Guides on Heart Disease


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Guides on Heart Disease

  1. 1. Ch01-F07260.qxd 5/9/07 10:57 AM Page 1 Diseases of the cardiovascular system 1 Eric Lim, Ziad Ali, Kevin Varty, John Wallwork, Philip Poole-Wilson PART 1A Diseases of the heart and great vessels SECTION 1.1 Introduction Applied basic sciences of rises (from pulmonary hypertension, right ventricular failure, tricuspid regurgitation) blood pools back into the the cardiovascular system venae cavae leading to an elevated jugular venous pressure Anatomy (JVP) and hepatomegaly. The right atrium and ventricle are supplied by the The heart right coronary artery. In approximately 70%, the right The heart is a four-chambered muscular pump with a valve coronary branches into the posterior interventricular artery that guards the outlet of each chamber. The heart (posterior descending artery), and this is termed a right is a pyramidal structure situated obliquely in the thorax. dominant coronary system; in the remaining 30%, the The base of the pyramid (which can be considered as coronary system is either left- or co-dominant. Infarction lying on its side) that consists of both the atria faces the of the right coronary artery can lead to right ventricular spine, and the apex points approximately to the 5th failure. Right coronary infarction is usually detected by intercostal space at the midclavicular line (where the apex abnormalities in the inferior leads (II, III and aVF) of the beat is situated). electrocardiogram (ECG). The anterior aspect of the heart is made up of the right The left atrium is situated on the most posterior aspect atrium and ventricle. Deoxygenated blood travels from of the (medial facing) base of the heart, and blood in the left the venae cavae into the right atrium, across the tricuspid atrium travels across the mitral valve into the left ventricle, valve into the right ventricle, across the pulmonary valve and then across the aortic valve into the aorta. and into the pulmonary arteries. Bacteria originating from The mitral valve has two leaflets, the anterior and the venous circulation (e.g. from contaminated syringes in posterior. The most common site of valve prolapse is intravenous drug use) predispose to right-sided endo- the middle aspect of the posterior leaflet. The mitral valve carditis. Moving backwards, when the right heart pressure complex consists of the leaflets, annulus, cordae tendineae, 1
  2. 2. Ch01-F07260.qxd 5/9/07 10:57 AM Page 2 Diseases of the cardiovascular system papillary muscles and left ventricle. Failure of any single volume replacement lowers the cardiac output and causes component can lead to mitral valve dysfunction, and usually back pressure on the left ventricle eventually resulting in mitral regurgitation. A better understanding of mitral valve pulmonary oedema. function has led to the ability to repair the individual com- ponents and restore mitral valve competence. Contractility The aortic valve is a semilunar valve with three cusps. Intrinsic contractility of the myocardium is influenced by The aortic valve complex consists of the valve leaflets, the sympathetic stimulation, and the treatment of circulatory sinuses of Valsalva (the dilated portion of the aorta that shock (in selected patients) includes the administration faces the valve leaflets), the annulus, the proximal ascend- of inotropic agents such as adrenaline. Drugs that inhibit ing aorta and the left ventricular outflow tract. Abnormal- the sympathetic system in general also impair contractility, ities of any of the components can similarly lead to aortic and include beta-blockers (β-blockers). The role of valve dysfunction, for example aortic regurgitation can be β-blockers in heart failure is complex, as overall survival due to dilatation of the proximal ascending aorta without benefit is thought to be achieved by attenuating the any aortic valve leaflet abnormality. adverse effects of intrinsic sympathetic overstimulation. The coronary artery supplies most of the blood to the The contractility of the heart can be assessed visually and is left heart. The left main artery branches into the anterior most commonly quantified as the ejection fraction on intraventricular (left anterior descending) and the circum- transthoracic echocardiography (p. 8). The normal ejection flex artery. The anterior intraventricular artery supplies the fraction is approximately 60%. septum and the branches (diagonal arteries) supply the left ventricular free wall. Branches of the circumflex artery Afterload (obtuse marginals) also supply the left ventricular free wall. Afterload is the load against which the heart must exert Infarction of the anterior intraventricular artery leads to a contractile force. The systolic pressure is normally abnormalities in the anterior and septal leads of the ECG, considered to be a measure of the afterload, although the left ventricular dysfunction and cardiogenic shock if suffi- systemic vascular resistance is often (loosely) considered. ciently extensive. Infarction of the circumflex artery leads to The cardiac