PRESENTING PROBLEMS IN CARDIOVASCULAR DISEASE

HYPERTENSION

High BP is a trait as opposed to a specific disease and represents a quantitative rather than a qualitative deviation from the norm.

Any definition of hypertension is therefore arbitrary.

Systemic BP rises with age, and the incidence of cardiovascular disease (particularly stroke and coronary artery disease) is closely related to average BP at all ages, even when BP readings are within the so-called ‘normal range’.

Randomised controlled trials have demonstrated that antihypertensive therapy can reduce the incidence of stroke and, to a lesser extent, coronary artery disease .

The cardiovascular risks associated with a given BP are dependent upon the combination of risk factors in an individual, such as age, gender, weight, physical activity, smoking, family history, serum cholesterol, diabetes mellitus and pre-existing vascular disease.

Effective management of hypertension requires a holistic approach, based on the identification of those at highest cardiovascular risk and the use of multifactorial interventions, targeting not only BP but all modifiable cardiovascular risk factors.

Thus a practical definition of hypertension is ‘the level of BP at which the benefits of treatment outweigh the costs and hazards’.

The British Hypertension Society classification of hypertension is consistent with those defined by the European Society of Hypertension and the World Health Organization–International Society of Hypertension.

Approach to newly diagnosed hypertension: Hypertension is predominantly an

asymptomatic condition and the diagnosis is usually made at routine examination or when a complication arises.

A BP check is advisable every 5 years in adults.

The objectives of the initial evaluation of a patient with high BP readings are:

-to obtain accurate and representative measurements of BP

-to identify contributory factors and any underlying cause (secondary hypertension)

- to assess other risk factors and quantify cardiovascular risk

-to detect any complications (target organ damage) that are already present

-to identify comorbidity that may influence the choice of antihypertensive therapy.

These goals are attained by a careful history, clinical examination and some simple investigations.

Syncope and Presyncope

The term ‘syncope’ refers to sudden loss of consciousness due to reduced cerebral perfusion.

‘Presyncope’ refers to lightheadedness where the individual thinks he or she may black out.

Syncope affects around 20% of the population at some time and accounts for more than 5% of hospital admissions.

Dizziness and presyncope are very common in old age.

Symptoms are disabling, undermine confidence and independence, and can affect an individual’s ability to work or to drive.

There are several mechanisms that underlie recurrent presyncope or syncope:

-cardiac syncope due to mechanical cardiac dysfunction or arrhythmia

-neurocardiogenic syncope in which an abnormal autonomic reflex causes bradycardia and/or hypotension.

Blackouts can also be caused by non-cardiac pathology such as epilepsy, cerebrovascular ischaemia or hypoglycaemia.

Differential diagnosis: History-taking, from the patient or a witness,

is the key to establishing a diagnosis. Attention should be given to potential

triggers (e.g. medication, exertion, posture), the victim’s appearance (e.g. colour, seizure activity), the duration of the episode and the speed of recovery.

Cardiac syncope is usually sudden but can be associated with premonitory lightheadedness, palpitation or chest discomfort.

The blackout is usually brief and recovery rapid.

Neurocardiogenic syncope will often be associated with a situational trigger, and the patient may experience flushing, nausea and malaise for several minutes afterwards.

Patients with seizures do not exhibit pallor, may have abnormal movements, usually take more than 5 minutes to recover and are often confused.

A history of rotational vertigo is suggestive of a labyrinthine or vestibular disorder.

The pattern and description of the patient’s symptoms should indicate the probable mechanism and help to determine subsequent investigations.

:Arrhythmia

Lightheadedness may occur with many arrhythmias, but blackouts (Stokes–Adams attacks) are usually due to profound bradycardia or malignant ventricular tachyarrhythmias.

The 12-lead ECG may show evidence of conducting system disease (e.g. sinus bradycardia, AV block, bundle branch block or axis deviation) which would predispose a patient to bradycardia, but the key to establishing a diagnosis is to obtain an ECG recording during symptoms.

Since minor rhythm disturbances are common, especially in old age, symptoms must occur at the same time as a recorded arrhythmia before a diagnosis can be made.

Ambulatory ECG recordings are helpful only if symptoms occur several times per week.

