The cardiovascular system

Chapter 4 The cardiovascular system




This chapter deals with the history and the examination of the heart and blood vessels, as well as other parts of the body where symptoms and signs of heart disease may appear. Not only is this fundamental to the assessment of any patient, but it is also an extremely common system tested in viva voce examinations. It is believed by cardiologists to be the most important system in the body.



The cardiovascular history



Presenting symptoms (Table 4.1)



Chest pain


The mention of chest pain by a patient tends to provoke more urgent attention than other symptoms. The surprised patient may find himself whisked into an emergency ward with the rapid appearance of worried-looking doctors. This is because ischaemic heart disease, which may be a life-threatening condition, often presents in this manner (Table 4.2). The pain of angina and myocardial infarction tends to be similar in character; it may be due to the accumulation of metabolites from ischaemic muscle following complete or partial obstruction of a coronary artery, leading to stimulation of the cardiac sympathetic nerves.1,2 Patients with cardiac transplants who develop coronary disease in the transplanted heart may not feel angina, presumably because the heart is denervated. Similarly, patients with diabetes are more likely to be diagnosed with ‘silent infarcts’.


TABLE 4.1 Cardiovascular history





































































Major symptoms
Chest pain or heaviness
Dyspnoea: exertional (note degree of exercise necessary), orthopnoea, paroxysmal nocturnal dyspnoea
Ankle swelling
Palpitations
Syncope
Intermittent claudication
Fatigue
Past history
History of ischaemic heart disease: myocardial infarction, coronary artery bypass grafting
Rheumatic fever, chorea, sexually transmitted disease, recent dental work, thyroid disease
Prior medical examination revealing heart disease (e.g. military, school, insurance)
Drugs
Social history
Tobacco and alcohol use
Occupation
Family history
Myocardial infarcts, cardiomyopathy, congenital heart disease, mitral valve prolapse, Marfan’s syndrome
Coronary artery disease risk factors
Previous coronary disease
Smoking
Hypertension
Hyperlipidaemia
Family history of coronary artery disease
Diabetes mellitus
Obesity and physical inactivity
Male sex and advanced age
Raised homocysteine levels
Functional status in established heart disease
Class I—disease present but no symptoms, or angina* or dyspnoea during unusually intense activity
Class II—angina or dyspnoea during ordinary activity
Class III—angina or dyspnoea during less than ordinary activity
Class IV—angina or dyspnoea at rest

* Canadian Cardiovascular Society (CCVS) classification.


New York Heart Association (NYHA) classification.


TABLE 4.2 Causes (differential diagnosis) of chest pain and typical features
































































































Pain Causes Typical features
Cardiac pain Myocardial ischaemia or infarction Central, tight or heavy; may radiate to the jaw or left arm
Vascular pain Aortic dissection Very sudden onset, radiates to the back
Aortic aneurysm  
Pleuropericardial pain Pericarditis +/− myocarditis Pleuritic pain, worse when patient lies down
Infective pleurisy Pleuritic pain
Pneumothorax Sudden onset, sharp, associated with dyspnoea
Pneumonia Often pleuritic, associated with fever and dyspnoea
Autoimmune disease Pleuritic pain
Mesothelioma Severe and constant
Metastatic tumour Severe and constant, localised
Chest wall pain Persistent cough Worse with movement, chest wall tender
Muscular strains Worse with movement, chest wall tender
Intercostal myositis Sharp, localised, worse with movement
Thoracic zoster Severe, follows nerve root distribution, precedes rash
Coxsackie B virus infection Pleuritic pain
Thoracic nerve compression or infiltration Follows nerve root distribution
Rib fracture History of trauma, localised tenderness
Rib tumour, primary or metastatic Constant, severe, localised
Tietze’s syndrome Costal cartilage tender
Gastrointestinal pain Gastro-oesophageal reflux Not related to exertion, may be worse when patient lies down—common
Diffuse oesophageal spasm Associated with dysphagia
Airway pain Tracheitis Pain in throat, breathing painful
Central bronchial carcinoma  
Inhaled foreign body  
Other causes Panic attacks Often preceded by anxiety, associated with breathlessness and hyperventilation
Mediastinal pain Mediastinitis  
Sarcoid adenopathy, lymphoma  

To help determine the cause of chest pain, it is important to ascertain the duration, location, quality, and precipitating and aggravating factors (the four cardinal features), as well as means of relief and accompanying symptoms (the SOCRATES questions; see Chapter 1).3


The term anginaa was coined by Heberden from the Greek and Latin words meaning ‘choking’ or strangling; and the patient may complain of crushing pain, heaviness, discomfort or a choking sensation in the retrosternal area or in the throat. It is best to ask if the patient experiences chest ‘discomfort’ rather than ‘pain’, because angina is often dull and aching in character and may not be perceived as pain.


The pain or discomfort is usually central rather



than left-sided. The patient may dismiss his or her pain as non-cardiac because it is not felt over the heart on the left side. It may radiate to the jaw or to the arms, but very rarely travels below the umbilicus. The severity of the pain varies.


Angina characteristically occurs with exertion, with rapid relief once the patient rests or slows down. The amount of exertion necessary to produce the pain may be predictable to the patient. A change in the pattern of onset of previously stable angina must be taken very seriously.


These features constitute typical angina (Table 4.3).4 Although angina typically occurs on exertion, it may also occur at rest or wake a patient from sleep. Ischaemic chest pain is usually unaffected by respiration. The use of sublingual nitrates characteristically brings relief within a couple of minutes, but this is not specific as nitrates may also relieve oesophageal spasm and also have a pronounced placebo effect.


TABLE 4.3 Clinical classification of angina from the European Society of Cardiology












Typical angina Meets all 3 of the following characteristics:


Atypical angina Meets 2 of the above characteristics
Non-cardiac chest pain Meets 1 or none of the above characteristics

The pain associated with an acute coronary syndrome (myocardial infarction or unstable angina) often comes on at rest, is usually more severe and lasts much longer. Acute coronary syndromes are usually caused by the rupture of a coronary artery plaque which leads to the formation of thrombus in the arterial lumen. Stable exertional angina is a result of a fixed coronary narrowing. Pain present for more than half an hour is more likely to be due to an acute coronary syndrome than to stable angina, but pain present continuously for many days is unlikely to be either. Associated symptoms of myocardial infarction include dyspnoea, sweating, anxiety, nausea and faintness.


Other causes of retrosternal pain are listed in Table 4.2. Chest pain made worse by inspiration is called pleuritic pain. This may be due to pleurisy (page 110) or pericarditis (page 78). Pleurisy may occur because of inflammation of the pleura as a primary problem (usually due to viral infection), or secondary to pneumonia or pulmonary embolism. Pleuritic pain is not usually brought on by exertion and is often relieved by sitting up and leaning forwards. It is caused by the movement of inflamed pleural or pericardial surfaces on one another.


Chest wall pain is usually localised to a small area of the chest wall, is sharp and is associated with respiration or movement of the shoulders rather than with exertion. It may last only a few seconds or be present for prolonged periods. Disease of the cervical or upper thoracic spine may also cause pain associated with movement. This pain tends to radiate around from the back towards the front of the chest.


Pain due to a dissecting aneurysm of the aorta is usually very severe and may be described as tearing. This pain is usually greatest at the moment of onset and radiates to the back. These three features—quality, rapid onset and radiation—are very specific for aortic dissection. A proximal dissection causes anterior chest pain and involvement of the descending aorta causes interscapular pain. A history of hypertension or of a connective tissue disorder such as Marfan’s syndrome or Ehlers-Danlos syndrome puts the patient at increased risk of this condition.


Massive pulmonary embolism causes pain of very sudden onset which may be retrosternal and associated with collapse, dyspnoea and cyanosis


Table 4.4a Differential diagnosis of chest pain

































Favours angina Favours pericarditis or pleurisy Favours oesophageal pain
Tight or heavy Sharp or stabbing Burning
Onset predictable with exertion Not exertional Not exertional
Relieved by rest Present at rest Present at rest
Relieved rapidly by nitrates Unaffected Unaffected unless spasm
Not positional Worse supine (pericarditis) Onset may be when supine
Not affected by respiration Worse with respiration Unaffected by respiration
Pericardial or pleural rub

(page 136). It is often pleuritic, but can be identical to anginal pain, especially if associated with right ventricular ischaemia.


Spontaneous pneumothorax may result in pain and severe dyspnoea (page 132). The pain is sharp and localised to one part of the chest.


