The Cardiovascular System | Approach to the patient with complaints



There is just a small number of presenting symptoms of cardiovascular disease, namely chest discomfort, breathlessness, palpitation, dizziness and syncope, and peripheral oedema. There are, however, a multitude of physical signs, but these are relatively straightforward to interpret as long as you bear in mind the underlying cardiovascular physiology and pathophysiology.




Presenting complaint


Chest discomfort

Patients with angina often say that the symptom they experience in the chest is not a pain but a feeling of discomfort. It’s important to recognize this – if you only ask the direct question ‘Do you get chest pain?’, and the patient answers ‘No’ ,you might move on and miss a vital part of the patient’s history.



If you must ask a leading question, enquire about chest discomfort rather than chest pain.


There are many different causes of chest discomfort, each of which has its own key characteristics (Table 7.1). 

Table 7.1 Common causes of chest discomfort and their characteristic features


Enquire about the following features:

location and radiation:

  • central (retrosternal), radiating to the arms,neck and jaw in angina and myocardial infarction
  •  retrosternal in gastro-oesophageal reflux and oesophageal spasm
  •  between the shoulder blades (interscapular) in aortic dissection
  •  tends to be localized with musculoskeletal or pleuritic pain, although the pain of massive pulmonary embolism can mimic that of angina


  • tight, heavy, crushing in angina or myocardial infarction
  • ‘tearing’ in aortic dissection
  •  sharp/stabbing with pleuritic pain (e.g. pulmonary embolism)
  •  sharp or ‘raw’ with pericarditis
  • sharp/stabbing or dull with musculoskeletal pain 


  • graded by the patient on a scale of 0–10, where 10 represents the worst pain ever

duration and onset:

  • angina – onset with exertion/emotional stress and usually lasting less than 10 minutes
  • myocardial infarction – onset often at rest, lasting more than 10 minutes
  •  pulmonary embolism – pleuritic chest pain of sudden onset
  • aortic dissection – sudden onset
  • musculoskeletal – may be of sudden onset (e.g. with movement) and lasts a few seconds, or be more gradual and chronic (e.g. costochondritis)

precipitating, exacerbating and alleviating factors:

  • angina – brought on by exertion/emotional stress, particularly in cold windy weather and/ or after a heavy meal, and rapidly relieved by rest or sublingual glyceryl trinitrate (GTN)
  • myocardial infarction – pain continues despite resting or using GTN
  • pericarditis – exacerbated by lying flat and respiration, relieved by sitting upright and leaning forwards
  • pleuritic pain – worsened by inspiration and coughing
  • musculoskeletal – worsened by movement

associated symptoms:

  • angina – breathlessness (which may be more of a feature than chest discomfort)
  • myocardial infarction – breathlessness, sweating, nausea and vomiting
  • pericarditis – breathlessness, fever
  • pulmonary embolism – breathlessness, haemoptysis
  • pneumonia – breathlessness, productive cough, fever
  • gastro-oesophageal reflux – waterbrash.


A degree of breathlessness (dyspnoea) is normal on heavy exertion, but breathlessness becomes abnormal when it is disproportionate to the level of activity undertaken. As with chest pain, you should ask about:

  • severity (heart failure symptoms can be graded using the New York Heart Association (NYHA) functional classification, see Table 7.2)
  • duration and onset
  • precipitating, exacerbating and alleviating factors
  • associated symptoms (e.g. chest discomfort).

Table 7.2 The New York Heart Association (NYHA) functional classification of heart failure symptoms


Left ventricular dysfunction is a common cardiac cause of breathlessness and can result from systolic dysfunction (a ‘weak’ ventricle with impaired contractility and a low ejection fraction), diastolic dysfunction (a ‘stiff ’ ventricle with impaired relaxation and filling), or a combination of the two. This leads to an elevation in filling pressures (end-diastolic pressure) which in turns raises left atrial pressure and pulmonary venous pressure. Pulmonary venous congestion occurs, ‘stiffening’ the lungs and exacerbating the sensation of breathlessness, and can ultimately progress to frank pulmonary oedema.

Orthopnoea is the sensation of breathlessness on lying flat. Orthopnoea occurs because of increased venous return and a redistribution of interstitial oedema throughout the lungs. Patients who are prone to orthopnoea may report using several pillows (ask how many) to prop themselves upright in bed, or may even resort to sleeping in a chair.

Paroxysmal nocturnal dyspnoea (PND) is the development of breathlessness while the patient is lying down asleep, waking the patient and usually forcing them to sit upright or even lean out of an open window to regain their breath. It results from the development of orthopnoea while the patient is sleeping. Patients often find PND an alarming symptom.

Breathlessness is also a feature of myocardial ischaemia, and indeed breathlessness may be the predominant (or even only) symptom. The respiratory causes of breathlessness are discussed in the Respiratory chapter.


Palpitation is an awareness of the heartbeat, but patients use the term in a variety of ways, so it is important to obtain a detailed description of what they are experiencing. It is particularly important to determine whether the palpitations are:

  • fast or slow
  •  regular or irregular.

Ask the patient to ‘tap out’ the rhythm by clapping their hands – this will usually make it clearer whether the rhythm is regular or irregular. If it is irregular, determine whether it is ‘regularly irregular’ (e.g. bigeminy) or ‘irregularly irregular’ (e.g. atrial fibrillation)

The patient’s description can give a strong clue as to the nature of the palpitation – intermittent ‘skipped beats’ are commonly ectopic beats, a rapid regular palpitation with gradual onset and termination and occurring with stress is commonly sinus tachycardia, whilst a rapid irregularly irregular palpitation is likely to be atrial fibrillation (which can occur in self-limiting episodes – ‘paroxysmal atrial fibrillation’ – as well as being persistent). In general, palpitations which have an abrupt onset and termination are more likely to be due to a ‘significant’ arrhythmia than palpitations which start gradually and later on fade away.



Sometimes the patient is aware of just a fleeting sensation, perceived as a ‘missed beat’ or ‘extra beat’, which is typically due to an ectopic beat – this is often described as the heart having ‘jumped’, ‘lurched’ or ‘skipped a beat’.


Palpitations are usually episodic, and so you should ask the following questions. 

  • How often do the episodes occur?
  • Do they occur at rest, during exercise or both?
  • How does each episode begin: 
    • sudden or gradual onset
    • any apparent triggers (e.g. alcohol, caffeine)?
  • How long does each episode last?
  • How does each episode terminate:
    •  sudden or gradual termination
    • does anything terminate an episode (e.g. Valsalva manoeuvre)?
  • Have they been prescribed any medication (e.g. β-blocker), and does it help?

Table 7.3 lists many of the commoner causes of palpitation and their key features. To make a definitive diagnosis, it is necessary to capture the heart rhythm on an electrocardiogram (ECG) during a typical episode.

Ask the patient whether they have any additional symptoms during an episode of palpitation, such as dizziness or syncope (see below), chest pain or breathlessness, as this will indicate how troublesome the episodes are and therefore guide the urgency of treatment . Some patients notice a need to pass urine just after an episode of supraventricular tachycardia.

Pre-syncope and syncope

Syncope refers to a transient loss of consciousness resulting from transient global cerebral hypoperfusion (in contrast to other causes of loss of consciousness, such as epilepsy). The cerebral hypoperfusion is a consequence of a fall in cardiac output and/or a fall in peripheral vascular resistance. Syncope is characterized by:

  • a rapid onset
  • a short duration 
  • a full recovery.

Patients with syncope may experience a prodrome (pre-syncope) in which they have a feeling of lightheadedness, ringing in the ears, visual disturbance, nausea and sweating. These prodromal symptoms last just a few seconds before the syncopal event occurs – if the patient is able to lie down (to improve cerebral perfusion) during that time, they might avoid a syncopal event altogether. Ask the patient about:

  •  frequency of pre-syncopal and syncopal episodes G any prodromal symptoms (pre-syncope)
  • specific triggers (e.g. pain, micturition, sudden, head-turning, exertion)
  • speed of onset of symptoms
  • any associated symptoms (e.g. palpitations, chest pain, fits, tongue biting, incontinence)
  • duration of event
  • rapidity of recovery
  • any residual symptoms after the event.



In a patient with syncope, make every effort to obtain a detailed description of the syncopal events from a witness. Patients typically recall little or nothing about the syncopal events themselves, so information from a witness can prove invaluable in making a diagnosis.


The cardiovascular causes of syncope can be classified as:

  • reflex (neurally mediated) syncope
  • syncope secondary to orthostatic hypotension 
  • cardiac syncope.

Reflex (neurally mediated) syncope can be predominantly vasodepressor (i.e. fall in blood pressure), predominantly cardio-inhibitory (i.e. fall in heart rate), or a mixed vasodepressor/cardio-inhibitory type. Examples include:

  • vasovagal syncope, which can occur with pain or emotional stress, or in specific situations such as during micturition or coughing
  • carotid sinus hypersensitivity, where pressure over the carotid sinus (e.g. tight collar, head turning) triggers syncope.

Syncope secondary to orthostatic hypotension (often called ‘postural hypotension’) is typically seen with hypovolaemia (e.g. haemorrhage or dehydration), autonomic failure or secondary to certain drugs (e.g. vasodilators such as angiotensinconverting enzyme inhibitors or a-receptor blockers). Patients with orthostatic hypotension report pre-syncopal symptoms and/or syncope occurring after suddenly standing.

Cardiac syncope is seen with some arrhythmias (e.g. bradycardia, such as complete heart block or sick sinus syndrome, and tachycardia, such as ventricular tachycardia) and also with structural heart disease where there is an obstruction to blood flow (e.g. aortic stenosis, hypertrophic obstructive cardiomyopathy, atrial myxoma). With obstruction to left ventricular outflow (aortic stenosis and hypertrophic obstructive cardiomyopathy) the presyncope/syncope typically occurs on exertion; with atrial myxoma it can occur at any time if the myxoma transiently obstructs flow through the mitral or tricuspid valve.



Dizziness is a vague term that can be used to refer to a feeling of vertigo, light-headedness, pre-syncope or unsteadiness (‘disequilibrium’). It is important to obtain as much detail as possible about the symptoms, and how and when they occur, to characterize the patient’s complaint more fully. Dizziness can be cardiovascular in origin, but can also result from inner ear pathology or a neurological disorder. Ask about associated symptoms such as vertigo (do the surroundings ‘spin round’?), hearing disturbance, muscle weakness and falls.


Peripheral oedema

Peripheral oedema is both a symptom and a sign, because it is a physical abnormality which is visible to the patient. It is typically noticed as ankle swelling, often worse in the evening, but can extend all the way up the legs and involve the abdomen (and, in recumbent patients, the sacrum). Peripheral oedema is most commonly associated with heart failure, but there are a number of other causes. Oedema is described as pitting (where finger pressure leaves an indentation) or non-pitting. The causes of pitting oedema are listed in Table 7.4. Non-pitting oedema is seen in hypothyroidism (pretibial myxoedema) and in lymphoedema.

Table 7.4 Causes of pitting oedema


The rest of the history


Past medical/surgical history

Enquire about:

  • a known diagnosis of angina or myocardial infarction
  •  how certain was the diagnosis?
  • previous investigations, such as coronary angiograms
    • xanthelasma – raised yellow deposits of cholesterol beneath the skin around the eyes
    • anaemia – which can exacerbate angina and breathlessness
    •  jaundice (yellow sclerae) – which in the context of cardiovascular disease may indicate hepatic congestion (in congestive cardiac failure)
    • corneal arcus – a white/yellow ring around the circumference of the cornea, which is seen in hyperlipidaemia (particularly when present in those aged <40 years) or in normal ageing (‘senile arcus’). previous cardiac operations or procedures:
        • coronary revascularization (coronary artery bypass grafting or percutaneous coronary intervention)
        • valve surgery (valvotomy, repair or replacement)
        • permanent pacemaker implant
        •  implantable cardioverter-defibrillator implant
          •  known congenital heart disease, and any corrective surgery
          • rheumatic fever in childhood
          • other known cardiovascular conditions, such as heart failure, arrhythmias, murmurs or palpitations.

      Cardiovascular risk factors

      These can be divided into modifiable and nonmodifiable risk factors.

      • Modifiable risk factors are: 
        • hypertension
        • diabetes mellitus
        • hyperlipidaemia
        • tobacco smoking.