output is increased with a lower afterload, and abnormalities in the lateral leads of the ECG and left this can be achieved by reducing the systemic vascular ventricular dysfunction. resistance and hence systolic pressure. Inodilators are a class of phosphodiesterase inhibitors (milrinone, enoximone) The pericardium that increase cardiac contractility whilst decreasing systemic The pericardium consists of two layers, a fibrous outer layer vascular resistance (afterload) to improve cardiac output. and an inner serous layer attached to the surface of the heart forming the epicardium. Normally there is Blood pressure approximately 50 mL of clear straw-coloured pericardial Blood pressure is influenced by the relationship between fluid within the pericardium. Normal intrapericardial the pre-load, contractility and afterload. The mean blood pressure is either negative or zero. Pericardial constraint pressure is calculated by adding a third of the pulse facilitates coupling of the ventricles; however, when a pressure to the diastolic blood pressure. The relationship pericardial effusion accumulates, the increase in pressure between arterial pressure, cardiac output and vascular will eventually impair diastolic relaxation of the ventricles resistance is: and cause cardiac tamponade. Arterial pressure = cardiac output × total peripheral Physiology resistance [1] Pre-load Cardiac output = stroke volume × heart rate [2] At rest, the heart pumps approximately 5 litres of blood per minute. The degree of tension of the heart muscle before Since stroke volume is influenced by pre-load and contrac- it begins to contract is the pre-load. End diastolic pressure tility, blood pressure increases if there is an increase in pre- is normally considered to be the measure of the pre-load. load, contractility, heart rate or total peripheral resistance. Within physiological limits, as pre-load increases, cardiac Often, manipulations of a combination of these factors are output increases. This is because the digitations of the actin undertaken in the intensive care unit (ICU) when managing and myosin filaments within the myocyte are optimized by a patient with low blood pressure. the increase in length. In severe haemorrhage, the pre-load With chronic hypertension, the kidney plays a major is reduced because of volume losses, cardiac output is role in maintaining the blood pressure. This is achieved suboptimal, and circulatory shock ensues when peripheral by changes in the extracellular fluid volume and the vasoconstriction can no longer sustain the blood pressure. renin–angiotensin system. Renin is secreted by the juxta- Fluid administration will increase the pre-load and restore glomerular cells in response to low blood pressure (secre- ventricular performance. In the setting of heart failure, tion is normally reduced in conditions of high blood cardiac output is low and once the optimum filling pressure pressure) and converts angiotensinogen to angiotensin I; (pre-load) is achieved, further distension results in reduced angiotensin I is converted to angiotensin II by the cardiac output, as the actin and myosin filaments are angiotensin-converting enzyme (ACE). Angiotensin II is a 2 distended to a point of sub-optimal coaptation. Further powerful vasoconstrictor that acts directly on the kidneys,
  3. 3. Ch01-F07260.qxd 5/9/07 10:57 AM Page 3 Introduction SECTION 1.1 causing salt and water retention, and also stimulates the Shortness of breath release of aldosterone that has the same effect on the Cardiac failure is an important cause of dyspnoea. Its kidneys. severity is often measured in relation to the New York Heart Antihypertensive medication can lower the blood Association (NYHA) functional class (p. 16). Symptoms of left pressure by a number of mechanisms. With equations [1] ventricular failure are dyspnoea, orthopnoea and Applied basic sciences of and [2] in mind, antihypertensive agents can lower the paroxysmal nocturnal dyspnoea. Orthopnoea refers to the cardiovascular system pre-load (diuretic agents decrease the extracellular volume), shortness of breath when lying flat, and is thought to be reduce contractility (β-blockers, non-dihydropyridine due to the redistribution of the interstitial oedema of the Symptoms of calcium antagonists), reduce heart rate (β-blockers), lungs. It is relieved by sitting upright, presumably facili- cardiac disease reduce total peripheral resistance (dihydropyridine calcium tating gravitational redistribution to the lung bases. Examination of the antagonists) and inhibit the renin–angiotensin system Paroxysmal nocturnal dyspnoea is sudden onset of cardiovascular system (ACE inhibitors). dyspnoea whilst sleeping that wakes the patient suddenly and is also relieved by sitting upright. Concomitant symp- Pressure and volume loading toms of right ventricular failure are peripheral oedema and The physiological response of the left ventricle to pressure abdominal distension (hepatomegaly, ascites). overload is concentric hypertrophy. Common conditions that lead to pressure overload include aortic stenosis Palpitations and chronic hypertension. In