Gastro-oesophageal reflux can quite commonly cause angina-like pain without heartburn. It is important to remember that these two relatively common conditions may co-exist. Oesophageal spasm may cause retrosternal chest pain or discomfort and can be quite difficult to distinguish from angina, but is rare. The pain may come on after eating or drinking hot or cold fluids, may be associated with dysphagia (difficulty swallowing) and may be relieved by nitrates.


Cholecystitis can cause chest pain and be confused with myocardial infarction. Right upper quadrant abdominal tenderness is usually present (page 170).


The cause of severe, usually unilateral, chest pain may not be apparent until the typical vesicular rash of herpes zoster appears in a thoracic nerve root distribution.



Dyspnoea


Shortness of breath may be due to cardiac disease. Dyspnoea (Greek dys ‘bad’, pnoia ‘breathing’) is often defined as an unexpected awareness of breathing. It occurs whenever the work of breathing is excessive, but the mechanism is uncertain. It is probably due to a sensation of increased force required of the respiratory muscles to produce a


Table 4.4b Differential diagnosis of chest pain






















































Favours myocardial infarction (acute coronary syndrome) Favours angina
Onset at rest Onset with exertion
May be severe Less severe
Sweating No sweating
Anxiety (angor) Mild or no anxiety
No relief with nitrates Rapid relief with nitrates
Associated symptoms (nausea and vomiting) Associated symptoms absent
Favours myocardial infarction Favours aortic dissection
Central chest pain Radiates to back
Subacute onset (minutes) Instantaneous onset
May be severe Very severe
Favours myocardial ischaemia Favours chest wall pain
Exertional Positional
Occurs with exertion Often worse at rest
Brief episodes Prolonged
Diffuse Localised
No chest wall tenderness (only discriminates between infarction and chest wall pain) Chest wall tenderness

volume change in the lungs, because of a reduction in compliance of the lungs or increased resistance to air flow. Cardiac dyspnoea is typically chronic and occurs with exertion because of failure of the left ventricular output to rise with exercise; this in turn leads to an acute rise in left ventricular end-diastolic pressure, raised pulmonary venous pressure, interstitial fluid leakage and thus reduced lung compliance. However, the dyspnoea of chronic cardiac failure does not correlate well with measurements of pulmonary artery pressures, and clearly the origin of the symptom of cardiac dyspnoea is complicated.5 Left ventricular function may be impaired because of ischaemia (temporary or permanent reduction in myocardial blood supply), previous infarction (damage) or hypertrophy (often related to hypertension). As it becomes more severe, cardiac dyspnoea occurs at rest.


Orthopnoea (from the Greek ortho ‘straight’; see Table 4.5), or dyspnoea that develops when a patient is supine, occurs because in an upright position the patient’s interstitial oedema is redistributed; the lower zones of the lungs become worse and the upper zones better. This allows improved overall blood oxygenation. Patients with severe orthopnoea spend the night sitting up in a chair or propped up on numerous pillows in bed. The absence of orthopnoea suggests that left ventricular failure is unlikely to be the cause of a patient’s dyspnoea (negative likelihood ratio [LR] = 0.046).


TABLE 4.5 Causes of orthopnoea

















Cardiac failure
Uncommon causes
Massive ascites
Pregnancy
Bilateral diaphragmatic paralysis
Large pleural effusion
Severe pneumonia

Paroxysmalbnocturnal dyspnoea (PND) is severe dyspnoea that wakes the patient from sleep so that he or she is forced to get up gasping for breath. This occurs because of a sudden failure of left ventricular output with an acute rise in pulmonary venous and capillary pressures; this leads to transudation of fluid into the interstitial tissues, which increases the work of breathing. The sequence may be precipitated by resorption of peripheral oedema at night while supine. Acute cardiac dyspnoea may also occur with acute pulmonary oedema or a pulmonary embolus.


Cardiac dyspnoea can be difficult to distinguish from that due to lung disease or other causes (page 109)7. One should inquire particularly about a history of any cardiac disease that could be responsible for the onset of cardiac failure. For example, a patient with a number of known previous myocardial infarctions who develops dyspnoea is more likely to have decreased left ventricular contractility. A patient with a history of hypertension or a very heavy alcohol intake may have hypertensive heart disease or an alcoholic cardiomyopathy. The presence of orthopnoea or paroxysmal nocturnal dyspnoea is more suggestive of cardiac failure than of lung disease.


