The chest X-ray
This is usually taken in the postero-anterior (PA) direction at maximum inspiration (p. 509). A PA chest film can aid the identification of cardiomegaly, pericardial effusions, dissection or dilatation of the aorta, and calcification of the pericardium or heart valves. A cardiothoracic ratio (p. 510) of greater than 50% on a PA film is abnormal and normally indicates cardiac dilatation or pericardial effusion. Examination of the lung fields may show signs of left ventricular failure (Fig. 10.1), valvular heart disease (e.g. markedly enlarged left atrium in mitral valve disease) or pulmonary oligaemia (reduction of vascular markings) associated with pulmonary embolic disease.
The electrocardiogram (ECG) is a recording from the body surface of the electrical activity of the heart. Each cardiac cell generates an action potential as it becomes depolarized and then repolarized during a normal cycle. Nor-mally, depolarization of cardiac cells proceeds in an orderly fashion beginning in the sinus node (lying in the junction between superior vena cava and right atrium) and spreading sequentially through the atria, AV node (lying beneath the right atrial endocardium within the lower inter-atrial septum), and the His bundle in the interventricular septum, which divides into right and left bundle branches (Fig. 10.2). The right and left bundle branches continue down the right and left side of the interventricular septum and supply the Purkinje network which spreads through the subendocardial surface of the right ventricle and left ventricle respectively. The main left bundle divides into an anterior superior division (the anterior hemi-bundle) and a posterior inferior division (the posterior hemi-bundle).
Fig. 10.1 The chest X-ray in acute left ventricular failure demonstrating cardiomegaly, hilar haziness, Kerley B lines, upper lobe venous blood engorgement and fluid in the right horizontal fissure. Hilar haziness and Kerley B lines (thin linear horizontal pulmonary opacities at the base of the lung periphery) indicate interstitial pulmonary oedema.
The standard ECG has 12 leads:
■ Chest leads, V1-V6, look at the heart in a horizontal plane (Fig. 10.3).
■ Limb leads look at the heart in a vertical plane (Fig. 10.4). Limb leads are unipolar (AVR, AVL and AVF) or bipolar (I, II, III).
The ECG machine is arranged so that when a depolarization wave spreads towards a lead the needle moves upwards on the trace (i.e. a positive deflec-tion), and when it spreads away from the lead the needle moves downwards.
Fig. 10.2 The conducting system of the heart. In normal circumstances only the specialized conducting tissues of the heart undergo spontaneous depolarization (automaticity) which initiates an action potential. The sinus (SA) node discharges more rapidly than the other cells and is the normal pacemaker of the heart. The impulse generated by the sinus node spreads first through the atria, producing atrial systole, and then through the atrioventricular (AV) node to the His-Purkinje system, producing ventricular systole.
ECG waveform and detinitions (Fig. 10.5)
Heart rate At normal paper speed (usually 25 mm/s) each ‘big square' measures 5 mm wide and is equivalent to 0.2 s. The heart rate (if the rhythm is regular) is calculated by counting the number of big squares between two consecutive R waves and dividing into 300.
P wave is the first deflection and is caused by atrial depolarization. When abnormal it may be:
■ Broad and notched (> 0.12 s, i.e. 3 small squares) in left atrial enlarge-ment (‘P mitrale', e.g. mitral stenosis)
■ Tall and peaked (> 2.5 mm) in right atrial enlargement (‘P pulmonale', e.g. pulmonary hypertension)
■ Replaced by flutter or fibrillation waves (p. 429)
■ Absent in sinoatrial block (p. 421).
The QRS complex represents ventricular activation or depolarization:
■ A negative (downward) deflection preceding an R wave is called a Q wave. Normal Q waves are small and narrow; deep (> 2 mm), wide (> 1 mm) Q waves (except in AVR and V1) indicate myocardial infarction (p. 453).
Fig. 10.3 ECG chest leads. (A) The V leads are attached to the chest wall overlying the intercostal spaces as shown: V4 in the mid-clavicular line, V5 in the anterior axillary line, V6 in the mid-axillary line. (B) Leads V and V2 look at the right ventricle, V3 and V4 at the interventricular septum, and V5 and V6 at the left ventricle. The normal QRS complex in each lead is shown. The R wave in the chest (precordial) leads steadily increases in amplitude from lead V to V6 with a corresponding decrease in S wave depth, culminating in a predominantly positive complex in V6.
Fig. 10.4 ECG limb leads. Lead I is derived from electrodes on the right arm (negative pole) and left arm (positive pole), lead II is derived from electrodes on the right arm (negative pole) and left leg (positive pole), and lead III from electrodes on the left arm (negative pole) and the left leg (positive pole).
■ A deflection upwards is called an R wave whether or not it is preceded by a Q wave.
