Non valvular atrial fibrillation and str

AN
Austra//an C r t t ~ 2 / C a r e

Non-valvular atrial fibrillation and stroke:
implications for nursing practice and I ralleltltk
University of W e ~ . ~ r d n e y

&W ~ H e a l t h

Service

Depax:h'mr~e~)~:ardiulmog.YeS:~of ~ v ~ ° S p l t a l , Sf/dney NSW
~A Brighton * MBBS FRACP FRACPA
D e p a r t m e n t of Haematology, St George Hospital, Sydney NSW
University of NSW
l E n i s * MBBS FRACP
D e p a r t m e n t of Neurology, St George Hospital, Sydney NSW
University of NSW

J M c C r o h o n " MBBS FRACP PhD
D e p a r t m e n t of Cardiology, St George Hospital, Sydney NSW.

University of NSW
D E l l l o t t • RN PhD
University of Sydney & Prince of Wales Hospital

l Cockburn • MSc PhD
University of Newcastle
G P a u l l • RN BN (Hans)
D e p a r t m e n t of Cardiology, St George Hospital, Sydney NSW.

J Da/y • RN PhD
University of Westem Sydney
Atrial fibriRation (AF) is the most common sustained cardiac rhythm disturbance and is increasing in prevalence due to the ageing of
the population, and rates of chronic heart failure. Haonodymnnic compromise and t h ~
events are responsible for signi~ant
morbidity and mortality in Australima communities. Non-valmdar A F is a s ~
predictor for both a higher incidence of stroke mad
increased mortality. Stroke affects approximately 40,000 Austral&ma every year and is Austra~n's third largest killer after cancer and
heart disease. The burden of illness associated with AF, the potential to decrease the risk of stroke and other embolic events by
thromboprophylaxis and the implications of this strategy for nursing care anti patient education, determine A F as a critical element of
nursing practice and research. A review of the literature was undertaken of the CINAHL, Medline, EMBASE and Cochrmae Databases

from 1966 until September 2002 focussing on , u n ~ e m e n t of atrial ~
to prevent thrombotic events. This review article
presents key elements of this literature review and the implications for nursing practice.
Davidson PM, Rees DM, Brighton TA, Enis J, McCrohon J, EUiott D, Co&burn J, Paull G & Daly J. Non-val~Aar atrid ~
implications for nursing, practice and therapeutics. Australian Critical Care 2004; 17(2): 65-73.

INTRODUCTION
Epidemiology and
atrial f i b r i l l a t i o n

prevalence

and stroke:

predictor for both a higher incidence of stroke and increased
mortality. In patients who also have rheumatic mitral stenosis, the
risk of stroke is 17 times higher 3'4. The Stroke Prevention in Atrial
Fibrillation (SPAF) investigators found that in the presence of two
or more risk factors the annual risk of stroke could rise to 17.6% s

of

Atrial fibrillation is the most common sustained cardiac rhythm
disturbance. The prevalence of AF in the adult population is 0.5%,
rising to 10% among people aged over 75 years and is associated
with a 5.6 times increase in the incidence of stroke 1. ~ The
cumulative incidence of stroke among patients 60 years or younger
with lone AF is not significantly different from that in a control
population matched for age and sex at a rate of 0.5 % per year. In
the elderly, however, risk is much higher, often exceeding 10% per
year. Non-valvular atrial fibrillation (NVAF) is a significant

In addition to age, the following factors have been identified as
independent predictors of stroke:
•
•
•
•
•
65

history of high blood pressure
diabetes mellitus
previous transient ischaemic attack (TIA), or stroke
left ventricular dysfunction
women older than 75 years'.~lz
Volume 17 Number 2

May 2004

Australian Critical Care

Determining which patients are at highest risk and the most
effective treatment for at-risk patients are important clinical issues.
Wadarin is one of the most common cause of death related to
prescription drugs ~3. However, judicious warfarin use affords
significant patient benefit in the prevention of thromboembolic
events. The incidence of NVAF will increase over the next decade
with the growing number of elderly Australians and the prevalence
of cardiovascular disease ~3. The social and economic burden

associated with stroke mandates a strong primary and secondary
prevention focus ~2.

Transesophagea[ echocardiography (TOE) is a useful strategy in
stratifying the risk of embolic complications in atrial fibrillation]7.1~.
TOE is the most sensitive clinical tool available for detecting left
atrial thrombus and spontaneous echo contrast. These factors
occur as a consequence of reduced atrial flow velocities and left
atrial contraction dysfunction caused by atrial fibrillation.
Spontaneous echo contrast (SEC), is characterised by a swirling
mass of fine echoes, also descritmd as echo "smoke" and indicates
blood stasis and the thrombus and is a predictor for increased risk of
thromboembolism. SEC is not easily imaged by transthoracic
echocardiography because the surface echocardiogram has a limited
view of the left atrial appendage where most atrial thrombi form in
patients with atrial fibrillation. However, an absence of left atrial
thrombus or spontaneous echo contrast does not necessarily infer a
lower risk in patients with atrial fibrillation ,7-~.

The National Heart Foundation Guidelines for management of AF

identify four key principles for patient management:
•
•
•

•

confirmation and documentation of the arrhythmia
identification and treatment of underlying causes
relief of symptoms precipitated by decreased cardiac output
achieved by the control of ventricular rate and restoration and
maintenance of sinus rhythm; and
reduction of the risk of systemic thrombocmbolism, particularly
stroke L

Thrombophi!Ja, NVAF a n d s t r o k e
incidence
There is limited evidence describing the pathophysiology and
aetiology of the hypercoagulable state associated with stroke and
other embolic events 2.