mitral stenosis, the chronic Palpitation is an awareness of the heartbeat. Arrhythmia pressure overload imposed by the narrowed mitral valve is the usual underlying cardiac cause (page 58). A variety of orifice leads to left atrial dilatation, and this predisposes to complaints are used to describe palpitations, including abnormal electrical pathways and atrial fibrillation. In the ‘fluttering’, ‘pounding’ and ‘skipping a beat’. Symptoms right heart, chronic pulmonary hypertension predisposes may also be experienced in the neck. Important aspects to dilatation of the thin-walled right ventricle. are the frequency, regularity of palpitation (e.g. fast and With volume overload, the response of the left ventricle irregular) and precipitating factors. is to dilate; therefore, in mitral or aortic regurgitation, the Knowledge of precipitating factors is important. Palpita- left ventricle dilates to accommodate the regurgitant tions can be a normal manifestation of anxiety or panic volume. Initially the dilatation improves the contractility, reactions. However, it is vitally important that an organic but later in the disease process gradual dilatation is asso- cause is excluded as it is common for anxiety disorders to ciated with ventricular impairment as the ventricular func- coexist in a patient with supraventricular tachycardia. Exer- tion approaches the far right-hand aspect of the Starling cise is associated with excess catecholamines and also a curve (Fig. 1.1). Therefore, when deciding the timing of precipitator of arrhythmia (supraventricular tachycardia, atrial intervention for aortic and mitral regurgitation, measure- fibrillation and ventricular tachycardia usually originating from ments of left ventricular end diastolic diameter are impor- the right ventricle). Excessive caffeine, smoking and alcohol tant, as increasing dimension is associated with disease intake are also thought to be precipitators of arrhythmia. progression. A history of any underlying heart disorder is important, as arrhythmia is associated with ischaemic heart disease (ventricular arrhythmia), hypertensive heart disease (atrial Symptoms of cardiac fibrillation), heart failure (ventricular arrhythmia) and heart disease valve disease. Early age of onset of arrhythmia (childhood or teenage Chest pain years) suggests the presence of a congenital abnormality Chest pain is a common symptom of cardiac disease. such as a bypass tract that can lead to supraventricular Cardiac ischaemia causes angina, a tight and crushing tachycardia. retrosternal pain that may radiate to the jaw and down into the arm. Angina may be precipitated by effort, emotion, Syncope Normal Heart failure food or cold weather. It is usually relieved by rest or glyceryl Syncope is often due to vasovagal reaction (simple faint) Ventricular performance trinitrate (GTN). If angina occurs at rest for more than but can also be a symptom of serious underlying disease. 20 minutes, a diagnosis of myocardial infarction should be Cardiac outflow obstruction, which occurs with aortic presumed until proven otherwise. The severity of angina is stenosis and hypertrophic obstructive cardiomyopathy, classified according to the Canadian Cardiovascular Society can result in syncope on effort as the cardiac output is Pulmonary oedema grade (p. 20). not increased on demand. Orthostatic hypotension causes Ventricular end Other cardiovascular causes of chest pains include a transient decrease in cerebral perfusion and if sufficiently diastolic volume pericarditis, often described as a sharp pleuritic chest severe can lead to loss of consciousness. This may result Fig. 1.1 Relationship pain that may radiate to the back (trapezius ridge pain) from the use of antihypertensive medications, and espe- between ventricular and is relieved by sitting forwards. The pain of aortic cially diuretics, in the elderly. In carotid sinus syndrome, the performance and end- dissection has a tearing quality and is usually described receptors of the carotid sinus are more sensitive than diastolic volume. as the most severe pain to be experienced by the patient. It normal; thus minor stimulation, such as turning the head or originates in the chest and may radiate to the back pressure from a tight collar, may elicit the carotid sinus or abdomen. reflex and precipitate syncope. 3
  4. 4. Ch01-F07260.qxd 5/9/07 10:57 AM Page 4 Diseases of the cardiovascular system Examination of the than half the diastolic pressure) may be indicative of cardiovascular system aortic stenosis. The JVP is examined: elevation occurs with congestive Inspection cardiac failure, tricuspid valve disease and pericardial The first impression can yield a lot of information: by tamponade. standing at the end of the bed it is easy to appreciate The precordium is palpated, and the apex beat located. dyspnoea at rest, evidence of cyanosis, the nodding of the The apex beat is displaced by conditions that lead to head with severe aortic regurgitation (de Musset’s sign), cardiomegaly (congestive heart failure, aortic valve disease, and cachexia of severe cardiac failure. mitral