Dyspnoea is also a common symptom of anxiety. These patients often describe an inability to take a big enough breath to fill the lungs in a satisfying way. Their breathing may be deep and punctuated with sighs.



Ankle swelling


Some patients present with bilateral ankle swelling due to oedema from cardiac failure. Patients with the recent onset of oedema and who take a serious interest in their weight may have noticed a gain in weight of 3 kg or more. Ankle oedema of cardiac origin is usually symmetrical and worst in the evenings, with improvement during the night. It may be a symptom of biventricular failure or right ventricular failure secondary to a number of possible underlying aetiologies. As failure progresses, oedema ascends to involve the legs, thighs, genitalia and abdomen. There are usually other symptoms or signs of heart disease.


It is important to find out whether the patient is taking a vasodilating drug (e.g. a calcium channel blocker), which can cause peripheral oedema. There are other (more) common causes of ankle oedema than heart failure that also need to be considered (page 71). Oedema that affects the face is more likely to be related to nephrotic syndrome (page 213).



Palpitations


This is not a very precise term. It is usually taken to mean an unexpected awareness of the heartbeat.8 Ask the patient to describe exactly what he or she notices and whether the palpitations are slow or fast, regular or irregular, and how long they last (Questions box 4.2).



There may be the sensation of a missed beat followed by a particularly heavy beat; this can be due to an atrial or ventricular ectopic beat (which produces little cardiac output) followed by a compensating pause and then a normally conducted beat (which is more forceful than usual because there has been a longer diastolic filling period for the ventricle).


If the patient complains of a rapid heartbeat, it is important to find out whether the palpitations are of sudden or gradual onset and offset. Cardiac arrhythmias are usually instantaneous in onset and offset, whereas the onset and offset of sinus tachycardia is more gradual. A completely irregular rhythm is suggestive of atrial fibrillation, particularly if it is rapid.


It may be helpful to ask the patient to tap the rate and rhythm of the palpitations with his or her finger. Associated features including pain, dyspnoea or faintness must be inquired about. The awareness of rapid palpitations followed by syncope suggests ventricular tachycardia. These patients usually have a past history of significant heart disease. Any rapid rhythm may precipitate angina in a patient with ischaemic heart disease.


Table 4.6 Causes (differential diagnosis) of dyspnoea, palpitations and oedema


















































































































































Favours heart failure   Favours lung disease
History of myocardial infarction   History of smoking
    Onset after some exertion (asthma)
No wheeze   Wheezing
PND   PND absent
Orthopnoea   Orthopnoea absent
Abnormal apex beat    
Third heart sound (S3)    
Mitral regurgitant murmur    
    Overexpanded chest
    Pursed-lips breathing
Early and mid-inspiratory crackles   Fine end-inspiratory crackles
Cough only on lying down   Productive cough
Palpitations differential diagnosis Ankle oedema differential diagnosis
Feature Suggests Favours heart failure
Heart misses and thumps Ectopic beats History of cardiac failure
Worse at rest Ectopic beats Other symptoms of heart failure
Very fast, regular SVT (VT) Jugular venous pressure elevated (+ve LR 9.0*)
Instantaneous onset SVT (VT) Favours hypoproteinaemia
Offset with vagal manoeuvres SVT Jugular venous pressure normal
Fast and irregular AF Oedema pits and refills rapidly, 2–3s
Forceful and regular—not fast Awareness of sinus rhythm (anxiety) Favours deep venous thrombosis or cellulitis
    Unilateral
    Skin erythema
    Calf tenderness
Severe dizziness or syncope VT  
Pre-existing heart failure VT  
    Favours drug-induced oedema
    Patient takes calcium channel blocker
    Favours lymphoedema
    Not worse at end of day
    Not pitting when chronic
    Favours lipoedema
    Not pitting
    Spares foot
    Obese woman

PND = paroxysmal nocturnal dyspnoea.


SVT = supraventricular tachycardia.


VT = ventricular tachycardia.


AF = atrial fibrillation.


* McGee S, Evidence-based clinical diagnosis, 2nd edn. St Louis: Saunders, 2007.


Khan NA, Rahim SA, Avand SS et al. Does the clinical examination predict lower extremity peripheral arterial disease? JAMA 2006 Feb 1; 295(5):536–546.



Table 4.7 Differential diagnosis of syncope and dizziness

















































































Favours vasovagal syncope (most common cause)
Onset in teens or 20s
Occurs in response to emotional distress, e.g. sight of blood
Associated with nausea and clamminess
Injury uncommon
Unconsciousness brief, no neurological signs on waking
Favours orthostatic hypotension
Onset when getting up quickly
Brief duration
Injury uncommon
More common when fasted or dehydrated
Known low systolic blood pressure
Use of antihypertensive medications
Favours ‘situational syncope’
Occurs during micturition
Occurs with prolonged coughing
Favours syncope due to left ventricular outflow obstruction (AS, HCM)
Occurs during exertion
Favours cardiac arrhythmia
Family history of sudden death (Brugada or long QT syndrome)
Anti-arrhythmic medication (prolonged QT)
History of cardiac disease (ventricular arrhythmias)
History of rapid palpitations
No warning (heart block—Stokes-Adams attack)
Favours vertigo
No loss of consciousness
Worse when turning head
Head or room seems to spin
Favours seizure
Prodrome—aura
Tongue bitten
Jerking movements during episode
Sleepiness afterwards
Head turns during episode
Follows emotional stress
Cyanosis
Muscle pain afterwards
Favours metabolic cause of syncope (coma)
Hypoglycaemic agents, low blood sugar

AS = aortic stenosis.


HCM = hypertrophic cardiomyopathy.


Patients may have learned manoeuvres that will return the rhythm to normal. Attacks of supraventricular tachycardia (SVT) may be suddenly terminated by increasing vagal tone with the Valsalva manoeuvre (page 70), carotid massage, by coughing, or by swallowing cold water or ice cubes.



Syncope, presyncope and dizziness


Syncope is a transient loss of consciousness resulting from cerebral anoxia, usually due to inadequate blood flow. Presyncope is a transient sensation of weakness without loss of consciousness. (See Questions box 11.4, page 326.)


Syncope may represent a simple faint or be a symptom of cardiac or neurological disease. One must establish whether the patient actually loses consciousness and under what circumstances the syncope occurs—e.g. on standing for prolonged



periods or standing up suddenly (postural syncope), while passing urine (micturition syncope), on coughing (tussive syncope), or with sudden emotional stress (vasovagal syncope). Find out whether there is any warning, such as dizziness or palpitations, and how long the episodes last. Recovery may be spontaneous or the patient may require attention from bystanders.


If the patient’s symptoms appear to be postural, inquire about the use of anti-hypertensive or anti-anginal drugs and other medications that may induce postural hypotension. If the episode is vasovagal, it may be precipitated by something unpleasant like the sight of blood, or occur in a crowded, hot room; patients often sigh and yawn and feel nauseated and sweaty before fainting and may have previously had similar episodes, especially during adolescence and young adulthood.


If syncope is due to an arrhythmia, there is a sudden loss of consciousness regardless of the patient’s posture; chest pain may also occur if the patient has ischaemic heart disease or aortic stenosis.10 Recovery is equally quick. Exertional syncope may occur with obstruction to left ventricular outflow by aortic stenosis or hypertrophic cardiomyopathy. Profound and sudden bradycardia, usually a result of complete heart block, causes sudden and recurrent syncope (Stokes-Adamsc attacksd). These patients may have a history of atrial fibrillation. Typically they have periods of tachycardia (fast heart rate) as well as periods of bradycardia (slow heart rate). This condition is called the sick sinus syndrome. The patient must be asked about drug treatment that could cause bradycardia, e.g. beta-blockers, digoxin, calcium channel blockers.


It is important to ask about a family history of sudden death. An increasing number of ion channelopathies are being identified as a cause of syncope and sudden death. These inherited conditions include the long QT syndrome and the Brugada syndrome. They are often diagnosed from typical ECG changes. In addition, certain drugs can cause the acquired long QT syndrome (Table 4.8).


