Myocardial ischaemia results from an imbalance be1ween the supply of oxygen to cardiac muscle and myocardial demand. The most common cause is coronary artery atheroma (coronary artery disease), which results in a fixed obstruction to coronary blood flow. Less common causes of myocardial ischaemia are coronary artery thrombosis, spasm or, rarely, arteritis (e.g. polyarteritis). Increased demand for oxygen due to an increase in cardiac output occurs in thyrotoxicosis or myocardial hypertrophy (e.g. from aortic stenosis or hypertension).
Coronary artery disease (CAD) is the single largest cause of death in many parts of the world, including the UK. However, in the last decade the mortality rate in the UK has fallen. Atheroma consists of atherosclerotic plaques (an accumulation of lipid, macrophages and smooth muscle cells in the intima of arteries) which narrow the lumen of the artery. The risk factors, listed below, contribute to the development of atheroma through vascular endo-thelial dysfunction, biochemical abnormalities, immunological factors and inflammation. Some of these risk factors cannot be changed, i.e. they are irreversible, and others can be modified.
Irreversible risk factors for coronary artery disease
Age CAD rate increases with age. It rarely presents in the young, except in familial hyperlipidaemia (p. 692).
Gender Men are more often affected than premenopausal women, although the incidence in women after the menopause is similar to that in men, possible due to the loss of the protective effect of oestrogen.
Family history CAD is often present in several members of the same family. It is unclear, however, whether family history is an independent risk factor as so many other factors are familial. A positive family history refers to those in whom a first-degree relative has developed ischaemic heart disease before the age of 50 years.
Potentially changeable risk factors
Hyperlipidaemia The risk of CAD is directly related to serum cholesterol levels, but there is an inverse relationship with high-density lipoproteins (HDLs). High triglyceride levels are also independently linked with coronary atheroma. Lowering serum cholesterol slows the progression of coronary atherosclerosis and causes regression of the disease.
Cigarette smoking increases the risk of CAD, more so in men. The risk from smoking declines to almost normal after 10 years of abstention.
Hypertension (systolic and diastolic) is linked to an increased incidence of cAD.
Metabolic factors Diabetes mellitus, an abnormal glucose tolerance, raised fasting glucose, lack of exercise, and obesity have all been linked to an increased incidence of atheroma.
Diets high in fats (particularly saturated fat intake) and low in antioxidant intake (fruit and vegetables) are associated with CAD.
Other risk factors Lack of exercise, psychosocial factors (work stress, lack of social support, depression), elevated serum C-reactive protein levels (as an inflammatory marker), high alcohol intake and coagulation factors (high levels of fibrinogen, factor VII and homocysteine) are also associated with CAD, while moderate alcohol consumption (1-2 drinks per day) is associated with a reduced risk of CAD.
Estimation of cardiovascular risk
Patients with symptomatic cardiovascular disease (coronary artery disease, stroke and peripheral vascular disease) have declared themselves to be at high risk for future vascular events. They require intense lifestyle and drug therapy to modify the changeable risk factors towards a more favourable profile, i.e. secondary prevention. The cardiovascular disease risk for asymp-tomatic apparently healthy people can also be estimated using prediction charts which take into account a number of risk factors, e.g. diabetes mel-litus, blood pressure and lipid profile (http://www.bhsoc.org/Cardiovascular_ Risk_Charts_and_Calculators.stm). Those individuals whose 10-year cardio-vascular risk exceeds 20% should also be targeted for preventative measures, i.e. primary prevention.
Angina pectoris is a descriptive term for chest pain arising from the heart as a result of myocardial ischaemia.