Patient activated ECG recorders are useful for examining the rhythm in patients with recurrent dizziness, but are not useful in assessing sudden blackouts.

In patients with presyncope or syncope in whom these investigations fail to establish a cause, an implantable ‘loop recorder’ can be placed subcutaneously in the upper chest.

This device continuously records the cardiac rhythm and will activate automatically if extreme bradycardia or tachycardia occurs.

The ECG memory can also be frozen by the patient using a hand-held activator. Stored ECGs can be accessed by the implanting centre, using a telemetry device.

Structural heart disease:

Severe aortic stenosis, hypertrophic obstructive cardiomyopathy and severe coronary artery disease can cause lightheadedness or syncope on exertion.

This is caused by profound hypotension due to a fall in cardiac output, or failure to increase output during exertion, coupled with exercise-induced peripheral vasodilatation. Exertional arrhythmias also occur in these patients.

Neurocardiogenic syncope:

This encompasses a family of syndromes in which bradycardia and/or hypotension occur because of a series of abnormal autonomic reflexes.

The two main conditions are hypersensitive carotid sinus syndrome (HCSS) and malignant vasovagal syncope.

Situational syncope:

This is the collective name given to some variants of neurocardiogenic syncope that occur in the presence of identifiable triggers (e.g. cough syncope, micturition syncope)

Vasovagal syncope:

This is normally triggered by a reduction in venous return due to prolonged standing, excessive heat or a large meal.

It is mediated by the Bezold–Jarisch reflex, in which there is an initial sympathetic activation that leads to vigorous contraction of the relatively underfilled ventricles.

This stimulates ventricular mechanoreceptors, producing parasympathetic (vagal) activation and sympathetic withdrawal, and causing bradycardia, vasodilatation or both.

Head-up tilt-table testing is a provocation test used to establish the diagnosis, and involves asking the patient to lie on a table that is then tilted to an angle of 60–70° for up to 45 minutes, while the ECG and BP are monitored.

A positive test is characterised by bradycardia (cardio-inhibitory response) and/or hypotension (vasodepressor response) associated with typical symptoms.

Initial management involves lifestyle modification (salt supplementation and avoiding prolonged standing, dehydration or missing meals).

In resistant cases, drug therapy can be used; fludrocortisone, which causes sodium and water retention and expands plasma volume, β-blockers, which inhibit the initial sympathetic activation, disopyramide (a vagolytic agent) or midodrine (a vasoconstrictor α-adrenoceptor agonist) may be helpful.

A dual-chamber pacemaker can be useful if symptoms are predominantly due to bradycardia. Patients with a urinary sodium excretion of less than 170 mmol/day may respond to salt loading.

Carotid sinus hypersensitivity:

This causes presyncope or syncope because of reflex bradycardia and vasodilatation.

Carotid baroreceptors are involved in BP regulation and are activated by increased BP, resulting in a vagal discharge that causes a compensatory drop in BP.

In HCSS the baroreceptor is sensitive to external pressure (e.g. during neck movement or if a tight collar is worn), so that pressure over the carotid artery causes an inappropriate and intense vagal discharge.

The diagnosis can be established by monitoring the ECG and BP during carotid sinus massage for 6 seconds.

This manœuvre should not be attempted in patients with a carotid bruit or with a history of cerebrovascular disease because of the risk of embolic stroke.

A positive cardio-inhibitory response is defined as a sinus pause of 3 seconds or more; a positive vasodepressor response is defined as a fall in systolic BP of more than 50 mmHg.

Carotid sinus pressure will produce positive findings in about 10% of elderly individuals but less than 25% of these experience spontaneous syncope.

Symptoms should not therefore be attributed to HCSS unless they are reproduced by carotid sinus pressure.

Dual chamber pacing usually prevents syncope in patients with the more common cardio-inhibitory response.

Postural hypotension:

This is caused by a failure of the normal compensatory mechanisms.

Relative hypovolaemia (often due to excessive diuretic therapy), sympathetic degeneration (diabetes mellitus, Parkinson’s disease, ageing) and drug therapy (vasodilators, antidepressants) can all cause or aggravate the problem.

Treatment is often ineffective; however, withdrawing unnecessary medication and advising the patient to wear graduated elastic stockings and get up slowly may be helpful.