Laboratory measures of this
hypercoagulability have included markers of increased coagulation
and platelet hyperactivity. Paroxysmal and persistent atrial
fibrillation have been associated with factors reflecting
intravascular thrombogenesis. Abnormalities of coagulation
include elevated fibrinogen (also an acute phase reactant),
increased coagulant VIII and von Willebrands factor (both acute
phase reactants and released in endothelial disturbances), elevated
D-dimer (suggesting indirectly increased fibrin formation),
increased levels of prothrombin fragments 1+2 or thrombinantithrombin complexes or other cleavage products of prothrombin
such as fibrinopeptides A (indicating increased thrombin
generation). Platelet hyperactivity has been proposed on the basis
of increased platelet factor 4 and thromboglobulin levels which are
released upon platelet activation =.z4.

Description of atrial fibrillation
In 1906, Einthoven reported the first electrocardiographic
demonstration of AF, a supraventricular tachyarrythmia
characterised by uncoordinated atrial activation 14. AF may be
paroxysmal, persistent, or permanent. Paroxysmal atrial fibrillation

is characterised by repeated, self-terminating episodes of
arrhythmia. Atrial fibrillation can be asymptomatic, especially in
the absence of tachycardia. Atrial fibrillation is the result of both
substrate and trigger. The substrate is most often a pathology that
affects the atria, such as hypertensive disease causing increased
stress on the atrial wall. Although an ectopic electrical focus can
originate anywhere in the atria, left atrial loci at or within the
pulmonary vein orifices are often responsible for episodes of atrial
fibrillation in patients without coronary pathology 3. Once
initiated, the arrhythmia is maintained by the mechanism of reentry. During atrial fibrillation many such re-entry circuits are
established in the atria, especially diseased or enlarged atria 3,IL

Novel markers of genetic thrombophilia have yet to be documented
in NVAE These potential mediators of common inherited
thrombophilia include: Activated protein C resistance (or AH2R),
Factor V Leiden mutation (Factor V G1691A, the cause of at least
95% of APCR), Prothrombin gene mutation G20210A, Plasma
homocysteine and mutations in homocysteine metabolism such as
the MTHFR C677T ~,~7. Further investigation of the
hypercoagulable state in NVAF may identify laboratory markers of

the hypercoagulable state that could be used to stratify patients' risk
of stroke. This empirical means of risk stratification is alluring,
particularly in individuals who are considered at high risk for
anticoagulation therapy.

H a e m o d y n a m l c effects o f a t r i a l
fibrillation
AF is associated with the loss of the atrial contribution to
ventricular filling. This may result in a decrease in ventricuiar
stroke volume of up to 20 percent. The irregularity of the
ventricular response may also contribute to haemodynamic
impairment. In some patients with a poorly controlled ventricular
rate, persistent tachycardia results in structural changes that cause
ventricular dysfunction. This tachycardia-mediated cardiomyopathy is often reversible after sinus rhythm has been restored or
when the heart rate during atrial fibrillation is controlled 3'16.

E m b o l i c events
Cerebral infarction in patients with atrial fibrillation may vary from
being clinically silent to catastrophic. The prevalence of silent
cerebral infarction and its effect as a risk factor for symptomatic

stroke are important considerations for the evaluation of patients
with atrial fibrillation. This also has implications for assessment of
cognitive function, particularly in the elderly patient ~ .

D i a g n o s i s a n d risk s t r a t i f i c a t i o n
Electrocardiographically, AF is characterized by the presence of
rapid, irregular, fibrillatory waves that vary in size, shape, and
timing. This set of findings is usually associated with an irregular
ventricular response, although regulansation may occur in patients
with complete heart block, an accelerated junctional or
idioventricular rhythm, or a ventricular paced rhythm 16 Moderate
to severe left ventricular dysfimction is an independent risk factor
for stroke in patients with atrial fibrillation, and these patients
should be strongly considered for anticoagulant therapy 2.2.
Vob~ne17 Number2

May2004

Management of atrial fibrillation
The therapeutic goals of atrial fibrillation therapy are to achieve

rate control, restore sinus rhythm where possible, prevent
cardiomyopathy, relieve symptoms and prevent embolic events.
66

Auxtrallon Critical Care

Electrical cardioversion

Both pharmacologic and non-pharmacologic strategies or a
combination of both may achieve these goals a4,5.

Direct current cardioversion involves delivery of an electrical
shock, synchronised with the electrical activity of the heart. The
aim of electrical cardioversion is to restore sinus rhythm in atrial
fibrillation, which is resistant to chemical cardioversion with
antiarrythmic drugs. Generally cardioversion is performed by the
application of external paddles, although transvenous electrical
cardioversion can be performed using a tight atrial catheter.
Cardioversion can be performed safely in patients with pacemakers
and implanted defibrillators. In this case, care should be taken to
position the paddles as far as possible from the device. For instance,
if the device is implanted anteriorly, paddles for cardioversion
should be positioned in an antetior-posterior manner. In the event
of electrical cardioversion of a patient with an electrical device, the
pacemaker should be checked immediately afterwards to ensure
adequate pacemaker function. Prophylactic antithrombotic
therapy is indicated for patients undergoing electrical cardioversion
due to the risk of thromboembolism ~3,3~.

Pharmacologic antiarrhythmic
therapy
Early drug therapy to restore sinus rhythm can be considered in
patients in whom the arrhythmia has lasted less than 48 hours or
who are receiving long-term warfarin therapy. The aims of
pharmacologic control of the heart rate in patients with persistent
atrial fibrillation are to minimise symptoms related to swings in
heart rate and prevent excessive tachycardia during normal daily
activities. Digoxin is not effective in converting atrial fibrillation
to sinus rhythm but antiarthythmic therapy increases the likelihood
of conversion to as much as 90 percent, if the drugs are
administered early and in adequate doses.
Considerable
information exists about the use of oral and intravenous
antiarrhythmic drugs for the conversion of recent-onset atrial
fibrillation to sinus rhythm and is beyond the context of this
discussion except to mention that patients with chronic heart
failure are prone to the proarryhthmic effects of antiarrythmic drugs
2,4.31.33. Dofetilide and amiodarone have been evaluated in patients
with HE I)igoxin may be acceptable as the sole therapy in an
elderly, sedentary patient, but it is not very effective for preventing
excessive tachycardia during moderate exertion. Beta-blockade is
potentially the drug class of choice in patients with both atrial
fibrillation and coronary artery disease, especially in the presence of
systolic dysfunction 2.3 Other common drugs used to treat atrial
fibrillation are described in Table 1.