Angina is usually described as central, crushing, retrosternal chest pain, coming on with exertion and relieved by rest within a few minutes. It is often exacerbated by cold weather, anger and excitement, and it frequently radi-ates to the arms and neck. Variants of classic angina include:
■ Decubitus angina- occurs on lying down
■ Nocturnal angina- occurs at night and may waken the patient from sleep
■ Variant (Prinzmetal’s) - angina is caused by coronary artery spasm and results in angina that occurs without provocation, usually at rest
■ Unstable angina- increases rapidly in severity, occurs at rest, or is of recent onset (less than 1 month) (see Acute coronary syndromes)
■ Cardiac syndrome X - patients with symptoms of angina, a positive exercise test and normal coronary arteries on angiogram. It is thought to result from functional abnormalities of the coronary microcirculation. The prognostic and therapeutic implications are not known.
Physical examination in patients with angina is often normal, but must include a search for risk factors (e.g. hypertension and xanthelasma occurring in hyperlipidaemia) and underlying causes (e.g. aortic stenosis).
The diagnosis of angina is largely based on the clinical history. Occasionally chest wall pain or oesophageal reflux causes diagnostic confusion (p. 408).
■ Resting ECG may show ST segment depression and T-wave flattening or inversion during an attack. The ECG is usually normal between attacks.
■ Exercise ECG testing is positive (p. 415) in most people with CAD, but a normal test does not exclude the diagnosis. ST segment depression (> 1 mm) at a low workload (within 6 minutes of starting the Bruce protocol) or a paradoxical fall in blood pressure with exercise usually indicates severe CAD and is an indication for coronary angiography.
■ Other testing protocols (pharmacological stress testing with myocardial perfusion imaging or stress echocardiography p. 419) are used in patients who cannot exercise or have baseline ECG abnormalities that can inter-fere with interpretation of the exercise ECG test. They may also be helpful in patients with an equivocal exercise test.
■ Coronary angiography (p. 420) is occasionally used in patients with chest pain where the diagnosis of angina is uncertain. More commonly it is used to delineate the exact coronary anatomy before coronary interven-tion (p. 448) or surgery is considered. CT coronary angiography and cardiovascular MR are also being increasingly used to provide information about coronary anatomy.
This is two-fold:
■ Identify and treat risk factors for CAD and offer secondary prevention
■ Symptomatic treatment of angina.
Secondary prevention Patients with angina are at a high risk of experien-cing subsequent cardiovascular events, including myocardial infarction, sudden death and stroke. Modification of risk factors has a beneficial effect on subsequent morbidity and mortality, and includes smoking cessation, control of hypertension, maintaining ideal bodyweight, regular exercise and glycaemic control in diabetes mellitus. In addition, aspirin and statins reduce subsequent risk:
■ Aspirin (75 mg daily, p. 242) inhibits platelet cyclo-oxygenase and forma-tion of the aggregating agent thromboxane A2, and reduces the risk of coronary events in patients with CAD. Clopidogrel (75 mg daily, p. 242) is an alternative when aspirin is not tolerated, or is contraindicated.
■ Lipid-lowering agents reduce mortality and incidence of myocardial infarction in patients with CAD and should be used in patients to achieve a cholesterol level of less than 5.0 mmol/L. Guidelines on introduction of lipid lowering therapy are illustrated on page 695. A statin (p. 700) is used unless the triglycerides are above 3.5 mmol/L, in which case a fibrate is indicated.
Symptomatic treatment Acute attacks are treated with sublingual glyceryl trinitrate tablet or spray (p. 499). Patients should be encouraged to use this before exertion, rather than waiting for the pain to develop. The main side-effect is a severe bursting headache, which is relieved by inactivating the tablet either by swallowing or spitting it out.
Most patients will require regular prophylactic therapy. Nitrates, β-blockers or calcium antagonists are most commonly used (p. 501), with treatment being tailored to the individual patient. Some patients will require combination therapy and revascularization for those not controlled on medical therapy:
■ β-Adrenergic blocking drugs (p. 495), e.g. atenolol and metoprolol reduce heart rate and the force of ventricular contraction, both of which reduce myocardial oxygen demand.
