of digoxin does vomiting occur?
0.5-2mcg/L
1mcg/L
1.8mcg/L
3mcg/L
What must be considered when interpreting TDM results for digoxin?
The clinical situation and the patient
What is the most common arrhythmia seen in clinical practice? What is the overall prevalence in the UK? Linked to how many deaths in the UK?
Atrial fibrillation (AF)
1.6%
1 in 12
What medication was historically prescribed for atrial fibrillation to control the arrhythmia? Atrial fibrillation is an important cause of morbidity and mortality from which conditions? In all AF patients, by what percentage is the risk of stroke increased? What percentage of all strokes are caused by AF?
Digoxin
HF, stroke, thromboembolism
Nearly 500%
15-20%
How much does AF and AF-related illness cost the NHS each year? What two factors increase the risk of AF? Why is the true prevalence of AF underestimated? How much does the prevalence of AF increase with each advancing decade of age?
Over £2.2 billion
Age and underlying heart disease
Subclinical AF is frequent
It doubles
What percentage of patients with AF are over 65 years old? In the next 20 years, how is the prevalence of AF (in those >55yrs) projected to change? Between which years did deaths from AF double? After adjusting for other factors, how much greater risk do men have of developing AF than women?
80%
Doubles
2007-2016
1.5x greater
What are the potential consequences of impaired cardiac performance due to AF? How does AF increase the risk of thrombotic stroke?
Myocardial ischaemia, cardiomyopathy, hypotension, heart failure
Blood stasis in the atria leads to clots
By how much can cardiac output be reduced in AF? How much higher is the mortality rate of people with AF compared to those in sinus rhythm? What is the relationship between heart disease and AF? Are the risks from paroxysmal AF similar to those from persistent or permanent AF?
10-20%
2x higher
Heart disease can cause and be induced by AF
Yes, they are similar
Name three cardiac causes of AF
Name three non-cardiac causes of AF
Name three aggravating factors for AF
Hypertension, valvular disease, IHD
Pyrexial illness, alcohol, thyrotoxicosis
Medications, electrolyte disturbances, caffeine
In people of African or Caribbean heritage, what is the most common cause of AF? In people of Indo-Asian heritage, what are the most common causes of AF?
Hypertension
Coronary artery disease and diabetes
What percentage of AF patients have “Lone AF”? What characterises “Lone AF”? In what percentage of patients with paroxysmal AF does Lone AF occur?
15%
Normal heart and normal investigations
30-40%
What is the fundamental characteristic of electrical activity in the atria during atrial fibrillation? What is the result of this?
Disorganised
Loss of synchrony
Where do rapidly firing cells often originate in atrial fibrillation? What is the response of the atrioventricular (AV) node to the electrical impulses in AF? What typically results in an irregular ventricular rhythm during AF?
Pulmonary veins in the left atrial musculature
Most impulses are blocked
Most impulses being blocked
What range can the ventricular rate vary from in AF? How might a patient initially present when they have asymptomatic AF?
50-200bpm
With a medical condition associated with AF
List four potential symptoms of AF
Palpitations, SOB, syncope, chest pain (angina)
What is the typical finding on physical examination in a patient with AF? What confirms this finding
Irregularly irregular pulse
ECG
What is paroxysmal AF? How long do episodes of paroxysmal AF last?
Intermittent and recurrent, terminates spontaneously
Longer than 30 seconds but less than 7 days
What is persistent AF? What is permanent AF? What criteria defines permanent AF?
Requires cardioversion to return to sinus rhythm
Not terminated by cardioversion
Lasting longer than 12 months and cardioversion not attempted
How does AF occurring in the context of an MI affect myocardial damage and left ventricular function? What initial step should be taken to assess for AF, especially if the patient is symptomatic?
Greater damage and poorer function
Manual pulse palpitation
What does the absence of an irregular pulse indicate? Do we currently perform population screening for AF among asymptomatic people?
Makes AF unlikely
No
How is a diagnosis of AF confirmed? What features confirm AF?
ECG
No P wave, chaotic baseline, irregular ventricular rate
What is the typical ventricular rate in AF? What do ventricular complexes typically look like on an ECG in AF?
160-180bpm
Normal unless there is a conduction defect
What does NICE recommend for people with an irregular pulse? When is 24-hour Holter monitoring recommended?
An ECG to confirm AF
For paroxysmal AF
Which scoring system is still recommended in the UK to assess stroke risk in AF? Which bleeding score risk is still recommended in the UK for AF?
CHA2DS2-VASc
ORBIT
What is the main difference between the CHA2DS2-VASc and CHA2DS2-VA scoring systems?
