Unit 562

July 2019

Cardiovascular

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Cardiovascular
Unit 562 July 2019

About this activity 2

Case 1 Henry recently attended the emergency department 4

Case 2 Kabir is tired and short of breath 9

Case 3 Vilija presents with difficulty writing 13

Case 4 Nicola is breathless 17

Multiple choice questions 22

The five domains of general practice

Communication skills and the patient–doctor relationship

Applied professional knowledge and skills
Population health and the context of general practice
Professional and ethical role
Organisational and legal dimensions
About this activity check Cardiovascular
About this activity
Cardiovascular disease is one of the
major causes of morbidity and mortality
in Australia.1,2 In 2016, it was reported
that 43,600 deaths were attributable to
cardiovascular disease – second only to
deaths from all types of cancer combined.3
There were 10,869 fatalities from stroke
in Australia in 2015, making it the third
leading cause of death in the country.4
Atrial fibrillation, which was associated
with 11% of stroke deaths in 2015,4
affects approximately 2% of the general
Australian population and 5% of adults
aged over 65 years.5
It is estimated that approximately 1–2%
of the Australian population have heart
failure,6 and hospitalisations due to
heart failure steadily increased in the
10 years prior to 2015.7
Idiopathic pulmonary arterial
hypertension (PAH) affects up to 30
Australian patients per million, in
addition to patients who develop PAH
secondary to other conditions.8
This edition of check considers the
investigation and management of
cardiovascular conditions in
general practice.
References
1. Australian Institute of Health and Welfare.
Cardiovascular disease, diabetes and
chronic kidney disease – Australian facts:
Morbidity – Hospital care. Canberra:
AIHW, 2014. Available at www.aihw.gov.
au/getmedia/0cdf3d37-1b29-47b5-abf5-
5f9bd28b79d5/18032.pdf.
aspx?inline=true [Accessed 30 May 2019].
2. Australian Institute of Health and Welfare.
Australian Burden of Disease Study:
Impact and causes of illness and death in
Australia 2011. Canberra: AIHW, 2016.
Available at www.aihw.gov.au/getmedia/
d4df9251-c4b6-452f-a877-
8370b6124219/19663.pdf.
aspx?inline=true [Accessed 30 May 2019].
3. Australian Institute of Health and Welfare.
Australia’s health 2016: In brief. Canberra:
AIHW, 2016. Available at www.aihw.gov.
au/getmedia/7752644b-e6f0-4793-
b4e0-74ef3093c589/19748-ah16-ib.pdf.
aspx?inline=true [Accessed 30 May 2019].
4. Australian Bureau of Statistics. Causes
of death, Australia, 2015. Canberra: ABS,
2017. Available at www.abs.gov.au/
ausstats/abs@.nsf/Lookup/by%20
Subject/3303.0~2015~Main%20
Features~Stroke~10003 [Accessed 30
May 2019].
2
5. National Heart Foundation of Australia.
Atrial fibrillation: Understanding
abnormal heart rhythm. Melbourne:
NHFA, 2016. Available at www.
heartfoundation.org.au/images/
uploads/publications/CON-175_Atrial_
Fibrillation_WEB.PDF [Accessed 30 May
2019].
6. Sahle BW, Owen AJ, Mutowo MP,
Krum H, Reid CM. Prevalence of heart
failure in Australia: A systematic review.
BMC Cardiovasc Disord 2016;16:32.
doi: 10.1186/s12872-016-0208-4.
7. Nichols M, Peterson K, Herbert J,
Allender S. Australian heart disease
statistics 2015. Melbourne: National
Heart Foundation of Australia, 2016.
Available at www.heartfoundation.org.
au/images/uploads/publications/RES-
115-Aust_heart_disease_statstics_2015_
WEB.PDF [Accessed 31 May 2019].
8. Keogh A. Pulmonary arterial
hypertension. Sydney: St Vincents &
Mater Health, 2009.
Learning outcomes
At the end of this activity, participants
will be able to:
• outline the investigations required for
suspected atrial fibrillation
• discuss the short-term and long-term
considerations for a patient following
stroke
• describe the diagnosis and
management of heart failure
• identify the pharmacological
therapies available to treat pulmonary
hypertension.
Authors
James Allan (Case 1) MBBS,
MFamMed, Dip Obs, FRACGP is a
general practitioner (GP) working in the
Adelaide Hills. He holds a Masters in
General Practice (by research) from
Monash University. He is currently
Assessment Panel Chair for the RACGP
fellowship exam in SA. In the past he
has been a Project Officer for the Hills
Division of General Practice (Diabetes)
and has been a medical education
officer for SA faculty QI&CPD program,
and he has been a medical officer
undertaking research in the
Department of General Practice
Adelaide University.
M Anne Hamilton-Bruce (Case 3) BSc,
MSc, MBA, PhD, LLB(Hons), CBiol
FRSB, CSci FIBMS, AFCHSE is a
Principal Medical Scientist, Co-Director
of the Stroke Research Programme,
Research and Education Co-lead in
Neurology at the Central Adelaide Local
Health Network, and Affiliate Associate
Professor, Adelaide Medical School,
University of Adelaide. She has an
interest in and researches stroke
prevention and management,
supervising stroke and transient
ischemic attack (TIA) research, which
includes genomics, proteomics and
services for clinical translation and
implementation. She also has a strong
community focus, being the
Chairperson of Stroke SA Inc., Deputy
Chairperson of Australian Neurology
Research, and an affiliate of the
Hospital Research Foundation Group’s
Cure For Stroke Australia co-founding
and current Advisory Committee
member.
Simon Koblar (Case 3) BMBS, FRACP,
PhD is a Professor of Neurology and
Neuroscience at the University of
Adelaide. He is also Director of the
Stroke Research Programme, which
researches prevention and treatment of
ischaemic stroke. Currently he works as
a neurologist with an interest in stroke
clinically at the Central Adelaide Local
Health Network. He was involved in
setting up stroke services in the
Adelaide metropolitan area and
continues to contribute.
Edmund Lau (Case 4) MBBS (Hons),
BSc, PhD, FRACP is a respiratory
physician at Royal Prince Alfred (RPA)
Hospital, Sydney. He is a member of the
Multidisciplinary Pulmonary
Hypertension Clinic at RPA Hospital.
He has a special interest in pulmonary
hypertension and has published widely
in this area.
Elaine Leung (Case 3) MBBS, BSc
(Med), FRACP, PhD is a general
practitioner in Adelaide and a senior
lecturer in General Practice at Flinders
University. She has a special interest in
stroke prevention.
Neil Strathmore (Case 2) BSc (Hons),
MBBS, FRACP, FCSANZ, FHRS, CCDS
trained at the University of Melbourne,
Royal Melbourne Hospital (RMH) and
the Massachusetts General Hospital.
He has been a member of the RMH
Cardiology Department since 1991 and

also works at Epworth Hospital. He has
a wide interest in cardiology and in
training junior doctors. He is particularly
interested in arrhythmias, especially the
management of atrial fibrillation and
bradycardias. He has extensive
experience in pacemaker and
defibrillator implantation, follow-up,
extraction and infection management.
Vivek Thakkar (Case 4) BSc, MBBS
(Hons), DMedSc, FRACP is a
Rheumatologist and Associate
Professor in Medicine at Macquarie
University, member of the
Multidisciplinary Pulmonary
Hypertension Services of Macquarie
University and Liverpool Hospital, and
practises in his rooms in South West
Sydney. His special interests are
cardiopulmonary complications of
autoimmune diseases and general adult
rheumatology.
Peer reviewers
Mark Beeby MBBS, FRACGP,
DipPallMed has been a general
practitioner (GP) for 37 years in Lalor
Plaza Medical Centre, Lalor, Victoria.
He is an examiner for the RACGP and a
clinical supervisor for general
practitioner registrars with Eastern
Victoria GP Training.
Mark Nelson MBBS (Hons), MFM, PhD,
FRACGP, FAFPHM is Professor and
Chair, Discipline of General Practice,
School of Medicine, and Senior Member,
Menzies Institute for Medical Research,
where he is also medical director of the
Blood Pressure Clinic, both at the
University of Tasmania. He is also an
Adjunct Professor, Department of
Epidemiology and Preventive Medicine,
Monash University. His research
interests focus on large-scale clinical
trials in primary care. He has 265 peer
reviewed scientific publications, has
been awarded more than AU$80 million
in competitive grants and is a principal
investigator on the National Institute of
Health–sponsored ASPREE/ASPREE-
XT study (N = 19,000) investigating if
aspirin extends healthy active life, and
the National Health and Medical
Research Council–sponsored STAREE
(recruitment to date >5000) similarly
investigating if statins extend healthy
active life. He is also an author of
multiple guidelines for cardiovascular
Cardiovascular check About this activity
disease prevention and treatment and Stroke, History of Bleeding,
remains in clinical general practice in Labile International
Hobart, Australia. Normalised Ratio, Age >65
years, Drugs, Alcohol
Atef Asham (Case 1) MBBS, FRACGP, Consumption
MSc Cardiology graduated medical INR International Normalised
school in 1992. He gained a Master’s Ratio
degree in Cardiology in 2000. He has JVP jugular venous pressure
worked at both Royal Melbourne MDI metered-dose inhaler
Hospital and Box Hill Hospital, as well NT-proBNP N-terminal pro b-type
as several general practice clinics natriuretic peptide
across Victoria. His medical interests NYHA New York Heart Association
include chronic disease management, PAH pulmonary arterial
cardiovascular care and diabetes. hypertension
Currently, he is the chair of the PBS Pharmaceutical Benefits
cardiology network at the RACGP and Scheme
is also an examiner there. He is also a PFT pulmonary function tests
research investigator at Baker Heart TIA transient ischaemic attack
and Diabetes Institute and is
collaborating with the National Heart
Foundation of Australia about
Cardiovascular Risk Assessment.
Abbreviations
AAA abdominal aortic aneurysm
ACEI angiotensin converting
enzyme inhibitor
AF atrial fibrillation
ARB angiotensin II receptor
blocker
AV atrioventricular
BNP b-type natriuretic peptide
bpm beats per minute
CHA2DS2-VASc
 ardiac failure or
C
ventricular dysfunction,
Hypertension, Age >65
years, Age >75 years,
Diabetes, Stroke or other
embolism, Vascular Disease
CHADS2 Cardiac failure or
ventricular dysfunction,
Hypertension, Age >75
years, Diabetes, Stroke or
other embolism
COPD chronic obstructive
pulmonary disease
CT computed tomography
CTEPH chronic thromboembolic
pulmonary hypertension
CXR chest X-ray
DOAC direct oral anticoagulant
ECG electrocardiogram
FAST Face, Arms, Speech, Time
GP general practitioner
HAS-BLED Hypertension, Impaired
Renal Function, Impaired
Liver Function, History of
3
Case 1 check Cardiovascular

CASE Question 1

1 Henry recently attended the

emergency department
On the basis of Henry’s presentation and his emergency
department discharge summary, what is the most likely
diagnosis?
Henry, aged 72 years, attends your clinic following a
recent emergency department attendance. Henry is a
choleric Scotsman who was recently widowed and
lives alone. He has a past history of mild chronic
obstructive pulmonary disease (COPD), a consequence
of being a pipe smoker for over 50 years. His peak
expiratory flow rate is 300 L/min. In the past two
years, you have seen Henry for benign prostatic
hypertrophy after he presented with nocturia, urinary
urgency and increased urinary frequency.

He stopped smoking two years ago and has been

prescribed salbutamol inhaler 500 mcg 4/24 as
needed and tamsulosin 400 mcg orally daily, both of
Question 2
which he takes infrequently.
What features would assist you to differentiate this
The emergency department summary is provided in Box 1.
diagnosis from the diagnosis of acute asthma given in the
emergency department?

Box 1. Emergency department

discharge summary
Present complaint: Male aged 72 years presents
by ambulance after developing sudden and severe
nocturnal dyspnoea
History of present complaint: Recent respiratory
infection with unproductive cough and increasing
exertional dyspnoea for two weeks
Examination: Afebrile, pulse rate 96 beats per minute
(bpm; irregular), blood pressure 105/60 mmHg,
respiratory rate 32 breaths per minute, peripheral
capillary oxygen saturation (SpO2) >96%, peak
expiratory flow rate 200 L/min, expiratory wheeze in all
Further information
areas, pitting oedema to the knees Henry’s N-terminal pro b-type natriuretic peptide
Investigations: Troponin 40 ng/L, electrocardiogram (NT-proBNP), measured shortly after his attendance at your
showed no ischaemic changes, normal electrolytes and
practice, is 30,000 ng/L, indicating significant heart failure.
complete blood examination, chest X-ray did not show
collapse/consolidation The electrocardiogram (ECG) indicates sinus rhythm with
Management: He was given salbutamol frequent atrial ectopic beats, lung function tests show mild
5 mg/2.5 mL via nebuliser × 2 with significant
COPD and radiology does not demonstrate an aortic aneurysm.
subjective improvement, and was discharged with
salbutamol 500 mcg metered-dose inhaler (MDI) × 2
puffs four-hourly when necessary, fluticasone 125 mcg Question 3
MDI × 2 puffs twice a day via spacer and a short course
of prednisolone 25 mg for five days then cease What investigations would you order?
Final diagnosis: Acute asthma

Henry has been asked to review the results with his

general practitioner (GP).

4
 Cardiovascular check Case 1

Question 4 Question 6
What is your immediate management? What is your immediate treatment?

Question 7
Henry returns from hospital and seems to be euvoloemic. His
Further information
current therapy is frusemide 20 mg in the morning and
Henry was started on frusemide 40 mg, one in the morning perindopril 4 mg in the morning. What are your goals in
and one in the middle of the day, and perindopril erbumine treatment at this stage?
2 mg once daily. A month later you are asked to visit Henry in
his home as he reports ‘feeling awful’. He fainted during the
night when he got up to go to the toilet and required
assistance from a neighbour. Apart from the trip to hospital,
he has not been outside his home for three months. His home
is cluttered but tidy and smells stale. You examine Henry and
record your findings as follows:

• afebrile, pale and sweaty

• pulse 102 beats per minute (bpm) irregular
• blood pressure 80/60 mmHg seated, 60/– mmHg standing
• respiratory rate 22 breaths per minute
• chest clear
• mild ankle oedema
• jugular venous pressure (JVP) not elevated.
Question 5
Further information
You increase Henry’s dose of perindopril to 4 mg daily over
the ensuing weeks and prescribe carvedilol 3.125 mg twice
daily for two weeks, doubling the dose every two weeks until
arriving at a dose of 25 mg twice daily.
Henry attends his cardiologist, who arranges an echocardiogram.
The echocardiogram shows severe left ventricular dysfunction
ejection fraction of 21% with moderate aortic regurgitation.

On the basis of your findings, what is your current diagnosis?

Question 8
What is the prognosis at this stage?

5
Case 1 check Cardiovascular
Further information
Three weeks later you are once more asked to visit Henry in
his home. He has had ‘asthma’ all night, and it has not been
improving following use of his inhalers. He complains of
worsening of his urinary incontinence. He tells you that he has
started taking zinc, folic acid, vitamin B12 and coenzyme Q10.
You examine Henry and record your findings as follows:
• afebrile
• pulse 102 bpm irregular
• blood pressure 120/60 mmHg
• respiratory rate 22 breaths per minute
• chest coarse crackles to the midzones
• pitting oedema to the knee
• JVP 4 cm.
Question 9
What could be causing Henry’s current symptoms?
Further information
On further questioning, Henry admits that worsening urinary
incontinence, dry mouth and a recent episode of hypovolaemia
had caused him to question the therapy. His daughter did
some internet research and suggested some natural
alternatives that he had tried. This has resulted in a
recurrence of Henry’s acute pulmonary oedema.
Question 10
What is the most appropriate management?
6
CASE 1 Answers
Answer 1
The most likely cause of this presentation is ‘cardiac asthma’.1
The bronchospasm is caused by interstitial oedema by an
unknown mechanism. It may be present in as many as 35% of
acute presentations of heart failure to emergency departments.1
Differential diagnoses include atrial fibrillation (AF; irregular
pulse), leaking abdominal aortic aneurysm (AAA; low blood
pressure and high pulse) or COPD (previous history).
Answer 2
The diagnosis of an initial presentation of acute asthma is
unusual in a person aged 72 years, despite Henry’s wheezing
and positive response to bronchodilators. A high level of
suspicion for acute pulmonary oedema is recommended. The
age of onset, presence of marked ankle oedema and
tachycardia support a diagnosis of heart failure. The absence
of JVP elevation and classical features on chest X-ray (CXR)
do not support this diagnosis.
Regarding the differential diagnoses: The diagnosis of AF is
suggested by the irregular pulse and can be confirmed by
ECG. This may coexist with heart failure. A leaking aortic
aneurysm is possible considering the relatively low blood
pressure and high pulse, but Henry lacks abdominal or back
pain, syncope or tenderness over the aneurysm. A CXR or
abdominal X-ray may show aortic widening, but a computed
tomography scan is a more appropriate emergency
department investigation.2 COPD is suggested by the
previous history and may be a comorbidity, but is not usually
responsible for this degree of ankle oedema. Formal lung
function testing would assist in diagnosis.
When uncertainty exists, the National Heart Foundation of
Australia Guidelines for the prevention, detection and
management of heart failure in Australia 2018 recommend
obtaining a b-type natriuretic peptide (BNP) estimation to
clarify the diagnosis (Table 1).3
Table 1. B-type natriuretic peptide and N-terminal pro
b-type natriuretic peptide diagnostic cut-off values3
  BNP (ng/L) NT-proBNP (ng/L)
Heart failure rule-out <100 <300
Heart failure rule-in >400 Age <50 years: >450
Age 50–75 years: >900
Age >75 years: >1,800
BNP, b-type natriuretic peptide; NT-proBNP, N-terminal pro b-type natriuretic peptide
Reproduced from Atherton JJ, Sindone A, De Pasquale CG, et al. National Heart
Foundation of Australia and Cardiac Society of Australia and New Zealand:
Guidelines for the prevention, detection and management of heart failure in Australia
2018 Heart Lung Circ 2018;27(10):1123–08. doi: 10.1016/j.hlc.2018.06.1042. Licence
at https://creativecommons.org/licenses/by-nc-nd/4.0/

Answer 3
In addition to serum BNP, the National Heart Foundation of
Australia suggests 12-lead ECG and a CXR are useful in the
emergency room diagnosis.3 If these have not already been
performed, it is appropriate to arrange these tests from general
practice. ECG and CXR may also identify underlying causes of
heart failure, such as AF and myocardial ischaemia. It is
recommended that blood screening includes cardiac enzymes
(acute ischaemia), electrolytes (hyponatraemia), renal function
(uraemia), blood count (anaemia), thyroid function and possibly
iron levels (deficiency/haemochromatosis).
The definitive investigation to diagnose heart failure is an
echocardiogram, and this is recommended for all patients
with suspected heart failure.3 Computed tomography coronary
angiography (non-invasive) for AAA, catheter angiography
(invasive), genetic studies for cardiomyopathy and bone
scintigraphy for amyloid are additional investigations that may
be arranged if indicated by Henry’s specialist.
Answer 4
Oxygen should be given in the acute setting, especially if oxygen
saturation falls below 97%. Nitrolingual spray may give some
short-term relief of dyspnoea. In extreme heart failure, ventilator
support, intravenous nitrate therapy and positive inotropes may
be used, but these are rarely initiated in general practice.4–6
Salt and fluid restriction and loop diuretics such as
furosemide (also known as frusemide) are important for
correcting fluid overload.3,6,7 Thiazides are not appropriate.
Angiotensin converting enzyme inhibitors (ACEIs) are
effective in providing symptomatic relief; however, care must
be taken to start at a small dose and gradually up titrate. For
example, perindopril erbumine may be prescribed for adults,
starting at 2 mg orally once daily; increasing to 4 mg orally
once daily.7 Where ACEIs are not tolerated, angiotensin II
receptor blockers (ARBs) may provide similar benefit.6,7
Comorbidities such as myocardial ischaemia, iron deficiency
anaemia, AF and poorly controlled hypertension should also
be treated.
Answer 5
The most likely diagnosis is hypovolaemia, caused by the loop
diuretic. It is important to review patients following initiation of
diuretic therapy as the dose may need to be reduced after 2–3
weeks to prevent over-correction. This is particularly important
in elderly patients and those with reduced renal reserve.
Answer 6
Henry requires urgent transfer to hospital by ambulance to
manage his acute hypovoloaemia. If detected earlier, Henry’s
diuretic should have been stopped and fluid correction
undertaken. Investigations of serum electrolytes and renal
function are required to look for electrolyte disturbance.
Measurement of Henry’s weight each day may be a useful
measure to indicate the return of normovolaemic status.
Henry will require frequent review.
Cardiovascular check Case 1
Answer 7
Diuretic therapy is insufficient to improve the outlook for
heart failure. It is possible that Henry’s next presentation
may be because of a recurrence of fluid overload as he
fluctuates from hypovolaemia to hypervolaemia. It is
important to treat the underlying heart failure and to address
any contributing comorbidities. First-line medicines that
improve heart failure survival are ACEIs (or ARBs if ACEIs are
not tolerated), selected beta blockers and aldosterone
antagonists (spironolactone).6,7
It is now important to add an appropriate beta blocker, and
increase its dosage. For instance, carvedilol initially 3.125 mg
once or twice daily for two weeks. The dose could then be
doubled every two weeks until arriving at a dose of 25 mg
twice daily.7 It is possible that Henry may become hypotensive,
and starting medicines that are also used as antihypertensives
may seem counterintuitive. Regardless, by starting with a low
dose and increasing it gradually, it is possible to achieve
therapeutic values in most patients. Elevated creatinine and
potassium retention are possible when a combination of ACEI
and aldosterone blocker is used. Rather than avoiding this
combination, it is advised to check the biochemistry frequently
and adjust accordingly.3
It is worth reviewing possible comorbidities. Comorbidities are
very frequent in heart failure. AF is suggested by Henry’s
irregular pulse. His ECG needs to be reviewed or repeated.
Correction to sinus rhythm (cardioversion or rhythm control
medicines like amiodorone) is the preferred option for severe
heart failure, but often rate control (digoxin or beta blocker) is all
that can be achieved in the short term. Henry’s cardiologist may
need to be consulted for advice. Iron deficiency is a common
precipitant of heart failure, and anaemia is suggested by Henry’s
pallor. Correction of anaemia will need to be accompanied by
investigation for the source of the iron deficiency. Acute
infection, valvular heart disease and thyroid disturbance are
other possible comorbidities that need to be investigated.
Answer 8
In the Rotterdam study, the five-year survival for patients
following admission for heart failure was 59%.8 This is worse
than the prognosis of many tumours. Factors that are associated
with poorer survival include age, AF, diabetes, renal failure,
hypotension and the severity of heart failure. Severity is
measured using the New York Heart Association (NYHA)
classification (Table 2).9
Table 2. New York Heart Association functional
classification of heart failure9
Class I Class II Class III Class IV
No limitation Slight limitation Marked Symptoms on
of ordinary of ordinary limitation any physical
physical activity physical activity of ordinary activity or at
No symptoms physical activity rest
at rest No symptoms
at rest
7
Case 1 check Cardiovascular
Henry is quite symptomatic and restricted in his activity, giving
him a rating of III or IV on the NYHA classification.
Answer 9
Heart failure is credited with one of the highest readmission
rates of all acute presentations to emergency
departments.10 In many instances, this occurs as a result of
the patient’s non-compliance and failure to adhere to
therapy. Henry’s use of mineral supplements and vitamin
therapies should alert you to the possibility that he has
stopped his heart failure medication.
Mineral supplements and antioxidant vitamins have not been
shown to benefit heart failure.11 There is some weak evidence
that coenzyme Q10 has a role in treating heart failure, but
requires further evaluation before it can be endorsed in
treatment guidelines.12
If Henry’s current presentation had occurred despite
maintaining and optimising his first-line therapy, there is a
place to consider second-line heart failure medication.13
It is also recommended to look for precipitants such as acute
infection, anaemia and AF.
Answer 10
Henry needs acute management of his heart failure and may
need to return to hospital for treatment.
A significant reduction of readmission has been achieved with
nurse-led heart failure clinics.14 These clinics provide
education about the disease and its management. They can
guide lifestyle management, including fluid restriction, salt
restriction and exercise therapies. Routine weighing may
prevent fluid mismanagement. These clinics can also assist in
up-titration of medicines like ACEI and beta blockers to
achieve therapeutic goals. Patients may need dosing aids
such as Webster packs.
It is recommended that Henry be enrolled in a suitable
program, if one exists. Alternatively, it might be possible to
emulate a similar strategy in your general practice, using
enhanced primary care strategies. The outcome is much
better than for ‘usual care’.
Second-line heart failure medicines include ivabradine and
substituting the ACEI or ARB with the combination medicines
sacubitril and valsartan. Survival may also be improved by
resynchronisation therapy, especially when it is combined
with an implanted defibrillator.
Ivabradine induces bradycardia and reduces myocardial load.
Sacubitril inhibits neprilysin, which is involved in the
breakdown of various peptides including naturitic peptide.
In randomised control trials comparing enalapril to sacubitril
with valsartan, there was reduced cardiovascular death or first
hospitalisation for heart failure by 4.7% and improved survival
by 2.8% in patients assigned to sacubitril with valsartan.15
Risks include hypotension and angioedema, but there was
reduced progression of heart failure, renal impairment and
hyperkalaemia.
8
These second-line therapies are worth exploring when first
line-therapy is not tolerated or has failed. First-line therapy
should be optimised through dose titration before it is
determined to have failed.
Conclusion
Although heart failure is a disease involving emergency room
management, hospital admission and specialist care, GPs play
an important part in coordinating care, optimising medical
treatment and preventing readmission and recurrence. This will
improve as GPs implement chronic disease management
strategies like recall systems, dedicated clinics, partnerships
with regional health providers and practice audits.
References
1. Jorge S, Becquemin MH, Delerme S, et al. Cardiac asthma in elderly
patients: Incidence, clinical presentation and outcome. BMC
Cardiovasc Disord 2007;7:16. doi: 10.1186/1471-2261-7-16.
2. Robinson D, Mees B, Verhagen H, Chuen J. Aortic aneurysms –
Screening, surveillance and referral. Aust Fam Physician
2013;42(6):364–69.
3. Atherton JJ, Sindone A, De Pasquale CG, et al. National Heart
Foundation of Australia and Cardiac Society of Australia and New
Zealand: Guidelines for the prevention, detection and management
of heart failure in Australia 2018. Heart Lung Circ
2018;27(10):1123–1208. doi: 10.1016/j.hlc.2018.06.1042.
4. Baird A. Acute pulmonary oedema – management in general
practice. Aust Fam Physician 2010;39(12):910–14.
5. Krum H, Driscoll A. Management of heart failure. Med J Aust
2013;199(5):334–39. doi: 10.5694/mja12.10993.
6. Expert Group for Cardiovascular. Heart failure. In: eTG complete
[Internet]. Melbourne: Therapeutic Guidelines Limited, 2017.
7. Australian Medicines Handbook 2019 (online). Adelaide: Australian
Medicines Handbook Pty Ltd, 2019. Available at https://
amhonline.amh.net.au/ [Accessed 15 May 2019].
8. Mosterd A, Cost B, Hoes AW, et al. The prognosis of heart failure
in the general population: The Rotterdam Study. Eur Heart
J 2001;22(15):1318–27.
9. Dolgin M, Association NYH, Fox AC, Gorlin R, Levin RI, New York
Heart Association. Criteria Committee. Nomenclature and criteria
for diagnosis of diseases of the heart and great vessels. 9th ed.
Boston, MA: Lippincott Williams and Wilkins, 1994.
10. Ziaeian B, Fonarow GC. The prevention of hospital readmissions in
heart failure. Prog Cardiovasc Dis 2016;58(4):379–85.
doi: 10.1016/j.pcad.2015.09.004.
11. Georgiopoulos G, Chrysohoou C, Vogiatzi G. Vitamins in heart
failure: Friend or enemy? Curr Pharm Des 2017;23(25):3731–42.
doi: 10.2174/1381612823666170321094711.
12. Ayers J, Cook J, Koenig RA, Sisson EM, Dixon DL. Recent
developments in the role of coenzyme Q10 for coronary heart
disease: A systematic review. Curr Atheroscler Rep 2018;20(6):29.
doi: 10.1007/s11883-018-0730-1.
13. Hopper I, Easton K. Chronic heart failure. Aust Prescr
2017;40:128–36. doi: 10.18773/austprescr.2017.044.
14. Cheng HY, Chair SY, Wang Q, Sit JW, Wong EM, Tang SW.
Effects of a nurse-led heart failure clinic on hospital readmission
and mortality in Hong Kong. J Geriatr Cardiol 2016;13(5):415–19.
doi: 10.11909/j.issn.1671-5411.2016.05.013.
15. M
cMurray JJV, Packer M, Desai AS, et al. Angiotensin-neprilysin
inhibition versus enalapril in heart failure. New Eng J Med
2014;371:993–1004. doi: 10.1056/NEJMoa1409077.
 Cardiovascular check Case 2

CASE Question 3

2
Does Kabir need immediate admission to hospital?
Kabir is tired and short of breath

Kabir is a retired metal worker aged 76 years who

presents with fatigue and shortness of breath on exertion
over the past month. He has not had any chest pain, is
not aware of palpitations and has had no syncope. He
does not have a cough or sputum and is a non-smoker.
He does have a past history of hypertension and has
taken lercandipine for several years. Kabir drinks four
stubbies of beer per night. He is overweight, with a body
mass index of 29 kg/m2, but remains quite active,
playing golf regularly and working around the house.

You examine Kabir. He does not appear unwell, is not

short of breath at rest and is not cyanosed or anaemic.
Question 4
You note that he has an irregular pulse at a rapid rate
of 130 beats per minute (bpm). His blood pressure is What other investigations would you do at this stage?
150/80 mmHg. He has some mild peripheral oedema
at the ankles. Kabir’s jugular venous pressure is not
increased, his heart sounds are normal without
murmurs and his chest is clear.

Question 1
What is the most likely diagnosis and how would you confirm it?

Further information

Kabir’s electrocardiogram (ECG) shows AF with a fast

ventricular rate of 130 bpm. You request blood tests, which
reveal that his urea and electrolytes, thyroid function and
blood sugar results are all normal.

You see Kabir immediately after the ECG is performed. You

explain that he has AF – ‘a fast, irregular heart beat’ – and that
it is very common for patients not to be aware of it. Kabir is
very concerned that he may have a heart attack or a stroke.

Question 2 Question 5
What are the causes of atrial fibrillation (AF) and the factors What is the likelihood that Kabir will have a heart attack or
predisposing to it? stroke related to his AF?

9
Case 2 check Cardiovascular

Further information
Question 8
Using an online calculator (eg available at www.mdcalc.com,
What general advice will you give Kabir?
or as a smartphone app), you determine Kabir’s Cardiac
failure or ventricular dysfunction, Hypertension, Age >75
years, Diabetes, Stroke or other embolism (CHADS2) score is
2 and his Cardiac failure or ventricular dysfunction,
Hypertension, Age >65 years, Age >75 years, Diabetes, Stroke
or other embolism, Vascular Disease (CHA2DS2-VASc) score
is 3. Based on these results, his annual risk of stroke is
approximately 3–4%.

Question 6
How can you reduce Kabir’s risk of thromboembolism and
stroke?

Question 9
What determines whether attempts should be made to
restore sinus rhythm, and what management strategies are
available?

Question 7
What are your management priorities for Kabir at this stage?

CASE 2 Answers

Further information
Kabir commences diltiazem sustained-release 180 mg and
apixaban 5 mg twice daily, and an echocardiogram is booked.
An appointment is made for an early consultation with a
specialist physician.
Answer 1
The physical examination is indicative of AF, but the time of
onset is unclear. Kabir does not appear to have significant
cardiac failure (although his cardiac function may be
impaired). AF is a very common arrhythmia and has increasing
prevalence with age.1,2 It is quite common for patients,
particularly older patients, to present without palpitations;
some patients may be completely asymptomatic, particularly
if the rate is controlled.3 A 12-lead ECG is essential to
diagnose an arrhythmia.4 A diagnosis of AF is made when the
rhythm shows irregular RR intervals and no discernible P
waves.4 Kabir appears to have persistent or permanent AF.
For paroxysmal AF, an episode lasting at least 30 seconds is
diagnostic.4 An ECG for Kabir should be performed
immediately if possible.

10

Given this is a new diagnosis of AF, a complete medical
history and evaluation is required, focusing on:
• more details of his symptoms, including shortness of breath,
chest pain, dizziness and syncope on exercise and at rest
• presence of precipitating factors (eg sepsis, recent surgery,
thyrotoxicosis, electrolyte imbalance) and underlying
cardiovascular conditions
• stroke risk and need for anticoagulation.
This will assist with making decisions regarding
immediate management, including hospital admission
and/or specialist referral, as well as long-term
management, which may involve control of ventricular
rate, heart rhythm and anticoagulation.
Answer 2
AF is caused by abnormal electrical activity in the atrium,
particularly starting in the posterior left atrium around the
connections with the pulmonary veins.
Thyrotoxicosis is an uncommon cause of AF, but AF may be
the only clinical manifestation of thyrotoxicosis, so it is
important to exclude it.
AF can be a feature of most forms of heart disease,
including ischaemic heart disease, valvular heart disease
– especially of the mitral valve – and cardiomyopathy.5
However, many patients with AF have no significant
underlying heart disease. This used to be called ‘lone
AF’.6 However, AF incidence is increased with
hypertension, obesity, alcohol use, obstructive sleep
apnoea and diabetes.5
Answer 3
Kabir does not appear to need immediate referral to a
hospital, which would be indicated if he:
• was unwell
• had chest pain
• was short of breath at rest
• had clear signs of cardiac failure with lung crackles.
Alternatively, if Kabir’s AF was symptomatic (ie causing
palpitations) and/or of recent onset (ie <48 hours), it may
be appropriate to consider cardioversion back to sinus
rhythm (which requires general anaesthesia and usually
specialist consultation).5
Answer 4
Kabir needs tests for urea and electrolytes, blood sugar and
thyroid function.4 The test for electrolytes is important
because cardiac medication toxicity may be exacerbated by
alterations in serum potassium. In the absence of chest pain, a
troponin or creatine kinase is not required.
An echocardiogram is very useful and should be ordered;
however, in Kabir’s context this can wait, and should not delay
initiation of treatment.
Cardiovascular check Case 2
Answer 5
Thromboembolism and, in particular, stroke are important
potential consequences of AF, and the risk increases with the
presence of other risk factors as expressed by the CHADS2
and CHA2DS2-VASc scores.7
A heart attack (ie myocardial infarction) is not likely to be
related to AF. If Kabir had chest pain with a rapid heart rate,
he would need to be assessed for coronary artery disease and
would probably require coronary angiography.
Heart failure can be a cause of AF, but ventricular dysfunction
can also be a consequence of a rapid, uncontrolled heart rate
for a prolonged (months) period. This is sometimes referred to
as tachycardia-induced cardiomyopathy. Given Kabir’s
shortness of breath, it is possible that he has ventricular
dysfunction, either as a cause or consequence of his AF. An
echocardiogram will be the best test to assess this.
Answer 6
The risk of thromboembolism would be reduced by 2/3 (to
1–1.5%) by anticoagulation with either warfarin or a direct (or
‘new’) oral anticoagulant (DOAC). Aspirin was used for this
purpose in the past but has little benefit and is no longer
recommended. Other anti-platelet medications, such as
clopidogrel, have not proved to be useful either.
Anticoagulation has been shown to be safe and effective in
reducing stroke in patients with an elevated risk of
thromboembolism as assessed by the CHADS2 and
CHA2DS2-VASc who have a low risk of bleeding. The
bleeding risk can be assessed by the HAS-BLED score
(Hypertension, Impaired Renal Function, Impaired Liver
Function, History of Stroke, History of Bleeding, Labile
International Normalised Ratios [INRs], Age >65 years,
Drugs, Alcohol Consumption). Note that many of the risks
of thromboembolism are also risks for bleeding. In
most patients, the balance of benefit versus risk favours
anticoagulation for a CHA2DS2-VASc score of 2 or more.4
The risk of causing ventricular dysfunction can be reduced by
controlling the ventricular rate.
Answer 7
The priorities are to slow the ventricular rate and initiate
anticoagulation. It is not clear when the AF started – possibly
some weeks or months before. A decision to cardiovert the
patient back to sinus rhythm and then initiate anti-arrhythmic
medicines to maintain sinus rhythm needs assessment – see
below. In general, for older patients who are not symptomatic
of palpitations, it is safer to control the ventricular rate rather
than try to maintain sinus rhythm.4
Ventricular rate control
The ventricular rate in AF is controlled by the atrioventricular
(AV) node; therefore, medications that slow the AV node are
indicated. In the past, digoxin was the medication of first
choice, but it is less effective in controlling the ventricular
rate during exercise and may have side effects.4,5 It is still
used as a second-line medicine.
11
Case 2 check Cardiovascular
The first-line medications are a beta blocker or non-
dihydropyridine calcium antagonist, such as:
• atenolol 25 mg daily, increasing to 50–100 mg daily
• metoprolol 25 mg twice daily, increasing to 100 mg twice daily
• diltiazem sustained-release 180–360 mg
• verapamil 180–480 mg.
Dihydropyridine calcium antagonists (eg amlodipine,
lercandipine) do not act on the AV node so do not provide any
rate control in AF.
Kabir’s peripheral oedema could be a side effect of
lercandipine. A reasonable first choice here would be to swap
it for diltiazem sustained-release 180 mg. Further increases in
medication doses will need to wait until after assessment of
left ventricular function with an ECG.
Anticoagulation
It is recommended that Kabir be commenced on an
anticoagulant such as warfarin or a DOAC (eg dabigatran,
rivaroxaban or apixaban). DOACs have been shown to be
equivalent to warfarin in preventing thromboembolism and
may have a lower risk of causing bleeding.4
In 2019, DOACs are available only on the Pharmaceutical
Benefits Scheme by Authority for AF with an additional
CHADS2 factor. Kabir qualifies for this.
If Kabir commences warfarin, his INR will need regular testing
to confirm a level between 2 and 3 is maintained. This may be
done by a pathology service, a general practitioner or the
patient using a point-of-care device (eg CoaguChek).
Answer 8
Explanation of the abnormal rhythm is important. Lifestyle
modification may be very helpful for some patients,
particularly those with significant symptomatic paroxysmal
AF. Alcohol reduction or abstinence, weight loss, increased
physical activity and control of obstructive sleep apnoea and
hypertension may reduce the frequency of recurrences.
When taking anticoagulation medication, the patient’s
self-care is vital. If Kabir injures himself, he will have
increased bleeding, and if he has a head injury, he may be
at high risk of intracranial bleeding. Explain to Kabir that
he should have a low threshold for presenting to you or to
a hospital emergency department if such a situation
arises. If Kabir requires surgery, the anticoagulant will
need to be managed – not necessarily ceased – both
preoperatively and postoperatively.5
Answer 9
Whether to adopt a rate-control strategy versus a rhythm-
control strategy (ie restoring and maintaining sinus rhythm)
depends on the patient’s symptoms, cardiac function and
comorbidities. There is considerable variation in the
management between patients (and between cardiologists).
Factors favouring a rhythm-control strategy include severe
symptoms, younger age and cardiac dysfunction. Factors
12
favouring a rate-control strategy include lack of symptoms,
older age (>70 years) and previous side effects with anti-
arrhythmic medicines.
Restoration of sinus rhythm may be initially achieved with
direct current reversion under general anaesthesia; however, for
sinus rhythm to be maintained, an anti-arrhythmic medicine
such as sotalol, flecainide or amiodarone is usually needed.4,5
Each of these medicines has side effects and should be used
carefully. Catheter ablation to achieve pulmonary vein isolation
has become increasingly common and effective in achieving
long-term sinus rhythm. 4,5 Catheter ablation requires referral
to a specialist electrophysiologist.
Conclusion
You arrange to review Kabir in three days’ time. His heart rate
has slowed to 100 bpm but remains irregular. He is feeling
less short of breath. You order an echocardiogram to assess
left ventricular dysfunction and refer him to a cardiologist for
further assessment. The echocardiogram shows mild left
ventricular dysfunction. The diltiazem dose is increased to
240 mg daily and his heart rate slows to 80 bpm. Kabir
continues to drink the same amount of alcohol. His exercise
capacity and symptoms improve. In consultation with the
cardiologist, it is decided to continue the ‘rate-control’
strategy with diltiazem and to continue the anticoagulation
with apixaban. A follow-up echocardiogram is booked for
three months’ time.
Resources for patients
• Heart Foundation – Atrial fibrillation, www.heartfoundation.
org.au/your-heart/heart-conditions/atrial-fibrillation
• Better Health Channel – Heart conditions – Atrial
fibrillation, www.betterhealth.vic.gov.au/health/
conditionsandtreatments/heart-conditions-atrial-fibrillation
References
1. Ball J, Carrington MJ, McMurray JJ, Stewart S. Atrial fibrillation:
Profile and burden of an evolving epidemic in the 21st century. Int J
Cardiol 2013;167(5):1807–24. doi: 10.1016/j.ijcard.2012.12.093.
2. Briffa T, Hung J, Knuiman M, et al. Trends in incidence and
prevalence of hospitalization for atrial fibrillation and associated
mortality in Western Australia, 1995–2010. Int J Cardiol
2016;208:19–25. doi: 10.1016/j.ijcard.2016.01.196.
3. Barbarossa A, Guerra F, Capucci A. Silent atrial fibrillation: A critical
review. J Atr Fibrillation 2014;7(3):1138. doi: 10.4022/jafib.1138.
4. Brieger D, Amerena J, Attia J, et al. National Heart Foundation and
the Cardiac Society of Australia and New Zealand: Australian
clinical guidelines for the diagnosis and management of atrial
fibrillation 2018. Heart Lung Circ 2018;27(10);1209–66.
doi: 10.1016/j.hlc.2018.06.1043.
5. Expert Group for Cardiovascular. Atrial fibrillation. In: eTG complete
[Internet]. Melbourne: Therapeutic Guidelines Limited, 2019.
6. Evans W, Swann P. Lone auricular fibrillation. Br Heart
J 1954;16(2):189–94.
7. MDCalc. CHADS2 score for atrial fibrillation stroke risk
[calculator]. Available at www.mdcalc.com/chads2-score-atrial-
fibrillation-stroke-risk [Accessed 20 May 2019]
 Cardiovascular check Case 3

CASE Question 2

3 Vilija presents with

difficulty writing
What components of the physical examination should you
focus on?

Vilija, a female patient aged 78 years, lives at home

with her husband. She is a regular patient of your
practice and independent in her activities of daily living.

Vilija has made an urgent appointment today. She is

concerned that when she attended her social club this
morning she had difficultly signing her name. She felt
that the letters were very small, and she was unable to
control her pen. Vilija is right-hand dominant and a
piano teacher. She also had trouble playing the piano
this morning, which was frustrating for her.

Further information

Your examination reveals Vilija’s blood pressure is

Question 1
166/99 mmHg, with a pulse rate of 50 beats per minute. She
What additional questions would you ask Vilija? has mild dysarthria and some mild dysmetria in her right
upper and lower limbs. There is no dysphasia, neglect or
weakness, and her reflexes are symmetrical and brisk. You ask
Vilija to write a sentence (Figure 1) and draw a clock face to
show a time of 11:10 am (Figure 2).

Figure 1. A sentence written by Vilija at her initial appointment

Question 3
What is your provisional diagnosis and how would you
Further information
manage this patient?
You know Vilija well and know that handwriting would
normally not be difficult for her. Vilija’s husband corroborates
that yesterday she was playing the piano as usual, supporting
Vilija’s claim that the symptoms began today. Vilija continues
to drive, although her husband drove her to the appointment
today. She has a significant past medical history including
atrial fibrillation (AF), hypertension, hypercholesterolaemia
and osteoarthritis.

Her medications include metoprolol 25 mg twice daily orally

and rivaroxaban 20 mg daily orally, treatment for her AF and
stroke prevention.

Vilija recently consulted her dentist regarding some dental

extractions, but he was concerned that she was taking
alendronate (for her osteoporosis) and rivaroxaban. Vilija
consulted her cardiologist, who advised her that she could
safely cease taking rivaroxaban four days before her dental
procedure if there were concerns regarding bleeding from
the procedure.
Further information
Given that Vilija’s symptoms and signs have not resolved, you
are concerned she may have had an acute ischaemic stroke.
You recommend that Vilija should present to a hospital for
further assessment.

13
Case 3 check Cardiovascular
Figure 2. Vilija’s drawing of a clock face showing a time of 11:10 am
Vilija is not keen to go to the hospital and, in particular, would
prefer to have her husband drive her there.
Question 4
How do you explain to Vilija the urgency of her condition and
how would you recommend she get to the hospital?
Further information
You arrange an ambulance for Vilija, and she is taken to the
closest hospital that has a stroke unit.
On presentation, a computed tomography brain scan is
performed that does not demonstrate any acute pathology. A
carotid duplex scan shows no significant stenosis bilaterally
14
but magnetic resonance imaging of the brain reveals a left
basal ganglia infarction with acute infarction of the putamen.
Vilija is discharged from hospital after three days and
presents to you for follow-up. The stroke team has changed
her rivaroxaban to apixaban, another direct oral anticoagulant
(DOAC). She still has some difficulty writing and is frustrated
that she is unable to play the piano.
Question 5
What are your next steps in caring for Vilija?
CASE 3 Answers
Answer 1
When assessing a patient with an uncommon presenting
symptom, a systematic approach is required. From Vilija’s
description of her symptoms, it sounds as though she has
micrographia and possibly a movement disorder. This
neurological symptom prompts further questioning regarding
other neurological symptoms including visual changes,
speech difficulties, weakness and numbness. In particular, the
onset and duration of symptoms should be elicited. Eliciting
history from family members and/or witnesses provides
additional information to establish a more accurate
assessment of the patient.
You should ask Vilija specific questions about her risk factors
for ischaemic stroke, including hypertension,
hypercholesterolaemia, diabetes, AF, smoking and a family
history of stroke. Other risk factors for ischaemic stroke
include oral contraception, hormone replacement therapy or a
history of patent foramen ovale. Vilija has some risk factors for
stroke, and enquiring about her adherence to therapy would
be useful.
Answer 2
A focused neurological examination is recommended, with
the addition of a limited cardiovascular examination. Given
the time restraints in general practice, and the need to
assess this patient urgently, we suggest the following

approach to cerebrovascular examination in primary care
(Box 1; video available at www.youtube.com/watch?v=BBJJ7-
0XE6c&list=PLwCU3RkP8J7aMBnyy9BkinjkrrHdLIuf0&inde
x=17&t=0s&frags=pl%2Cwn).
Box 1. A suggested approach to cerebrovascular
examination in primary care
Alert: Yes/No/Confused
Mental state: Orientation = Time, Person, Place / Where? / Why?
Speech: Slurred (Dysarthria) / Wrong words (Dysphasia)
Confusion: Disorientation or receptive dysphasia (Not
understanding speech)
Vitals: Heart rate (Regular = Yes/No) / Blood pressure /
Temperature / Glucose level
Face
Visual fields: Hemianopia (Yes/No) and both left and right visual
inattention (Middle cerebral artery [MCA] = Cerebral hemisphere)
Smile: Symmetrical – Yes/No (MCA = Cerebral hemisphere)
Extra-ocular movements: Horizontal and vertical planes –
diplopia / abnormal (Vertebrobasilar artery system [VBA] =
Brainstem or cerebellum)
Nystagmus: Yes/No (VBA = Brainstem or cerebellum)
Mouth: ‘Ah’ – Look at soft palate rise – yes or no (VBA = Brainstem)
Tongue extend: Midline / deviated – left and right (VBA = Brainstem)
Arms
Observe
Outstretched arms (eyes open and eyes closed) – Arm drift (MCA
= Cerebral hemisphere)
Finger/nose test: Yes/No (VBA = Cerebellum)
Tone: Normal or increased
Reflexes: Biceps only
Sensation: Touch – left and right (MCA = Cerebral hemisphere)
Sensory inattention: Yes/No (MCA = Cerebral hemisphere)
Legs
Observe
Walk into room: Drag leg? Unsteady? Needs assistance?
(Yes or no for each)
Lift up leg from chair: Yes/No (MCA = Cerebral hemisphere)
Tone: Normal or increased
Reflexes: Knees
Plantars: Up or down
If unsteady walk: Heel to shin – normal or ataxia (VBA = Cerebellum)
Sensation: Touch left/right (MCA = Cerebral hemisphere)
Sensory inattention: Yes/No (MCA = Cerebral hemisphere)
Answer 3
Vilija has a number of risk factors for stroke and has
persistent signs and symptoms. You refer her to an
emergency department via ambulance.
Micrographia is an uncommon presentation of stroke.1–3
The most common symptoms of ischaemic stroke are
facial or arm weakness and dysphasia, with micrographia
more commonly being a sign of Parkinson’s disease.4
However, in Vilija’s case, the acute onset and associated
dysmetria and dysarthria would suggest a suspected acute
ischaemic stroke.
Cardiovascular check Case 3
Answer 4
Vilija and her husband need to have the seriousness of her
condition explained, as all patients with suspected stroke
should be managed as an emergency. The Stroke
Foundation recommends that patient are transferred by
ambulance services to a hospital with reperfusion therapies
and a stroke unit.5
Public awareness of the signs and symptoms of stroke in
Australia has improved with the success of the Stroke
Foundation’s Face, Arms, Speech, Time (FAST) campaign
(https://strokefoundation.org.au/About-Stroke/Stroke-
symptoms).6
As a general practitioner (GP), your role is to provide ongoing
education to patients in recognising stroke signs and
symptoms, particularly for patients with an increased risk of
cerebrovascular disease.7 This role also extends to educating
reception staff about stroke symptom recognition (FAST) and
to triage calls from patients with suspected stroke symptoms
to the ambulance service.5
For patients in remote and rural areas who present with stroke
symptoms, access to telehealth services may be available.8
Answer 5
All patients with AF who have had a stroke or transient
ischaemic attack (TIA) should be prescribed long-term
anticoagulation medication.9 It is recommended that patients
with normal renal function and non-valvular AF be
commenced on a DOAC; in this case, Vilija has been
prescribed apixaban by the stroke team.10
Following Vilija’s discharge after her ischaemic stroke,
secondary prevention falls to you as her GP. Growing evidence
suggests that cognitive decline can occur in the five years
following TIA or a small stroke presentation; therefore, it is
important to continue management of risk factors to prevent
further infarction.11 This involves the management of risk
factors for recurrent stroke including addressing smoking,
diet, physical activity, obesity and alcohol.5 Patients should
also be screened for depression.5 Blood pressure, antiplatelet
therapy/anticoagulation, cholesterol and diabetes can be
managed comprehensively through a GP Chronic Disease
Management Plan and a Team Care Arrangement. Vilija may
be taking multiple new medications following discharge. A
Home Medicines Review with the community pharmacist
could address her adherence to therapy and Vilija’s (and her
husband’s) understanding of her condition.
Conclusion
Vilija required ongoing rehabilitation with outpatient speech
therapy and occupational therapy, as she was keen to return
to playing her piano. Patients are instructed not to return to
driving private vehicles for at least four weeks post-stroke.12
All patients should be screened for depression following a
stroke.5 In this case, Vilija had found her inability to play the
piano or drive frustrating. Groups such as those listed by the
Stroke Foundation can provide peer support, and patients
15
Case 3 check Cardiovascular

discharged from stroke units are offered a My Stroke Journey

Information Pack, a resource to assist in the transition back to
the community (https://strokefoundation.org.au/What-we-
do/Support-programs/My-Stroke-Journey).13

Resources for patients

• Stroke Foundation – My Stroke Journey, https://
strokefoundation.org.au/What-we-do/Support-programs/
My-Stroke-Journey

References
1. Capone F, Pilato F, Profice P, Pravatà E, Di Lazzaro V. Neurological
picture. A case of stroke induced micrographia. J Neurol
Neurosurg Psychiatry 2009;80(12):1356. doi: 10.1136/
jnnp.2009.175208.
2. Marinella MA. Subcortical stroke presenting as micrographia. Am
J Emerg Med 2007;25(1):89–90. doi: 10.1016/j.ajem.2006.03.033.
3. Montero Escribano P, Catalán Alonso MJ, Alonso French F,
López Valdés E, García Ramos R, Parees Moreno I. Isolated
micrographia following stroke [abstract]. Mov Disord
2016;31(Suppl 2).
4. Inzelberg R, Plotnik M, Harpaz NK, Flash T. Micrographia, much
beyond the writer’s hand. Parkinsonism Relat Disord 2016;26:1–9.
doi: 10.1016/j.parkreldis.2016.03.003.
5. The Stroke Foundation. Clinical guidelines for stroke management.
Melbourne: Stroke Foundation, 2017.
6. Bray JE, Johnson R, Trobbiani K, et al. Australian public’s
awareness of stroke warning signs improves after national
multimedia campaigns. Stroke 2013;44(12):3540–43. doi: 10.1161/
STROKEAHA.113.002987.
7. The Royal Australian College of General Practitioners. Guidelines
for preventive activities in general practice. 9th edn. East
Melbourne, Victoria: RACGP, 2018. Available at www.racgp.org.
au/download/Documents/Guidelines/Redbook9/17048-Red-
Book-9th-Edition.pdf [Accessed 6 June 2019].
8. Cadilhac DA, Moloczij N, Denisenko S, et al. Establishment of an
effective acute stroke telemedicine program for Australia: Protocol
for the Victorian Stroke Telemedicine project. Int J Stroke
2014;9(2):252–58. doi: 10.1111/ijs.12137.
9. Saxena R, Koudstaal PJ. Anticoagulants for preventing stroke in
patients with nonrheumatic atrial fibrillation and a history of stroke
or transient ischaemic attack. Cochrane Database Syst Rev
2004;(2):CD000185.
10. Ruff CT, Giugliano RP, Braunwald E, et al. Comparison of the
efficacy and safety of new oral anticoagulants with warfarin in
patients with atrial fibrillation: A meta-analysis of randomised
trials. Lancet 2014;383(9921):955–62. doi: 10.1016/s0140-
6736(13)62343-0.
11. Pendlebury ST, Rothwell PM. Incidence and prevalence of
dementia associated with TIA and stroke: Analysis of the
population-based Oxford Vascular Study. Lancet Neurol
2019;18(3):248–58. doi: 10.1016/S1474-4422(18)30442-3.
12. Austroads and National Transport Commission (NTC) Australia.
Assessing fitness to drive: For commercial and private vehicle
drivers: 2016 medical standards for licensing and clinical
management guidelines [amended 2017]. 5th edn. Sydney, NSW:
Austroads, NTC Australia, 2017.
13. The Stroke Foundation. My Stroke Journey. Melbourne: Stroke
Foundation, 2017. Available at https://strokefoundation.org.au/
What-we-do/Support-programs/My-Stroke-Journey [Accessed 15
May 2019].

16
 Cardiovascular check Case 4

CASE Further information

4
Nicola’s progressive history of breathlessness, transthoracic
Nicola is short of breath echocardiogram results suggestive of pulmonary
hypertension, and underlying risk factor of scleroderma (which
results in at least 10% of patients developing Group 1
Nicola, aged 66 years, is a retired nurse with an eight-
pulmonary arterial hypertension [PAH] across their lifetime)
year history of limited scleroderma who presents to
are all suggestive of the development of clinically significant
you with 12 months of progressive exertional
pulmonary hypertension.2
shortness of breath. She is breathless after
100 metres of walking on flat ground but comfortable
Question 3
at rest. She has no associated cough, chest pain or
fever; she has noticed mild ankle swelling over recent What are the next steps in your assessment?
months. On clinical examination, Nicola has features
of limited scleroderma, is in sinus rhythm, has a loud
second heart sound, no basal crepitations and 1+ of
mild pitting peripheral oedema to her mid tibia.

Question 1
What investigations would you conduct at this stage?

Further information

You know that screening for PAH is an important part of

optimal clinical care for patients with scleroderma.

Question 4
Further information
Outline the rationale and your key recommendations for
You arrange a full blood count, bedside spirometry and a
screening for Nicola.
transthoracic echocardiogram. The full blood count shows no
anaemia, and bedside spirometry is unremarkable. The
transthoracic echocardiogram shows results consistent with
pulmonary hypertension, with a systolic pulmonary artery pressure
estimate of 58 mmHg, a moderately dilated right ventricle, a short
pulmonary acceleration time, normal left-sided cardiac
assessment and no significant valvular heart disease.

Question 2
What is meant by pulmonary hypertension? Outline the key
classification criteria, which consider the pathophysiology,
treatment options and prognosis.

Further information

You refer Nicola to an expert pulmonary hypertension centre.

The ventilation–perfusion scan for pulmonary embolism is
negative, and a high-resolution computed tomography (CT)
scan does not reveal any parenchymal lung disease. Pulmonary
function tests (PFTs) show normal spirometry, normal static
lung volumes and reduced diffusing capacity for carbon

17
Case 4 check Cardiovascular
monoxide (46% predicted). A right heart catheter showed
elevated pulmonary artery pressure (mean pulmonary artery
pressure = 40 mmHg), normal pulmonary artery wedge
pressure (12 mmHg) and cardiac output (5.1 L/min), and
elevated pulmonary vascular resistance (5.5 Wood units).
Based on these investigations, Nicola is diagnosed with Group
1 PAH due to limited scleroderma.
Question 5
What specific pharmacological therapies are available to treat
pulmonary hypertension? When should these agents be used
to treat pulmonary hypertension?
Question 6
What is the current pharmacotherapeutic approach to
managing Group 1 PAH?
Question 7
While specific pharmacotherapies for Nicola’s Group 1 PAH
will be directed by the expert pulmonary hypertension centre,
how can you, as the general practitioner, help with
co-management of Nicola?
18
CASE 4 Answers
Answer 1
The clinical assessment is suspicious for the development of
pulmonary hypertension, although interstitial lung disease and
anaemia are common in scleroderma. A full blood count and
bedside spirometry should be arranged, with view to
performing a transthoracic echocardiogram.
Answer 2
Pulmonary hypertension refers to an abnormally elevated
pulmonary arterial pressure and is caused by a variety of
different conditions and mechanisms.1,2 Haemodynamically,
pulmonary hypertension is defined as a mean pulmonary
artery pressure (mPAP) >25 mmHg at right heart
catheter, which is well above what is considered ‘normal’
(mPAP 14.0 mmHg ± 3.3 mmHg).
The clinical consequences of pulmonary hypertension vary
from no symptoms to minimal symptoms, usually due to
milder disease and cardiopulmonary adaptation, through to
marked dyspnoea and fatigue associated with progressive
disease and right heart failure.
Importantly, there are distinctly different mechanisms that can
drive elevations in pulmonary artery pressure, which have major
treatment and prognostic implications. Therefore, it is vital to
determine the main groups of pulmonary hypertension. The
classification of pulmonary hypertension is as follows:
1. Group 1 or PAH. In this group, the distal pulmonary arterioles
(and some venules) obstruct and obliterate over time,
resulting in an increased pulmonary vascular resistance.
Although rare, affecting up to 100 patients per million,
this group currently has the most available treatment
options.2 Idiopathic and autoimmune connective tissue
diseases are the two most common causes, respectively.
2. Group 2 or pulmonary hypertension due to left heart
disease. Referred to as post-capillary pulmonary
hypertension or pulmonary venous hypertension,
this group is the most common cause of pulmonary
hypertension and usually reflects conditions that cause
dysfunction of the left ventricle or valvular problems.
3. Group 3 or pulmonary hypertension due to lung disease
or hypoxia. In these conditions, primary respiratory
conditions such as chronic obstructive pulmonary disease,
interstitial lung disease and obstructive sleep apnoea are
the chief causes. Notably, only a small number of patients
with these conditions develop pulmonary hypertension,
but a history of these conditions often signifies a worse
prognosis.
4. Group 4 or pulmonary hypertension due to chronic
thomboembolic disease (CTEPH) reflects non-
resolving occlusive pulmonary thromboembolic disease.
Importantly, surgical resection can greatly improve the
condition, and select vasodilators may be helpful.
5. Group 5 or pulmonary hypertension due to multifactorial
or unclear mechanisms.

Answer 3
It is recommended that Nicola is referred to an expert
pulmonary hypertension centre. These centres, which are
usually multidisciplinary, bring together coordinated expertise in
the assessment and management of pulmonary hypertension.
A detailed assessment would determine the main factors
contributing to Nicola’s pulmonary hypertension. Aside from a
clinical assessment, this will usually involve detailed review of
the echocardiogram; high-resolution CT of the chest to
evaluate for significant parenchymal lung disease, ventilation–
perfusion study to evaluate for chronic thromboembolic
pulmonary embolism (as distinct from acute pulmonary
embolism), and PFTs to evaluate for parenchymal disease and
gas transfer. Additional tests such as autoimmune serology
(eg anti-nuclear antibody and extractable nuclear antigen) and
a sleep study are often considered.
A right heart catheter procedure, while invasive, is considered a
safe and essential test with a much lower morbidity when
compared with the much more commonly performed left heart
catherisation for coronary artery disease. It is also a requisite
for accessing high specialised Group 1 PAH (and less
commonly Group 4 CTEPH) therapy via the Pharmaceutical
Benefits Scheme (PBS).3 The haemodynamic variables also
inform the likely aetiology, especially when coupled with a
detailed assessment, and provide important prognostic
information, including response to treatment.
Answer 4
Scleroderma is an autoimmune connective tissue disease
characterised by fibrosis and vasculopathy affecting the skin
and internal organs. At least one in 10 patients with
scleroderma will develop PAH during their lifetime, and as a
treatable complication with an untreated mortality of 50% at
12 months, Australian and international guidelines recommend
annual screening for pulmonary hypertension with a
transthoracic echocardiogram.4 A systolic pulmonary artery
pressure ≥40 mmHg is a useful cut-off point to keep in mind,
though echocardiography can underestimate and overestimate
pressures and must be considered with the clinical features.
Additional tests, such as a disproportionately low diffusing
capacity of the lung for carbon monoxide on full PFT, are also
very useful. Importantly, non-invasive tests can only suggest
pulmonary hypertension, and right heart catheter is necessary
for a definitive diagnosis (Table 1).
Answer 5
Currently, four main classes of pulmonary hypertension–
specific agents are available in Australia. These are:
• endothelin receptor 1 antagonists (bosentan, macitentan
and ambrisentan)
• phosphodiesterase type-5 inhibitors (sildenafil and tadalafil)
• soluble guanylate cyclase stimulators (riociguat)
• prostacyclin derivatives (epoprostenol and iloprost).
Cardiovascular check Case 4
Table 1. Important investigations in the work-up
of pulmonary hypertension
Investigation Key utility and interpretation
Echocardiography This is the most important screening test
for pulmonary arterial hypertension (PAH).
Echocardiography will reveal elevated
pulmonary artery pressure and signs of right
ventricular dysfunction. Left ventricular systolic
function is usually preserved.
Electrocardiogram Signs of right heart strain are seen in PAH.
(ECG) Ischaemic changes may suggest coronary artery
disease. Normal ECG does not exclude PAH.
Chest X-ray Enlarged central pulmonary arteries and/or
enlarged right heart chambers occur in PAH.
Ventilation– Mismatched perfusion defects suggest
perfusion thromboembolic disease. Ventilation–perfusion
scintigraphy scintigraphy is more sensitive than computed
tomography (CT) pulmonary angiogram in
detecting chronic thromboembolic PAH.
Computed Enlarged main pulmonary artery and enlarged
tomography (CT) right heart chambers occur in PAH. CT
pulmonary angiogram may detect signs
of chronic thromboembolic disease. Lung
disease can be detected with high-resolution
chest CT.
Lung function test Isolated reduction in diffusing capacity
of the lungs for carbon monoxide is the
classic pattern seen in PAH. Mild restrictive
ventilatory defect may be seen in PAH. Severe
derangement in spirometry or lung volumes
suggests lung disease.
Sleep study Sleep disordered breathing and nocturnal
desaturation are seen in PAH.
Six-minute walk A simple test to assess exercise capacity and
distance monitor therapeutic response, the six-minute
walk distance is associated with prognosis
in PAH.
Connective tissue These tests search for an underlying cause
disease screen of PAH.
and human
immunodeficiency
virus serology
N-terminal pro- Elevated NT-pro BNP occurs in PAH
b-type natriuretic because of right ventricular strain. NT-pro
peptide (NT-pro BNP is prognostic and used to monitor the
BNP) patient.
Coronary This test is used if coronary artery disease is
angiography suspected clinically or there are risk factors
for coronary artery disease.
Right heart This test is required for definitive diagnosis
catheterisation of PAH. Acute vasoreactivity testing can be
performed with inhaled nitric oxide.
19
Case 4 check Cardiovascular

These medications all exert vasodilatory action on the
pulmonary arteries (Table 2).
In general, these medicines should only be used to treat Group 1
PAH. These medicines are non-efficacious and potentially
harmful when used to treat other groups of pulmonary
hypertension. Therefore, accurate diagnosis is paramount, and it
is recommended that patients undergo diagnostic assessment
and treatment at an expert pulmonary hypertension centre. In
fact, only designated pulmonary hypertension centres are
allowed to prescribe these therapies via the PBS Specialised
Drug Access Scheme.
For patients with non–Group 1 PAH, therapy is directed at the
underlying cause of pulmonary hypertension, such as
optimising left ventricular function and treating lung disease,
as appropriate.
Answer 6
For patients diagnosed with Group 1 PAH, the current
standard of care is combination therapy.5 Agents from
different classes are combined to maximise therapeutic
benefit (with the exception of combining soluble guanylate
cyclase stimulators and phosphodiesterase type-5 inhibitors,
which is contraindicated because of systemic hypotension
and no evidence of positive risk–benefit ratio). There is also
good evidence that combination therapy should be used at the
time of diagnosis, rather than waiting for deterioration before
additional agents are added.2
Patients must be reviewed regularly at their pulmonary
hypertension expert centre. At each visit, patients will usually
undergo an echocardiogram, six-minute walk test and
measurement of N-terminal pro b-type natriuretic peptide. If
required, a repeat right heart catheter will be performed.
Additional treatment can be introduced if treatment targets
are not reached. The aim is to ensure that the patient has
minimal or mild symptoms, good exercise capacity and no
signs of right heart failure. Patients who are potentially
eligible for lung transplantation should be referred if the
disease is not controlled despite maximal therapy.
Answer 7
Nicola should receive an annual influenza vaccination and be
considered for the pneumococcal polyvalent vaccine. She will
require diuretics for relief of symptoms caused by her right
heart failure. Although patients with PAH traditionally receive

Table 2. Specific pulmonary arterial hypertension therapies available via the Pharmaceutical Benefits Scheme

Drug class Generic name Route/dosage Common side effects/comments

Prostacyclins Epoprostenol Continuous Tachycardia, bradycardia, nervousness, chest pain, fever, myalgia, abdominal pain,
intravenous; up to pain at injection site
30 ng/kg/min Catheter-related infections

Iloprost Inhaled; up to 5 mcg Fainting, dyspnea, cough, trismus

6–9 times/day Short half-life requires frequent inhalations

Endothelin Bosentan Oral; 125 mg twice Fatigue, itch, muscle cramps, palpitations, hepatotoxicity (transaminitis); may
antagonists daily require cessation in ~5% of patients
Teratogenic

Ambrisentan Oral; 5 mg Anaemia, nasopharyngitis, fluid retention, palpitations, constipation

(maximum Teratogenic
10 mg) daily

Macitentan Oral; 10 mg daily Anaemia, nasopharyngitis, fluid retention, cholelithiasis, hypotension,

thrombocytopaenia, influenza, itch, insomnia, hepatotoxicity (transaminitis)
Teratogenic

Phosphodiesterase Sildenafil Oral; 20 mg three Headache, flushing, nasal congestion (nosebleeds), dizziness, visual disturbance
5 inhibitors times daily Must not be combined with nitrates (severe hypotension)
Drug–drug interaction with bosentan via CYP3A4; concomitant administration
decreases serum levels of both drugs

Tadalafil Oral; 40 mg daily Hypotension, nausea, vomiting, blurred vision, increased uterine bleeding
Must not be combined with nitrates (severe hypotension)

Soluble guanylate Riociguat Oral; up to 2.5 mg Hypotension, palpitations, peripheral oedema, bleeding (nosebleeds and serious
cyclase stimulator three times daily respiratory tract bleeding), anaemia, reduced haemoglobin, headache, dizziness,
nasal congestion, gastro-oesophageal reflux disease, dyspepsia, dysphagia, nausea,
vomiting, diarrhoea, abdominal pain, constipation
Must not be combined with nitrates or phosphodiesterase 5 inhibitors because of
increased risk of symptomatic hypotension
May cause fetal harm; contraindicated in pregnancy.

20
 Cardiovascular check Case 4

anticoagulation, the evidence for this is weak. In patients with

high bleeding risk (such as patients with systemic sclerosis
who have reflux oesophagitis and vascular ectasias of the
bowel), anticoagulation should be avoided. PAH can affect
women of child-bearing age, and pregnancy must be avoided
given the high risk of poor maternal and fetal outcomes.
Furthermore, endothelin-1 antagonists are teratogenic.
Oestrogen-containing contraceptives should be avoided
because of the increased risk of venous thromboembolism.
Depot progesterone and intra-uterine devices are acceptable
forms of contraception. If a patient requires elective surgery, it
is recommended that this be coordinated with the expert
pulmonary hypertension centre, and surgery should ideally be
performed at the expert pulmonary hypertension centre in
case of complications. Patients should be encouraged to be
physically active. Most expert pulmonary hypertension centres
offer pulmonary/cardiac rehabilitation so patients can
undertake supervised structured exercise.6 Finally, there is a
significant psychological burden associated with a potentially
life-threatening disease such as PAH, and psychological
support is best offered when necessary.

References
1. Moonen A, Thakkar V, Rachael C, Lau E. Pulmonary hypertension:
What you need to know. Cardiology today 2018;8(2):64–73.
2. Galiè N, Humbert M, Vachiery JL, et al. 2015 ESC/ERS Guidelines
for the diagnosis and treatment of pulmonary hypertension: The
Joint Task Force for the Diagnosis and Treatment of Pulmonary
Hypertension of the European Society of Cardiology (ESC) and
the European Respiratory Society (ERS): Endorsed by: Association
for European Paediatric and Congenital Cardiology (AEPC),
International Society for Heart and Lung Transplantation (ISHLT).
Eur Respir J 2015;46(4):903–75. doi: 10.1183/13993003.01032-2015.
3. Department of Human Services. Pulmonary hypertension –
arterial. Canberra: DoHS, 2019. Available at www.humanservices.
gov.au/organisations/health-professionals/services/medicare/
written-authority-required-drugs/drug-program-or-condition/
pulmonary-hypertension-arterial [Accessed 4 June 2019].
4. Lau EMT, Celermajer DS, Keogh A, Thakkar V. Screening
of pulmonary arterial hypertension. Semin Respir Crit Care
Med 2017;38(5):596–605. doi: 10.1055/s-0037-1606202.
5. Klinger JR, Elliott CG, Levine DJ, et al. Therapy for pulmonary
arterial hypertension in adults: Update of the CHEST Guideline
and Expert Panel Report. Chest 2019;155(3):565–86. doi: 10.1016/j.
chest.2018.11.030.
6. Lavender M, Chia KS, Dwyer N, et al. Safe and effective exercise
training for patients with pulmonary arterial hypertension: Putting
current evidence into clinical practice. Expert Rev Respir
Med 2018;12(11):965–77. doi: 10.1080/17476348.2018.1527687.

21
Multiple choice questions check Cardiovascular

ACTIVITY ID 161065 Question 2

Which one of the following is the definitive
Cardiovascular investigation to diagnose heart failure?

This unit of check is approved for six Category 2 A. Chest X-ray

points in the RACGP QI&CPD program. The
B. Computed tomography coronary angiography
expected time to complete this activity is three
hours and consists of: C. Echocardiogram

• reading and completing the questions for each D. Blood screening for cardiac enzymes
case study

–– you can do this on hard copy or by logging on Further information

to the gplearning website, http://gplearning.
You ask Francis about his symptoms, and he says he
racgp.org.au
feels like he is slightly limited in his daily activities, but
• answering the following multiple choice questions does not have any symptoms when he is relaxing.
(MCQs) by logging on to the gplearning website,
http://gplearning.racgp.org.au

–– you must score ≥80% before you can mark the Question 3
activity as ‘Complete’
Which of the following ratings of the New York Heart
• completing the online evaluation form. Association classification is the most appropriate to
describe Francis’s symptoms?
You can only qualify for QI&CPD points by
completing the MCQs online; we cannot process A. Class I
hard copy answers.
B. Class II
If you have any technical issues accessing this
C. Class III
activity online, please contact the gplearning
helpdesk on 1800 284 789. D. Class IV

If you are not an RACGP member and would like to

access the check program, please contact the
Case 2 – Haleema
gplearning helpdesk on 1800 284 789 to purchase
access to the program. Haleema, aged 72 years, has recently been diagnosed
with atrial fibrillation (AF). She is having a difficult
time adjusting to her diagnosis and comes to you for
advice on how she can best modify her lifestyle to
Case 1 – Francis manage her symptoms.

Francis, aged 79 years, has recently been diagnosed with

cardiac asthma. You note he has marked ankle oedema and
tachycardia. Combined with Francis’s age, these factors lead Question 4
you to suspect a diagnosis of heart failure. You decide to
Incidence of atrial fibrillation is not increased by:
perform further tests to clarify the diagnosis.
A. alcohol use

B. hypotension
Question 1
C. obstructive sleep apnoea
Which one of the following results for a b-type natriuretic peptide
(BNP) estimation would rule in a diagnosis of heart failure? D. obesity.

A. <300 ng/L
Further information
B. >450 ng/L
Your management priorities for Haleema are to slow
C. >900 ng/L
her ventricular rate and reduce the frequency of
D. >1800 ng/L recurrences of paroxsysmal AF.

22
 Cardiovascular check Multiple choice questions

C. At least three weeks

Question 5
D. At least four weeks
Which one of the following is a first-line medication for
ventricular rate control?

A. Rivaroxaban Case 4 – Micah

B. Amlodipine Micah, aged 60 years, has a history of limited scleroderma
and comes to see you complaining of being out of breath after
C. Lercandipine
her morning walk. You conduct a clinical assessment and the
D. Diltiazem results are suggestive of pulmonary hypertension.

Question 6 Question 9
Which one of the following would not be helpful to reduce the Which one of the following tests would be recommended to
frequency of recurrences of paroxysmal AF? confirm pulmonary hypertension?

A. Alcohol reduction A. 12-lead electrocardiogram

B. Decreased physical activity B. Ventilation–perfusion scintigraphy

C. Management of hypertension C. Lung function test

D. Weight loss D. Right heart catheter

Case 3 – Alfie Question 10

Alfie, aged 70 years, has been recently diagnosed as having an For patients with scleroderma, screening for pulmonary
acute ischaemic stroke and has come to see you for a follow-up hypertension is recommended:
appointment after discharge from the hospital. He comments
A. every three months
to you that he was surprised by his diagnosis as his symptoms
were not what he understood were ‘typical’ for stroke. B. every six months

C. every year

Question 7 D. every two years.

Which of the following is an uncommon presentation of stroke?

A. Dysphasia

B. Ataxia

C. Dysarthria

D. Micrographia

Further information

Alfie has recovered well from his stroke. He likes to go to a

local social club to meet with his friends, but he is worried he
will not be able to get there if he cannot drive his car.

Question 8
After having a stroke, how long should a patient wait before
returning to drive a private vehicle?

A. At least one week

B. At least two weeks

23
Independent learning program for GPs

Independent learning program for GPs