■ Calcium antagonists, (p. 501) e.g. diltiazem, amlodipine, block calcium influx into the cell and the utilization of calcium within the cell. They relax the coronary arteries and reduce the force of left ventricular contraction, thereby reducing oxygen demand. The side-effects (postural dizziness, headache, ankle oedema) are the result of systemic vasodilatation. High-dose nifedipine increases mortality and should not be used in this situation.
■ Nitrates (p. 499) reduce venous and intracardiac diastolic pressure, reduce impedance to the emptying of the left ventricle, and dilate coronary arter-ies. They are available in a variety of slow-release preparations, including infiltrated skin plasters, buccal pellets and long-acting oral nitrate prepara-tions, e.g. isosorbide mononitrate, isosorbide dinitrate. The major side-effect is headache, which tends to diminish with continued use.
■ Other treatments are usually reserved for patients where there are con-traindications or inadequate response to the above agents. Nicorandil combines nitrate-like activity with potassium channel blockade; it has both arterial and venous vasodilating properties. Ranolazine interacts with sodium channels and can improve exercise tolerance but causes QT prolongation. Ivabradine inhibits the cardiac pacemaker If current and lowers the heart rate. It is used in patients who have a contraindication or intolerance of β-blockers.
When angina persists or worsens in spite of general measures and optimal medical treatment, patients should be considered for coronary artery bypass grafting (CABG) or percutaneous coronary intervention.
Percutaneous coronary intervention (PCI) Localized atheromatous lesions are dilated at cardiac catheterization using small inflatable balloons. Stent placement reduces the risk of acute vessel closure and restenosis rates. This technique is widely applied for angina resulting from isolated, proximal, non-calcified atheromatous plaques. Complications include death, acute myocardial infarction, the need for urgent CABG and restenosis. Dual antiplatelet therapy with aspirin and clopidogrel is routinely given (p. 242). The addition of the antiplatelet glycoprotein IIb/IIIa antagonists (tirofiban, eptifibade, abciximab) has further reduced peri-procedural complications. Drug-eluting stents which release antiproliferative agents (sirolimus, paclit-axel) reduce restenosis rates still further but there is a risk of late stent thrombosis.
Coronary artery bypass grafting The left or right internal mammary artery is used to bypass stenoses in the left anterior descending or right coronary artery respectively. Less commonly, the saphenous vein from the leg is anastomosed between the proximal aorta and coronary artery distal to the obstruction. Surgery successfully relieves angina in about 90% of cases and, when performed for left main stem obstruction or three-vessel disease, an improved lifespan and quality of life can be expected. Operative mortality rate is less than 1%. In most patients the angina eventually recurs because of accelerated atherosclerosis in the graft (particularly vein grafts), which can be treated by stenting.
Acute coronary syndromes
Acute coronary syndromes (ACS) encompass a spectrum of unstable coronary artery disease. The common mechanism to all ACS is rupture or erosion of the fibrous cap of a coronary artery atheromatous plaque with subsequent formation of a platelet-rich clot and vasoconstriction produced by platelet release of serotonin and thromboxane A2. Patients with ACS include those whose clinical presentations cover the following diagnoses:
■ Unstable angina
■ Non-ST-elevation myocardial infarction (NSTEMI)
■ ST-elevation myocardial infarction (STEMI).
Unstable angina differs from NSTEMI in that in the latter the occluding thrombus is sufficient to cause myocardial damage and an elevation in serum markers of myocardial injury (troponin and creatine kinase). In patients pre-senting with symptoms suggestive of ACS, serum troponin should be meas-ured on arrival at hospital and at 12 hours after the onset of symptoms; a normal serum troponin at 12 hours suggests unstable angina rather than myocardial infarction. In both unstable angina and NSTEMI the ECG may be normal or show evidence of ischaemia with T wave inversion and/or ST segment depression. Both unstable angina and NSTEMI may be complicated by myocardial infarction with ST segment elevation (STEMI) if treatment is inadequate. In STEMI there is complete occlusion of the coronary artery by thrombus with usually more severe symptoms, typical ECG changes of myo-cardial infarction (see below) and elevated troponin and creatine kinase.