■ A negative deflection following an R wave is termed an S wave. Ventricular depolarization starts in the septum and spreads from left to right (Fig. 10.2). Subsequently the main free walls of the ventricles are depolarized. Thus, in the right ventricular leads (V1 and V2) the first deflection is upwards (R wave) as the septal depolarization wave spreads towards those leads. The second deflection is downwards (S wave) as the bigger left ventricle (in which depolarization is spreading away) outweighs the effect of the right ventricle (see Fig. 10.3). The opposite pattern is seen in the left ventricular leads (V5 and V6), with an initial downwards deflection (small Q wave reflecting septal depolarization) followed by a large R wave caused by left ventricular depolarization.
Fig. 10.5 The waves and elaboration of the normal ECG. (From Goldman MJ (1976) Principles of Clinical Electrocardiography, 9th edn. Los Altos: Lange.)
Left ventricular hypertrophy with increased bulk of the left ventricular myocardium (e.g. with systemic hypertension) increases the voltage-induced depolarization of the free wall of the left ventricle. This gives rise to tall R waves (> 25 mm) in the left ventricular leads (V5, V6) and/or deep S waves (> 30 mm) in the right ventricular leads (Vi, Vị). The sum of the R wave in the left ventricular leads and the S wave in the right ventricular leads exceeds 40 mm. In addition to these changes there may also be ST-segment depres-sion and T wave flattening or inversion in the left ventricular leads.
Right ventricular hypertrophy (e.g. in pulmonary hypertension) causes tall R waves in the right ventricular leads.
The QRS duration reflects the time that excitation takes to spread through the ventricle. A wide QRS complex (> 0.10 s, 2.5 small squares) occurs if conduction is delayed, e.g. with right or left bundle branch block, or if conduc-tion is through a pathway other than the right and left bundle branches, e.g. an impulse generated by an abnormal focus of activity in the ventricle (ventricular ectopic).
T waves result from ventricular repolarization. In general the direction of the T wave is the same as that of the QRS complex. Inverted T waves occur in many conditions and, although usually abnormal, they are a non-specific finding.
The PR interval is measured from the start of the P wave to the start of the QRS complex whether this is a Q wave or an R wave. It is the time taken for excitation to pass from the sinus node, through the atrium, atrioventricular node and His-Purkinje system to the ventricle. A prolonged PR interval (> 0.22 s) indicates heart block (p. 422).
The ST segment is the period between the end of the QRS complex and the start of the T wave. ST elevation (> 1 mm above the isoelectric line) occurs in the early stages of myocardial infarction (p. 453) and with acute pericarditis (p. 479). ST segment depression (> 0.5 mm below the isoelectric line) indicates myocardial ischaemia.
The QT interval extends from the start of the QRS complex to the end of the T wave. It is primarily a measure of the time taken for repolarization of the ventricular myocardium, which is dependent on heart rate (shorter at faster heart rates). The QT interval, corrected for heart rate (QTc = QT/V2(R-R)), is normally < 0.44 s in males and < 0.46 s in females. Long QT syndrome (p. 432) is associated with an increased risk of torsades de pointes ventricular tachycardia and sudden death.
The cardiac axis refers to the overall direction of the wave of ventricular depolarization in the vertical plane measured from a zero reference point (Fig. 10.6). The normal range for the cardiac axis is between -30° and +90°. An axis more negative than -30° is termed left axis deviation and an axis more positive than +90° is termed right axis deviation. A simple method to calculate the axis is by inspection of the QRS complex in leads I, II and III. The axis is normal if leads I and II are positive; there is right axis deviation if lead I is negative and lead III positive, and left axis deviation if lead I is positive and leads II and III negative. Left axis deviation occurs due to a block of the anterior bundle of the main left bundle conducting system (p. 409), inferior myocardial infarction and the Wolff-Parkinson-White syndrome. Right axis deviation may be normal and occurs in conditions in which there is right ventricular overload, dextrocardia, Wolff-Parkinson-White syndrome and left posterior hemiblock.
This assesses the cardiac response to exercise. The 12-lead ECG and blood pressure is recorded whilst the patient walks or runs on a motorized treadmill. The test is performed according to a standardized method (e.g. the Bruce protocol). Myocardial ischaemia provoked by exertion results in ST segment depression (> 1 mm) in leads facing the affected area of ischaemic cardiac muscle. Exercise normally causes an increase in heart rate and blood pres-sure. A sustained fall in blood pressure usually indicates severe coronary artery disease. A slow recovery of the heart rate to basal levels has also been reported to be a predictor of mortality. Contraindications include unstable angina, severe hypertrophic cardiomyopathy, severe aortic stenosis and malignant hypertension. A submaximal exercise test can be performed within
4 days of a myocardial infarction. A positive test and indications for stopping the test are:
Fig. 10.6 Cardiac vectors. (A) The hexaxial reference system, illustrating the six leads in the frontal plane, e.g. lead I is 0°, lead II is +60°, lead III is 120°. (B) ECG leads showing the predominant positive and negative deflection with axis deviation.
■ Chest pain
■ ST segment depression or elevation > 1 mm
■ Fall in systolic blood pressure > 20 mmHg
■ Fall in heart rate despite an increase in workload
■ BP > 240/110
■ Significant arrhythmias or increased frequency of ventricular ectopics.