regurgitation). A thrill (palpable murmur) will occur Inspection of the fingers may reveal clubbing (cyanotic with the associated heart valve disease. heart disease, endocarditis), splinter haemorrhages, Osler’s nodes (painful erythematous lesions on the pulps of the Auscultation fingers) and Janeway lesions (flat erythematous lesions on The heart is auscultated in the apex with the bell and the palms of the hands). Peripheral infarctions of the digits diaphragm of the stethoscope and then over the second can be due to emboli from atrial fibrillation or prosthetic right intercostal space (aortic area), the second left inter- heart valves. costal space (pulmonary area), down the left border of the sternum (for the diastolic murmur of aortic regurgitation) Palpation and over the tricuspid area. A summary of the heart valve The peripheral pulse reveals the rate and rhythm (pulse lesions and corresponding murmurs is provided in Table 1.1. volume should be assessed at the carotids). In addition the character of the pulse may be bounding in aortic Peripheral examination regurgitation, giving a water hammer quality. Symmetry At the end of the examination it is also important to of the pulses is important and may be affected by aortic auscultate the lung bases for pulmonary oedema and to dissection and coarctation (radio-femoral delay). The blood examine the liver for hepatomegaly and the legs for pressure is obtained and a narrow pulse pressure (less peripheral oedema. Table 1.1 Summary of cardiac murmurs Valve disease Murmur Location of greatest intensity Other features Systolic murmurs Aortic stenosis Ejection systolic Right second interspace Radiates to the carotids Mitral regurgitation Pansystolic Apex Radiates to the axilla Tricuspid regurgitationa Pansystolic Left lower sternal edge Elevated JVP, right ventricular heave, pulsatile hepatomegaly Ventricular septal defectb Pansystolic ‘tearing’ Left sternal edge b Coarctation of the aorta Systolic Over precordium (collateral flow) Radio-femoral delay and the back Diastolic murmurs Aortic regurgitationa Early diastolic Left sternal edge Accentuated by expiration Mitral stenosisa Mid diastolic rumbling Apex Accentuated by expiration with the patient turned to the left a Uncommon conditions b Rare conditions 4
  5. 5. Ch01-F07260.qxd 5/9/07 10:57 AM Page 5 Investigations for cardiac disease SECTION 1.2 SECTION 1.2 Investigations for cardiac disease Blood tests Electrocardiogram Diagnostic imaging Blood tests the entire coronal axis can be analyzed in multiples of 30° (Fig. 1.2a). The electrical axis of the heart is analyzed in the Cardiac radionuclide Serum cardiac markers coronal plane and the normal axis is defined to lie within imaging The cardiac enzymes (creatine kinase and lactase dehydro- –30° to +120°. genase) have largely been superseded by troponin (T or I) The precordial leads look at the heart in a horizontal as the serum cardiac marker of choice (troponin is a plane (Fig. 1.2b). Each lead is made positive in turn: V1 is peptide). The almost absolute specificity of troponin to in the 4th intercostal space to the right of the sternum, V4 cardiac muscle has led to the recent re-definition of is in the 5th intercostal space to the left of the sternum, and myocardial infarction using elevated serum troponin as V6 lies in the midaxillary line. the primary diagnostic criterion. Troponin is detected in Grouping of the leads allows the different aspects of the the serum approximately 4–10 hours after the onset of heart to be analyzed. The main regions are the anterior, myocardial infarction, peaks at 12–48 hours and remains inferior and left lateral surfaces (Table 1.3). Each small elevated for 4–10 days.1 CK-MB (myocardium-bound square on the ECG represents 0.04 seconds and each fraction of creatine kinase) is a suitable alternative when large square (5 small squares) is 0.20 seconds. troponin assay is not available. CK-MB is elevated 4–8 hours after myocardial infarction, peaks at approximately 12 hours and returns to normal after 2–3 days. CK-MB remains a –90 elevated for a much shorter time than troponin, is a useful –120 –60 indicator for early re-infarction and provides an estimate of the size of the infarct. aVR(–150) aVL(–30) Electrocardiogram +180 I (0) The standard 12 lead ECG is obtained by the analysis of electrical current generated by the heart and analyzed in two planes. The first plane is the coronal plane of the limb leads. There are six different leads (Fig. 1.2a). Lead I is +150 +30 created by making the left arm positive and the right arm negative, giving the angle of orientation of 0°. The angles of orientation of the subsequent leads are created similarly, III (+120) II (+60) giving rise to different angles (Table 1.2). By extrapolation, aVF (+90) b Table 1.2 Electrical axis of the limb leads of the ECG Lead Positive Negative Angle of electrode electrode orientation I Left arm Right arm 0° II Legs Right arm 60° V6 III Legs Left arm 120° V5 V4 aVL* Left arm All other leads –30° V1 V2 V3 aVR* Right arm All other leads –150° aVF* Legs All other leads 90° The limb leads are in multiples of 60° from 0° * The augmented limb leads are in multiples of 30° from 0° Extrapolating from all the leads, the angle of orientation of the entire Fig. 1.2a Orientation of the limb leads. The standard leads are coronal axis can be analyzed in multiples of 30° in black, and the extrapolations that can be used are in grey. Fig. 1.2b Orientation of the precordial leads. 5