The diagnosis of ACS is made in a patient with known angina and worsening pain on minimal exertion, chest pain at rest, or chest pain unrelieved in the usual time by nitrates or rest. In some patients, chest pain is absent and presentation is with collapse, arrhythmia or new onset heart failure. Patients without previous angina may also present for the first time with ACS. Other causes of chest pain must be considered in all patients, e.g. aortic dissection, musculoskeletal pain, gastro-oesophageal reflux disease.
Emergency Box 10.3 summarizes the initial investigation and management of patients presenting with suspected ACS.
■ Antiplatelet therapy. In the absence of contraindications, aspirin (300 mg initially, then 75 mg daily, p. 242) is indicated in all patients. It reduces the risk of subsequent vascular events and deaths and is continued indefinitely. Clopidogrel (300 mg initially, then 75 mg daily, p. 242) is also given and continued for 12 months. Platelet glycoprotein IIb/IIIa receptor inhibitors are added for high-risk patients (see below).
■ Antithrombins. Heparin interferes with thrombus formation at the site of plaque rupture and reduces the risk of ischaemic events and death. Low molecular weight heparin, e.g. enoxaparin 1 mg/kg s.c. twice daily (p. 244), has better efficacy than unfractionated heparin. Treatment should be for at least 48 hours. The synthetic pentasaccharide, fonda-parinux, inhibits factor Xa of the coagulation cascade. It has a lower risk of bleeding than heparin and may become the antithrombin of choice in ACS.
■ Anti-ischaemia agents. Nitrates (p. 499) are given sublingually or by intravenous infusion with continuing pain for 24-48 hours. β-blockers (p. 495), e.g. metoprolol are the first line oral anti-anginal of choice given their secondary preventative effects in CAD.
■ Plaque stabilization. Statins (p. 700) and an ACE inhibitor (p. 497) are continued long term and reduce future cardiovascular events.
Oral medication is continued indefinitely after hospital discharge, with the exception of clopidogrel, which is stopped after 12 months.
There are several risk stratification scoring systems (e.g. Thrombolysis in Myocardial Infarction (TIMI) and the Global Registry of Acute Coronary Events (GRACE)) that can predict subsequent risk of STEMI and death in patients with unstable angina/NSTEMI and provide a basis for therapeutic decision-making. The TIMI score is shown in Table 10.8. Early coronary angiography with a view to surgery or PCI is recommended in patients at intermediate/ high risk. Coronary stenting may stabilize the disrupted coronary plaque and reduces angiographic restenosis rates compared to angioplasty alone. Low-risk patients should have a cardiac stress test (p. 447), usually an exercise ECG, if they remain pain-free with no evidence of ischaemia, heart failure or arrhythmias.
STEMI, ST segment elevation myocardial infarction; LMWH, low molecular weight heparin.
|Table 10.8 The TIMI risk score in acute coronary syndrome|
|More than three coronary artery disease risk factors – hypertension, hyperlipidaemia, family history, diabetes, smoking||1|
|Known CAD (stenosis of ≥ 50% on angiography||1|
|Aspirin use in the last 7 days||1|
|At least two episodes of rest pain in the last 24 hours||1|
|ST deviation on admission ECG (horizontal ST depression or transient ST elevation > 1 mm)||1|
|Elevated cardiac markers (creatine kinase-myocardial bound or troponin)||1|
|CAD, coronary artery disease. Low risk = score 0–2; Intermediate risk = score 3–4; High risk = score 5–7|
ST segment elevation myocardial infarction (STEMI)
Myocardial infarction is the most common cause of death in developed countries. It is almost always the result of rupture of an atherosclerotic plaque, with the development of thrombosis and total occlusion of the artery.