Radiofrequency ablation
Radiofrequency ablation is the targeted cautery of cardiac tissue by
local application of radiofrequency energy. Target zones are
identified during an electrophysiological study, in which a series of
catheters are placed in the heart. Recording the cardiac electrical
activation sequence identifies arthythmia circuits and accessory
pathways. Once a target zone is identified, ablation is performed by
heating the interface between catheter and endocardium until cell
death occurs. Radiofrequency ablation is used for patients with
paroxysmal atrial fibrillation. However, persistent atrial fibrillation
usually affects patients with structural or ischaemic heart disease.
Sinus rhythm can be restored with electrical or pharmacological
cardioversion, but fibrillation tends to recur because of the
persistence of triggering foci and underlying atrial disease,
rendering focal ablation less successful. For patients with
paroxysmal atrial fibrillation, focal ablation may be an option ff
antiarrhythmic drugs are ineffective or not tolerated. Individuals
demonstrating frequent atrial ectopic beats with a consistent P
wave morphology indicating a single ectopic focus are most suited
to focal ablation a t6.3:.

Non-pharmacological therapy
Although usually prescribed when phamxacologic therapy is not
effective, not tolerated, or contraindicated, non-pharmacologic
therapies namely: catheter ablation, cardiac pacing, internal
defibrillation, and dysrhythmia surgery are playing an increasingly
important role in the overall management of AE It is also
important to recognise the importance of treating reversible
conditions, particularly, the control of hypertension, weight and
avoidance of known stimulants such as alcohol and caffeine.

Pacemaker therapy

Dual-site pacing is considered preferable over single-site pacing for
the prevention of paroxysmal atrial fibrillation 2.16,39.

Pacing techniques are being investigated for the prevention of
paroxysmal atrial fibrillation. These are based on the concept that
inhomogeneous or delayed interatrial or inixaatrial conduction
times predispose persons to the development of arthythmia. Both
dual-site atrial pacing and biatrial pacing reduce the duration of the
P wave and result in a more homogeneous atrial depolarization. In
patients with atrial fibrillation that is refractory to pharmacological
therapy data from uncontrolled trials suggest a benefit of dual-site
pacing over single-site pacing for the prevention of paroxysmal
atrial fibrillation a 16.39

Implantable atrial defibrillators
Successes with implantable ventricular defibrillation have led to
trials aimed at terminating atrial fibrillation by means of internal
cardioversion. Newer models of implantable atrial defibrillators
combines the option of atrial defibrillation wi[h the capacity for
ventricular defibrillation. This device permits the termination of
atrial arrhythmias in patients with coexisting paroxysmal atrial
fibrillation and ventricular tachycardia, and it can act as a safety
device in the very rare event that an atrial shock precipitates
ventricular fibrillation. In addition to the capability of delivering
an atrial shock, the new device offers the option of applying
antitachycardia pacing and burst atrial pacing in a tiered fashion, as
programmed by the physician. However, unless a ventricular
defibrillator is also required for coexisting ventricular arthythmias,
it is unlikely that the atrial defibrillator will be used, with the
potential exception of highly symptomatic paroxysmal atrial
fibrillation that is resistant to conventional therapy 16,38.39.

Surgical intervention
In 1987, Cox and colleagues introduced a surgical procedure that
they called the Maze procedure. In this procedure the atrial
appendages are excised and the pulmonary veins isolated. With the
use of additional, carefully placed incisions, a narrow, tortuous path
of atrial tissue is created that directs the sinus-node impulses across
the atria to the atrioventticular node. The incisions are made so
that no areas are able to sustain multiple reentry circuits. A mazelike pathway is constructed to permit atrial conduction. The
67

Volume17

Number2

May2004

Au.~'allm~ Critical Care

associated risks of cardiopulmonary bypass inhibit high utilisation.
However, surgical adaptations using minimally invasive techniques
are currently under investigation 3.~¢,0.

clinics or the emergency department. This highlights the need for
flagging and referral mechanisms to ensure assessment of these
patients for invest/gation and as.w.ssment for ant/coagulation. In a
Cochrane systematic review, Benavente et al identified that
anticoagulation for primary prevention in AF patients who have an
average stroke rate of 4% per year, about 25 strokes and 12 disabling
fatal strokes would be prevented yearly for every 1000 treated6t As
in most clinical decisions, judicious balancing of risks and benefits
need to be undertaken, particularly in an elderly population where
the potential for iatrogenesis is greater. Appropriate use of drugs to
prevent thromboembolism in patients with AF involves comparing
the patient's risk of stroke to the risk of haemorrhage from
medication use~ Warfarin is particularly prone to interactions with
other drugs (including herbal medicines) and foods. This
underscores the importance of patient education and monitoring.
One of the most common causes of over-coagulation is
concomitant antibiotic use.
The Australasian Society of
Thrombosis and Haemostasis has published guidelines for the
management of over-coagulation, including administration of
Vitamin K. It is important to note that the approach to a raised
INR should be individualised to the patient's clinical condition and
risk of bleeding. Peti-procedural management of the chronically
anticoagulated patient is a complex issue, and requires
consideration of the following issues:

Prevention of embolic complications
with anti-thrombin and ant/-platelet
therapy
A body of compelling evidence from prospective, randomised trials
of patients with atrial fibrillation evaluating either warfarin or
aspirin or both, dictates anti-coagulation as a Level 1 based therapy
for stroke prevention in atrial fibrillation. Table 2 describes the
current risk-based approach to anti-thombotic therapy in patients
with AF of an expert group from the National Heart Foundation,
following a systematic review of the evidence 2.5. Reflected in these
recommendations, adjusted-dose warfarin has been demonstrated
to be effective; aspirin is less effective, reducing mainly nondisabling, non-cardioembolic strokes and low-intensity warfarin
(INR < 1.5), alone or combined with aspirin, offers little
protection. Selection of an antithombotic agent should be based
upon an individualised assessment of the risks of stroke and
bleeding 4~.42. An important part of the nurses' role in caring for
patients with AF is to provide information regarding the treatment
rationale and assistance in formulation of a self-management action
plan 3,41s3. Warfarin inhibits the vitamin-K dependent synthesis of
factors II, VII, IX and X in the liver. The low level of these factors
leads to a reduction in thrombus formation. Aspirin induces an
antithrombotic effect by blocking platelet cycloxygenase L