Fludrocortisone, which can expand blood volume through sodium and water retention, may be of value.

Palpitation

Palpitation is a very common and sometimes frightening symptom. Patients use the term to describe a wide variety of sensations including an unusually erratic, fast, slow or forceful heart beat, or even chest pain or breathlessness.

Initial evaluation should concentrate on determining its likely mechanism, and whether or not there is significant underlying heart disease.

A detailed description of the sensation is essential and patients should be asked to tap out the heart beat they experience, on their chest or a table.

A provisional diagnosis can usually be made on the basis of a thorough history.

It helps to obtain an ECG recording during an episode using an ambulatory monitor or a patient-activated ECG recorder.

Recurrent but short-lived bouts of an irregular heart beat are usually due to atrial or ventricular extrasystoles (ectopic beats).

Some patients will describe the experience as a ‘flip’ or a ‘jolt’ in the chest, while others report dropped or missed beats. Extrasystoles are often more frequent during periods of stress or debility; they can be triggered by alcohol or nicotine.

Episodes of a pounding, forceful and relatively fast (90–120/min) heart beat are a common manifestation of anxiety.

They may also reflect a hyperdynamic circulation, such as anaemia, pregnancy and thyrotoxicosis, and can occur in some forms of valve disease (e.g. aortic regurgitation).

Discrete bouts of a very rapid (> 120/min) heart beat are more likely to be due to a paroxysmal tachyarrhythmia.

Supraventricular and ventricular tachycardias may all present in this way.

In contrast, episodes of atrial fibrillation typically present with irregular and usually rapid palpitation.

Palpitation is usually benign and, even if the patient’s symptoms are due to an arrhythmia, the outlook is good if there is no underlying structural heart disease.

Most cases are due to an awareness of the normal heart beat, a sinus tachycardia or benign extrasystoles, in which case an explanation and reassurance may be all that is required.

Palpitation associated with presyncope or syncope may reflect more serious structural or electrical disease and should be investigated promptly.

Cardiac arrest and sudden cardiac death

Cardiac arrest describes the sudden and complete loss of cardiac output due to asystole, ventricular tachycardia or ventricular fibrillation, or loss of mechanical cardiac contraction (pulseless electrical activity).

The clinical diagnosis is based on the victim being unconscious and pulseless; breathing may take some time to stop completely after cardiac arrest.

Death is virtually inevitable unless effective treatment is given promptly.

Sudden cardiac death is usually caused by a catastrophic arrhythmia and accounts for 25–30% of deaths from cardiovascular disease, claiming an estimated 70000–90000 lives each year in the UK.

Many of these deaths are potentially preventable.

Arrhythmias complicate many types of heart disease and can sometimes occur in the absence of recognisable structural abnormalities

Sudden death less often occurs because of an acute mechanical catastrophe such as cardiac rupture or aortic dissection.

Coronary artery disease, especially acute MI, is the most common condition leading to cardiac arrest.

Ventricular fibrillation or ventricular tachycardia is common in the first few hours of MI and many victims die before medical help is sought.

Up to one-third of people developing MI die before reaching hospital, emphasising the importance of educating the public to recognise symptoms and to seek medical help quickly.

Acute myocardial ischaemia (in the absence of infarction) can also cause these arrhythmias, although less commonly.

Patients with a history of MI may be at risk of sudden arrhythmic death, especially if left ventricular function is impaired or there is ongoing myocardial ischaemia.

In these patients, the risk is reduced by the appropriate treatment of heart failure with β-blockers and ACE inhibitors, and by coronary revascularisation, and many require implantation of a cardiac defibrillator.

Aetiology of cardiac arrest: Cardiac arrest may be caused by ventricular

fibrillation, pulseless ventricular tachycardia, asystole or pulseless electrical activity.

Ventricular fibrillation and pulseless ventricular tachycardia: These are the most common and most easily

treatable cardiac arrest rhythms. Ventricular fibrillation produces rapid ineffective uncoordinated movement of the ventricles, which therefore produce no pulse.

The ECG shows rapid, bizarre and irregular ventricular complexes.

Ventricular tachycardia can cause cardiac arrest if the ventricular rate is so rapid that effective mechanical contraction and relaxation cannot occur, especially if it occurs in the presence of severe left ventricular impairment.