Central chest pain similar to that occurring in angina is the most common presenting symptom. Unlike angina it usually occurs at rest, is more severe and lasts for some hours. The pain is often associated with sweating, breath-lessness, nausea, vomiting and restlessness. There may be no physical signs unless complications develop (see later), although the patient often appears pale, sweaty and grey. About 20% of patients have no pain, and such ‘silent' infarctions either go unnoticed or present with hypotension, arrhythmias or pulmonary oedema. This occurs most commonly in elderly patients or those with diabetes or hypertension.
The diagnosis is made on the basis of the clinical history and early ECG appearances. Serial changes (over 3 days) in the ECG and serum levels of cardiac markers confirm the diagnosis and allow an assessment of infarct size (on the magnitude of the enzyme and protein rise, and extent of ECG changes). A normal ECG in the early stages does not exclude the diagnosis.
The ECG shows a characteristic pattern. Within hours there is ST segment elevation (> 1 mm in two or more contiguous leads) followed by T-wave flattening or inversion (Fig. 10.16). Pathological Q waves are broad (> 1 mm) and deep (> 2 mm, or > 25% of the amplitude of the following R wave) nega-tive deflections that start the QRS complex. They develop because the infarcted muscle is electrically silent so that the recording leads ‘look
Fig. 10.16 Electrocardiographic evolution of myocardial infarction. After the first few minutes the T waves become tall, pointed and upright and there is ST segment elevation. After the first few hours the T waves invert, the R wave voltage is decreased and Q waves develop. After a few days the ST segment returns to normal. After weeks or months the T wave may return to upright but the Q wave remains.
through' the infarcted area. This means that the electrical activity being recorded (on the opposite ventricular wall) is moving away from the electrode and is therefore negative. New left bundle branch block is also an indicator of acute myocardial infarction.
Typically ECG changes are confined to the leads that ‘face' the infarct. Leads II, III and AVF are involved in inferior infarcts; I, II and AVL in lateral infarcts; and V2-V6 in anterior infarcts. As there are no posterior leads, a posterior wall infarct is diagnosed by the appearance of reciprocal changes in V, and V2 (i.e. the development of tall initial R waves, ST segment depression and tall upright T waves). New or presumed new left bundle branch block is also compatible with a diagnosis of myocardial infarction.
Cardiac markers Necrotic cardiac muscle releases several enzymes and proteins into the systemic circulation:
■ Troponin T and troponin I are regulatory proteins, highly specific and sensitive for cardiac muscle damage. They are released early (within hours of event onset) and persist for several days, and are more sensitive and cardiac specific than CK-MB (see below).
■ Creatine kinase (CK), which is also produced by damaged skeletal muscle and brain, is less sensitive than troponin for myocardial damage. The myocardial-bound (MB) isoenzyme fraction of CK is specific for heart muscle damage and the size of the enzyme rise is broadly proportional to the infarct size.
Other investigations These include a chest X-ray, full blood count, serum urea and electrolytes, blood glucose and lipids (lipids taken within the first 12 hours reflect preinfarction levels, but after this time they are altered for up to 6 weeks).
The aims of treatment are relief of pain, limitation of infarct size and treat-ment of complications. The immediate and subsequent management is sum-marized in Emergency Boxes 10.3 and 10.4. Treatment is urgent: prolonged times between symptom onset and treatment to recanalize the artery are associated with impaired ST-segment resolution, larger infarct sizes and higher mortality (‘time is muscle')
Limitation of infarct size
Immediate primary angioplasty is the optimal treatment for recanalization of the infarct-related arterys (p. 420). When compared with thrombolysis (see below) PCI reduced mortality, re-infarction, recurrent ischaemia, stroke and the need for coronary artery bypass grafting. However, it is only a thera-peutic option when rapid access to a catheterization laboratory is possible, the cardiologist is experienced in interventional cardiology and a full support team is immediately available. PCI is also used as ‘rescue' therapy in patients who have received thrombolysis and who seem on clinical grounds not to
|Emergency Box 10.4|
|Management of ST elevation myocardial
• Immediate investigations and treatment (Emergency Box 10.3)
• Reperfusion therapy for patients presenting within 12 hours of onset > primary angioplasty with GP11b/111a inhibitor, e.g. abciximab, or > thrombolysis, e.g. streptokinase: 1.5 million units in 100 mL 0.9% sodium chloride over 1 h by intravenous infusion pump
• Metoprolol 5 mg slow i.v. injection if heart rate > 100 b.p.m. Repeat every 15 minutes, titrated against heart rate and BP. Do not give if hypotension, heart failure, bradycardia, asthma
• Insulin infusion if blood glucose > 11 mmol/L, aim for blood glucose of 7–10 mmol/L
• Treat complications (p. 456).