•
•
•
•
•
•
•

Despite the evidence base guidelines advocating antithrombotic
therapy, adherence to these recommendations is far from optimal ~~. Earlier work from our institution demonstrates an uptake of le~s
than 10% m patients with NVAF without contraindications to
therapySL In a managed care environment an uptake of up to 85%
has been documented 58. This high rate of utilisation reflects the
potential benefits of providing infrastructure to facilitate uptake.
The success of disease management strategies in CHF is likely
worthy of emulation in this patient group ~9.

Evaluation of attempts to involve patients in this clinical decision
making process have rendered mixed results, this is likely due to the
complexity of the issues and fears of catastrophic complications,
particularly in high risk populations ~-~. The potential for rebound
thrombotic events following cessation of warfarin is to be
considered. It is also important to note that factors such as
advanced age, valvular heart disease and elevated post-operative
adrenergic tone, render patients more vulnerable to post operative
AF followmg myocardial revascularisation~.

Anecdotally, reluctance to anticoagulate patients is based upon fear
of adverse effects and poor compliance with monitoring,
particularly in the elderly. There is a paucity of data describing
anticoagulation therapy and documenting adverse event rates in
the Australian community s¢ sT. Further, recommendations for
management of warfarin therapy in the perioperative period and in
the presence of a bleed is poorly defined and creates a dilemma for
clinicians 6% It is clear that management of this therapy in the
elderly, particularly in a context of high rates of comorbid
conditions and potentially less than optimal level of cognition and
functional status, is a complex issue. Major haemorthage occurs in
1 to 5% of patients per year and has a fatality rate of 25-30%.
These high rates of morbidity and mortality underscore the
importance of careful patient selection and monitoring of
antithrombotic therapy ~,6~%

The i m p o r t a n c e o f m o n i t o r i n g
The Stroke Prevention in Atrial Fibrillation (SPAF) III study and
the Coumadin Aspirin Reinfarction Study (CARS) study using
fixed doses of warfarin in their warfarin/aspirin arms, without
International Normalised Ratio (INR) adjusted dosage, failed to
show benefit because the average LNRs were below the therapeutic
range ~' 4~ ~0 However, in the Stroke Prevention in Atrial
Fibrillation (SPINAF) study, where a monitoring schedule (INR
performed weekly during a 12-week induction period and monthly
thereafter during a maintenance period for a total follow-up of 36
month) a 79% reduction in stroke rate was achieved among the
warfarin-assigned patients without an increase in bleeding
complications. From the results of several studies, it appears that
anticoagulation therapy with warfarin should be monitored
carefully. An INR of between 2.0 and 3.0 is the optimum range to
achieve thromboprophylaxis.
As in many other chronic
conditions, patients should be empowered for self-management and
nurses play an important role and patient education in this process.

Nursing i m p l i c a t i o n s for care o f
p a t i e n t s w i t h AF
Nurses play an important role in the identification of patients with
AF and the facilitation of therapeutic options, particularly
anticoagulation. AF is often an incidental finding, not related to a
cardiovascular admission. For instance, it is not uncommon for the
first documentation of NVAF to occur in surgical preadmission
Volume17 N u m b s 2

Mew2004

severity of underlying condition and urgency of surgery
baseline risk profile
risk of thromboembolism in the absence of anticoagulation
risk of bleeding with the procedure
consequences of bleeding
ability to control bleeding by manual pressure and
duration of bleeding risks after the procedure t

68

Australian Critical Cant

The patient's action plan for warfarin therapy must involve a
written plan of specific self-care strategies. This plan should
involve the patient's primary care physician and include
information that is socially and culturally relevant to their needs
and situation. In particular, information should be sought from
patients regarding cultural practices such as prolonged fasting,
which may effect the INR. Patients need to be reminded to
maintain a consistent intake of foods containing vitamin K and
minimise alcohol intake. When giving patients informaticm it is
important to avoid assumptions regarding literacy and
comprehension and provide clear, unambiguous advice and
strategies. A number of specific techniques have been used to
enhance patients' recall and knowledge of advice. These include
presenting the most important information first, as people tend to
remember this advice better. Giving simple concrete advice, and
repeating it, also enhances recall.
Explicit categorising
information, for example, dividing the instructions into categories
and announcing the categories before giving the patient
information pertaining to each category, is another strategy to help
ensure people remember information 70.

High risk (6%-12% per year riak of ~d~oke)
•

Age >65 years and hypertension or diabetes
ischaemic attack (TIA) or stroke

•

Previous tran~en!

•

VaJvular heart disease or heart failure

•

Recent rnyocardL~l infarction

•

Impaired k~t ventdcular function on e c h ~ : : a r d l o ~

•

Thyroid disease Left atrial thrombu8 or left atrial spontaneous echo
contrast (TOE done on basis of d4nicaf susptdon)

T~nt:

Warfadn (target INR 2.0-3.0) if possible end not

contTalndlcated.

Moderate risk (2%.5% per year risk of stroke)
•

Age 65 year8 and h ' , ~

•

Age >65 years and not In

or ~

high dsk group

Treatwmnt: Wartadn (target INR 2.0-3.0) or aspidn 75-300rng daily,
depending on individual case and echocardiograpt-ry findings

Ort and colleagues explored the relationship between atrial
fibrillation and dementia in a population-based study ~0 A
significant positive association of both dementia and impaired
cognitive function with atrial fibrillation was found. These
findings emphasise the importance of establishing systems to allow
monitoring and facilitation of behaviouml strategies to promote
compliance.