      Non-modifiable risk factors are: 

      • age
      • gender
      • family history (see below).

      Drug history

      Note down the drugs currently being taken by the patient. Also enquire about drugs taken previously, together with any adverse effects they might have had.

      Allergies and adverse reactions

      Document details of any known allergies and adverse reactions. Examples with particular relevance to cardiology include:

      • aspirin allergy
      • aspirin intolerance (e.g. excessive bleeding, gastrointestinal upset, worsening asthma)
      • β-blocker intolerance (e.g. bronchospasm)
      • angio-oedema, intolerable cough or renal impairment with angiotensin-converting enzyme inhibitors
      • rhabdomyolysis with statins
      • allergy to iodine-based contrast agents (e.g. during coronary angiography).

      Social history


      • Smoking is strongly associated with the development of cardiovascular disease.
      • Record whether the patient is a current or exsmoker, or has never smoked.
      •  For cigarette smokers, calculate the lifetime consumption in terms of ‘pack-years’. Thus 40 cigarettes (2 packs) per day for 15 years is a 30 pack-year smoking history


      • Excessive alcohol consumption can be a causative factor in hypertension, atrial fibrillation and dilated cardiomyopathy
      • Record alcohol consumption in terms of units per week, but also describe the pattern of drinking (e.g. 14 units per week could equal 2 units every day or ‘binge’ drinking of 14 units all in 1 day).


      Caffeine consumption can be a factor in palpitations, so document the patient’s consumption of caffeine containing drinks (e.g. coffee, cola drinks)

      Recreational drug use

      • Cocaine can cause coronary artery spasm, which further causes myocardial ischaemia and infarction.
      • Volatile substance (e.g. butane gas) misuse can cause arrhythmias.
      • Infective endocarditis affecting the right heart can occur in intravenous drug users.


      Ask about the patient’s occupation. A diagnosis of cardiovascular disease can have serious career implications (e.g. pilots, military personnel, ‘occupational’ drivers). Where appropriate, patients should seek advice from their occupational health department.


      • Ask whether the patient drives a vehicle, and the type of driver’s license that they hold (e.g. ‘standard’ license, heavy goods or public service vehicle license).
      • Rules vary according to the nature of the driving (e.g. there are special rules for ‘occupational’ driving) and the underlying cardiovascular condition.
      • In the UK, detailed guidance is available from the Driver and Vehicle Licensing Agency (DVLA) in its regularly updated ‘At a Glance’ document on Medical Standards of Fitness to Drive (see www.

      Effects of the cardiovascular condition on home and family life

      • Impaired mobility due to chest pain or breathlessness.
      • Psychological effects (e.g. fear of dying).
      • Sexual function (e.g. impotence due to use of b-blockers).

      Family history

      Enquire about any family history of sudden cardiac death, which may indicate a familial disorder that predisposes to arrhythmias (e.g. long QT syndrome, Brugada syndrome).

      Other cardiovascular conditions with a genetic basis include:

      • Marfan’s syndrome
      • hypertrophic cardiomyopathy 
      • familial hypercholesterolaemia (see



      A family history of coronary artery disease increases an individual’s risk by half, but only where it affects a first-degree relative at a ‘premature’ age (younger than 55 years for male relatives and 65 years for female relatives). If more than one first-degree relative is affected, the patient’s risk is doubled.




      General examination

      Begin the cardiovascular examination by ensuring that the patient is reclining comfortably on a couch at an angle of 45°. Take a step back, and inspect the patient’s general appearance.

      Do they appear:

      • comfortable at rest
      •  breathless
      • sweaty or clammy (‘diaphoretic’)
      • cachectic (e.g. as a result of longstanding heart failure – cardiac cachexia)?

      Be alert to the features of specific genetic and endocrine diseases that can be associated with cardiac problems:

      • Marfan’s syndrome
        • tall stature, high-arched palate, lens dislocation
        • mitral valve prolapse, aortic dilatation, aortic dissection
      • Ehlers–Danlos syndrome
        • joint hypermobility, elastic skin, easy bruising G mitral valve prolapse, aortic (and other arterial) aneurysms
      • Down’s syndrome
        • microgenia, macroglossia, epicanthic folds, single transverse palmar crease
        • complete atrioventricular septal defects
      • Turner’s syndrome
        • short stature, broad chest, webbed neck
        • bicuspid aortic valve, coarctation of the aorta
      • thyrotoxicosis
        • heat intolerance, weight loss, tremor
        • tachycardia
      • hypothyroidism
        • cold intolerance, fatigue, weight gain, depression
        • bradycardia
      • acromegaly
        • enlargement of hands and feet, prominent brow
        •  cardiomyopathy.


      The hands

      Look for signs of:

      • cyanosis (e.g. right-to-left intracardiac shunt)
      • clubbing – causes are listed in Table 7.5
      •  splinter haemorrhages (Fig. 7.1) – narrow red/brown lines beneath the nails, aligned in the direction of nail growth, most commonly due to trauma but also found in infective endocarditis
      • Osler’s nodes – an uncommon manifestation of infective endocarditis, these are tender, red lesions that occur on the fingertips, palms and soles
      • Janeway lesions (Fig. 7.2) – also seen in infective endocarditis (infrequently), these are maculopapular lesions that occur on the palms and soles but, unlike Osler’s nodes, are non-tender
      •  tendon xanthoma – yellowish cholesterol deposits in the tendons, often in the hands or at the elbow/knee, seen in hyperlipidaemia
      • staining of the fingers as a consequence of cigarette consumption.

      Table 7.5 Causes of clubbing

      Figure 7.1 Splinter haemorrhages.

      Figure 7.2 Multiple Janeway lesions on the hand in Staphylococcus aureus endocarditis.


      Arterial pulses

      During or after your examination of the hands, check the patient’s radial pulse at the wrist using the tips of your forefinger and middle finger. Assess:

      • pulse rate
      •  pulse rhythm.

      Rate and rhythm can also be assessed at the brachial pulse in the antecubital fossa, medial to the biceps tendon.

      Pulse rate

      Count the number of pulsations over a period of 30 seconds, and then double this figure to obtain the pulse rate in beats per minute (bpm). A normal pulse rate is between 60 and 100bpm. A rate <60bpm is termed bradycardia, and >100bpm is called tachycardia.


      Bradycardia may result from slowing of the heart’s sinoatrial node (‘sinus bradycardia’), which may be due to a normal physiological cause (as seen in athletes, or during sleep), a problem within the node itself (e.g. sick sinus syndrome) or an external factor (e.g. hypothyroidism, hypothermia). Several drugs slow the sinoatrial node, including b-blockers, verapamil, diltiazem and digoxin. Alternatively, the sinoatrial node itself may be working normally but not all its impulses are reaching the ventricles (e.g. in second or third-degree atrioventricular block). Abnormal rhythms such as atrial fibrillation or flutter may also be associated with bradycardia if there is a high degree of atrioventricular block.

      Bradycardia may also be an ‘apparent’ bradycardia rather than a ‘true’ bradycardia. This can occur when the patient is experiencing ventricular ectopic beats – these are ‘weaker’ than normal beats, and so palpation of the radial pulse may fail to detect them, leading to an underestimation of the true heart rate.


      Tachycardia may result from a high sinoatrial rate (‘sinus tachycardia’), which may be due to a normal physiological cause (as seen with pregnancy, anxiety, or pain), a problem with the node itself (e.g. ‘inappropriate sinus tachycardia’) or an external factor (e.g. thyrotoxicosis, blood loss). Several drugs increase the sinoatrial rate, including atropine, dobutamine and salbutamol. Abnormal rhythms such as supraventricular tachycardia or ventricular tachycardia cause a fast heart rate, as do (usually) atrial fibrillation or flutter.

      Pulse rhythm

      The pulse rhythm can be described as:

      • regular
      • irregular:
        • ‘regularly irregular’
        •  ‘irregularly irregular’.

      Sinus rhythm is usually regular, although in younger patients there can be a noticeable variation in heart rate with respiration (sinus arrhythmia) – this is normal. Several abnormal rhythms can be regular too, including supraventricular tachycardia (atrioventricular re-entry tachycardia and atrioventricular nodal re-entry tachycardia (AVNRT)), atrial tachycardia, atrial flutter (with regular block), and ventricular tachycardia.

      A ‘regularly irregular’ rhythm is one in which there is a predictable change in rhythm – this can be seen in second-degree Mobitz I heart block (Wenckebach’s phenomenon), where a beat is ‘dropped’ on a regular basis, or with regular ventricular ectopic beats (e.g. ventricular bigeminy, trigeminy, etc.). An ‘irregularly irregular’ rhythm is one in which the occurrence of each beat is chaotic and unpredictable, and is usually the result of atrial fibrillation.


      Pulse character and volume

      With the exception of a collapsing pulse, pulse character and volume are not easily assessed at the radial pulse because it is so far from the heart (so the pulse has become quite ‘damped’). In most cases it is easier and better to assess pulse character and pulse volume using the brachial pulse or, even better, the carotid pulse.

      Several types of abnormal pulse character are recognized.

      • Slow-rising pulse (‘pulsus parvus et tardus’) – with a gradual ‘upslope’ which peaks in late systole, this pulse is also weak and is characteristic of severe aortic stenosis.
      • Collapsing pulse – assessed by raising the patient’s arm above their head while palpating the radial pulse, this pulse has an early peak followed by a sharp descent and indicates aortic regurgitation. It is also known as a ‘water hammer’ pulse.
      • Biphasic pulse (‘pulsus bisferiens’) – this describes a ‘double peak’ pulse and is classically found in mixed aortic stenosis and regurgitation, and also in hypertrophic obstructive cardiomyopathy.
      • Alternating pulse (‘pulsus alternans’) – this describes alternate strong and weak beats, and is found in severe left ventricular systolic dysfunction.
      • Pulsus paradoxus – this refers to an exaggeration of the normal variation in pulse volume with respiration (which decreases on inspiration and increases on expiration). It is seen in cardiac tamponade, and also in severe asthma and chronic obstructive pulmonary disease.



      A large volume pulse is seen with increased cardiac output (e.g. pregnancy, anaemia, thyrotoxicosis, sepsis) and in aortic regurgitation. A small volume pulse is seen with reduced cardiac output (e.g. severe left ventricular failure, severe aortic stenosis) and/ or reduced circulating volume (e.g. haemorrhage, dehydration).

      Finally, check for radio-femoral delay by palpating the radial and femoral pulses simultaneously. Normally the two pulses occur together, but the femoral pulse is delayed relative to the radial pulse in the presence of coarctation of the aorta.


      Blood pressure

      Before taking a patient’s blood pressure (BP), explain what you are about to do and try to ensure that the patient is as relaxed as possible. Standard BP measurements are made in a warm environment, with the patient sitting and the arm supported at the level of the heart. Patients should be seated for 5 minutes before the measurement is taken. Which arm is used is unimportant, but it is a good idea to check BP in both arms on a patient’s first visit.



      • A standard cuff (bladder 12 × 26 cm) for most adults.
      • A large cuff (bladder 12 × 40 cm) for obese arms.
      • A small cuff (bladder 12 ×18 cm) for lean adult arms and children.


      Locate the position of the brachial artery in the antecubital fossa and position the BP cuff 2–3cm above the antecubital fossa with the centre of the cuff ’s bladder over the line of the artery. Using a cuff that is too small leads to an overestimation of blood pressure, and vice versa (see Box 7.1).

      Before using the stethoscope, estimate the systolic pressure by palpating the brachial artery and inflating the cuff until the brachial pulse disappears – this is the systolic pressure estimated by palpation.

      Next, place your stethoscope over the brachial artery (without applying excessive pressure) and reinflate the cuff to 30mmHg above the systolic pressure estimated by palpation. Gradually reduce the pressure at 2–3mmHg per second and listen carefully for the point at which repetitive, clear tapping sounds first appear for two or more consecutive beats – this marks the systolic blood pressure (Korotkoff phase 1, Table 7.6). Continue to deflate the cuff, and the point where the sounds finally disappear marks the diastolic blood pressure (Korotkoff phase 5). Both measurements should be taken to the nearest 2 mmHg.