It may degenerate into ventricular fibrillation.

Defibrillation will restore cardiac output in more than 80% of patients if delivered immediately.

However, the chances of survival fall by at least 10% with each minute’s delay, and by more if basic life support is not given; thus provision of these is the key to survival.

Asystole: This occurs when there is no electrical

activity within the ventricles and is usually due to failure of the conducting tissue or massive ventricular damage complicating MI.

A precordial thump, external cardiac massage, or administration of intravenous atropine or adrenaline (epinephrine) may restore cardiac activity.

When due to conducting tissue failure, permanent pacemaker implantation will be required if the individual survives.

Pulseless electrical activity: This occurs when there is no effective

cardiac output despite the presence of organised electrical activity.

It may be caused by reversible conditions, such as hypovolaemia, cardiac tamponade or tension pneumothorax , but is often due to a catastrophic event such as cardiac rupture or massive pulmonary embolism, and therefore carries an extremely poor prognosis.

Management of cardiac arrest:The Chain of Survival: This term refers to the sequence of events that are

necessary to maximise the chances of a cardiac arrest victim surviving.

Survival is most likely if all links in the chain are strong, i.e. if the arrest is witnessed, help is called immediately, basic life support is administered by a trained individual, the emergency medical services respond promptly, and defibrillation is achieved within a few minutes.

Good training in both basic and advanced life support is essential and should be maintained by regular refresher courses.

In recent years, public access defibrillation has been introduced in places of high population density, particularly where traffic congestion may impede the response of emergency services, e.g. railway stations, airports and sports stadia.

Designated individuals can respond to a cardiac arrest using basic life support and an automated external defibrillator.

Basic life support (BLS):

BLS encompasses manœuvres that aim to maintain a low level of circulation until more definitive treatment with advanced life support can be given.

Management of the collapsed patient requires prompt assessment and restoration of the airway, maintenance of breathing using rescue breathing (‘mouth-to-mouth’ breathing) and maintenance of the circulation using chest compressions.

Advanced life support (ALS):

ALS aims to restore normal cardiac rhythm by defibrillation when the cause of cardiac arrest is due to a tachyarrhythmia, or to restore cardiac output by correcting other reversible causes of cardiac arrest.

ALS can also involve administration of intravenous drugs to support the circulation, and endotracheal intubation to ventilate the lungs.

If cardiac arrest is witnessed, a precordial thump may sometimes convert ventricular fibrillation or tachycardia to normal rhythm, but this is futile if cardiac arrest has lasted longer than a few seconds.

The priority is to assess the patient’s cardiac rhythm by attaching a defibrillator/monitor.

Ventricular fibrillation or pulseless ventricular tachycardia is treated with immediate defibrillation.

Defibrillation is more likely to be effective if a biphasic shock defibrillator is used, where the polarity of the shock is reversed midway through its delivery.

Defibrillation is usually administered using a 150 Joule biphasic shock, and CPR resumed immediately for 2 minutes without attempting to confirm restoration of a pulse, because restoration of mechanical cardiac output rarely occurs immediately after successful defibrillation.

If after 2 minutes a pulse is not restored, a further biphasic shock of 150–200 joules is given.

Thereafter, additional biphasic shocks of 150–200 joules are given every 2 minutes after each cycle of cardiopulmonary resuscitation (CPR).

During resuscitation, adrenaline (epinephrine, 1 mg i.v.) should be given every 3–5 minutes and consideration given to the use of intravenous amiodarone, especially if ventricular fibrillation or ventricular tachycardia reinitiates after successful defibrillation.

Ventricular fibrillation of low amplitude, or ‘fine VF’, may mimic asystole.

If asystole cannot be confidently diagnosed, the patient should be regarded as having ‘fine VF’ and defibrillated.

If an electrical rhythm is present that would be expected to produce a cardiac output, ‘pulseless electrical activity’ is present.

There are several potentially reversible causes that can be easily remembered as a list of four Hs and four Ts.

Pulseless electrical activity is treated by continuing CPR and adrenaline (epinephrine) administration whilst seeking such causes.

Asystole is treated similarly, with the additional support of atropine and sometimes external or transvenous pacing in an attempt to generate an electrical rhythm.