CHA2DS2-VA is genderless
What are the two main considerations in the treatment of AF? What are the two main aims in the treatment of AF? What are AF patients at high risk of, especially with chronic AF?
Thromboembolic prophylaxis and arrhythmia treatment
Rhythm control or rate control
Thromboembolic events especially stroke
How many times more likely are patients with non-valvular AF to have a stroke compared to a matched population? How many times more likely are patients with valvular AF to have a stroke compared to a matched population?
5x
17x
Through what mechanism does AF itself rarely cause death? What has treatment with anticoagulants been proven to do?
Thromboembolic complications
Reduce mortality and morbidity
Approximately what percentage of patients per year can major bleeds occur in with warfarin therapy? What monitoring is required for warfarin therapy?
About 1%
INR monitored daily until therapeutic
Name four Newer Oral AntiCoagulants (NOACs) or Direct Oral AntiCoagulants (DOACs)
Dabigatran, Rivaroxaban, Edoxaban, Apixaban
What was Dabigatran compared with in the RE-LY study? In the RE-LY study, what did low-dose dabigatran show? In the RE-LY study, what did high-dose dabigatran show?
Warfarin
As effective as warfarin, low bleeding risk
Greater stroke protection, equivalent bleeding risk
What reduction in stroke risk does Aspirin give versus placebo?
About 20% reduction
For patients with valvular AF, what is the recommended oral anticoagulant? What conditions constitute valvular AF?
Warfarin
Rheumatic valvular disease or prosthetic valves
What is the first step when considering anticoagulation for patients with non-valvular AF? What scoring system should be used for this?
Assess stroke risk
CHA2DS2-VASc
What initial step should be taken in AF patients requiring anticoagulation?
Identify and correct reversible bleeding factors
What risk factors are modifiable for bleeding in AF patients?
- Hypertension (SBP>160mmHg)
- Labile INR
- Concomitant meds e.g. Antiplatelet agents and NSAIDs
- Excess alcohol (>8 drinks/week)
What risk factors are potentially modifiable for bleeding in AF patients?
- Anaemia
- Impaired renal function
- Impaired Liver function
- Hx of frailty and falls
- Dialysis dependent kidney disease
What risk factors are non-modifiable for bleeding in AF patients?
- Advanced age
- Hx of major bleeds
- Previous stroke
- Cirrhotic liver disease
- Malignancy
- Genetic or racial variations
According to NICE, what scoring system can be used to assess a patient’s risk of bleeding in AF?
ORBIT
What is a characteristic of strokes caused by AF? In some countries, what is the approximate prevalence of AF? In what populations is the incidence of AF often higher?
Tend to be more severe
~3%
First Nations peoples in Pacific
What is the relationship between heart disease and AF?
Heart disease can cause and be induced by AF
Name two medications that can aggravate AF
L-thyroxine, salbutamol
When is 24 hr Holter monitoring usually recommended in AF? Why have other countries switched to the CHA2DS2-VA score?
Paroxysmal AF
Standardises treatment thresholds
How effective is aspirin compared to anticoagulants for stroke risk reduction?
1/3 as effective
What are the risk factors and points for each in the CHA2DS2-VASc scoring system?
- CCF - 1 point
- Hypertension (including Hx HTN) - 1 point
- Age 75yrs or over - 2 points
- Diabetes - 1 point
- Stroke/TIA - 2 points
- Vascular disease - 1 point
- Age 65-74yrs - 1 point
- (Sc) Female gender - 1 point
What does ICH stand for in the context of bleeding risk?
Intracranial haemorrhage
What ORBIT scores correspond to low, medium, and high risk for bleeds per 100 patient-years?
0-2: Low (2.4 bleeds)
3: Medium (4.7 bleeds)
4-7: High (8.1 bleeds)
List some risk factors and points for bleeding used in the HAS-BLED score
- Hypertension (>160mmHg systolic) 1
- Abnormal liver or renal function 1-2
- Stroke 1
- Hx of Bleeding 1
- Labile INR 1
- > 65 yrs 1
- Drugs (antiplatelets or NSAIDs) or concomitant alcohol use (1pt each) 1-2
In which patient population is intracranial hemorrhage (ICH) more prevalent when taking anticoagulants?
Aboriginal patients
What does NICE recommend to assess a patient’s bleeding risk in Atrial Fibrillation management? According to this score, what haemoglobin level in males indicates a bleeding risk factor? What haematocrit level in females is considered a bleeding risk factor? What age is considered a risk factor for bleeding?
ORBIT
<13g/dL
<36%
>74 years
According to the ORBIT score, how many points are assigned for a history of GI bleed, intracranial bleed, or hemorrhagic stroke? According to the ORBIT score, how many points are assigned for a GFR <60ml/min/1.73m^2? According to the ORBIT score, what is the bleeding risk per 100 patient-years for a patient with a score of 3?