      In pregnancy, determining diastolic pressure is trickier as the sounds often continue all the way to zero. In this case, take the diastolic pressure as the point at which the sounds become muffled (Korotkoff phase 4).

      Table 7.6 Korotkoff phases.

      Orthostatic hypotension

      Normally on standing there is a modest drop in systolic BP and a modest rise in diastolic BP, keeping mean arterial pressure constant. Orthostatic hypotension refers to a fall in blood pressure on standing, and can occur in volume depletion (e.g. as a result of haemorrhage) and be a cause of syncope. However, testing for orthostatic hypotension is often performed incorrectly. When checking for a ‘postural drop’, it is important to check the pulse as well as the BP – a rise in pulse rate of ≥30bpm or an inability to complete the test due to postural dizziness is a sensitive indicator of hypovolaemia (Brostoff, 2009). A drop in systolic BP of ≥20 mmHg or diastolic BP ≥10mmHg is also often taken as an indicator of a ‘significant’ postural drop, but such a measurement must be taken after at least 1 minute of standing.


      Face and eyes

      Inspect the patient’s face for signs of a malar flush – a reddish colour over the cheeks, seen in mitral stenosis with pulmonary hypertension. Next, take a closer look at the patient’s eyes. Look for:

    • xanthelasma – raised yellow deposits of cholesterol beneath the skin around the eyes
    • anaemia – which can exacerbate angina and breathlessness
    •  jaundice (yellow sclerae) – which in the context of cardiovascular disease may indicate hepatic congestion (in congestive cardiac failure)
    • corneal arcus – a white/yellow ring around the circumference of the cornea, which is seen in hyperlipidaemia (particularly when present in those aged <40 years) or in normal ageing (‘senile arcus’).

      Using an ophthalmoscope, carefully inspect the fundi, looking for:

      • Roth spots – retinal haemorrhages with a pale centre, seen in infective endocarditis (but also in several other disorders, including leukaemia, anaemia and vascular diseases)
      • hypertensive retinopathy (Table 7.7, Fig. 7.5). 

      Table 7.7 Grades of hypertensive retinopathy

      Figure 7.5 Hypertensive retinopathy.

      Ask the patient to open their mouth. Look for:

      • central cyanosis (blue tongue)
      •  poor dentition – which may pose a risk of bacteraemia and infective endocarditis
      • high arched palate – a feature of Marfan’s syndrome.


      Jugular venous pressure

      Examination of the jugular venous pressure (JVP) tells you about the pressure within the right atrium (judged from the ‘height’ of the JVP) and about right heart function (judged from the JVP waveform). With the patient reclining at an angle of 45° and with the neck muscles relaxed (use a pillow), inspect the right side of the neck to assess venous pulsation in the right internal jugular vein. This runs from the angle of the jaw, down the neck (passing deep to the sternocleidomastoid muscle), to the sternoclavicular joint. Avoid using the left internal jugular vein (which provides a less accurate guide to the JVP) or the external jugular veins (which are more superficial, and therefore more easily visible, but are more likely to ‘kink’).

      Sometimes it can be tricky to distinguish between pulsation in the internal jugular vein and the carotid artery. Table 7.8 lists some helpful pointers.

      Table 7.8 Distinguishing characteristics of venous and arterial neck pulsation.

      Height of the JVP



      Normal mean right atrial pressure is ≤ 9cm H2O (which equates to ≤7 mmHg), so the height of the normal JVP is no more than 4 cm above the sternal angle.


      As there are no valves between the right atrium and the internal jugular veins, there is effectively a column of blood which acts as a manometer, the height of which reflects right atrial pressure. With the patient reclining at 45°, measure the height of the JVP (taken as the maximum height of pulsation in the right internal jugular vein) vertically in relation to the angle of the sternum, which itself lies approximately 5cm above the centre of the right atrium (Fig. 7.6). Thus a JVP which lies exactly at the level of the sternal angle (0cm) equates to a right atrial pressure of 5 cm H2O.

      Figure 7.6 Positioning the patient to assess the JVP.


      You can state the height of the JVP either in relation to the sternal angle (‘The JVP lies 2cm above the sternal angle’) or in terms of right atrial pressure (in cm H2O) by adding 5 cm H2O to your measurement (‘The right atrial pressure is 7 cm H2O’, i.e. 2 + 5). Whichever way you choose to express the JVP, be clear and consistent with your terminology – simply writing ‘JVP + 5’ in the case notes does not make it clear whether the JVP is 5 cm above the sternal angle (abnormally elevated) or the right atrial pressure is 5 cm H2O (normal). Box 7.2 lists the causes of raised JVP.



      • Heart failure
      • Fluid overload
      • Superior vena cava obstruction
      • Pulmonary embolism
      • Constrictive pericarditis
      • Cardiac tamponade


      An additional manoeuvre that can be performed is the ‘abdomino-jugular test’, widely known as ‘hepato-jugular reflux’ (see Box 7.3). This tests the ability of the right heart to deal with an increase in venous return, and is positive if the right heart fails to do so, as in right ventricular failure, pericardial constriction, cardiac tamponade and tricuspid valve disease. The test is performed by applying firm pressure with your right hand over the patient’s periumbilical area for 30 seconds while observing the height of the JVP. A sustained elevation of ≥4cm in the JVP throughout the test represents a positive (abnormal) result.



      The term ‘hepato-jugular reflux’ is widely used but rather misleading. First, pressure should be applied over the peri-umbilical area, not specifically the liver, to cause splanchnic (not hepatic) blood to return to the circulation. Second, the physiological mechanism is still not fully understood, so to call it ‘reflux’ may not be correct. Third, some textbooks refer to it as the ‘hepato-jugular reflex’, which is definitely incorrect. The best term may be ‘abdomino-jugular test’. For an excellent discussion of this, and other topics, see Brostoff JM. Re-examining examination: misconceptions in clinical medicine. Journal of the Royal Society of Medicine 2009; 102: 11–15. 

      Character of the JVP

      The character or waveform of the JVP can be challenging to assess. The normal waveform has three peaks (a, c, v) and two descents (x, y), as shown in Figure 7.7.

      Figure 7.7 The normal JVP waveform.


      • ‘a’ wave – represents right atrial contraction:
        •  ‘a’ waves are prominent when right atrial pressure is raised (e.g. pulmonary hypertension, tricuspid stenosis)
        • giant ‘a’ waves (‘cannon waves’) are seen when atrial systole occurs against a closed tricuspid valve (e.g. complete heart block, ventricular tachycardia with retrograde atrial depolarization)
        •  ‘a’ waves are absent in atrial fibrillation (no atrial systole).
      •  ‘x’ descent – represents atrial relaxation:
        • ‘x’ descent is prominent in cardiac tamponade and constrictive pericarditis.
      •  ‘c’ wave – interrupts the ‘x’ descent and represents a transmitted pulsation from the carotid artery; it also happens to mark the moment of tricuspid valve closure at the onset of ventricular systole.
      • ‘v’ wave – represents atrial filling while the tricuspid valve is closed (during ventricular systole)
        •  ‘v’ waves are prominent in tricuspid regurgitation due to regurgitation of blood from the right ventricle back into the right atrium.
      • ‘y’ descent – represents rapid ventricular filling after the tricuspid valve opens:
        • ‘y’ descent is slow in tricuspid stenosis
        •  ‘y’ descent is prominent in tricuspid regurgitation and constrictive pericarditis



      Normally the height of the JVP falls on inspiration. However, if right ventricular filling is impaired (e.g. right ventricular infarction, constrictive pericarditis, cardiac tamponade) the opposite can happen – the JVP rises on inspiration. This is called Kussmaul’s sign.


      Inspection of the precordium

      Carefully inspect the chest wall, looking for:

      • chest wall deformities:
        • pigeon chest deformity (pectus carinatum) 
        • funnel chest deformity (pectus excavatum)
      • operation scars:
        • midline sternotomy (e.g. coronary artery bypass and/or valve surgery)
        • left lateral thoracotomy (mitral valvotomy)
      • devices:
        • permanent pacemaker
        • implantable cardioverter-defibrillator (ICD) 
        • implantable loop recorder
      • visible pulsation: 
        • apex beat.


      Palpation of the praecordium

      Using the flat of your hand and with your fingers outstretched, palpate the praecordium to:

      •  locate and characterize the apex beat
      • check for a left parasternal heave
      • check for thrills (apex, pulmonary and aortic areas).


      The apex beat

      The apex beat refers to the most lateral and inferior position in which the cardiac impulse can be palpated – usually the fifth left intercostal space in the left midclavicular line. Locate the apex with the index finger of your right hand and then, with your left hand, ‘count down’ the rib spaces until you reach the space in which the apex beat lies. You may need to ask the patient to roll to their left (the ‘left lateral position’) to make the apex beat more easily palpable.

      Having located the apex beat (see Box 7.4), determine its character with your fingertips. Normally the pulsation of the apex beat is relatively gentle. However, a number of abnormalities are recognized. It is easy to tie yourself in knots over the terminology used to describe apex beat character, but essentially there are five distinct abnormalities you need to recognize.

      • Pressure-loaded apex – a localized, heaving and sustained apex beat, which is found in pressure overload (e.g. left ventricular hypertrophy due to aortic stenosis or hypertension).
      •  Volume-loaded apex – a diffuse, thrusting and non-sustained apex beat, which is found in volume overload (e.g. mitral regurgitation).
      • Tapping apex – a palpable loud first heart sound, found in mitral stenosis.
      • Double impulse apex – two beats are felt during each systole. This is found in hypertrophic cardiomyopathy.
      • Dyskinetic apex – an uncoordinated and diffuse apex beat, usually due to myocardial infarction.



      An impalpable apex beat may be a consequence of:

        • overweight
        • hyperinflated lungs (e.g. chronic obstructive pulmonary disease)
        • pericardial effusion
        • dextrocardia (in which case the apex beat is palpable on the right side of the chest).

      Displacement of the apex beat (laterally and/or inferiorly) can result from:

      •  left and/or right ventricular enlargement
      •  mediastinal shift (so check tracheal position too)
        •  tension pneumothorax
        • large pleural effusion
        •  lung collapse
      • funnel chest deformity (pectus excavatum).

      Left parasternal heave

      Use the heel of your right hand to check for a heave just to the left of the sternum (‘left parasternal heave’) which lifts your hand during systole. The presence of a left parasternal heave indicates right ventricular hypertrophy or dilatation.


      Finally, place the heel of your right hand in the aortic area with your fingers lying across the pulmonary area, and feel for a thrill (a vibrating sensation) in both areas. A thrill is caused by turbulent blood flow and represents a palpable murmur. Thrills may also be felt at the apex and left sternal edge (so be alert to them while palpating in these areas too). Apical thrills are more easily felt with the patient in the left lateral position; aortic and pulmonary area thrills are best felt with the patient leaning forwards and in end-expiration. Determine whether the thrill is systolic or diastolic by simultaneously palpating the right internal carotid artery with your left hand.



      Auscultation of the heart begins by using the bell in the mitral area (apex, Fig. 7.8), pressing lightly so as not to make the underlying skin taut. The bell is good for low-pitched sounds such as the diastolic murmur of mitral stenosis (see below). Having listened with the bell, now listen again in the same area with the diaphragm of your stethoscope to pick up higher pitched sounds.

      Figure 7.8 Areas in which to auscultate the heart.


      Sticking with the diaphragm, move on to the tricuspid area (lower left sternal edge), pulmonary area (second left intercostal space) and aortic area (second right intercostal space) in turn. As you auscultate in each area, palpate the carotid pulse to time the heart sounds with the cardiac cycle.

      Auscultate also in the axilla (particularly to detect the radiation of a mitral regurgitation murmur) and over both carotid arteries (for the radiation of an aortic stenosis murmur, and for carotid bruits).

      Next ask the patient to roll into the left lateral position and auscultate again with the bell in the mitral area, checking for mitral stenosis. Then ask the patient to sit upright and to lean forwards, and auscultate (during end-expiration: ask the patient to ‘Takeabreathin–Andout–Andstopthere’–auscultate – ‘Now breathe normally’) with the diaphragm in the aortic area and lower left sternal edge for the early diastolic murmur of aortic regurgitation.