24-Hour ambulatory taped electrocardiography
A 12-lead ECG is recorded continuously over a 24-hour period and is used to record transient changes such as a brief paroxysm of tachycardia, an occasional pause in rhythm or intermittent ST segment shifts. It is also called ‘Holter' electrocardiography after its inventor. Event recording is used to record less frequent arrhythmias in which the patient triggers ECG recording at the time of symptoms. They are both outpatient investigations.
This is performed to investigate unexplained syncope when cardiac (usually echocardiogram and 24-hour ECG) and other tests have not provided a diagnosis. It is specifically used to diagnose neurocardiogenic (vasovagal) syncope in which patients give a history of repeated episodes of syncope which occur without warning and are followed by a rapid recovery. The patient lies on a swivel motorized table in a flat position with safety straps applied across the chest and legs to hold them in position. Blood pressure, heart rate, symptoms and ECG are recorded after the table is tilted +60O to the vertical for 10-60 minutes - thus simulating going from a flat to an upright position. Reproduction of symptoms, bradycardia or hypotension indi-cates a positive test.
This is an ultrasound examination of the heart (Fig. 10.7). Different modalities (e.g. M mode, two- and three-dimensional) are used to provide information about cardiac structure and function. The examination is performed in two ways:
■ Transhioracic echo is the most common method and involves the place-ment of a handheld transducer on the chest wall. Ultrasound pulses are emitted through various body tissues, and reflected waves are detected by the transducer as an echo. The commonest reasons for undertaking an echocardiogram are to assess ventricular function in patients with symptoms suggestive of heart failure, or to assess valvular disease. Left ventricular function is assessed by the ejection fraction (percentage of
Fig. 10.7 Echocardiogram: an example of a two-dimensional long-axis view. (A) Diagram showing the anatomy of the area scanned and a diagrammatic representation of the echocardiogram. (B) Two-dimensional long-axis view.
■ Transoesophageal echo uses miniaturized transducers incorporated into special endoscopes. It allows better visualization of some structures and pathology, e.g. aortic dissection, prosthetic valve endocarditis.
Further refinements of the echocardiogram are Doppler and stress echo-cardiography. Doppler echocardiography uses the Doppler principle (in this case, the frequency of ultrasonic waves reflected from blood cells is related to their velocity and direction of flow) to identify and assess the severity of valve lesions, estimate cardiac output and assess coronary blood flow. Stress (exercise or pharmacological) echocardiography is used to assess myocardial wall motion as a surrogate for coronary artery perfusion. It is used in the detection of coronary artery disease, assessment of risk post-myocardial infarction and perioperatively, and in patients in whom routine exercise ECG testing is non-diagnostic. For those who cannot exercise, pharmaco-logical intervention with dobutamine is used to increase myocardial oxygen demand.
Cardiac nuclear imaging
This is used to detect myocardial infarction or to measure myocardial func-tion, perfusion or viability, depending on the radiopharmaceutical used and the technique of imaging. A variety of radiotracers can be injected intra-venously and these diffuse freely into myocardial tissue or attach to red blood cells.
Thallium-201 is taken up by cardiac myocytes. Ischaemic areas (produced by exercising the patient) with reduced tracer uptake are seen as ‘cold spots' when imaged with a Y camera.
Technetium-99m is used to label red blood cells and produce images of the left ventricle during systole and diastole.
Cardiac computed tomography (CT)
CT is useful for the assessment of the thoracic aorta and mediastinum and multidetector thin slice scanners can assess calcium content of coronary arteries as an indicator of the presence and severity of coronary artery stenoses. CT coronary angiography has high sensitivity for the detection of coronary artery diseases and may become part of the assessment of patients presenting with acute chest pain to look for aortic dissection, pulmonary embolism as well as coronary artery disease.
Cardiovascular magnetic resonance (CMR)
CMR is a non-invasive imaging technique that does not involve harmful radiation. It is increasingly utilized in the investigation of cardiovascular disease to provide both anatomical and functional information. Contra-indications are permanent pacemaker or difibrillator, intracerebral clips and significant claustrophobia. Coronary stents and prosthetic valves are not a contraindication.
A small catheter is passed through a peripheral vein (for study of right-sided heart structures) or artery (for study of left-sided heart structures) into the heart, permitting the securing of blood samples, measurement of intracardiac pressures and determination of cardiac anomalies. Specially designed cath-eters are then used to selectively engage the left and right coronary arteries, and contrast cine-angiograms are taken in order to define the coronary cir-culation and identify the presence and severity of any coronary artery disease. Coronary artery stenoses can be dilated (angioplasty) and metal stents also placed to reduce the rate of restenosis - this is referred to as percutaneous coronary intervention (PCI). A further development is the introduction of stents coated with drugs (sirolimus or paclitaxel) to reduce cellular proliferation and restenosis rates still further. However, there is a risk of late-stent thrombosis.
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