Subsequent management of uncomplicated infarction
• Repeat ECG, serum cardiac markers and electrolytes at 24 and 48 hours after admission
• Initiate secondary prevention therapy: aspirin, clopidogrel, statin, metoprolol, ACE inhibitor and modification of CAD risk factors (as for ACS)
• Transfer from CCU to medical ward after 48 h
• Mobilize gradually and discharge from hospital after 5 days
• Submaximal exercise ECG test prior to discharge if primary angioplasty not performed
• Refer to cardiac rehabilitation programme
• No driving for 1 month; special assessment is required for heavy goods or public service licence holder before driving. Usually return to work in 2 months.
have reperfused (ongoing chest pain and < 50% resolution of ST elevation 45-60 minutes after start of thrombolysis).
Fibrinolytic agents (thrombolysis) enhance the breakdown of occlusive thromboses by the activation of plasminogen to form plasmin. They are indicated where primary PCA is not available and there are no contraindica-tions to thrombolysis (p. 248). Maximum benefit is derived from thrombolytic agents if they are given early (‘time is muscle' - minutes count) and in some centres pre-hospital thrombolysis is used. There is little benefit of thromboly-sis more than 12 hours after the onset of symptoms. Of the four thrombolytic agents available, reteplase and tenecteplase are preferred in the pre-hospital setting because they can be administered as a bolus intravenous injection.
Streptokinase and alteplase are given by intravenous infusion. Streptokinase is the cheapest thrombolytic agent available but may induce the development of antistreptokinase antibodies and reduce the effectiveness of subsequent treatment. It should not be used beyond 4 days after first administration.
Mortality is increased in diabetic patients with MI, largely owing to the high incidence of heart failure. This is due in part to metabolic changes which occur in the early stages of MI, and is reduced by rigorous control of blood glucose with insulin infusion, and monitoring with 2-hourly BM Stix. This regimen is also indicated in patients not known to be diabetic who have an admission blood glucose of > 11 mmol/L. β-blockers reduce infarct size and the incidence of sudden death. Metoprolol (5-10 mg i.v) should be given, particularly if the heart rate is greater than 100 b.p.m. and there is persistent pain.
Subsequent management ACE inhibitors (or angiotensin receptor blocker if intolerant) reduce mortality and prevent the development of heart failure and should be started on the first day after MI. Treatment with ACE inhibitors, aspirin, statin and β-blockers is continued indefinitely (see ACS for doses). Aldosterone antagonist, e.g. eplerenone 25 mg/day (p. 350) is given to patients with clinical evidence of heart failure and reduced ejection fraction on echocardiogram. Gradual mobilization takes place on the second day and if the patient is fully ambulant and pain-free, a submaximal exercise tolerance test is performed (70% of age-predicted maximal heart rate) before hospital discharge on day 5 or 6 in uncomplicated cases. Patients with test results suggesting ischaemia are referred for coronary angiography.
Complications (Table 10.9)
Disturbances of rate, rhythm and conduction (p. 420)
■ Atrial arrhyhimias. Sinus tachycardia is common; treatment is that of the underlying cause, particularly pain, anxiety and heart failure. Sinus brady-cardia is especially associated with acute inferior wall myocardial infarc-tion. Treatment is initially with intravenous atropine (p. 421). Temporary transcutaneous or transvenous pacemaker insertion is used if there are adverse signs (heart failure, hypotension, ventricular arrhythmias). Atrial fibrillation occurs in about 10% of cases and is usually a transient rhythm disturbance. Treatment with digoxin or amiodarone is indicated if the fast rate is exacerbating ischaemia or causing heart failure.