      Heart sounds

      First heart sound

      Strictly speaking, the first heart sound (S1) has two components (mitral and tricuspid) and is best heard at the apex. Mitral closure occurs a fraction earlier than tricuspid closure, but for all practical purposes the two occur so closely together that they are heard as a single sound.

      A loud S1 is heard in:

      • mitral stenosis (mitral leaflets are still widely open at the onset of systole)
      • short PR interval (mitral leaflets are still widely open at the onset of systole)
      •  hyperdynamic circulation.

      A soft S1 is heard in:

      • mitral regurgitation (mitral valve leaflets fail to close properly)
      •  long PR interval (mitral leaflets already partly closed at the onset of systole)
      •  low cardiac output.

      A variable-intensity S1 is heard in:

      • atrial fibrillation
      •  ectopic beats
      • complete heart block.

      Second heart sound

      The second heart sound (S2) is made up of two separate sounds that result from aortic valve (A2) and pulmonary valve (P2) closure. In expiration A2 and P2 are almost indistinguishable in adults and so are heard as a virtually single sound (S2), but in inspiration P2 is delayed (by an increase in venous return to the right heart) and so S2 becomes split, with P2 occurring about 50 ms after A2 (Fig. 7.9). Splitting is easiest to hear when auscultating over the pulmonary area.

      Figure 7.9 Splitting of the second heart sound.

      Table 7.9 Grading of murmur intensity


      This normal or ‘physiological’ splitting of S2 becomes wider if P2 occurs later (due to delayed or prolonged right ventricular emptying caused by right bundle branch block or pulmonary stenosis), or if A2 occurs earlier (due to shortened left ventricular emptying due to ventricular septal defect or mitral regurgitation).

      Reversed splitting of S2 (A2 occurring after P2) is heard in delayed or prolonged left ventricular emptying caused by left bundle branch block or aortic stenosis, and in this situation the splitting is best heard in expiration (as P2 occurs, as normal, later during inspiration and therefore moves closer to the late A2).

      Fixed splitting occurs when there is no variation with respiration and is a characteristic feature of

      atrial septal defect. The communication between right and left atria means that pressure changes with respiration affect both right and left heart equally.

      A loud A2 is heard in:

      • systemic hypertension (forceful aortic valve closure).

      A soft A2 is heard in:

      • calcific aortic stenosis (reduced cusp mobility)
      • aortic regurgitation (failure of cusp coaptation).

      A loud P2 is heard in:

      • pulmonary hypertension (forceful pulmonary valve closure).

      Third heart sound

      The third heart sound (S3) is low-pitched and occurs in early diastole soon after S(Fig. 7.10). It coincides with rapid ventricular filling and can be normal in younger patients, particularly athletes and in pregnancy, but in older patients it usually represents reduced left ventricular compliance as seen in heart failure and aortic or mitral regurgitation.

      Figure 7.10 Additional heart sounds.


      The combination of S1 + S2 + S3 is like the cadence of the word ‘Kentucky’. When the patient is tachycardic (as is usually the case when S3 is pathological), this ‘triple rhythm’ is described as a ‘gallop rhythm’. An S3 arising from the left ventricle is best heard at the apex; from the right ventricle, an S3 is best heard at the left sternal edge.

      Fourth heart sound

      The fourth heart sound (S4) is also low-pitched and quite soft, occurring in late diastole just before S1. It is caused by atrial contraction against a poorly compliant left ventricle and is therefore always pathological (e.g. left ventricular hypertrophy, ischaemic heart disease, hypertension, aortic stenosis). The combination of S4 + S1 + S2 is like the cadence of the word ‘Tennessee’. S4 is best heard at the apex.

      Additional heart sounds

      Other heart sounds (Fig. 7.10) that may be heard include:

      • Opening snap – a high-pitched sound best heard at the apex or left sternal edge just after the second heart sound. It occurs in mitral stenosis (and rarely tricuspid stenosis), due to sudden opening of the valve, and is followed by a mid-diastolic murmur.
      • Ejection click – a high-pitched sound best heard in the aortic/pulmonary areas or left sternal edge just after the first heart sound. It occurs in aortic or pulmonary stenosis due to sudden opening of the valve (if the valve is still relatively mobile), and is followed by an ejection systolic murmur.
      • Mid-systolic click – a high-pitched sound best heard at the apex in mid-systole. It occurs in mitral valve prolapse and is usually followed by a late systolic murmur.
      • Prosthetic mitral valve sounds – a mechanical mitral valve will make a metallic opening sound (just after S2) and closing sound (which coincides with S1).
      • Prosthetic aortic valve sounds – a mechanical aortic valve will make a metallic opening sound (just after S1) and closing sound (which coincides with S2).
      • Pericardial rub – a ‘scratchy’ sound heard in both systole and diastole in pericarditis. Pericardial rubs can come and go quite rapidly, and are enhanced with the patient sitting upright and at end-expiration.

      Heart murmurs

      For any heart murmur, describe:

      • timing – where it occurs in the cardiac cycle (Fig. 7.11); palpate the carotid pulse at the same time as auscultating the murmur to assess the timing
      • duration – how long it lasts (e.g. ejection systolic, pansystolic, late systolic)
      • character – high or low pitch, harsh, blowing
      •  loudness – graded on a scale of 1–6 (Table 7.9)
      •  location – the area of maximal intensity
      • radiation – where else it can be heard beyond the area of maximal intensity.

      Figure 7.11 Heart murmurs



      When assessing the intensity of a murmur, bear in mind that intensity is often a poor guide to the severity of the underlying valve lesion.

      Systolic murmurs

      There are three types of systolic murmur:

      • ejection systolic
      • pansystolic
      • late systolic.

      An ejection systolic murmur grows in loudness during early systole, peaks in mid-systole, and diminishes during late systole (‘crescendo-decrescendo’). Ejection systolic murmurs result from:

      • aortic stenosis
      • pulmonary stenosis
      • hypertrophic obstructive cardiomyopathy
      • increased flow (‘flow murmur’)
        • pregnancy
        • anaemia
        • fever
        • atrial septal defect (left-to-right shunt).

      The ejection systolic murmur of aortic stenosis is usually best heard in the aortic area, and radiates to the carotid arteries. The murmur of pulmonary stenosis is best heard in the pulmonary area. In hypertrophic obstructive cardiomyopathy the murmur is usually loudest at the lower left sternal edge. Flow murmurs are generally best heard in the aortic area, except in the case of atrial septal defect in which case it is loudest in the pulmonary area.

      A pansystolic murmur begins with S1 and continues throughout systole to S2. Pansystolic murmurs result from:

      • mitral regurgitation
      •  tricuspid regurgitation
      •  ventricular septal defect.

      The pansystolic murmur of mitral regurgitation is usually best heard at the apex and radiates to the axilla. The murmurs of tricuspid regurgitation and ventricular septal defect are best heard at the lower left ster

      A late systolic murmur begins after S1 and then continues throughout systole to S2. Late systolic murmurs result from mitral regurgitation secondary to:

      • mitral valve prolapse
      •  papillary muscle dysfunction.

      Innocent murmurs

      Innocent murmurs (also known as ‘functional’ or ‘physiological’ murmurs) are those which occur in the absence of any significant structural heart disease. They always occur in systole, are soft, and there are no other symptoms or signs of heart problems. Such murmurs are commonest in children.

      Diastolic murmurs

      There are two types of diastolic murmur:

      • early diastolic
      • mid-diastolic.

      An early diastolic murmur peaks at the start of diastole and then gradually diminishes in loudness. Early diastolic murmurs result from:

      • aortic regurgitation
      • pulmonary regurgitation.

      The early diastolic murmur of aortic regurgitation is usually best heard at the lower left sternal edge, and is enhanced with the patient sitting forward and in expiration. The murmur of pulmonary regurgitation is sometimes called a Graham Steell murmur and is generally found in the context of pulmonary hypertension.

      A mid-diastolic murmur is a low-pitched ‘rumbling’ murmur which is loudest in the middle of diastole. Mid-diastolic murmurs result from:

      • mitral stenosis
      • tricuspid stenosis (rare).

      The mid-diastolic murmur of mitral stenosis is best heard at the apex, and is enhanced with the patient rolled onto their left side. If the patient is in sinus rhythm, there may be an increase in the loudness of the murmur (‘pre-systolic accentuation’) at the end of diastole, coinciding with the ‘kick’ of atrial contraction which increases flow across the stenotic valve.


      Continuous murmur

      A continuous or ‘machinery’ murmur is heard during systole and diastole, and is most commonly due to a persistent (patent) ductus arteriosus (which connects the aorta to the pulmonary artery). The murmur is best heard at the upper left sternal edge and over the left scapula.


      The chest and back

      Ask the patient to lean forwards and perform a chest examination (Chapter 8). In particular, auscultate at the lung bases for the presence of inspiratory crackles, indicating the presence of pulmonary oedema. As pulmonary oedema worsens,

      the crackles may extend higher in the lung fields. A degree of bronchospasm may be evident causing an expiratory wheeze (‘cardiac asthma’). Heart failure may also cause a pleural effusion, usually bilaterally but occasionally unilaterally.

      While the patient is sitting forward, take this opportunity to check the sacral area for pitting oedema. Like ankle oedema, this is a sign of right heart/congestive cardiac failure, and is commonly found when such patients have been confined to bed.


      A number of bedside manoeuvres can affect the intensity of heart murmurs, and this can help in the diagnosis.

        • Inspiration makes right heart murmurs louder (due to an increase in venous return).
        • A Valsalva manoeuvre increases the loudness of the ejection systolic murmur of hypertrophic obstructive cardiomyopathy.
        •  Rapid squatting from a standing position diminishes the murmur of hypertrophic obstructive cardiomyopathy. It also delays the mid-systolic click of mitral valve prolapse.
        •  Sustained handgrip increases the intensity of the pansystolic murmur of mitral regurgitation and ventricular septal defect, but does not affect (or may diminish) the ejection systolic murmur of aortic stenosis.


      The abdomen

      Ask the patient to lie flat and perform an abdominal examination. In particular, check for:

      • hepatomegaly (as a sign of congestive cardiac failure)
      • hepatic pulsatility (in tricuspid regurgitation or, rarely, aortic regurgitation)
      • splenomegaly (in infective endocarditis)
      • ascites (in congestive cardiac failure)
      • abdominal aortic aneurysm.


      The lower limbs

      Examine the lower limbs to assess:

      • the arterial circulationthe venous circulation
      • peripheral oedema.

      Check for the presence of pitting peripheral oedema by applying finger pressure for 15 seconds:

      • pitting is confirmed if a pit (indentation) remains after the finger is removed
      • be gentle – pitting oedema can make the overlying skin very tender.



      If pitting oedema is present, assess how far up the leg it extends (it can sometimes involve the abdominal wall and scrotum). Remember to check for sacral oedema.






      12-lead ECG

      The 12-lead ECG is a relatively simple, safe and widely available tool that can reveal considerable amounts of information about the heart (Fig. 7.12). A detailed discussion of ECG interpretation is outside the scope of this chapter, but helpful textbooks are available. In short, the 12-lead ECG uses information from 10 electrodes (four limb electrodes, one on each limb, and six chest electrodes) to generate 12 different ‘leads’ (or ‘views’) of the heart. Using this information, the ECG can provide information on:

      • heart rate
      • heart rhythm
      • structural heart abnormalities (e.g. atrial enlargement, ventricular hypertrophy)
      • myocardial ischaemia
      • myocardial infarction
      • electrolyte abnormalities
      • drug effects on the heart
      • miscellaneous abnormalities (e.g. hypothermia).

      Figure 7.12 12-lead ECG showing an acute anterolateral ST-segment elevation myocardial infarction.


      In reporting on a 12-lead ECG, always adopt a structured approach:

      • check the patient’s identification details
      • check the date and time of the recording
      • assess the heart rate
      • assess the heart rhythm
      • measure the cardiac axis (normally between –30° and +90°)
      • inspect the P waves (= atrial depolarization, Fig. 7.13)
      • measure the PR interval (normally between 120 and 200 ms)
      • check for abnormal Q waves
      • inspect the QRS complexes (= ventricular depolarization)
      • assess the ST segments
      •  inspect the T waves
      • measure the QT interval
      • check for any additional features, e.g. J waves, U waves.

      Figure 7.13 Components of the normal ECG.