2
1
4.7
According to the ORBIT score, how many points are assigned for treatment with antiplatelets? According to the ORBIT score, what risk group corresponds to a score of 0-2? According to the ORBIT score, what risk group corresponds to a score of 4-7?
1
Low
High
What score can also be used to assess a patient’s risk of bleeding in Atrial Fibrillation management, other than ORBIT? How many points are assigned for hypertension with systolic BP >160mmHg? How many points are assigned for a Hx of stroke?
HAS-BLED score
1
1
According to the HAS-BLED score, what point range is assigned for abnormal liver or renal function? According to the HAS-BLED score, how many points are assigned for a history of bleeding? According to the HAS-BLED score, how many points are assigned for labile INR? According to the HAS-BLED score, how many points are assigned for being >65 years old? According to the HAS-BLED score, what point range is assigned for drugs (antiplatelets or NSAIDs) or concomitant alcohol use?
1-2
1
1
1
1-2
What is the maximum score achievable on the HAS-BLED scoring system? Which scoring system is UK recommended for deciding when to anticoagulate in Atrial Fibrillation?
9
CHA2DS2-VASC
According to the CHA2DS2-VASC score, what action should be taken for men with a score of 1? According to the CHA2DS2-VASC score, what action should be taken for men and women with a score of 2 or more? According to the CHA2DS2-VASC score, what action should be taken for women with a score of 1? According to the CHA2DS2-VASC score, what action should be taken for men and women with a score of 0?
Consider anticoagulants
Offer anticoagulants
NO anticoagulants
NO anticoagulants
In Atrial Fibrillation management, which medication is no longer recommended according to the guidelines? What has often been underused in the past in the management of AF, especially in the elderly, leading to increased stroke risk?
Aspirin
Warfarin
What concerns exist regarding Warfarin use that can lead to undertreatment or overtreatment? In trials, how have Novel Anticoagulants (NOACs) or Direct-acting Oral Anticoagulants (DOACs) compared to warfarin?
Poor compliance
As effective or better
How are DOACs typically dosed? What happens to DOAC levels if a patient’s renal function changes quickly and isn’t regularly monitored?
Based on age, bleeding risk, renal function
Levels can become unsafe
What percentage of patients take at least 80% of their prescribed doses of chronic medications?
<50%
Why would the effects of poor compliance be more rapid with DOACs compared to Warfarin? What is a key difference between DOACs and Warfarin regarding antidotes in overdose situations?
DOACs have shorter half-lives
DOACs do not have effective antidotes
What patient-specific factors should be considered when selecting an anticoagulant?
- Patient preference
- Tolerability
- Potential for DIs
- Likely compliance/adherence
- Monitoring requirements
- Concomitant medications
What are the clinical advantages and disadvantages of Warfarin?
A:
- Gold standard therapy for >50 years
- Long half-life
- Cheap, effective antidote available (Vit K)
- Prescribers familiar with its management and DIs
- Potentially better compliance due to once daily dosing
- Well established guidelines for reversal in emergencies
D:
- Narrow therapeutic index
- Unpredictable therapeutic response
- Multiple drug-drug and drug-food interactions
- Slow onset and offset of action
- Frequent INR monitoring required
- Dietary restrictions
- Bridging therapy required
What are the clinical advantages of DOACs?
A:
- Specific coagulation enzyme target
- Rapid onset of action
- Predictable therapeutic response
- Fixed dosing
- Fewer drug-drug or drug-food interactions
- As effective as warfarin with a lower intracranial haemorrhage risk
- Less likelihood of uncommon warfarin-related side effects
- No need for bridging
- Regular coagulation monitoring is not required
- No dietary restrictions
What are the clinical disadvantages of DOACs?
- Shorter half life
- Accumulation in renal impairment
- No evidence for efficacy (and some evidence for harm) in patients with valvular AF
- No reliable anticoagulation monitoring available
- ‘New’ DIs – CYP450, P-glycoprotein inhibitors/inducers
- Lack of long term safety data
- No commercially available antidote for factor Xa inhibitors and the reversal agent for dabigatran (idarucizumab) is expensive
- Higher drug costs to the government
- Twice daily dosing (Dabigatran and apixaban), less forgiving to non-adherence, potentially increasing thromboembolic risk
- Monitoring of renal function and dosage adjustment in renal impairment is required. Contraindicated in severe renal impairment
- Not indicated in patients with valvular AF
- Risk of non-detection of suboptimal patient adherence
- Inability to titrate doses
- Cannot easily assess the degree of anticoagulation
- Lack of prescriber awareness, therefore risk of bleeding or thromboembolic events due to DIs
- Unknown potential for long term side effects
- Reversal of anticoagulation more complicated in patients with bleeding or requiring emergency surgery
What is the current international consensus regarding anticoagulant preference in AF? When is Warfarin typically used in AF management according to current guidelines?
DOACs/NOACs are preferred
When DOACs aren’t tolerated or C/Is
Summarise the stroke prevention treatment pathway in AF
- MHVs or moderate/severe mitral stenosis
Y: warfarin
N: proceed - Estimate stroke risk based on CHA2DS2-VASC
0: OAC or antiplatelet NOT recommended
1: Men consider OAC, Women no OAC
2 or >: OAC recommended (NOAC preferred) - Assess C/Is
- Correct reversible bleeding factors
- Consider patient’s values and preferences
- Left Atrial Appendage occluding devices may be considered for patients with clear C/Is to OACs
What are the two main management goals for Atrial Fibrillation relating to the arrhythmia itself?
Rate or Rhythm Control
What is the choice between rate or rhythm control dependent on?
Acute vs chronic AF and patient tolerance
List factors favouring rhythm control in AF
Patients who are:
- Younger, more physically active, highly symptomatic
- Those with paroxysmal or early persistent AF
- Those with left ventricular dysfunction
- No severe left atrial enlargement
- Those in whom adequate rate control of the ventricle is difficult to achieve
List factors favouring rate control in AF
Preferred in patients:
- With minimal symptoms
- Or those in which attempts at achieving and maintaining sinus rhythm are likely to be or are futile
When is rate control often recommended in AF patients? When is rate control considered first-line therapy? In what situation is rhythm control not “indicated”? When is rate control a treatment option?
Adjunctive treatment in nearly all AF patients
Patients not requiring sinus rhythm for symptom control
Asymptomatic patients
After failure of rhythm control
In what scenario does the risk of restoring sinus rhythm outweigh the benefits?
When rate control is preferred
In rate control, what is the target ventricular rate at rest? What medications are used to obtain and maintain long term control of ventricular rate?
<110bpm
Beta blocker or non-dihydropyridine CCB
Which beta blockers are mentioned for long term RATE control? Which calcium channel blockers are mentioned for long term rate control?
- Bisoprolol, atenolol (25-100mg daily) or metoprolol (25-100mg BD) (NOT sotalol)
- Diltiazem (180-360mg daily) or verapamil SR (160-480mg daily)
DO NOT USE beta blockers in combination with verapamil so use diltiazem if there is a possibility of adding a beta blocker in future
Why is Digoxin alone relatively ineffective in slowing rapid ventricular rate?
Increased sympathetic tone (exercise and fever)
If monotherapy for rate control is ineffective, what combination of medications is suggested? Which combination of medications should be avoided for rate control? What is a non-pharmacological approach to rate control in AF?
Digoxin with beta blocker/CCB
Beta Blockers with verapamil
AV node ablation
What must be considered before attempting cardioversion? How long should a patient be anticoagulated prior to elective cardioversion? What is the purpose of anticoagulation before cardioversion?
Risk of thromboembolism
2-6 weeks
Dissolve or adhere thrombus
What can transoesophageal echocardiography detect, potentially reducing the need for prolonged warfarin therapy before cardioversion? Which drugs are used for pharmacological conversion to sinus RHYTHM?
Arterial thrombus
Flecainide or amiodarone (IV or oral)
What pretreatment might be considered if using flecainide for cardioversion? Why is Sotalol not frequently used for attempted conversion?
Digoxin, beta blocker, or non-dihydropyridine CCB
No more effective than placebo, RATE and RHYTHM control not selective
What is the rationale for pretreatment with digoxin, a beta blocker, or a non-dihydropyridine calcium channel blocker when using flecainide?
Prevent increase in ventricular rate
What should be considered if drug therapy fails to convert a patient to sinus rhythm?
Synchronised electrical cardioversion
What anticoagulation strategy is preferred for non-valvular AF? What anticoagulation strategy is used for valvular AF?
NOAC
Warfarin
How quickly should a transoesophageal echocardiography be performed to reduce the need for prolonged warfarin therapy prior to cardioversion?
Within 12 hours
The classes of Vaughan Williams classification and what they do?:
Class I
Class II
Class III
Class IV
- Sodium blockers
- Beta blockers
- Potassium blockers
- Calcium channel blockers
What factors and points are involved in the ORBIT score?
Haemoglobin (<13g/dL for males & 12g/dL for females) OR haematocrit (<40% men and <36% women) 2
Age >74 1
Bleeding Hx (GI or intracranial bleed or haemorrhagic stroke) 2
GFR <60ml/min/1.73^2 1
Antiplatelet treatment 1