TABLE 4.8 Drugs and syncope



























Associated with QT interval prolongation and ventricular arrhythmias
Anti-arrhythmics; flecainide, quinidine, sotalol, procainamide, amiodarone
Gastric motility promoter; cisapride
Antibiotics; clarithromycin, erythromycin
Antipsychotics; chlorpromazine, haloperidol
Associated with bradycardia
Beta-blockers
Some calcium channel blockers (verapamil, diltiazem)
Digoxin
Associated with postural hypotension
Most antihypertensive drugs, but especially prazosin and calcium channel blockers
Anti-Parkinsonian drugs

Neurological causes of syncope are associated with a slow recovery and often residual neurological symptoms or signs. Bystanders may also have noticed abnormal movements if the patient has epilepsy. Dizziness that occurs even when the patient is lying down or which is made worse by movements of the head is more likely to be of neurological origin, although recurrent tachyarrhythmias may occasionally cause dizziness in any position. One should attempt to decide whether the dizziness is really vertiginous (where the world seems to be turning around), or whether it is a presyncopal feeling.



Intermittent claudication and peripheral vascular disease


The word claudicatione comes from the Latin meaning to limp. Patients with claudication notice pain in one or both calves, thighs or buttocks when they walk more than a certain distance. This distance is called the ‘claudication distance’. The claudication distance may be shorter when patients walk up hills. A history of claudication suggests peripheral vascular disease with a poor blood supply to the affected muscles. The most important risk factors are smoking, diabetes, hypertension and a history of vascular disease elsewhere in the body, including cerebrovascular disease and ischaemic heart disease. More severe disease causes the feet or legs to feel cold, numb and finally painful at rest. Rest pain is a symptom of severely compromised arterial supply. Remember the six P’s of peripheral vascular disease:








Popliteal artery entrapment can occur, especially in young men with intermittent claudication on walking but not running. Also, lumbar spinal stenosis causes pseudo-claudication: unlike vascular claudication, the pain in the calves is not relieved by standing still, but is relieved by sitting (flexing the spine) and may be exacerbated by extending the spine (e.g. walking downhill).




Risk factors for coronary artery disease


An essential part of the cardiac history involves obtaining detailed information about a patient’s risk factors—the patient’s cardiovascular risk factor profile (Questions box 4.4).



Previous ischaemic heart disease is the most important risk factor for further ischaemia. The patient may know of previous infarcts or have had a diagnosis of angina in the past.


Hypercholesterolaemia is the next most important risk factor for ischaemic heart disease. Many patients now know their serum cholesterol levels because widespread testing has become fashionable. The total serum cholesterol is a useful screening test, and levels above 5.2 mmol/L are considered undesirable. Cholesterol measurements (unlike triglyceride measurements) are accurate even when a patient has not been fasting. Patients with established coronary artery disease benefit from lowering of total cholesterol to below 4 mmol/L. An elevated total cholesterol level is even more significant if the high-density lipoprotein (HDL) level is low (less than 1.0 mmol/L). Significant elevation of the triglyceride level is a coronary risk factor in its own right and also adds further to the risk if the total cholesterol is high. If a patient already has coronary disease, hyperlipidaemia is even more important. Control of risk factors for these patients is called ‘secondary prevention’. Patients who have multiple risk factors for ischaemic heart disease (e.g. diabetes and hypertension) should have their cholesterol controlled aggressively. If the patient’s cholesterol is known to be high, it is worth obtaining a dietary history. This can be very trying. It is important to remember that not only foods containing cholesterol but those containing saturated fats contribute to the serum cholesterol level. High alcohol consumption and obesity are associated with hypertriglyceridaemia.


Smoking is probably the next most important risk factor for cardiovascular disease and peripheral vascular disease. Some patients describe themselves as non-smokers even though they stopped smoking only a few hours before. The number of years the patient has smoked and the number of cigarettes smoked per day are both very important (and are recorded as packet-years, page 6). The significance of a history of smoking for a patient who has not smoked for many years is controversial. The risk of symptomatic ischaemic heart disease falls gradually over the years after smoking has been stopped. After about 2 years the risk of myocardial infarction falls to the same level as for those who have never smoked. After 10 years the risk of developing angina falls close to that of non-smokers.


Hypertension is another important risk factor for coronary artery disease. Find out when hypertension was first diagnosed and what treatment, if any, has been instituted. The treatment of hypertension probably does reduce the risk of ischaemic heart disease, and certainly reduces the risk of hypertensive heart disease, cardiac failure and cerebrovascular disease. Treatment of hypertension has also been shown to reverse left ventricular hypertrophy.


A family history of coronary artery disease increases a patient’s risk, particularly if it has been present in first-degree relatives (parents or siblings) and if it has affected these people below the age of 60. Not all heart disease, however, is ischaemic; a patient whose relatives suffered from rheumatic heart disease is at no greater risk of ischaemic heart disease than anybody else.


A history of diabetes mellitus increases the risk of ischaemic heart disease very substantially. A diabetic without a history of ischaemic heart disease has the same risk of myocardial infarction as a non-diabetic who has had an infarct. It is important to find out how long a patient has been diabetic and whether insulin treatment has been required. Good control of the blood sugar level of diabetics reduces this risk. An attempt should therefore be made to find out how well a patient’s diabetes has been controlled.


Chronic kidney disease is associated with a very high risk of vascular disease. This is possibly related to high calcium-times-phosphate product and may be reduced by dietary intervention, ‘phosphate binders’, efficient dialysis, in renal transplant. Ischaemic heart disease is the most common cause of death in renal failure patients on dialysis.


The presence of multiple risk factors makes control of each one more important. Aggressive control of risk factors is often indicated in these patients.


It is interesting to note that in the diagnosis of angina the patient’s description of typical symptoms is more discriminating than is the presence of risk factors which only marginally increase the likelihood that chest pain is ischaemic. Previous ischaemic heart disease is an exception. Certainly a patient who has had angina before and says he or she has it again, is usually right.





Past history


Patients with a history of definite previous angina or myocardial infarction remain at high risk for further ischaemic events. It is very useful at this stage to find out how a diagnosis of ischaemic heart disease was made and in particular what investigations were undertaken. The patient may well remember exercise testing or a coronary angiogram, and some patients can even remember how many coronary arteries were narrowed, how many coronary bypasses were performed (having more than three grafts often leads to a certain amount of boasting). The angioplasty patient may know how many arteries were dilated and whether stents (often called coronary stunts by patients and cardiac surgeons) were inserted. Acute coronary syndromes are now usually treated with early coronary angioplasty.


Patients may recall a diagnosis of rheumatic fever in their childhood, but many were labelled as having ‘growing pains’.11 A patient who was put to bed for a long period as a child may well have had rheumatic fever. A history of rheumatic fever places patients at risk of rheumatic valvular disease.


Hypertension may be caused or exacerbated by aspects of the patient’s activities and diet (Questions box 4.5). A high salt intake, moderate or greater alcohol use, lack of exercise, obesity and kidney disease may all be factors contributing to high blood pressure. Non-steroidal anti-inflammatory drugs cause salt and fluid retention and may also worsen blood pressure. Ask about these, about previous advice to modify these factors, and about any drug treatment of hypertension when interviewing any patient with high blood pressure.





Examination anatomy


The contraction of the heart results in a wringing or twisting movement that is often palpable (the apex beat) and sometimes visible on the part of the chest that lies in front of it—the praecordium (from the Latin prae ‘in front of’, and cor ‘heart’). The passage of blood through the heart and its valves and on into the great vessels of the body produces many interesting sounds, and causes pulsation in arteries and movement in veins in remote parts of the body. Signs of cardiac disease may be found by examining the praecordium and the many accessible arteries and veins of the body.


The surface anatomy of the heart and of the cardiac valves (Figure 4.1) and the positions of the palpable arteries (Figure 4.2) must be kept in mind during the examination of the cardiovascular system. In addition the physiology of blood flow through the systemic and pulmonary circuits need to be understood if the cardiac cycle and causes of cardiac murmurs are to be understood (Figure 4.3).





The cardiac valves separate the atria from the ventricles (the atrioventricular or mitral and tricuspid valves) and the ventricles from their corresponding great vessels. Figure 4.4 shows the fibrous skeleton that supports the four valves and their appearance during systole (cardiac contraction) and diastole (cardiac relaxation).



The filling of the right side of the heart from the systemic veins can be assessed by inspection of the jugular veins in the neck (Figure 4.5) and by palpation of the liver. These veins empty into the right atrium.


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Oct 26, 2017 | Posted by in GENERAL SURGERY | Comments Off on The cardiovascular system

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