      Ambulatory ECG

      When investigating a patient who has episodic palpitations, there is no substitute for obtaining an ECG recording during an episode of palpitation. This usually requires some form of ambulatory ECG monitoring, with the patient wearing or carrying an ECG monitor for an extended period until a symptomatic event occurs. This can be achieved using one of the following methods:

      • 24-hour ambulatory ECG recording
      • event recorder
      • implantable loop recorder.

      The appropriate choice of method depends upon how frequently symptomatic episodes occur – there is little point in a 24-hour recording if the patient only experiences palpitations once every 3 months, for instance.

      Exercise ECG

      Exercise ECG testing can be useful in:

      • diagnosing chest pain
      • risk stratification in stable angina
      • risk stratification after myocardial infarction
      • assessing exercise-induced arrhythmias
      • assessing the need for a permanent pacemaker
      • assessing exercise tolerance
      • assessing response to treatment.

      Exercise ECG testing is usually performed using treadmill or bicycle exercise, with continuous 12-lead ECG and blood pressure monitoring. Any relevant symptoms (e.g. chest tightness and/or breathlessness) are noted, together with any ischaemic ECG changes (classically ST-segment depression, but sometimes T wave inversion), arrhythmias or abnormal blood pressure response.


      Chest X-ray

      The chest X-ray has many roles in cardiac assessment.

      • Assessing heart size – the cardiothoracic ratio, which compares the transverse diameter of the heart to that of the thoracic cage, is normally <50 per cent. An increased cardiothoracic ratio indicates enlargement of the heart (cardiomegaly), e.g. due to dilated cardiomyopathy or pericardial effusion.
      • Assessing heart shape – in certain conditions the cardiac silhouette may be abnormal (e.g. the ‘boot-shaped’ heart of tetralogy of Fallot, Fig. 7.14).
      • Assessing lung fields:
        • left ventricular failure (upper lobe venous diversion, Kerley B lines, diffuse lung shadowing, pleural effusions)
        • enlarged pulmonary arteries (left-to-right shunts).
      • Miscellaneous features:
        • rib notching in coarctation of the aorta
        • sternal sutures following cardiothoracic surgery
        • prosthetic heart valves.

      Figure 7.14 Chest X-ray showing the ‘boot-shaped’ heart of tetralogy of Fallot. This X-ray also shows right upper lobe collapse secondary to previous tuberculosis.



      Cardiac ultrasonography (echocardiography) is one of the most versatile of cardiac investigations, revealing detailed information about cardiac structure and function (Fig. 7.15). In transthoracic echo (TTE) an ultrasound probe is applied to the anterior chest wall to obtain 2-D (and, where available, 3-D) moving images of the heart, and also to assess blood flow using the Doppler principle. There are many indications for TTE, including the assessment of:

      • breathlessness (e.g. left ventricular failure, pulmonary hypertension)
      • heart murmurs
      • infective endocarditis
      • prosthetic valves
      • cardiomyopathy
      • pericardial disease (e.g. pericardial effusion)
      • congenital heart disease.

      TTE can be combined with stress (using exercise or a pharmacological stressor) to assess left ventricular function for signs of myocardial ischaemia or infarction (‘stress echo’).

      Figure 7.15 A normal echocardiogram (‘apical 4-chamber view’ ). LA, left atrium; LV, left ventricle; Ra, right atrium; RV, right ventricle.


      Transoesophageal echo (TOE or TEE) uses the same principles as TTE, but the probe is passed into the patient’s oesophagus. This provides clearer images, making TOE particularly useful when higher resolution imaging is necessary (such as the detection of small vegetations in suspected infective endocarditis). The commonest indications for a TOE study include assessment of:

      • cardiac source of emboli
      • suspected or proven infective endocarditis
      • aortic diseases (e.g. aortic dissection/trauma)
      • regurgitant heart valves, to judge suitability for surgical repair
      • prosthetic valves (especially those in the mitral position)
      • cardiac masses
      • congenital heart disease and intracardiac shunts.


      Nuclear cardiology

      Myocardial perfusion imaging uses a radiopharmaceutical (e.g. thallium-201 or a technetium-99m-labelled radiopharmaceutical), administered intravenously, to assess myocardial blood flow, providing valuable information about coronary artery disease with a high degree of sensitivity and specificity (Fig. 7.16).

      Figure 7.16 Myocardial perfusion imaging.

      Radionuclide ventriculography assesses ventricular function using red blood cells labelled with technetium-99m. The count-rate of the radioactivity can be measured using a gamma camera at different stages of the cardiac cycle, and from this an accurate measure of ejection fraction can be derived.


      Cardiac magnetic resonance imaging

      Cardiac magnetic resonance imaging (MRI) is a highly versatile technique for cardiac imaging and provides both anatomical and functional information. Examples of its many uses include the assessment of:

      • cardiac chamber dimensions and function
      • valvular heart disease
      • cardiomyopathies
      • cardiac masses
      • congenital heart disease
      • pericardial disease
      • aortic abnormalities.



      Although cardiac MRI does not involve exposure to ionizing radiation, it does use a powerful magnetic field and is therefore contraindicated in patients with certain types of metallic implants (e.g. pacemakers, implantable defibrillators and cerebrovascular aneurysm clips).


      Cardiac computed tomography

      Multislice computed tomography (MSCT) is used to image the heart. MSCT scanners contain a gantry carrying an X-ray source that rotates around the patient, and multiple image ‘slices’ are obtained as the patient is moved through the gantry during the scan. The slices are then processed to generate images of the heart in any plane and from any angle, either as a three-dimensional volume rendered image (Fig. 7.17) or as cross-sectional slices.

      Cardiac CT scanning is very fast (it takes just a few seconds to acquire the images) but processing and reporting the images usually takes 10–30 minutes.

      The main use of cardiac CT is in assessment of the coronary arteries. A calcium score can be obtained (reflecting the amount of calcification present in the coronary arteries) and this correlates with the patient’s risk of future cardiovascular events. With the injection of an intravenous contrast agent, the coronary arteries themselves can be imaged (CT coronary angiography).

      Figure 7.17 Cardiac computed tomography (CT) scan (volume rendered image) of a patient with coronary aneurysms resulting from Kawasaki disease.



      Cardiac catheterization

      Cardiac catheterization is an invasive technique, requiring a catheter to be passed to the heart via a peripheral vessel such as the radial or femoral artery. By injecting a contrast agent, the operator can image the coronary arteries (Fig. 7.18) and cardiac chambers. The catheter can also be used to measure intracardiac pressures and oxygen saturations.

      Figure 7.18 Coronary angiogram (showing a normal left coronary artery).




      The discomfort of myocardial ischaemia (angina) is typically felt as a heavy, tight, squeezing or band-like sensation in the centre of the chest (retrosternal), and may radiate to the left and/or right arm, to the neck (causing a ‘choking’ discomfort) and to the jaw. When asked to indicate the location of the discomfort, patients with angina will often hold a clenched fist in front of the sternum (Levine’s sign). Pain which is left sided and/or can be ‘pointed to’ with a finger is unlikely to be angina.



      Myocardial ischaemia can cause breathlessness as well as chest discomfort, and in many cases breathlessness is the predominant symptom (particularly in women). Be sure to ask about breathlessness in patients with suspected myocardial ischaemia, and similarly be sure to consider myocardial ischaemia in the differential diagnosis in patients presenting with breathlessness.


      Angina is typically precipitated and/or exacerbated by physical exertion and is often reproducible, such that patients find that a certain amount of exertion under the same conditions predictably brings on their symptoms. However, some patients notice that their exercise tolerance improves for a while after an angina attack, a characteristic known as ischaemic preconditioning (or the ‘warm-up phenomenon’). Conversely, angina is more easily provoked by exertion after a heavy meal, or by exercising in a cold environment. Many patients will say that their angina is at its worst when trying to walk into a cold headwind. The degree of functional limitation can be categorized as grade I to grade IV according to the Canadian Cardiovascular Society (CCS) angina grading scale statements/Grading%20of%20Angina.pdf

      Anginal symptoms are usually relieved quickly by rest or by the use of sublingual GTN – normally in less than 5 minutes. GTN will also relieve the symptoms of oesophageal spasm, but usually takes longer than 5 minutes to do so.

      Chest pain is regarded as ‘typical’ of angina if it is retrosternal, brought on by stress, and relieved by rest or GTN. Pain which has just two of these characteristics is termed ‘atypical’, and pain with just one characteristic is termed ‘non-specific’.



      A patient’s response to GTN given as a ‘test of treatment’ can sometimes help with the diagnosis of angina. Angina usually improves rapidly with GTN. A response within 5 minutes has a sensitivity of around 60 per cent and a specificity of around 70 per cent for the diagnosis of angina. (Chun AA, McGee SR. Bedside diagnosis of coronary artery disease: a systematic review. Am J Med 2004; 117: 334–43.


      Physical examination is usually unremarkable in stable angina, although there may be signs of associated risk factors such as hyperlipidaemia (tendon xanthoma, periorbital xanthelasma, corneal arcus) or hypertension. Look for evidence of vascular disease elsewhere (carotid artery bruits, diminished peripheral pulses). Auscultation of the heart during an angina attack may reveal evidence of ischaemic left ventricular dysfunction (third or fourth heart sound, ischaemic mitral regurgitation).

      Angina usually occurs in the presence of coronary atheroma, but it can occur in the presence of normal coronary arteries if there is increased myocardial oxygen demand (e.g. hypertrophic cardiomyopathy) or reduced cardiac output (e.g. severe aortic stenosis). It can also result from coronary artery spasm (‘Prinzmetal’s angina’) – the symptoms are similar in character to exertional angina, but typically occur at rest (particularly during the night) and are associated with transient ST segment elevation (rather than depression) on the ECG during episodes of pain. The occurrence of anginal symptoms and myocardial ischaemia in the absence of any anatomical obstruction to blood flow (e.g. coronary atheroma, aortic stenosis) or coronary artery spasm is termed syndrome X and is thought to result from microvascular dysfunction.

      The investigation of angina can be physiological (stress testing with an exercise treadmill test, stress echocardiogram, stress cardiac MRI scan or nuclear myocardial perfusion scan) or anatomical (CT coronary angiogram or cardiac catheterization).



      Acute coronary syndrome

      The chest discomfort of an acute coronary syndrome (ACS) has similar characteristics to that of angina. However, the chest discomfort of ACS is typically:

      • more severe (‘crushing’)
      • longer lasting
      • lacking an obvious precipitant (often occurring at rest)
      • not relieved by GTN
      • associated with sweating, nausea and vomiting.

      Acute coronary syndrome is a medical emergency and you should advise patients to call the emergency medical services when they experience prolonged central chest pain that does not respond to GTN. ACS can be categorized as:

      • unstable angina
      • non-ST-segment elevation myocardial infarction (NSTEMI)
      • ST-segment elevation myocardial infarction (STEMI).

      The clinical features of all three types of ACS are the same, and the diagnosis is based initially on the ECG findings and subsequently on levels of cardiac markers in the blood (e.g. troponin I or T). 

      Physical examination in ACS will often reveal the patient to be unwell and obviously in pain, with sweating (‘diaphoresis’), nausea and vomiting. The remainder of the examination should assess:

      • heart rate:
        • bradycardic if parasympathetic overactivity/ heart block

      tachycardiac if sympathetic overactivity/ tachyarrhythmias

      • blood pressure:
        • low if parasympathetic overactivity/heart failure
        • high if pre-existing hypertension/sympathetic overactivity
      •  JVP – elevated JVP with right ventricular infarction
      • heart sounds:
        • third or fourth heart sound in ischaemic left ventricular dysfunction
        •  mid-late systolic murmur from ischaemic mitral regurgitation
        • pan-systolic murmur from papillary muscle rupture or acute ventricular septal defect
        • pericardial rub from pericarditis
      • evidence of left ventricular failure.



      Aortic dissection

      Aortic dissection, a tear between the layers in the wall of the aorta, usually presents with pain that is:

      • severe
      • of sudden onset
      • interscapular
      • ‘tearing’ in character.