Low risk (1% per year risk of =lToke)
•

Age 65 and no hypertension, diabetes, T1A, stroke, or oltmr clinical risk
factors
T~nt:

None, or aspirin 75-300mg daily.

Source: Hankey G.I. Non-valvular atTial fibrillation and stroke prevention
[Position Statement]. Meal J Aust 2001; 174: 234-348.

Adverse effects o f o r a l
anttcoagulation

h tip :.//~ww. mJa.com .akgpublic/-.~es/174 05 05030 l/ban key/hart key.html
Accessed on October 4, 20G2.

Bleeding is the most important complication of anticoagulant
therapy. The intensity of anticoagulation, the concomitant use of
aspirin, non-steroidal anti-inflammatory drugs and underlying

69

Vo~ume l7

Numbs2

May2004

Austrn;~n C d t / c ~ Care

l,d,I," I. t',,mm,., I.h,nm..',,I.,'.'i,
MEDICATION

,d ,~a,'~,t. l'" th," m,m,._'Cm,'.l ,,/',.~ial fil,iill,.i,,~

ACTION

NURSING CONSIDERATIONS

Lengthens depoladeation
Decreases automatictty

Monitor for atriove~tricular block. Monitor electrolytes
particularly magnealum and potassium

Slows conduction
InhlNts sodium channels

May be proan'yfithmic, particularly In patients with left
ventricular dysfunctk~. Monitor renal function closely with flecantde

"[ype IA
Procanamide,
Quinidine
Type IC
Flecanide
Propafenone
Type III
Sotalol
Dofe'dlide
Ibulttde
Amiodarone

Increase action potential duration Sotalol and amiodarone hav~ some beta blocking prope~es
and refractory period
Care with sotalot In patients with reactive airways disease
and left ventdcular dysfunction; sotalol is more u~eful for rate control than cardK~v~rslo~.
Consider potential for toraade de pointa with Ibultlde
Amiodarone:- monitor for hepatic, pulmonary and thyroid toxicity;
Inform patient regarding potential for p h o t o s e n ~

REFERENCES

clinical disorders, are common factors influencing the risk of
bleeding. Skin rash and alopecia are uncommon adverse effects and
may be managed by changing oral anticoagulants. Skin necrosis is
a rare complication and usually appears within a few days of the
start of oral anticoagulation therapy. Drug interactions are the
commonest cause of significant change in the INR value. Patients
should be advised not to change any medication without a
physician or pharmacist's advice. Adequate monitoring is the key
to a s u c c ~
and safe warfarin therapy 7~'~.

Conclusions and implications for
nursing practice

1.

Kannel WB, Abbott RD, Savage DD et d. Coronary heart disease and
atrial fibrillation: the Framing,ham Study. American Heart Journal
1983; 106-389-396.

2.

FrosterV, Reiden LE, Asinger RW eta/. ACC/AHA/ESC guidelines
for the management of patients with atrial fibrillation; a report of the
American College of Cardiology/American Heart Association Task
Force on practice guidelines and the European Society of Cardiology
Committee for Practice guidelines and policy conferences
(Committee to develop guidelines for the management of patients
with atrial fibrillation) Journal of American College of Cardiology
2001; 38:4:1266ii-1266lx.
Mc'CabePJ & Geoffroy S. Atrial fibrillation: The newest frontier in
arryhthmia rnanagernent. Progress in Cardiovascular Nursing 2002;
17:110-123.
Stroke Prevention in atrial fibrillation investigators. Warfarin versus
aspirin for prevention of thromboembolism in atrial fibrillation: SPAF
II study. Lancet 1994; 343:687-691.

3.

Increased understanding of the aetiology and risks associated with
thromboembolism related to atrial fibrillation have led to
antithrombotic therapy recommendation to prevent stroke in
patients with atrial fibrillation a 4. 5. All patients with atrial
fibrillation should be evaluated for factors associated with
additional risk and their stroke risk should be estimated.
Integrating available evidence into practice remains problematic
and likely requires systems and processes to support clinicians and
patients in this high-risk polmlation ~a. Patients at high risk for
stroke and many of those at moderate risk should be considered for
anticoagulation. Further studies are needed of low molecular
weight heparin and aspirin in lower risk patients and many of these
trials are currently ongoing. Novel antithrombotic agents that are
more efficacious than aspirin and more easily administered than
warfarin agents offer some promise and are currently under
investigation ~. Clinical studies on a novel oral anticoagulant
ximelagatran, for stroke prevention in patients with non-valvular
atrial fibrillation are currently ongoing. Ximelagatran is an oral
direct thrombin inhibitor, without the need for dosage adjustment
and routine coagulation monitoring 84.

4.

5.

Hankey GJ. Non-valvular atrial fibrillation and stroke prevention
[Position Statement]. Medical Journal of Australia 2001; 174: 234348. htrp://qa~vw.mja.com.au/public/issues/174_05_050301/hankey/
hankey.html Accessed on October 4, 2002.

6.

Dries DL, Exner DV, Gersh BJ, Domanski MJ, Waclawiw MA &
Stevenson LW. Atrial fibrillation is associated with an increased risk
for mortality and heart failure progression in patients with
asymptomatic and symptomatic left ventricular systolic dysfunction: a
retrospective analysis of the SOLVD trials. Journal of American
College of Cardiology 1998; 32:695-703.

Langenberg M, Hellemons BS, van Ree JW et & Atrial fibrillation in
elderly patients: prevalence and comorbiclity in general practice.
British Medical Journal 1996; 313:1534.
8. Gajew~kiJ & Singer RB. Mortality in an insured population with
atrial fib~llation. Journal of American Medical Association 1981;
245:1540-1544.
9. Wolf PA, Abbott RD & Kannel WB. Atrial fibrillation as an
independent risk factor for stroke: the Framingham Study. Stroke.
1991; 22:983-988.
10. Benjamin EJ, Wolf PA, D'Agostino RB, Silbershatz H, Kannel WB &
Levy D. Impact of atrial fibrillation on the risk of death: the
Framingham Heart Study. Cirmalation 1998; 98:946-52.
7.