Survivors of cardiac arrest:

Patients who survive a cardiac arrest caused by acute MI need no specific treatment beyond that given to those recovering from an uncomplicated infarct, since their prognosis is similar.

Those with reversible causes, such as exercise-induced ischaemia or aortic stenosis, should have the underlying cause treated if possible.

Survivors of ventricular tachycardia or ventricular fibrillation arrest in whom no reversible cause can be identified may be at risk of another episode, and should be considered for an implantable cardiac defibrillator and anti-arrhythmic drug therapy.

Abnormal heart sounds and murmurs

The first clinical manifestation of heart disease may be the discovery of an abnormal sound on auscultation.

This may be incidental—for example, during a routine childhood examination—or may be prompted by symptoms of heart disease.

Clinical evaluation is helpful but an echocardiogram is often necessary to confirm the nature of an abnormal heart sound or murmur.

Is the sound cardiac?

Additional heart sounds and murmurs demonstrate a consistent relationship to a specific part of the cardiac cycle but extracardiac sounds (e.g. pleural rub or venous hum) do not.

Pericardial friction produces a characteristic scratching or crunching noise, which often has two components corresponding to atrial and ventricular systole, and may vary with posture and respiration.

Is the sound pathological?

Pathological sounds and murmurs are the product of turbulent blood flow or rapid ventricular filling due to abnormal loading conditions.

Some added sounds are physiological but may also occur in pathological conditions; for example, a third sound is common in young people and in pregnancy but is also a feature of heart failure.

Similarly, a systolic murmur due to turbulence across the right ventricular outflow tract may occur in hyperdynamic states (e.g. anaemia, pregnancy) but may also be due to pulmonary stenosis or an intracardiac shunt leading to volume overload of the RV (e.g. atrial septal defect).

Benign murmurs do not occur in diastole and systolic murmurs that radiate or are associated with a thrill are almost always pathological.

Auscultatory evaluation of a heart murmur:

Timing, intensity, location, radiation and quality are all useful clues to the origin and nature of a heart murmur:

Radiation of a murmur is determined by the direction of turbulent blood flow and is only detectable when there is a high-velocity jet, such as in mitral regurgitation (radiation from apex to axilla) or aortic stenosis (radiation from base to neck).

Similarly, the pitch and quality of the sound can help to distinguish the murmur, such as the ‘blowing’ murmur of mitral regurgitation or the ‘rasping’ murmur of aortic stenosis.

The position of a murmur in relation to the cardiac cycle is crucial and should be assessed by timing it with the heart sounds, carotid pulse and apex beat.

Systolic murmurs associated with ventricular :outflow tract obstruction

These occur in mid-systole and have a crescendodecrescendo pattern, reflecting the changing velocity of blood flow.

Pansystolic murmurs maintain a constant intensity and extend from the first heart sound throughout systole (up to and beyond the second heart sound).

They occur when blood leaks from a ventricle into a low-pressure chamber at an even or constant velocity.

Mitral regurgitation, tricuspid regurgitation and ventricular septal defect are the only causes of a pansystolic murmur.

Late systolic murmurs are unusual but may occur in mitral valve prolapse, if the mitral regurgitation is confined to late systole, hypertrophic obstructive cardiomyopathy if dynamic obstruction occurs late in systole.

Mid-diastolic murmurs:

These are due to accelerated or turbulent flow across the mitral or tricuspid valves.

They are low-pitched noises that are often difficult to hear and should be evaluated with the bell of the stethoscope.

A mid-diastolic murmur may be due to mitral stenosis (located at the apex and axilla), tricuspid stenosis (located at the left sternal edge), increased flow across the mitral valve (e.g. the to-and-fro murmur of severe mitral regurgitation) or increased flow across the tricuspid valve (e.g. left-to-right shunt through a large atrial septal defect).

Early diastolic murmurs have a soft, blowing quality with a decrescendo pattern and should be evaluated with the diaphragm of the stethoscope.

They are due to regurgitation across the aortic or pulmonary valves and are best heard at the left sternal edge with the patient sitting forwards in held expiration.

Continuous murmurs:

These result from a combination of systolic and diastolic flow (e.g. persistent ductus arteriosus), and must be distinguished from extracardiac noises such as bruits from arterial shunts, venous hums (high rates of venous flow in children) and pericardial friction rubs.