      However, not all of these features will necessarily be present, and sometimes other features (such as those relating to compromised flow in vessels arising from the aorta, see below) may predominate. Such ‘atypical’ presentations mean that aortic dissection is a commonly overlooked diagnosis. You need to maintain a high index of suspicion so as not to miss the diagnosis.   Assess the patient for the presence of risk factors for aortic dissection:

      •  hypertension
      • Marfan’s syndrome
      • Ehlers–Danlos syndrome
      • chest trauma (e.g. blunt injury from a car accident)
      • pregnancy
      • bicuspid aortic valve
      • aortic coarctation
      • syphilitic aortitis.

      A number of vessels arise from the aorta and these may be compromised by the dissection. Patients may therefore have features of:

      • myocardial ischaemia/infarction (coronary artery involvement)
      • neurological deficits (cerebral or spinal artery involvement)
      • renal ischaemia
      • mesenteric ischaemia.

      The aortic dissection can involve the aortic root, causing aortic regurgitation, or rupture into the pericardium, leading to cardiac tamponade. If the aortic dissection compromises flow down one or other subclavian artery, there may be a difference in blood pressure between the two arms – however, such a blood pressure deficit is found in less than a third of cases of dissection.

      A chest X-ray may show a widened mediastinum. Investigations to image the aorta directly and confirm aortic dissection include MRI, CT angiography or transoesophageal echocardiography.



      Aortic dissection is a medical emergency, and must be distinguished from myocardial infarction – the use of a thrombolytic drug is absolutely contraindicated by the presence of an aortic dissection. Remember that the two conditions can occur at the same time, if the dissection involves the origin of one of the coronary arteries.



      Heart failure and cardiomyopathy

      Heart failure is common, affecting 1–2 percent of the population (and is particularly common in the elderly, affecting over 10 per cent of those aged over 85 years). Heart failure is regarded as a clinical syndrome in which patients have the symptoms and signs of heart failure together with objective evidence of a structural or functional cardiac abnormality at rest. It can be classified

      • left and/or right ventricular failure
      • systolic and/or diastolic
      • acute or chronic
      • high output (e.g. thyrotoxicosis) or low output.

      The functional status of patients with heart failure can be graded according to the NYHA scale (Table 7.2). When assessing the patient for symptoms and signs of heart failure, remember to look for evidence of the underlying cause (Box 7.5).



        • Coronary artery disease
        • Hypertension
        • Valvular disease
        •  Viral myocarditis
        • Cardiomyopathy
        • Cardiotoxic drugs e.g. anthracyclines
        • Alcohol.



      Left ventricular failure may be asymptomatic or it may manifest as:

      • exertional breathlessness
      • orthopnoea
      • paroxysmal nocturnal dyspnoea
      • cough (sometimes with pink frothy sputum)
      • fatigue.

      Right ventricular failure:

      • ankle swelling
      • abdominal symptoms (due to hepatic congestion and/or ascites)
        •  loss of appetite
        • abdominal discomfort
        •  abdominal swelling.


      Left ventricular failure:

      • tachycardia
      • alternating pulse (‘pulsus alternans’)
      • hypotension with a narrow pulse pressure
      • displaced, volume-loaded apex beat
      • S3 and/or S4 (gallop rhythm)
      • tachypnoea
      • inspiratory crackles at lung bases
      • pleural effusion (sometimes).

      Right ventricular failure: 

      • elevated JVP
      • ankle and/or sacral oedema
      • hepatomegaly
      •  ascites.

      In advanced heart failure patients may develop muscle wasting and weight loss (‘cardiac cachexia’). Remember that the clinical features of left and right heart failure can co-exist.


      The cornerstone of investigating heart failure is an echocardiogram. Left ventricular size and function (commonly expressed in terms of ‘ejection fraction’) can be assessed, together with right ventricular size and function. Co-existent structural abnormalities (e.g. valvular heart disease), which may be causing or contributing to the heart failure, can be assessed at the same time. The chest X-ray may show an enlarged heart (cardiomegaly), pulmonary venous congestion, pulmonary oedema or pleural effusions.


      Hypertrophic cardiomyopathy

      Hypertrophic cardiomyopathy (HCM) is an autosomal dominant condition affecting 1 in 500 of the population and is a common cause of sudden cardiac death, particularly in the young. The left ventricular hypertrophy in HCM is usually asymmetrical (in contrast to the concentric left ventricular hypertrophy seen in hypertension or aortic stenosis) and systolic function is preserved but diastolic function is impaired. If the hypertrophy is located in the left ventricular outflow tract it may obstruct the flow of blood out of the left ventricle into the aorta – this is hypertrophic obstructive cardiomyopathy (HOCM).

      Hypertrophic cardiomyopathy may be asymptomatic, but can present with:

      • breathlessness
      • chest pain
      • palpitations
      • pre-syncope/syncope
      • (sudden cardiac death).

      Ask about any known family history of the condition (or of sudden death) – family screening is important, so compile a list of first-degree relatives. The clinical features include:

      • ‘jerky’ pulse (pulsus bisferiens)
      • double impulse apex beat
      • fourth heart sound (S4)
      • ejection systolic murmur (if obstruction is present), usually best heard at the lower left sternal edge. The murmur increases in loudness with a Valsalva manoeuvre (in contrast to aortic stenosis, where the murmur becomes quieter).

      The diagnosis of hypertrophic cardiomyopathy can be confirmed with echocardiography.



      • Renal parenchymal disease (e.g. polycystic kidney disease)
      • Renovascular disease (e.g. renal artery stenosis)
      • Endocrine/metabolic:
        • phaeochromocytoma
        • acromegaly
        • Conn’s syndrome
        • Cushing’s syndrome
      • Drugs:
        • steroids
        •  non-steroidal anti-inflammatory drugs
        • oral contraceptives
        • liquorice
      •  Coarctation of the aorta




      Hypertension is arbitrarily defined as a blood pressure >140/90mmHg and is a major risk factor for cardiovascular disease. In 95 percent of cases hypertension is idiopathic (‘essential’ hypertension), but in 5 per cent there is an identifiable underlying cause (Box 7.6).


      Hypertension is usually asymptomatic and discovered as an incidental finding during a ‘routine’ examination. However, it may present with features resulting from end-organ damage:

      • myocardial ischaemia or infarction
      • heart failure
      • peripheral vascular disease
      • aortic dissection
      • cerebrovascular disease (e.g. stroke)
      •  renal failure.


      • Measure blood pressure:
        • grade the severity of hypertension (Table 7.10).
      • Loud aortic component to second heart sound (A2).
      • Look for evidence of an underlying cause of hypertension:
        • renal parenchymal disease
        • renovascular disease
        • endocrine/metabolic disease
        • coarctation of the aorta.
      • Look for evidence of end-organ damage:
        • hypertensive retinopathy
        • left ventricular hypertrophy
        • heart failure
        • cerebrovascular disease (e.g. stroke, transient ischaemic attack, carotid artery bruits)
        • hypertensive encephalopathy
        • peripheral vascular disease.

      Table 7.10 British Hypertension Society classification of blood pressure levels



      Investigations in the hypertensive patient should include:

      • urine dipstick analysis for protein and blood
      • serum urea and electrolytes, glucose, lipid profile
      • ECG
      • echocardiogram, if left ventricular hypertrophy is suspected.

      Ambulatory blood pressure monitoring can be useful in cases of ‘white coat’ hypertension.



      Accelerated (‘malignant’) hypertension is rare, affecting around 1 per cent of hypertensive patients, but is a medical emergency. It is characterized by severe hypertension and the presence of grade III/ IV hypertensive retinopathy and/or hypertensive encephalopathy (seizures, blurred vision, altered mental state).


      Atrial fibrillation

      Atrial fibrillation (AF) is the commonest sustained arrhythmia and affects 5–10 percent of elderly people. It can be classified as paroxysmal, persistent or permanent:

      • paroxysmal AF – spontaneously terminating episodes of AF on a background of sinus rhythm
      • persistent AF – continuous AF with no intervening sinus rhythm
      • permanent AF – continuous AF where there is no expectation of restoring sinus rhythm (e.g. by DC cardioversion).


      Atrial fibrillation may be asymptomatic (incidental finding). However, it may present with:

      • palpitations (irregular and often fast)
      • breathlessness
      • fatigue
      • dizziness or syncope
      • reduced exercise tolerance
      • symptoms arising from systemic embolism (e.g. stroke, peripheral embolism)
      • symptoms of an underlying cause (see Box 7.7).



      • Hypertension
      • Ischaemic heart disease
      • Hyperthyroidism
      • Sick sinus syndrome
      • Alcohol
      • Mitral or tricuspid valve disease
      • Cardiomyopathy
      • Atrial septal defect
      • Pericarditis
      • Myocarditis
      • Pulmonary embolism
      • Pneumonia
      • Cardiac surgery
      • Idiopathic (‘lone’) atrial fibrillation


      Systemic embolism is a significant risk in AF and may also be a presenting feature. The risk of stroke can be estimated using the CHADS2 score (see Box 7.8).



      The CHADS2 score predicts stroke risk in patients with non-rheumatic AF (patients with rheumatic valve disease already have a high stroke risk). The CHADS2 score assigns 1 point for each of the following characteristics:

      • Congestive heart failure
      • Hypertension
      • Age ≥75 years
      • Diabetes mellitus

      and assigns 2 points for:

      • Stroke or transient ischaemic attack.

      Thus patients can have a total CHADS2 score between 0 and 6. A score of 0 is taken to indicate a low risk, 1 a moderate risk, and 2 or more a high risk of stroke.

      Reference: Gage BF et al. Validation of clinical classification schemes for predicting stroke results from the National Registry of Atrial Fibrillation. JAMA 2001; 285: 2864–70.



      The signs of atrial fibrillation include:

      • irregularly irregular pulse, often with tachycardia
      • blood pressure:
        • may be high if underlying hypertension
        • may be low if AF is poorly tolerated
      • absent ‘a’ wave in JVP (absent atrial systole)
      • variable intensity S1
      • signs of left ventricular failure if AF is poorly tolerated
      • signs of underlying conditions (e.g. hyperthyroidism, mitral or tricuspid valve disease).


      The diagnosis of AF can be confirmed with an ECG, which will show absent P waves and an irregularly irregular rhythm, often with a fast ventricular rate. Ambulatory ECG monitoring may be required if the AF is paroxysmal. An echocardiogram will identify underlying structural heart disease, and thyroid function tests are essential, as AF may be the only sign of a thyroid disorder.



      Atrial flutter

      Atrial flutter causes similar symptoms to AF and carries similar implications in terms of ventricular rate control, anticoagulation and cardioversion. However, in atrial flutter the underlying atrial rhythm is regular (approximately 300 atrial depolarizations per minute) as opposed to irregularly irregular in AF. Patients with atrial flutter will often have 2:1, 3:1 or 4:1 atrioventricular block, which gives them a ventricular rate of 150 bpm, 100 bpm or 75 bpm respectively. Unlike AF, the pulse will usually be regular on examination (unless the patient has variable block). Thus from the pulse alone it can be impossible to distinguish between atrial flutter and sinus rhythm, and an ECG should be recorded to confirm the diagnosis.


      Aortic stenosis

      Calcific degeneration of the aortic valve is one of the commonest causes of aortic stenosis and is characterized by progressive fibrosis and calcification of the aortic valve. Bicuspid aortic valve is also common, and is thought to be responsible for around half of cases of severe aortic stenosis in adults (particularly when aortic stenosis occurs at a young age). Rheumatic aortic stenosis is less common than rheumatic mitral stenosis, and the two often co-exist in the same patient. There is fusion of the commissures of the aortic valve cusps and the cusps themselves become fibrotic and eventually calcified.


      Aortic stenosis may be asymptomatic (incidental finding) or it may present with:

      • exertional chest pain
      • exertional dizziness and/or syncope
      • exertional breathlessness.

      The development of symptoms has prognostic implications: those with chest pain as a result of aortic stenosis have an average life expectancy of 5 years, those with exertional syncope 3 years, and those with heart failure just 1 year.


      The signs of aortic stenosis include:

      • slow-rising, small volume pulse
      • low systolic blood pressure and narrow pulse pressure
      • hyperdynamic apex beat (as a result of left ventricular hypertrophy)
      • soft or absent aortic component (A2) to second heart sound
      • reversed splitting of S2 (A2 occurring after P2)
      • ejection click (if cusps remain mobile)
      • harsh ejection systolic murmur
        • loudest in the aortic area
        • may cause a systolic thrill
        • may radiate to the carotid arteries
      • signs of left ventricular failure in advanced cases.

      Indicators of severity

      • Slow-rising pulse.
      • Presence of a systolic thrill.
      •  Soft or absent aortic component (A2) to second heart sound.
      •  Late peaking in the intensity of the ejection systolic murmur.
      •  Symptoms and/or signs of left ventricular failure.

      Differential diagnosis

      An ejection systolic murmur may also be heard with:

      • increased flow across a normal valve (‘innocent’ murmur, e.g. due to fever, anaemia, pregnancy)
      • supravalvular aortic stenosis
      • subvalvular aortic stenosis
      • pulmonary stenosis
      • hypertrophic obstructive cardiomyopathy



      The term ‘aortic sclerosis’ is often used when there is an ejection systolic murmur and on echo some thickening of the aortic valve cusps is evident, but there is no significant pressure gradient across the valve. Many cases of aortic sclerosis subsequently go on to develop stenosis.


      Aortic regurgitation

      Aortic regurgitation can result from a problem with the aortic valve itself or from a problem with the aortic root affecting an otherwise normal valve. Valvular causes include:

      • bicuspid aortic valve, causing incomplete closure of the valve
      • calcific degeneration of the aortic valve
      • rheumatic aortic valve disease
      •  infective endocarditis
      • connective tissue diseases (e.g. rheumatoid arthritis, systemic lupus erythematosus).

      Aortic root causes result from dilatation and/or distortion of the aortic root. These include:

      • hypertension
      • Marfan’s syndrome
      • Ehlers–Danlos syndrome
      • osteogenesis imperfecta
      • aortic dissection
      • sinus of Valsalva aneurysm
      • cystic medial necrosis
      • syphilitic aortitis
      • Behçet disease.


      Aortic regurgitation may be asymptomatic (incidental finding), or may present with symptoms of left ventricular failure:

      • breathlessness
      • orthopnoea
      • paroxysmal nocturnal dyspnoea.

      Symptoms may also indicate the aetiology (e.g. tearing interscapular pain in aortic dissection; fever and sweats in infective endocarditis).


      The signs of aortic regurgitation include:

      • collapsing pulse
      • low diastolic blood pressure and wide pulse pressure G prominent arterial pulsation (Table 7.11)
      • displaced and hyperkinetic apex beat
      • presence of a diastolic thrill in the aortic area/lower left sternal edge
      • soft aortic component (A2) to second heart sound G early diastolic murmur in the aortic area and lower left sternal edge.

      Table 7.11 Eponymous signs in aortic regurgitation.


      There may also be additional murmurs:

      • an ejection systolic murmur, reflecting hyperdynamic flow across the aortic valve
      • an Austin Flint murmur (an apical low-pitched mid-diastolic murmur caused by the regurgitant jet impinging on the anterior mitral leaflet).

      Signs of left ventricular failure may be seen in advanced cases. Signs may also indicate the aetiology, such as:

      • fever and splinter haemorrhages in infective endocarditis
      • clinical features of Marfan’s syndrome
      • signs of aortic dissection.

      Indicators of severity

      • Collapsing pulse
      • Wide pulse pressure
      • Soft aortic component (A2) to second heart sound
      • Presence of a third heart sound (S3)
      • Long diastolic murmur
      • Presence of an Austin Flint murmur
      • Symptoms and/or signs of left ventricular failure.

      Differential diagnosis

      An early diastolic murmur may also be heard with pulmonary regurgitation.

      Mitral stenosis

      Rheumatic valve disease most commonly affects the mitral valve, causing thickening and fusion along the leaflet edges. Other causes of mitral stenosis are rare and include congenital mitral stenosis, mitral annular calcification, systemic lupus erythematosus, rheumatoid arthritis, carcinoid syndrome and infective endocarditis. Some conditions can mimic mitral stenosis by obstructing the mitral orifice, such as left atrial myxoma or infective endocarditis with a large vegetation.

      Rheumatic mitral stenosis usually presents 20–40 years after an episode of rheumatic fever and is now relatively uncommon in developed countries. Most patients are female, and most will have other co-existent valve disease. The symptoms can build up insidiously over a long period, but a new event (such as pregnancy or the onset of atrial fibrillation) can cause a sudden deterioration. Once a patient develops symptoms, if left untreated their 10-year survival is around 50–60 per cent.


      The symptoms often have a gradual onset and include:

      • breathlessness (including orthopnoea and paroxysmal nocturnal dyspnoea)
      • cough
      • haemoptysis
      • peripheral oedema
      • peripheral emboli.


      The signs of mitral stenosis include:

      • malar flush (‘mitral facies’)
      •  low-volume pulse
      • AF (is common)
      • tapping apex beat (palpable S1)
      • loud S1
      • opening snap
      • low-pitched mid-diastolic murmur (with presystolic accentuation if in sinus rhythm) loudest at the apex (use the bell of the stethoscope).

      If you suspect pulmonary hypertension, look for:

      • large ‘a’ wave in the JVP (but the ‘a’ wave is absent if in AF)
      •  left parasternal heave (right ventricular hypertrophy)
      • loud P2.

      Indicators of severity

      • Low-volume pulse
      • Soft S1
      • Early opening snap
      • Long diastolic murmur
      • Signs of pulmonary hypertension.

      Differential diagnosis

      A diastolic murmur may also be heard with:

      • tricuspid stenosis
      • aortic regurgitation (and/or Austin Flint murmur)
      • pulmonary regurgitation
      • left atrial myxoma (listen for a ‘tumour plop’ as the myxoma obstructs the mitral orifice).


      Mitral regurgitation

      Mitral regurgitation can result from dysfunction of any part of the mitral valve apparatus: the leaflets, annulus, papillary muscles or chordae tendineae. Causes include:

      • myxomatous degeneration/mitral valve prolapse
      • rheumatic valve disease
      • infective endocarditis
      • ischaemic heart disease (papillary muscle dysfunction/rupture)
      • mitral annular dilatation (‘functional’ mitral regurgitation, secondary to left ventricular dilatation).


      Mitral stenosis may be asymptomatic. The symptoms may be insidious (chronic MR) or abrupt (acute MR) and include:

      • breathlessness (including orthopnoea and paroxysmal nocturnal dyspnoea)
      • fatigue.

      The symptoms may also indicate the aetiology (e.g. myocardial infarction, infective endocarditis).


      The signs of MR include:

      • AF (may be present)
      • displaced apex beat with hyperdynamic character
      • soft or absent S1
      • S3 present
      • pansystolic murmur
        •  loudest at the apex
        • may cause a systolic thrill
        • may radiate to the axilla
      • signs of heart failure in advanced (or acute) cases.



      Mitral valve prolapse is the single commonest cause of mitral regurgitation in the developed world, and as well as being a result of degenerative valve disease can also occur in collagen disorders such as Ehlers–Danlos syndrome or Marfan’s syndrome, or papillary muscle dysfunction/rupture. Characteristic signs of mitral valve prolapse are a mid-systolic click followed by a late systolic murmur.


      Indicators of severity

      • Displaced apex beat
      • Soft or absent S1
      • Loud S3
      • Early A2
      • Loud pansystolic murmur
      • Signs of pulmonary hypertension
      • Symptoms and/or signs of left ventricular failure

      Differential diagnosis

      A systolic murmur may also be heard with:

      •  tricuspid regurgitation
      • ventricular septal defect
      • aortic stenosis
      • pulmonary stenosis.


      Atrial septal defect

      Atrial septal defect (ASD) can remain asymptomatic for many years and may present late in adult life. It can also be an incidental finding. In advanced cases, the increased pulmonary blood flow eventually leads to pulmonary hypertension and right heart failure.


      Atrial septal defect may be asymptomatic or may present with:

      • breathlessness
      • recurrent respiratory infections
      • palpitations (atrial fibrillation)
      • paradoxical embolism.


      The signs of ASD include:

      • AF – can occur
      • fixed splitting of S2
      • low-pitched diastolic (flow) murmur in tricuspid area
      • ejection systolic (flow) murmur in pulmonary area
      • pulmonary hypertension and right heart failure (advanced cases).


      Ventricular septal defect

      A ventricular septal defect (VSD) permits oxygenated blood flow from the left ventricle into the right ventricle. In advanced cases, the increased pulmonary blood flow eventually leads to pulmonary hypertension and right heart failure. These defects can be congenital or acquired (e.g. post myocardial infarction).


      Ventricular septal defect may be asymptomatic or may present with:

      • breathlessness
      • recurrent respiratory infections.


      The signs of VSD include:

      • systolic thrill at lower left sternal edge
      • wide splitting of S2
      • loud P2 if pulmonary hypertension
      • harsh pansystolic murmur at lower left sternal edge (louder with small defects)
      • pulmonary hypertension and right heart failure (advanced cases).



      Persistent (patent) ductus arteriosus

      A persistent (patent) ductus arteriosus (PDA) is an abnormal connection between the aorta and pulmonary artery, allowing shunting of oxygenated blood to the lungs. The increased pulmonary blood flow eventually leads to pulmonary hypertension and right heart failure.


      A PDA may be asymptomatic or may present with:

      • breathlessness
      • recurrent respiratory infections.


      The signs of PDA include:

      • bounding pulses with a widened pulse pressure
      • systolic thrill in first left intercostal space
      • loud P2 if pulmonary hypertension
      • continuous (‘machinery’) murmur in first left intercostal space
      • pulmonary hypertension and right heart failure (advanced cases).


      Eisenmenger’s syndrome

      The presence of a left-to-right shunt (such as an ASD, VSD or PDA) allows blood to pass directly from the left side of the circulation to the right, increasing the volume of blood flowing through the pulmonary circulation. Over time this leads to pulmonary hypertension and right heart failure. Once right-sided pressures exceed left-sided pressures, the shunt reverses, causing blood to start shunting from right-to-left instead. At this point, the patient is said to have developed Eisenmenger’s syndrome (or reaction). Venous (deoxygenated) blood entering the right heart starts crossing directly into the left heart, bypassing the lungs. Clinical signs include:

      • cyanosis
      • clubbing
      • signs of pulmonary hypertension.


      Coarctation of the aorta

      Coarctation of the aorta is a narrowing that typically occurs just distal to the origin of the left subclavian artery. Patients presenting in adulthood are usually asymptomatic.


      The signs of coarctation of the aorta include:

      • radio-femoral delay with weak lower limb pulses
      • upper body hypertension (arms but not legs)
      • systolic murmur in left infraclavicular area and near left scapula
      • continuous murmur may be present if there are large collateral vessels (which cause rib notching on the chest X-ray).

      There may be features of associated Turner’s syndrome or bicuspid aortic valve (ejection click and possibly murmurs of aortic stenosis and/ or regurgitation).


      Infective endocarditis

      Infective endocarditis refers to an infection of the endocardium (e.g. Staphylococcus aureus, Streptococcus viridians) usually on a background of pre-existing structural heart disease (e.g. valve disease or valve prosthesis, congenital heart disease). In the past, infective endocarditis has been classified as acute or subacute (‘SBE’,subacute bacterial endocarditis) but this terminology is outdated and should no longer be used.


      `The symptoms of infective endocarditis include:

      • fever
      • fatigue
      • anorexia
      • weight loss
      • ’flu-like symptoms.


      The signs of infective endocarditis include:

      • anaemia
      •  fever
      • clubbing
      • splinter haemorrhages
      • Janeway lesions
      • Osler’s nodes
      • Roth spots
      • evidence of underlying structural heart disease, and there may be a new or changing heart murmur
      • splenomegaly
      • peripheral emboli.




      Acute pericarditis

      Acute inflammation of the pericardium can result from viral infection (e.g. Coxsackie), tuberculosis, myocardial infarction (early or late – Dressler’s syndrome), autoimmune disorders (e.g. rheumatoid arthritis), uraemia, malignancy and following cardiac surgery.


      The symptoms of pericarditis include:

      • chest pain
      • sharp or ‘raw’
      • worsened by lying flat
      • eased by sitting forwards
      • varies with respiration
      • cough
      • breathlessness
      • fatigue.


      The signs of pericarditis include:

      • fever
      •  tachycardia
      • pericardial friction rub.



      A pericardial effusion can exert sufficient pressure on the heart to cause haemodynamic compromise – this is called cardiac tamponade. The three ‘classical’ signs of tamponade – known as Beck’s triad – comprise: hypotension; raised JVP; and quiet heart sounds.

      Cardiac tamponade also causes: tachycardia; pulsus paradoxus; prominent x descent in the JVP; and an impalpable apex beat.

      The diagnosis can be confirmed by echocardiography. Cardiac tamponade is a medical emergency, requiring urgent drainage of the pericardial effusion.


      Constrictive pericarditis

      Thickening and fibrosis of the myocardium may follow an episode of acute pericarditis, and this can constrict the heart, restricting the filling of the cardiac chambers. It is particularly common after tuberculous pericarditis.


      The symptoms of constrictive pericarditis include:

      • history of prior acute pericarditis
      • fatigue
      • breathlessness
      • abdominal swelling
      • peripheral oedema.


      The signs of constrictive pericarditis include:

      • pulsus paradoxus
      • raised JVP
        • prominent x and y descents (the sudden ‘collapse’ of the raised JVP is termed Friedreich’s sign)
        • Kussmaul’s sign
      • quiet heart sounds
      • early S3
      • pericardial ‘knock’
        • due to sudden termination of ventricular filling
        • heard early in diastole, after S2
        • occurs earlier, and is a higher pitch than, an S3 added sound
      • hepatomegaly
      • splenomegaly
      • ascites
      • peripheral oedema.


      Constrictive pericarditis or restrictive cardiomyopathy?

      The diagnosis of constrictive pericarditis is notoriously difficult to make, and is often missed. It can be particularly difficult to distinguish between constrictive pericarditis and restrictive cardiomyopathy. Clinical features in favour of constrictive pericarditis include:

      • history of prior pericarditis
      • early S3
      • pericardial ‘knock’
      • absence of mitral or tricuspid regurgitation.

      Echocardiography can be very useful in making the distinction between constrictive pericarditis and restrictive cardiomyopathy.




      Clinical history

      Peripheral arterial disease is usually a consequence of atherosclerosis. The cardinal symptom is intermittent claudication – a sensation of aching, cramping or pain, most commonly in the calf muscle, which is brought on by exercise and relieved by rest. Less commonly, claudication affects the thigh muscles or the buttocks.

      Ask the patient about the character and location of their symptoms, and enquire about functional limitation – how far can they walk before the symptoms occur, and what impact does this have upon their activities of daily living?

      More severe limb ischaemia causes rest pain, often described as a burning discomfort in the foot and toes particularly when lying in bed at night. The patient may also present with non-healing wounds and gangrene.

      Ask about cardiovascular risk factors, particularly diabetes mellitus, and any history of other cardiovascular conditions such as ischaemic heart disease or cerebrovascular disease.


      Physical examination

      Perform a full cardiovascular examination, with a particular emphasis on the arterial pulses. Record the presence or absence of each pulse, and if a pulse is present describe whether it is normal, diminished or aneurysmal. With the patient lying supine on an examination couch, assess the:

      • radial pulse
      • brachial pulse
      • carotid pulse:
        • auscultate for bruits 
      • abdominal aorta:
        •  inspect the abdomen for obvious aortic pulsation
        • palpate the abdomen for the presence of a pulsatile mass – in thin patients a normal aorta may be palpable
        • auscultate for bruits
      • femoral pulse:
        •  palpate with your fingertips in the inguinal crease, midway between the pubic tubercle and anterior superior iliac spine

      auscultate for bruits

      • popliteal pulse:
        •  flex the knee and reach behind, with your thumb on the patella, to palpate the popliteal pulse with your fingertips
      • posterior tibial pulse:
        • palpate with your fingertips just posterior to the medial malleolus
      •  dorsalis pedis pulse:
        • palpate with your fingertips on the dorsum of the foot lateral to the tendon of extensor hallucis longus.

      Inspect the legs for general signs of chronic ischaemia:

      • cool feet/toes
      • shiny, hairless skin
      • toenail dystrophy
      • arterial ulceration, most commonly found on the foot and the mid-shin
        • commoner in men
        • painful
        • has a regular margin
      • gangrene (tissue necrosis, usually affecting the toes).

      Look for evidence of co-existent peripheral venous disease.



      Buerger’s test is used to assess the arterial supply to the leg.

        1. With the patient lying supine on an examination couch, raise both legs to an angle of 45° for 1–2 minutes.
        2. Observe the colour of the feet – pallor while elevated indicates ischaemia.
        3. Ask the patient to sit upright on the edge of the couch, with their legs hanging over the side.
        4. Observe the colour of the feet again. Normally the feet should turn pink. Redness (reactive hyperaemia) indicates peripheral arterial disease.



      The ankle:brachial pressure index (ABPI) is a simple method for assessing the peripheral arterial circulation. A blood pressure cuff is applied around the lower calf (above the ankle) and inflated while a Doppler ultrasound probe is applied to the dorsalis pedis and posterior tibial artery in turn. Record the maximum cuff pressure at the point at which flow in each artery is detected. Then, use the cuff to measure systolic blood pressure at the brachial artery in the right and left arms. Calculate the ratio between the highest pedal artery pressure (dorsalis pedis or posterior tibial) and the highest brachial artery pressure (right or left arm) – this is the ABPI and is normally >1.0. An ABPI <0.9 indicates some degree of arterial disease, and typical values in intermittent claudication lie in the range 0.5–0.8. An ABPI <0.5 indicates severe ischaemia and can be associated with rest pain, arterial ulcers and gangrene. Arterial calcification causes spuriously high ABPIs, often >1.3.

      Other important investigations in peripheral arterial disease are:

      • arterial ultrasound scan (e.g. carotid artery stenosis)
      • CT scan (e.g. abdominal aortic aneurysm)
      • MRI scan (e.g. renal artery stenosis)
      • angiography (e.g. limb ischaemia).


      Common diagnoses


      Acute limb ischaemia

      Acute limb ischaemia is an emergency and commonly results from thrombosis or peripheral embolism. It requires urgent assessment and intervention. The clinical features are summarized by the ‘rule of Ps’:

      • painful (but becoming painless later)
      • paraesthesiae
      • paralysed
      • pale
      • pulseless
      • perishing cold.

      As time passes, the initially pale limb becomes mottled and then dark purple or black.

      Chronic limb ischaemia

      The key features of chronic limb ischaemia are discussed above.


      Mesenteric ischaemia

      See Chapter 9, p. 112.


      Stroke and transient ischaemic attack

      See Chapter 12, p. 203.


      Raynaud’s phenomenon

      Raynaud’s phenomenon occurs when there is an exaggerated vasomotor response, primarily affecting the fingers, in cold weather or as a response to emotional stress. A sequence of changes affects the fingers:

      1. on exposure to cold, the fingers turn pale (white) and become numb due to digital arterial spasm
      2. next, the fingers turn blue (cyanosis) as the blood in the fingers becomes desaturated
      3. onre-warming,thefingersturnredduetoareactive hyperaemia, and this phase can be associated with finger paraesthesiae and swelling, before eventually returning to norm

      Primary Raynaud’s phenomenon (sometimes termed Raynaud’s disease) is idiopathic and is most commonly seen in young women. Secondary Raynaud’s phenomenon is seen in association with such conditions as systemic lupus erythematosus, systemic sclerosis or rheumatoid arthritis.



      The commonest peripheral venous disorders are:

      • varicose veins
      • superficial thrombophlebitis
      • deep vein thrombosis (DVT)
      • chronic venous insufficiency (including ulceration).


      Varicose veins

      Normally the superficial veins of the leg drain into the deep veins via communicating veins. Incompetence of the valves within these communicating veins leads to retrograde filling of the superficial veins, causing the veins to become dilated and tortuous (varicose veins). Varicose veins can be painful (usually an aching or heavy discomfort) and cause itching. Enquire about ankle swelling or any history of leg ulceration or DVT. Ask if the patient has previously had any varicose vein surgery (e.g. sclerotherapy, vein stripping).

      Examine the legs while the patient is standing as well as lying supine. Look for:

      • dilated, tortuous superficial veins
      • ankle swelling
      • venous eczema (also known as gravitational, stasis or varicose eczema), a red-brown discoloration of the skin, often scaly, mainly around the ankle but sometimes more widespread
      • venous ulceration. 


      Trendelenburg’s test

      Trendelenburg’s test assesses the competency of the valves in the communicating leg veins. Ask the patient to lie supine on an examination couch, and then raise the leg as far as practical to empty the superficial veins. Keeping the leg elevated, apply a tourniquet around the upper thigh (compressing the superficial veins) and ask the patient to stand. Normally, the superficial veins will refill slowly from below. If however, there is incompetence of a valve in a communicating vein below the level of the tourniquet, the superficial veins will fill more quickly. If the superficial veins fill rapidly on removal of the tourniquet, the incompetence is above the tourniquet at the level of the sapheno-femoral junction. The test can be repeated with the tourniquet applied at different levels of the leg to precisely locate incompetent valves.


      Superficial thrombophlebitis

      Superficial thrombophlebitis is inflammation of a superficial vein, often with associated thrombosis, causing pain. It most commonly occurs in leg veins (especially varicose veins) but any vein can be affected. Examine the affected vein(s) for redness, swelling, warmth and tenderness. Superficial thrombophlebitis can infrequently lead to deep vein thrombosis and pulmonary embolism. Migratory thrombophlebitis is recurrent, affects otherwise normal veins, and can be associated with underlying malignancy (Trousseau’s sign of malignancy).


      Deep vein thrombosis

      Deep vein thrombosis can be asymptomatic, but commonly presents with pain and swelling in the affected leg. It is usually unilateral and most commonly affects the calf veins, but may extend more proximally. It can also affect the arm (axillary or subclavian vein thrombosis), particularly in patients with a central venous catheter in situ. The main acute risk of a DVT is that the clot embolizes to the lungs, causing pulmonary embolism. In the long term, DVT can result in chronic venous insufficiency (post-thrombotic syndrome).

      Risk factors for DVT include:

      •  immobility
        • recent surgery
        • bed rest
        • prolonged travel
      • age >60 years
      • acute medical illness
      • pregnancy
      • obesity
      • malignancy
      • thrombophilia
      • personal or family history of venous thromboembolism
      • oral contraceptives or hormone replacement therapy.

      When examining a patient with suspected DVT, look for swelling in the affected limb – measure the limb circumference with a tape measure and compare it with the opposite side. Examine for tenderness and assess whether the limb looks red or feels warm. The clinical appearance of a DVT can be mimicked by a ruptured Baker’s (popliteal) cyst – the two conditions can be distinguished with an ultrasound scan.



      Chronic venous insufficiency (including ulceration)

      Chronic venous insufficiency can result from previous DVT, varicose veins or reduced contraction of leg muscles (chronic immobility). It may be asymptomatic, but can cause a feeling of aching and ‘heaviness’ in the legs. Examine the patient for evidence of:

      •  varicose veins
      • ankle swelling (which may be only slightly pitting)
      • venous eczema
      • lipodermatosclerosis (fibrosis of subcutaneous fat, leading to ‘tightening’ of the skin and narrowing of the leg just above the ankle – the so-called ‘beer bottle leg’)
      • venous ulceration.

      Venous ulcers are most commonly found above the medial malleolus, and can occur following trauma or spontaneously.

      Venous ulcers:

      • are commoner in women and the elderly
      • have an irregular margin
      • have a pink (granulation tissue) base, with green slough.

      In contrast to arterial ulceration, the leg is usually warm with palpable pulses in the presence of venous ulceration.



      Key features of the presenting history are:

      • chest discomfort
      • breathlessness
      • palpitation
      • pre-syncope and syncope
      • peripheral oedema.

      Include the following in your physical examination:

      •  general examination
      •  the hands
      • arterial pulses
        • rate
        • rhythm
        • character and volume
      • blood pressure
      • face and eyes
      • jugular venous pressure
        • height of the JVP
        • character of the JVP
      • praecordium
        • inspection
        • palpation
          •  apex beat
          •  left parasternal heave
          •  thrills
        • auscultation
          • heart sounds
          • heart murmurs
      • chest and back
      • abdomen
      • lower limbs
        • arterial circulation
        • venous circulation
        • peripheral oedema.


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SA Bos, M.D.

Lead Author