■ Ventricular arrhythmias. Ventricular ectopic beats are common and may precede the development of ventricular tachycardia (VT) or fibrillation (VF). Antiarrhythmic drug treatment has not been shown to affect progres-sion to these more serious arrhythmias. VT may degenerate into VF (p. 432) or may itself produce shock or heart failure. Treatment of VT is with intravenous lidocaine (p. 492) or amiodarone (p. 491) or direct current cardioversion if there is hypotension. VF may be primary (occur-ring in the first 24-48 hours) or secondary (occurring late after infarction
|Table 10.9 Complications of myocardial infarction|
Rupture of free wall of iníarcted ventricle (usually fatal)
Rupture of the interventricular septum (ventricular septal defect)
May deveOp weeks or months after MI
and associated with large infarcts and heart failure). Treatment is with immediate DC cardioversion. Recurrences may be prevented with intra-venous lidocaine or amiodarone. Late VT/VF is associated with a poor prognosis and a high incidence of sudden death, and is an indication for an implantable cardiac debrillator.
■ Heart block occurring with inferior infarction is common and usually resolves spontaneously. Some patients respond to intravenous atropine, but a temporary pacemaker may be necessary if the rhythm is very slow or producing symptoms.
■ Complete heart block occurring with anterior wall infarction indicates the involvement of both bundle branches by extensive myocardial necrosis, and hence a very poor prognosis. The ventricular rhythm in this case is unreliable and a temporary pacing wire is necessary. Heart block is often permanent and a permanent pacing wire may be necessary.
Heart failure in a mild form occurs in up to 40% of patients following myocardial infarction. Extensive infarction may cause acute heart failure (p. 443), which may also occur following rupture of the ventricular septum or mitral valve papillary muscle. Both conditions present with worsening heart failure, a systolic thrill and a loud pansystolic murmur. Mortality is high, and urgent surgical correction is often needed. Hypotension with a raised JVP is usually a complication of right ventricular infarction, which may occur with inferior wall infarcts. Initial treatment is with volume expansion, and peri-cardial effusion (which produces similar signs) should be ruled out on an echocardiogram.
Embolism Patients with severe left ventricular dysfunction, persistent AF or mural thrombus on echocardiography are at risk of embolism from left
ventricular or left atrial clot and should be anticoagulated with warfarin to achieve a target INR of 2-3.
Pericarditis is characterized by sharp chest pain and a pericardial rub. Treatment is with non-steroidal anti-inflammatory drugs until spontaneous resolution occurs within 1-2 days. Late pericarditis (2-12 weeks after) with fever and a pericardial effusion (Dressler's syndrome) is rare and corticos-teroids may be necessary in some patients.
Prognosis is variable depending on factors such as age and size of infarct. Fifty per cent of patients die during the acute event, many before reaching hospital. A further 10% die in hospital, and of the survivors a further 10% die in the next 2 years.
1. Ethics and communication
2. Infectious diseases
3. Gastroenterology and nutrition
4. Liver, biliary tract and pancreatic disease
Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER DISEASE IN PREGNANCY
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS
5. Haematological disease
Assessment and treatment of suspected neutropenic sepsis
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
6. Malignant disease
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
8. Water, electrolytes and acid–base balance
WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
9. Renal disease
INVESTIGATION OF RENAL DISEASE
URINARY TRACT INFECTION
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
10. Cardiovascular disease
COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
ISCHAEMIC HEART DISEASE
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
ARTERIAL AND VENOUS DISEASE
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS
11. Respiratory disease
12. Intensive care medicine
13. Drug therapy, poisoning, and alcohol misuse
14. Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
15. Diabetes mellitus and other disorders of metabolism
16. The special senses
COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES