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name stages of cardiac cycle, and the role of atrial kick,? When do chambers dilate? Why do
cardiac chamber walls hypertrophy?

The cardiac cycle refers to the events that occur between heart beats and can be considered to have 5 phases:
1. late diastole: ventricles fill passively as both chambers are relaxed
2. atrial systole: atria contract and force additional blood into the ventricles (also known as ‘atrial kick’)
3. isovolumetric ventricular contraction: ventricular contraction begins pushing the AV valves closed but not creating enough pressure to open the pulmonary/aortic valves (S1 – the first heart sound, is made by the closing of the AV valves
4. ventricular ejection: ventricular pressure rises and exceeds that of arterial pressure causing the opening of the semilunar valves and ejection of blood
5. isovolumic ventricular relaxation: pressure in the ventricles falls as they begin to relax. The back flow of blood into the cusps of the semilunar valves closes them (S2 – second heart sound) while also supplying blood to the coronary arteries.
Answer: Chambers dilate due to volume overload (increased end diastolic volume) --> excessive preload
answer: Cardiac walls undergo hypertrophy due to? due to pressure overload ((hypertension, stenosis etc)

When do cardiac chambers dilate? (Volume overload)
Volume overload equates to an excessive preload, which affects how efficiently the heart can eject blood. The frank-starling law dictates that the greater end-diastolic volume (preload) present, the greater potential for more forceful ventricular contraction. However, this is only true up to a certain point; as the myocardium becomes excessively stretched (dilated), myofibrils (within sarcomeres) are unable to form cross-bridges. This occurs in volume overload leading to systolic dysfunction and cardiac failure.
To compensate, sarcomeres are added in series with existing sarcomeres, increasing the number of cross bridges formed. This is known as eccentric hypertrophy, where chamber volume enlarges without a relative increase in wall thickness. This helps the ventricle resist over-dilating in diastole when challenged by volume overload.
Causes include congenital defects (patent ductus arteriosus, atrial and septal defects), valvular disorders (stenosis and regurgitation), excessive alcohol consumption, iron overload (haemochromatosis), postpartum, hyperthyroidism, post-viral and certain drugs (i.e. doxorubicin).

Why do cardiac chamber walls hypertrophy? (Pressure overload)
Pressure overload equates to an excessive afterload. In affect, the ventricles need to overcome a greater systolic pressure to eject blood. To achieve this, concentric hypertrophy develops whereby wall thickness increases without chamber enlargement (sarcomeres are added in parallel). A positive inotropic effect results as myocardial contractility increases in strength and is able to overcome the afterload.
However, increased wall thickness without chamber enlargement can lead to low stroke volume due to a smaller end-diastolic volume. This is referred to as diastolic dysfunction and is precipitated by the rigid hypertrophied myocardium.
Commonly seen in chronic arterial hypertension or obstruction to left ventricular outflow (i.e. coarctation of the aorta). Also caused by aortic stenosis, pulmonary stenosis and pulmonary hypertension.


explain the basics of micro circulation and fluid balance?

Haemodynamics of Circulation (including microcirculation & fluid balance)
- Blood flow through the heart is as follows:
 Left atrium (mitral valve) Left ventricle (aortic valve)  aorta  body  vena cava  right atrium (tricuspid valve)  right ventricle (pulmonary valve)  pulmonary artery  lungs  pulmonary veins  left atrium
- There are 3 major types of blood vessels
 Arteries – carry blood away from the heart (elastic, muscular, arterioles)
 Capillaries – small blood vessels that are responsible for exchange of material
 Venous system – carry blood towards the heart (venules, veins)

Microcirculation & Fluid Balance
- Capillary beds provide microcirculation: blood flow from arteriole to venule
- The amount of blood entering a capillary bed is regulated by vasomotor fibres & local chemicals
- Nutrient and gas exchange occurs by diffusion along a concentration gradient
- The relative amount of extracellular fluid between plasma & interstitial space is determined by balance of hydrostatic & colloid osmotic pressures across capillary membrane:


How does oedema form? (list mechanisms) Common causes of pedal oedema? Common causes of
pulmonary oedema? 

Six factors can contribute to the formation of edema:

1) increased hydrostatic pressure;
2) reduced colloidal or oncotic pressure within blood vessels;
3) increased tissue colloidal or oncotic pressure;
4) increased blood vessel wall permeability (e.g., inflammation);
5) obstruction of fluid clearance in the lymphatic system;
6) changes in the water retaining properties of the tissues themselves. Raised hydrostatic pressure often reflects retention of water and sodium by the kidney

Generation of interstitial fluid is regulated by the forces of the Starling equation. Hydrostatic pressure within blood vessels tends to cause water to filter out into the tissue. This leads to a difference in protein concentration between blood plasma and tissue. As a result, the colloidal or oncotic pressure of the higher level of protein in the plasma tends to draw water back into the blood vessels from the tissue.

common causes of pedal oedema?
- The most common cause of pedal edema is increased hydrostatic pressure, as occurs in right-sided heart failure (increased pressure in RV causes blood to backup in RA and systemic system)
- Increased blood concentration in capillary --> blood ‘pushed out’ into the interstitium
- Most commonly occurs in legs/feet due to the effects of gravity
(also renal failure, nephrotic syndrome, liver disease, diuretic induced)

Common causes of pulmonary oedema?

Pulmonary edema is fluid accumulation in the tissue and air spaces of the lungs. It leads to impaired gas exchange and may cause respiratory failure. It is due to either failure of the left ventricle of the heart to remove blood adequately from the pulmonary circulation (cardiogenic pulmonary edema), or an injury to the lung parenchyma or vasculature of the lung (noncardiogenic pulmonary edema).

--> Classically it is cardiogenic (left ventricular) but fluid may also accumulate due to damage to the lung. This damage may be direct injury or injury mediated by high pressures within the pulmonary circulation. When directly or indirectly caused by increased left ventricular pressure pulmonary edema may form when mean pulmonary pressure rises from the normal of 15 mmHg to above 25 mmHg.


What are the upstream and downstream effect of
1) valvular regurgitation? (on auscultation) aortic/pulmonary regurgitation
2) stenosis (aortic and mitral)

3) what would you hear on auscultation for each

valvular regurgitation:
Mitral regurgitation:
The symptoms associated with Mitral regurgitation are symptoms of acute decompensated congestive heart failure (i.e. shortness of breath, pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea, as well as symptoms of cardiogenic shock (i.e., shortness of breath at rest).

Aortic regurgitation:
Aortic insufficiency (AI), also known as aortic regurgitation (AR), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle. As a consequence the cardiac muscle is forced to work harder than normal
Symptoms include (from back log into the left ventricle: dyspnoea, orthopnea, PND, volume overload and hypertrophy

Aortic stenosis:
The three main symptoms of aortic stenosis are loss of consciousness, anginal chest pain and shortness of breath with activity or other symptoms of heart failure such as shortness of breath while lying flat, episodes of shortness of breath at night, or swollen legs and feet
--> can lead to angina from hypertrophy of the cardiac tissue decreasing the ability of the heart to supply blood to itself While the muscular layer of the left ventricle thickens, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may not receive enough blood supply to meet its oxygen requirement
--> congestive cardiac failure due to a combination of left ventricular hypertrophy with fibrosis, systolic dysfunction (a decrease in the ejection fraction) and diastolic dysfunction (elevated filling pressure of the LV).
--> syncope: due to decreased ejection fraction thus decreasing blood supply to brain

Mitral valve stenosis: Signs and symptoms
Heart failure symptoms (end stage), such as dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea (PND)
Palpitations, Chest pain,Hemoptysis
Thromboembolism in later stages when the left atrial volume is increased (i.e., dilation). The latter leads to increase risk of atrial fibrillation, which increases the risk of blood stasis (motionless). This increases the risk of coagulation. (this is due to increaed left atrial pressure causing AF)hen atrial fibrillation develops, the atrial kick is lost (since it is due to the normal atrial contraction)

What would be heard on auscultation to different murmurs?
aortic regurgitation auscultation:Soft S2: Decrescendo high-pitched diastolic murmur begins after S2 (early diastolic murmur)

Aortic stenosis: crescendo decrescendo (ejection systolic murmur)

Mitral/tricuspid regurgitation: pan-systolic S1-S2

Mitral stenosis: mid diastolic (opening snap)

By area to auscultate:
aortic area: ejection type murmur (aortic stenosis, flow murmur)
Pulmonic area:ejection type murmur: pulmonary stenosis (flow murmur)
Tricuspid area: pan-systolic murmur: triscuspid regurgitation,VSD, also mid to late diastolic (triscupid stenosis)
Mitral area: Pansystolic murmur (mitral regurgitation), mid to late diastolic (mitral stenosis)

Left sternal border: early diastolic murmur (aortic reguritation and pulmonic regurgitation)


what are the effects of tachycardia? hyper dynamic state?

How does pulmonary tension develop? what is the clinical consequences?

What causes AF and what are the consequences?

- Increased heart rate (due to increased rate of ventricular contraction)
- Usually results from increased sympathetic stimulation to meet the body’s increasing needs (eg. during exercise) or to compensate for a decreased cardiac output (eg. in left-heart failure)

Hyper dynamic state: Hyperdynamic circulation is abnormally increased circulatory volume. Systemic vasodilation and the associated decrease in peripheral vascular resistance results in decreased pulmonary capillary wedge pressure and decreased blood pressure, presenting usually with a collapsing pulse, but sometimes a bounding pulse. In effort to compensate the heart will increase cardiac output and heart rate, which accounts for the increased pulse pressure and sinus tachycardia.The condition sometimes accompanies septic shock, preeclampsia, and other physiological and psychiatric conditions

Pulmonary Hypertension
- Causes: left sided atrial or ventricular heart disease, left sided valvular heart disease, COPD, sleep-apnoea, inflammation, etc.
-->Left sided heart failure--> build up of blood in pulmonary circulation--> pulmonary hypertension. This can then lead to right sided heart failure as harder for right ventricle to pump blood into the pulmonary circulation.
- Symptoms: breathlessness, chest pain, fatigue, palpitation, syncope, elevated JVP
- Management: warfarin, oxygen, diuretics & digoxin as appropriate

What causes AF and what are the consequences?
Atrial Fibrillation
1) Ischaemic heart disease, Hypertension, Valvular heart disease (esp. mitral stenosis / regurgitation), Acute infections, Electrolyte disturbance (hypokalaemia, hypomagnesaemia), Thyrotoxicosis, Drugs (e.g. sympathomimetics), Pulmonary embolus, Pericardial disease, Acid-base disturbance, Pre-excitation syndromes, Cardiomyopathies: dilated, hypertrophic., Phaeochromocytoma
Atrial fibrillation (key features on ECG)
- Irregularly irregular rhythm.
- No P waves.
- Absence of an isoelectric baseline.
- Variable ventricular rate.
-QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction.
- Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm).
- Fibrillatory waves may mimic P waves leading to misdiagnosis.
AF is:
- The most common cardiac arrhythmia
- Determined by absence of P waves on an ECG
- Completely irregular rhythm  irregular cardiac output
--> Is often asymptomatic and not life-threatening
--> May result in palpitations, fainting, chest pain or congestive heart failure
--> Thromboembolism (as lack of organised atrial contraction can result in some stagnant blood in the left atrium – lack of movement can lead to thrombus formation)
-->Mitral regurgitation – normally, the coordinated contraction of the atria acts like a sphincter to assist in closing the mitral valve but during atrial fibrillation this doesn’t happen. This combined with an increased left atrium size can result in regurgitation.


What is left heart failure? What is right heart failure? What is bi‐ventricular cardiac
failure? What are their main causes and the clinical features?

LHF; stasis of blood in the left sided chambers of the heart and inadequate perfusion of down stream tissues leading to organ dysfunction.
RHF; stasis of blood in the right sided chambers of the heart and inadequate perfusion of lung tissues leading to dysfunction.
Biventricular cardiac failure; stasis of blood in the chambers of the heart and inadequate perfusion of systemic and pulmonary tissues leading to organ dysfunction.

Left sided heart failure: Failure of the left side of the heart causes blood to back up (be congested) into the lungs, causing respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood. Common respiratory signs are increased rate of breathing and increased work of breathing (non-specific signs of respiratory distress). Rales or crackles, heard initially in the lung bases, and when severe, throughout the lung fields suggest the development of pulmonary edema (fluid in the alveoli). Cyanosis which suggests severe low blood oxygen, is a late sign of extremely severe pulmonary edema.
additional signs include: Displaced apex beat, Gallop rhythm, additional heart sounds (aortic stenosis, mitral valve regurgitation)
--> backward failure of the heart consues: causing congestion in the lungs, causing dyspnoea (due to increased osmotic pressure and fluid in lungs (on exertion and then then progressing to rest), also SOB when laying flat (orthopnea) measured by number of pillows needed, also PND, easy fatigability and excercise intolerance
clinical signs:
- Dyspnoea, orthopnoea, tachypnoea
- Mitral regurgitation
- Signs of pulmonary congestion
- Sinus tachycardia

Right sided heart failure:
Right-sided heart failure is often caused by pulmonary heart disease (cor pulmonale), which is usually caused by difficulties of the pulmonary circulation, such as pulmonary hypertension or pulmonic stenosis.
Physical signs on examination: examination may reveal pitting peripheral edema, ascites, and liver enlargement. Jugular venous pressure is frequently assessed as a marker of fluid status, which can be accentuated by eliciting hepatojugular reflux. If the right ventricular pressure is increased, a parasternal heave may be present, signifying the compensatory increase in contraction strength.
--> backward failure of the right side leads to systemic congestion of capillaries: This generates fluid accumulatio due to increased hydrostatic forces--> leading peripheral oedema --> starting with your pedal, sacral when people are lying down. Nocturia (frequent nightime urination) when fluid from legs returns to blood stream while laying down at night. progressively, ascites, and hepatomegaly may incure due t pumonary hypertension. significant liver congestion can lead to impaired liver function and (congestive hepatopathy) and jaundice

Biventricular heart failure:
Bi-Ventricular Cardiac Failure
- Because the right and left ventricles are connected, failure of one ventricle chamber leads to failure of the other. Bi-ventricular cardiac failure is therefore a ‘late stage’ cardiac failure.
- Aetiology: Ischaemic heart disease, systemic hypertension, valvular heart disease (mitral stenosis is a common cause of right(?) heart failure), lung disease
- Pathogenesis:
-->The heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or can only do so at elevated filling pressure.
Compensatory mechanisms include:
-Frank-Starling mechanism – increase stroke volume to increase CO
-Hypertrophy with or without cardiac chamber dilation
-Activation of neurohumoral systems
• release of adrenaline
• activation rennin-angiotensin-aldosterone system
• release atrial natriuretic peptide
- Morphology: Findings in heart vary depending on disease progression myopathy, dilatation, hypertrophy, fibrosis (eg. evidence of MI, etc.)
- Clinical Symptoms: Dyspnoea, pulmonary oedema, systemic venous congestion & oedema

Dullness of the lung fields to finger percussion and reduced breath sounds at the bases of the lung may suggest the development of a pleural effusion (fluid collection between the lung and the chest wall). Though it can occur in isolated left- or right-sided heart failure, it is more common in biventricular failure because pleural veins drain into both the systemic and pulmonary venous systems. When unilateral, effusions are often right sided.

If a person with a failure of one ventricle lives long enough, it will tend to progress to failure of both ventricles. For example, left ventricular failure allows pulmonary edema and pulmonary hypertension to occur, which increase stress on the right ventricle. Right ventricular failure is not as deleterious to the other side, but neither is it harmless


what clinical and biochemistry is needed for the diagnosis of ARF and RHD (the Australian Guidelines compared to the Modified
Jones Criteria).

first presentation of ARF requires both:
laboratory evidence of prior group A streptococcus infection
2 major criteria or 1 major and 2 minor criteria
recurrent presentations;
laboratory evidence of group A streptococcus infection
2 major or 3 minor or 1 major and 1 minor
where laboratory evidence is positive throat culture or increased/rising anti-streptolysin O titer or streptococcal antibodies (anti-DNase B)
Major criteria are subclinical/clinical carditis, mono/polyarthritis, polyarthralgia, chorea, erythema marginatum, subcutaneous nodules,
minor criteria are monoarthralgia, prolonged PR interval, elevated ESR/CRP, fever.

Suspect with/without prior ARF presenting with heart valve abnormalities
Diagnosis by cardiac auscultation and confirmed by echocardiogram with mitral regurgitation, mitral stenosis, aortic regurgitation, aortic stenosis.
A. Pathological MR* and at least 2 morphological features of RHD of the mitral valve†
B. MS mean gradient ≥4 mmHg (must exclude congenital mitral valve anomalies)
C. Pathological AR‡ and at least two morphological features of RHD of the aortic valve§ (must exclude bicuspid aortic valve and dilated aortic root)
D. Pathological AR‡ and at least two morphological features of RHD of the mitral valve†


What is the Aetiology, signs, symptoms and diagnosis of bacterial endocarditis (ABE and SBE).and first line management

Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the valves. Endocarditis is characterised by lesions known as vegetations which is a mass of platelets, fibrin, microorganisms and scant inflammatory cells.
over 3/4ths of cases are caused by strep or staph
the viridans group of strep are commensals in the URT that may enter the blood stream on chewing or teeth brushing, or at the time of dental treatment
Staph infections have overtaken strep infections as a common cause of acute endocarditis – it originates from skin infections, abscesses or vascular access sites (IV/central lines) or from IV drug use

SIgns and symptoms:
Infective Endocarditis
General signs: fever, weight loss, pallor (anaemia)
Hands: splinter haemorrhages, clubbing (within 6 weeks of onset), osler nodes (rare), janeway lesions (very rare)
Arms: evidence of intravenous drug use
Eyes: pale conjunctivae (anaemia); retinal or conjunctival haemorrhages – roth spots are fundal vasculitic lesions with a yellow centre surrounded by a red ring
Mouth: Mucosal petechial haemorrhages, poor dentition
Heart- signs of underlying heart disease 1. Acquired (mitral regurgitation, mitral stenosis, aortic stenosis, aortic regurgitation), 2. Congential (PDA, VSD, coarctation of the aorta), 3. Prosthetic valves
Abdomen: splenomegaly
Peripheral evidence of embolisation to limbs or CNS


How urgent is referral and investigation of this patient? Who should provide definitive

Referral and investigation is quite urgent in this patient as it is evident her exertional dyspnoea is worsening – thus indicating progression of her RHD. It is clear her dyspnoea is worsening as she is now in a position where she can no longer play basketball, which has a profound effect on her lifestyle. The presence of raised JVP, an irregularly irregular HR and bibasilar crackles in the patient are all of significant concern (right sided heart failure and progressive cardaic failure) and should be approached with the necessary caution. JM should have access to a specialist physician and/or cardiologist, preferably the same specialist, for regular follow up visits to minimize likelihood of progression of her RHD. Needs to undergo surgical interventions and associated pharmaocotherapies to manage complications and symptoms


What features of this case may cause concern at initial presentation, for example, if this
woman is triaged by an experienced RN?

At initial presentation there are not a lot of characteristics that would cause too much concern for an experienced RN undertaking triage. This is because of the fact that her dyspnoea has not progressed to the stage where it comes on at rest, and waiting in the ED waiting room to be triaged is unlikely to trigger an episode of dyspnoea due to lack of exertion.
Patterns of Rheumatic Fever
- Is more common in Indigenous communities due to overcrowding, lower SES and poorer living standards which all contribute to the spread of group A streptococci infection
- Therefore, patients presenting with a sore throat should be given antibiotics in these communities (need to educate doctors)
- Is also more common in tropical communities as these promote survival of streptococci
- Patterns of rheumatic heart disease follow similar trends


What is the likely immediate management for her condition? How would you explain this to Ms. JM and her family? What sort of prognosis would you propose – without immediate intervention and with intervention?

The likely immediate course of action in terms of management of JM would be to handle the factors that may worsen and thus impact the RHD negatively. These would include her dental caries, which should indicate immediate access to oral healthcare services for JM in order to prevent further attacks of ARF, or even the development of infective endocarditis, a complication of RHD. Adequate access to a specialist physician and/or a cardiologist, preferably the same specialist, for regular follow up visits is also essential so as to handle the cardiac issues at hand, and to provide JM and her family with the appropriate information to take home to prevent future ARF attacks or the development of complications of RHD which include infective endocarditis, heart failure or myocardial infarction. Assuming JM and her family are not too familiar with the significance and dire nature of RHD, it is important to explain it to them in a simple manner, whilst still stressing the importance of adequate care of her condition and the severe negative repercussions if she were to dismiss advice on managing her condition. With regards to prognosis, with immediate intervention a good prognosis is likely in that her condition has not worsened to the point of dyspnoea coming on at rest, and the development of orthopnoea/PND is not evident as of yet. In many cases, the prevention of recurrent ARF attacks in long-term management of RHD allows for the resolution of heart disease. Without intervention, prognosis is quite poor as JM’s dyspnoea is likely to worsen. Furthermore, the fact she has dental caries opens her up to increase likelihood of getting future ARF attacks or infective endocarditis. JM’s living situation is also undesirable and without intervention it is highly likely future attacks of ARF will occur, thus causing progression of her RHD.


How would you explain RHD, atrial fibrillation and endocarditis to Ms. JM and her

It is important to use simple lay language with Ms. JM, who identifies as an Aboriginal, as well as maintain respect, cultural sensitivity and awareness. Simple lay terms can be used to explain acute rheumatic fever and its symptoms and effects on the heart valves and how ongoing infections from this bug further valve damage over the years, developing into RHD.
The use of visual aids such as videos, brochures and drawings etc can be an effective way to educate JM and her family about ARF, RHD, AF and their relationship.


What is likely short and long term prognosis of her RHD? 

Rheumatic mitral valve disease is inconsistently reparable, and the long-term outcomes after surgical repair are not as good as for valve repair for mitral valve prolapse due to leaflet and chordal scarring. In addition, leaflet scarring may be progressive after repair. However, rheumatic mitral valve stenosis that is not associated with severe chordal fusion or shortening or with calcification may be treated with either percutaneous or open mitral commissurotomy with a high degree of long-term success.


what does the concepts of primordial, primary and secondary prevention of ARF/RHD – and tertiary management mean? How would you explain some of
these concepts to Ms. JM and her family?

Patient education regarding the recurrent nature of ARF and the serious potential long-term consequences of the disease is essential.

Primordial: broad social, economic and environmental strategies in a community, undertaken to limit GAS infections.

Primary: educating JM and her family about the importance of maintaining hygiene to prevent further GAS infections.Primary Prevention
 Improve living conditions to prevent GAS infections
 Early recognition & treatment of GAS infections
E.g. washing hands, covering the mouth while coughing, taking day off from school if sick. Therefore primary infection involves limiting acquiring the infection in areas with increased risk factors.

Secondary: early detection of RHD and early treatment to prevent further attacks of GAS infections and worsening of symptoms.  Accurate & timely diagnosis of ARF
 Secondary prophylaxis (penicillin)*
 health education
 Screening for undiagnosed RHD
It is crucial to Educate JM and her family about the importance of regular prophylactic antibiotic administration so as to prevent GAS infections and thus control progression of her disease

Tertiary management: providing JM and her family with further potential interventions to reduce symptoms and prevent premature death in the long run, e.g. medical management (anticoagulants, diuretics) , valve replacement, balloon valvuloplasty.

* Current guidelines indicate that penicillin prophylaxis should be given every 3-4 weeks for a period of 10 years to patients who have had rheumatic fever to prevent them from developing rheumatic heart disease with further strep infections.


what is the meaning of Primary, secondary, Tertiary and Quaternary prevention?

Primary: the promotion of health and the prevention of illness, for example, immunisation and making physical environments safe

Secondary: the early detection and prompt intervention to correct departures from good health or to treat the early signs of disease, for example, cervical screening, mammography, blood pressure monitoring and blood cholesterol checking

Tertiary: reducing impairments and disabilities, minimising suffering caused by existing departures from good health or illness, and promoting patients’ adjustment to chronic or irremediable conditions, for example, prevention of complications


What are the likely long‐term challenges of secondary prophylaxis for ARF/RHD?

- Rheumatic Fever is common in rural indigenous communities which lack health care services
- Lack of understanding about the importance of taking antibiotics (not biomedical approach to health nor responsibility for own health)
- Staff shortages and staff not understanding the community
- Youth may move to larger centres for educational opportunities
- Compliance problems (coming in to centre for IM)


What would you advise Ms. JM about family planning? What about her teeth?   

· In RHD, oestrogen-containing contraceptives may carry a slight higher risk of thrombosis but this has not yet been confirmed in published studies
· Circulatory changes will exacerbate any pre-existing valvular diseases
· If immediate pregnancy is not planned a full history and examination with functional assessment and detailed ECG to monitor pregnancy and complications
· If patient is already symptomatic, serious consideration should be given to interventional therapy or surgery prior to pregnancy
· Prevention of infective endocarditis – maintain good personal hygiene, brush teeth at least twice a day and have a bath and shower daily


Name the basic method for Interpretation of ECGs rate and rhythm?
define and describe sinus tachycardia, p mitrale and atrial fibrillation?

Interpretation of ECG
1- Rhythm – is the SA node driving the rhythm (P waves present = sinus)? Ectopic beats?
2- Rate – 300/ number of large squares = beats/min
3- P wave – present? absent? normal height and duration (<0.10sec)?
4- PR interval – duration(0.12-0.22sec)?
5- QRS complex – duration (<0.12sec)? height? deflection?
6- ST segment – with baseline or depressed? elevated?
7- T wave – height? shape? duration?
8- QT axis – how long (<0.44sec)?
9- Electrical axis – is QRS positive in both leads I and aVF? (if so, normal)

Sinus Tachycardia
- Rate >100bpm
- Regular rhythm
- P waves present & normal
- PR interval shortened
(addtional information Causes Pain anxiety
Hypoxia, hypercarbia Hyperthyroidism Pulmonary embolism
Sepsis, pyrexia Exercise Pharmacological causes:
Beta-agonists: adrenaline, isoprenaline, salbutamol, dobutamine
Sympathomimetics: amphetamines, cocaine, methylphenidate
Antimuscarinics: antihistamines, TCAs, carbamazepine, atropine
Others: caffeine, theophylline, marijuana)
Handy tip:
With very fats heart rate the P waves may be hidden in the preceding T wave, producing a camel hump appearance

Atrial Fibrillation
- Rate >100bpm
- Absent P waves
- Irregular PR intervals
Key features in AF:
Irregularly irregular rhythm.
No P waves.
Absence of an isoelectric baseline.
Variable ventricular rate.
QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction.
Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm).
Fibrillatory waves may mimic P waves leading to misdiagnosis

P mitrale
- P wave shaped like an M
- Indicative of bulky left atrium (eg. atrial hypertrophy)
(additional infromation: P mitrale. The presence of broad, notched (bifid) P waves in lead II is a sign of left atrial enlargement, classically due to mitral stenosis. Bifid P waves (P mitrale) in left atrial enlargement
Left atrial hypertrophy, left atrial abnormality.
Left atrial enlargement (LAE) is due to pressure or volume overload of the left atrium.
It is often a precursor to atrial fibrillation
Diagnostic criteria: In lead II
Bifid P wave with > 40 ms between the two peaks
Total P wave duration > 110 ms
Most commonly seen in mitral stenosis:
Or can be associated with left ventricular hypertrophy:
(Systemic hypertension, Aortic stenosis, Mitral incompetence, Hypertrophic cardiomyopathy)


what are normal heart rates in paedetric patients? (different ages)

Normal heart rate in children:
Newborn: 110 – 150 bpm
2 years: 85 – 125 bpm
4 years: 75 – 115 bpm
6 years+: 60 – 100 bpm


How important is ARF/RHD as a cause of cardiac disease worldwide?  

ARF and RHD are diseases of poverty, low SES and poor access to health care that remain endemic in developing and emerging economies.
It is estimated that there are over 15 million cases of RHD worldwide, with 282,000 new cases and 233,000 deaths annually. Consequently, there is a need to focus on prevention and control methods that can help stem the tide of ARF/RHD.


Who gets ARF and RHD? Why is ARF/RHD so common in Aboriginal Australians, Torres Strait Islanders and Pacific Islanders?

In Australia, the vast majority of people with ARF/RHD are Aboriginal people and Torres Strait Islanders, many of whom live in remote areas of central and northern Australia. Pacific Islanders, and migrants from high-prevalence countries, are also at high risk.
Prevalence of RF/RHD has been attributed to overcrowding and unhygienic living related to low SES. Unhygienic living results in persistent GAS in the environment. Since GAS spreads by droplet dissemination, overcrowding causes cross infection from person to person. Low SES may undermine nutrition and seriously limit access to medical treatment. Poor nutritional status is also believed to contribute to a decreased immune response. The result is not only endemic RF but also a more severe or virulent disease.
Additionally, Indigenous people do not receive the same level of primary prevention and management, emergency and acute care, rehabilitation, ongoing management, and secondary prevention care for CVD as do non-Indigenous people


Why does so much RHD go undetected until late in the disease?

It is possible that an initial attack of ARF is mild, resulting in mild carditis, which remains subclinical, undiagnosed and as such the patient does not get prophylaxis to prevent recurrences. In low SES settings, recurrences can cause further cardiac damage resulting in symptomatic RHD with multivalve involvement and congestive failure. Therefore, it is the recurrences of the disease in the absence of secondary prophylaxis that is responsible for patients presenting with severe disease.


What approaches do we take to address ARF/RHD in Australia? Are they successful?

What approaches do we take to address ARF/RHD in Australia? Are they successful?
There are 3 approaches to addressing ARF/RHD in Australia: primordial prevention, primary prevention and secondary prevention.

Primordial prevention: Preventing the development of risk factors in the community to prevent the disease in the population and thus protect individuals. E.g. prevention of overcrowding, improving nutritional status and public education regarding the risk of ARF from sore throat especially below the age of 15 years.

Primary prevention: Identifying symptomatic GAS pharyngitis in those individuals most at risk (5-14 years), and eradicate the bacterium with antibiotic treatment before the immune responses associated with ARF has been initiated. Studies show that ARF associated with GAS pharyngitis can be prevented if treatment is commenced within 9 days of symptoms appearing.

Secondary prevention: Secondary prophylaxis of ARF in someone who is known to have had ARF is the only RHD control strategy shown to be effective and cost effective at both individual and population levels. The recommended method is a four-weekly benzathine penicillin G (BPG) injection. The appropriate duration of secondary prophylaxis is determined by a number of factors, including age, time since the last episode of ARF and potential harm from recurrent ARF. For individuals, the duration of secondary prophylaxis is at least 10 years.

Furthermore, effective RHD management involves regular clinical follow up, with specialist review and echocardiography.

While strategies for controlling RHD have been proven to be simple, cheap and cost-effective, they must be adequately implemented in the populations at highest risk of disease. Persistent high rates of recurrent ARF in high-risk populations highlight the continued barriers to prevention

"“While acute rheumatic fever (ARF) has become a rare curiosity in Australia’s non‐Indigenous population, its incidence in Indigenous Australians living in remote areas remains among the highest reported in the world. It is unlikely that such a stark contrast between two populations living within the same national borders exists for any other disease or on any other continent."


How do you know when to come to terms Acceptance and limits of your ability and need to seek advice? The patient needs specialist care.  How do you know when you have reached your level of competence and need to seek further advice or refer on?

 Be aware of own knowledge and stage of development
 Compare yourself with your peers
 Keep up to date
 Do not be afraid to admit ignorance
 When in doubt seek help
 Constantly assess and reflect on your experiences
 Listen to advice from your colleagues


What is a mitral valve prolapse? Aetiology? pathogenesis? morphology? Clinical symtpoms?

Floppy Valve Syndrome (aka: mitral valve prolapsed):
- Occurs when one or both mitral valve leaflets are ‘floppy’ & bulge into left atrium during systole.
- Aetiology: Congenital abnormalities (inc. marfan’s syndrome), degenerative myxomatous changes
- Pathogenesis:
 The basis for changes that weaken the valve leaflets and associated structures is unknown
 One or both mitral valve leaflets are ‘floppy’ and bulge into the left atrium during systole
 Can lead to mitral regurgitation - blood ‘leaks backwards’ from ventricle into atrium
- Morphology:
o Interchordal ballooning of the mitral leaflets
o Affected leaflets often enlarged, redundant, thick and rubbery
o Tendinous cords may be elongated, thinned or ruptured o Myxomatous degeneration
o Fibrous thickening of valve (when rub against each other)
o Attenuation of collaganeous fibrosa layer of valves

- Clinical Symptoms: Many are asymptomatic, midsystolic click, benign arrhythmias, atypical chest pain & small risk of embolic stroke
- Complications: Low risk (increased risk if mitral regurgitation develops)