Currently, treating 1000 AF patients, with a 5% per year risk of
stroke, with warfarin prevents about 30 strokes and causes at least
two episodes of major haemorthage each year and treating 1000 AF
patients with aspirin prevents about 15 strokes each yearL With
the lifetime risk esttmated at 1 in 4 for males and 1 in 5 for females,
these figures underscore the development of reliable schemes to
identify individuals with atrial fibrillation and predict stroke risk
together with strategies to achieve adherence to evidence based
therapy in order to improve clinical outcomes of an ageing sotalol
is more useful for rate control than cardioversion population.

11. EzekowitzMD & Levine A. Preventing stroke in patients with atrial
fibrillation. Journal of American Medical Association 1999;
281:t830-1835.
12. Hart RG & Halperin JL Atrial fibrillation and thromboembolisrn: a
decade of progress in stroke prevention. Annals of Internal Medicine
1999; 131(9): 688-695.

71

Volume l 7

Number2

May2004

Australian Critical Care

13.

CampbeLL P, Roberts G, Eaton V, Coghlan D & Gallus A. Managing
warfarin therapy in the community.
24:86-89.

32.

Hohnk~er SH, Kuck KH & Lilienthal J. Rhythm or rate control in
atrial fibrillation - pharmacological intervention in atrial fibrillation
(PIAF): a randomised trial. Lancet 2000; 356:1789-1794.

Australian Prescriber 2001;

14.

Silverman ME. From rebellious palpitations to the discovery of
auricular fibrillation: contributions of Meccans, Lewis and Einthoven.
American Journal of Cardiology. 1994; 73".384-389.

33.

Wyse DG, Anderson JL, Antman EM et d. Atrial fibrillation followup investigation of rhythm management - the AFFIRM study design.
American Journal of Cardiology 1997; 79:1198-1202.

15.

Bubien RS & Sanchez JE. Atrial fibrillation: treatment rationale and
clinical utility of nonpharmacologic therapies. AACN Clinical
Ismes: Advanced Practice in Acute & Critical Care 2001; 12(1):140155.

34.

16.

Falk RH. Medical Progress: Atrial Fibrillation. New England Journal
of Medicine 2001; 344(14):1067-1078

Tieleman RG, Van Gelder IC, Crijins HJGM, de Kam PJ, Van den
Berg MP, Haaksma Jet a.k Early recurrence of atrial fibrillation after
electrical cardioversion: a result of fibrillation-induced electrical
remodelling of the atria? Journal of American College of Cardiology
1998; 31:167-173.

35.

17.

Klein AL, Grimm RA, Black IW et aL Cardioversion guided by
transesophageal echocardiography: the ACUTE pilot study: a
randomized, controlled trial. Annals of Internal Medicine 1997;
126:200-209.

Stoddard MF, Dawkins PR, Prince CR & Longaker RA.
Transesophageal echocardiographic guidance of cardioversion in
patients with atrial fibrillation. American Heart Journal 1995;
129:1204-1215.

36.

Hobbs WJC, Fyrm S, Todd DM, Wolfson P, Galloway M & Garratt
CJ. Reversal of atrial electrical remodeling after cardioversion of
persistent atrial fibrillation in humans. Circulation 2000; 101:11451151.

37.

Wood MA, Bmwn-Mahoney C, Kay N & Ellentx)gen KA. Clinical
outcomes after ablation and pacing therapy for atrial fibrillation: a
meta-analysis. Circulation 2000; 101: 1138-1144.

38.

Tse HF, Lau CP, Yu CM et a/. Effect of the implantable atrial
defibrillator on the natural history of atrial fibrillation. Journal of
Cardiovascular Electmphysiology 1999; 10:1200-1209.

39.

Swerdlow CD, Schsls W, Dijkman B et al. Detection of atrial
fibrillation and flutter by a dual-chamber implantable cardioverterdefibrillator. Circulation 2008; 101:878-885.

40.

Lee R, Nitta T, Schuessler RB, Johnson 12(2, Boineau JP & Cox JL.
The closed heart MAZE: a nonbypass surgical technique. Annals of
Thoracic Surgery 1999; 67:1696-1702.

41.

Petersen P, Boysen G, Godtfredsen J, Andersen ED & Andersen B.
Placelx>-controlled, randomised trial of warfarin and aspirin for
prevention of thromboembolic complications in chronic atrial
fibrillation: the Copenhagen AFASAK study. Lancet 1989; I: 175-179.

42.

Boston Area Anticoagulation Trial for Atrial Fibrillation
Investigators. The effect of low-dove warfarin on the risk of stroke in
nonrheumatic atrial fibrillation. New England Journal of Medicine
1990; 323:1505-1511.

43.

Connolly SJ, Laupacis A, Gent M et d. Canadian Atrial Fibrillation
Anticoagulation (CAFA) study. Journal of American College of
Cardiology 1991; 18:349-355.

44.

Ezekowitz MD, Bridgers SL, James KE et aL Warfarin in the
prevention of stroke associated with nonrheumatic atrial fibrillation:
the Veterans Affairs Cooperative Study. New England Journal of
Medicine 1992; 327:1406-1412.

45.

European Atrial Fibrillation Trial Study Group. Secondary
prevention in non-rheumatic atrial fibrillation after transient
ischemic attack or minor stroke. Lancet 1993; 342:1255-1262.

46.

Stroke Prevention in Atrial Fibrillation Investigators. Adjusted-dose
warfarin versus low intensity, fLxeddose, warfarin plus aspirin for highrisk patients with atrial fibrillation: Stroke prevention in atrial
fibrillation III randomized clinical trials. Lancet 1996; 348:633-638.

47.

GulLov AL, Koe.foel DG, Petersen P et al. Fixedminidosewarfarinand

18.

19.

20.

21.

22.

Fatkin D & Feneley M. Stratification of thromboembolic risk of atrial
fibrillation by transthoracic echocardiography and transesophageal
echocardiography: the relative role of left atrial appendage fimction,
mitral valve disease, and spontaneous echocardiographic contrast.
Progress in Cardiovascular Disease 1996; 39:57-68.
Martmng WJ, Silverman DI, Gordon SP, Krumholz HM & Douglas
PS. Cardioversion from atrial fibrillation without prolonged
anticoagulation with use of transesophageal echocardiography to
exclude the presence of atrial thrombi. New England Journal of
Medicine 1993; 328:750-755.
Leung DY, Davidson PM, Cranney GB & Walsh WF.
Thromboembolic risks of left atrial thrombu~ detected by
transesophageal echocardiogram. American Journal of Cardiology
1997; 79(5):626-629.
Atrial Fibrillation Investigators. Echocardiographic predictors of
stroke m patients with atrial fibrillation. Archives of Internal
Medicine 1998; 158:1316-1320.
Feinberg WM, Comell ES, Nightingale SD, Peaxce LA, Tracy RP,
Hart RG & Bovill EG. relationship between prothombin activation
fragment F1.2 and international normalised ratio in patients with
atrial fibrillation. Stroke 1997; 28:1101-1106.

23.

Demellis J & Panaretou M. C-reactive protein and paroxysmal atrial
fibrillation: evidence of the implication of an inflammatory process in
paroxysmal atrial fibrillation. Acta Cardiologica 2001; 56(6):375-780.

24.

Lip GY, Lowe GD, Rumley A & Dunn F-(3. D-dimer levels in
paroxysmal atrial fibrillation: evidence for intermediate elevated
levels of intravascular thrombogenesis. American Heart Journal 1996;
131:724-730.

25.

Lip GY. Hypercoaguability and hemodynamic abnormalities in atrial
fibrillation (comment). Heart 1997; 77:395-396.

26.

Feinberg WM, Comell ES, Nightingale SD, Pearce LA, Tracy RP,
Hart RG & Bovill EG. relationship between pmthombin activation
fragment F1.2 and International Normalised Ratio in Patients with
Atrial Fibrillation. Stroke 1997; 28:1101-1106.

27.

Heppel RM, Berkin KE, McLenachan & Davies JA. Haemostatic and
haemodynamic abnormalities associated with left atrial thrombosis in
non-rheumatic areal fibrillation. Heart 1997; 77:407-411.

28.

Stroke Prevention in Atrial Fibrillation Investigators. Design of a
multicenter randomized trial for the stroke prevention in areal
fibrillation study. Stroke. 1990; 21:538-545.

29.

Ezekowitz MD, James KE, Nazanan SM et d. Silent cerebral
infarction in patients with nonrheumatic atrial fibrillation.
Circulation 1995; 92: 2178-2182.

30.

Ott A, Breteler M, de Bruyne MC eta/. Atrial fibrillation and
dementia in a population-based study: The Rotterdam Study. Stroke
1997; 28: 316-321.

31.

Larrue V, von Kummer R, del Zoppo G & Bluhmki E. Hemorrhagic
transformation in acute ischemic stroke: potential contributing factors
in the European Cooperative Acute Stroke Study. Stroke 1997;
28:957-960.

Volum~ 17 Number 2

May 2004

aspirin alone and in combination vs adjusted-dose wan%tin for stroke
prevention in atrial fibrillation: Second Copenhagen Atrial
Fibrillation, Aspirin, and Anticoagulation Study. Archives of
Internal Medicine 1998; 158:1513-1521.

72

48.

Stroke Prevention tn Atrial Fibrillation Investigators. Patients with
nonvalvular atrial fibrillation at low risk of stroke during treatment
with aspirin. Journal of American Medical Association 1998;
279:1273-1277.

49.

Atrial Fibrillation Investigators. Risk factors for stroke and efficacy of
antithrombotic therapy in atrial fibrillation: analysis of pooled data
from five randomized controlled trials. Archives of Internal Medicine
1994; 154:1449-1457.

At,,
Au,rtrallan Critical Care

69.

Ruben DB, Frank JC, Hirsute SH, McGuigan KA & Maly RC. A
randomized clinical trial of outpatient comprehensive geriatric
assessment coupled with an intervention to increase adherence to
recommendations. Journal of the American Geriatrics Society 1999;
47:269-276.

70.

Cockburn J. Patient education and strategies to improve compliance.
In Walls R, Jenkins C. (Eds). Understanding Asthma. Sydney:
McLelland and Petty, 2000.

71.

Man-Son-Hing M, Laupacis A. Balancing the risks of stroke and
upper gastrointestinal tract bleeding in older patients with atrial
fibrillation. Archives of Internal Medicine 2002; 162(5):541-550

72.

Segal JB, McNamam RL, Miller MR, Powe NR, Goodman SN &
Robinson KA. Bass anticoagulants or antiplatelet therapy for nonrheumatic atrial fibrillation and flutter. The Cochrane Library
(Oxford) 2001.

73.

Go, AS et al. Warfarin use among ambulatory patient with
nonvalvular atrial fibrillation. The anticoagulantion and risk factors
in atrial fibrillation (ATRIA) study. Annals of Internal Medicine
1999; 131:927-934.

74.

Effectiveness of anticoagulation among patients discharged from
hospital on warfarin. The Newcastle Anticoagulation Study. Medical
Journal of Australia 1998; 169(5):243-246.

Gage BE Fihn, SD & White RH. Warfarin therapy for an
octogenarian who has atrial fibrillation. Annals of Internal Medicine
2001; 134(6):465-474.

75.

Enis J. Stroke prevention in patients with non-valvular atrial
fibrillation: a current community perspective. Journal of Clinical
Neuroscience 1997; 4: 320-325.

Laupacis A, Albers G, Dalen J, Dunn MI, Jacobson AK & Singer DE.
Antithrombotic therapy in atrial fibrillation. Chest 1998; 114: 579S589S.

76.

Yuan Z, Bowlin S, Einstadter D, Cebul RD, Conners AR & Rimm A.
Atrial fibrillation as a risk factor for stroke: a retrospec~ve cohort
study of hospitalized Medicare beneficiaries. American Journal of
Public Health 1998; 88(3)'395-400.

77.

Davis DA, Thomson MA, Oxman AD & Haynes RB. Changing
physician performance: a systematic review of the effect of continuing
medical education strategies. Journal of American Medical
Association 1995; 274:700-705.

78.

Thompson O'Brien MA, Oxman AD, Davis DA, Haynes RB.
Freemantle N & Harvey EL. Educational outreach visits: effects on
professional practice and health care outcomes. Cochrane Database
of Systematic Reviews 2000 (2):C[XXX)409.

79.

Oxman AD, Thomson MA, Davis DA & Haynes RB. No magic
bullets: a systematic review of 102 trials of intervention to maprove
professional practice. Canadian MedAJ 1995; 153:1423-1431.

80.

Ho, LL & Brighton T. Warfarin, antiplatelet drugs and their
interactions. Australian Prescriber 2002; 25:81-85.

81.

Hart RG & Halperin JL. Atrial fibrillation and thromboembolism: a
decade of progress in stroke prevention. Annals of Internal Medicine
1999; 131(9): 688-695.

82.

Laupacis A, Albers G, Dalen J, Dunn MI, Jacobson AK & Singer DE.
Antithrombotic therapy in atrial fibrillation. Chest 1998; 114: 579S589S.

83.

Hirsh J, Warkentin TE, Slxaughnessy SG et at. Heparin and low
molecular heparin: mechanisms of action, pharmacokinetics, dosing,
monitoring, efficacy and safety. Chest 2001; 119:64S-94S.

84.

Olsson B & Petersen E Fixed dose oral direct thrombin inhibitor
ximelagatran as an alternative for dose-adjusted warfarin in patients
with non-valvular atrial fibrillation. Poster Number:. 1761 ESC
Stockholm 2001. htrp://www.pslgroup.com/dg/20563a.htm October
29, 2002
•

50.

Coumadin Aspirin Reinfarction Study (CARS) Investigators.
Randomized double-blind trial of fixed low-dose warfarin with aspirin
after myocardial infarction. Lancet 1997; 350:389-396.

51.

Stroke Prevention in Atrial Fibrillation Investigators. Design of a
multicenter randomized trial for the Stroke Prevention in Atrial
Fibrillation Study. Stroke 1990;, 21:538-545.

52.

Boston Area Anticoagulation Trial for Atrial Fibrillation
Investigators. The effect of low-dose warfarin on the risk of stroke in
nortrheumatic atrial fibrillation- New England Journal of Medicine
1990; 323:1505-1511.

53.

Connolly SJ, Laupacis A, Gent Met aL Canadian Atrial Fibrillation
Anticoagulation (CAFA) study. Journal of American College of
Cardiology 1991; 18:349-355.

54.

Gottleib LK & Salem-Schatz S. Anticoagulation in atrial fibrillation:
does efficacy in clinical trials translate into effectiveness in practice?
Archives of Internal Medicine 1994; 154:1945-1953.

55.

56.

57.

58.

Go, AS et al. Warfarin use among ambulatory patient with
nonvalvular atrial fibrillation. The Anticoagulantion and Risk factors
in Atrial Fibrillation (ATRIA) Study. Annals of Internal Medicine
1999; 131:927-934.

Chesebro JH, Wiebers DO, Holland AE et aL Bleeding during
antithrombotic therapy in patients with atrial fibrillation. Archives of
Internal Medicine 1996; 156:409-416.

59.

Gage B, Fihn SD & White RH. WarFarin therapy for an octogenarian
who has atrial fibrillation. Annals of Internal Medicine 2001;
134(6):465-474.

60.

Ruben DB, Frank JC, Hirsute SH, McGuigan KA & Maly RC. A
randomized clinical trial of outpatient comprehensive geriatric
assessment coupled with an intervention to increase adherence to
recommendations. Journal of the American Geriatrics Society 1999;
47: 269-276.

61.

62.

HyleckEM, SkatesSJ, SheehanMAezaL An analysis of the lowest dose
of prophylactic anticoagulation for patients with nonrheumatic atrial
fibrillation. New England Journal of Medicine 1996; 335:540-546.
McAlister FA, Lawson FM, Teo KK & Armstrong R A systematic
review of randomized trials of disease management programs in heart
failure. American Journal of Medicine 2001; 110 (5):378-384.

63.

Ezekowitz MD, James K, Radford M, RicHes F & Redmond N.
Initiating and maintaining patients on warfarin anticoagulation: the
importance of monitoring. Journal of Cardiovascular Pharmacolgical
Therapeutics 1999; 43-48.

64.

Heit JA. Perioperative management of the chronically anticoagulatecl
patient. Journal of Thrombosis & Thrombolysis 2001; 12(1):81-87.

65.

Benavente O, Hart R, Koudstaal, Laupacis A & McBride R. Oral
anticoagulants for preventing stroke in patients with non-valvular
atrial fibrillation and no previous history of stroke or transient
ischemic attacks. The Cochrane Library (Oxford) 2001.

66.

Whifford DL & Scott TA. Quality improvement in the prevention of
thromboembolic complications in atrial fibrillation in one general
practice. Journal of Clinical Governance 2000; 8(2):102-106.

67.

Sawicki PT, for the working group for the study of patient selfmanagement of oral anticoagulation. A structured teaching and selfmanagement program for patients receiving oral anticoagulation: a
randomized controlled trial.
Journal of American Medical
Association 1999; 281:145-150.

68.

Sabatini T, Frisoni GB, Barbisoni P, Belletli G, Roazini R & Tralmcchi
M. Atrial fibrillation and cognitive disorders in older people. Journal
of American Geriatrics Society 2000; 48:387-390.

73

Volume l 7

Number2

May2004