  6. 6. Ch01-F07260.qxd 5/9/07 10:57 AM Page 6 Diseases of the cardiovascular system Table 1.3 Grouping of the leads of the ECG previously thought that ST segment elevation was asso- ciated with infarction whilst ST segment depression was Group Lead combination associated with ischaemia. It is now recognized that either configuration can be associated with infarction and Anterior V1, V2, V3, V4 troponin release. Left lateral I, V5, V6 Inferior II, III, aVF T wave and QT interval The T wave (Fig. 1.3) is due to repolarization of the ven- tricles. Peaked T waves can result from hyperkalaemia. The QT interval (from the onset of the Q to the end of P wave the T wave) measures the duration from the start of The P wave (Fig. 1.3) results from atrial depolarization. depolarization to the end of repolarization (Fig. 1.3). The The current flows from right atrium to left atrium and in normal QT interval varies with the heart rate, therefore the a slightly inferior direction; it is therefore positive in the corrected QT interval is normally estimated as QT interval left and inferior leads. The duration of the P wave is divided by the square root of the R to R interval of a 0.12–0.20 seconds (3–5 small squares). A short P wave is successive beat and is normally less than 0.45 seconds. usually due to an accessory pathway into the ventricle that Drugs (antihistamines, tricyclic antidepressants) and elec- bypasses the normal conduction, hence shortening the trolyte abnormalities (hypokalaemia, hypocalcaemia) that P wave. Two such common pathways are the bundle of prolong the QT interval predispose to a form of ventricular Kent in Wolff–Parkinson–White syndrome and James fibres tachycardia (torsade de pointes) with a risk of progression in Lown–Ganong–Levine syndrome, the pre-excitation to ventricular fibrillation. syndromes. Conduction blocks QRS complex First-degree heart block is defined as a prolonged PR The QRS complex (Fig. 1.3) is caused by depolarization interval (more than 0.20s) without any dropped beats of the ventricles. From the atrio-ventricular node, the (Fig. 1.4a). This is a common finding and may be associated conducting system (the sites of fastest conduction) with drugs such as β-blockers. In general, first-degree heart comprises the bundle of His, which divides into the right block is a benign rhythm due to delay in conduction at the and left bundle branches and finally the terminal Purkinje AV node or bundle of His. fibres. The QRS duration is normally less than 0.12 seconds Second-degree heart block occurs when not every atrial (3 small squares) and the QRS axis normally lies within –30° impulse passes through the AV node into the ventricles. to +90°. Left axis deviation is associated with left ven- There are two types of second degree heart block: Mobitz tricular enlargement (loosely termed hypertrophy, but type I (or Wenckebach block) that occurs within the AV the ECG cannot distinguish between myocardial hyper- node and causes the PR interval to become progressively trophy and ventricular dilatation). Right axis deviation is longer resulting in a dropped beat (Fig. 1.4b), and Mobitz much less common and is associated with right ventricular type II conduction block that occurs below the AV node dilatation. where a dropped beat occurs after 2 to 3 normal beats without a prolonged PR interval (Fig. 1.4c). Mobitz type II The ST segment second degree heart block is usually associated with The ST segment (Fig. 1.3) represents the time from ven- more serious underlying disease compared to Mobitz type tricular depolarization to repolarization. The height of the I block. ST segment is affected by ischaemia and infarction. It was Complete heart block occurs when the atria and ventri- cles are conducting independently of each other (Fig. 1.4d). The ventricle usually generates an escape rhythm at a rate of 40 beats per min. A wide QRS results (Fig. 1.4d) as the ‘new’ pacemaker originates within the ventricular tissue QRS complex and not the conducting system. T wave Partial conduction block can also occur below the P wave bundle of His, resulting in right or left bundle branch block. It is associated with a normal heart rate with a wide QRS complex (more than 0.12 s). A right bundle branch block results in an RSR’ pattern in lead V1 and left bundle branch block is associated with notched R waves in V6; PR interval the pattern is not usually as pronounced as in right bundle ST segment branch block. QT interval Cardiac enlargement Left ventricular hypertrophy (more accurately, enlarge- 6 Fig. 1.3 Standard ECG complex. ment) is suggested when the sum of the S wave amplitude
  7. 7. Ch01-F07260.qxd 5/9/07 10:57 AM Page 7 Investigations for cardiac disease SECTION 1.2 with uncontrolled angina, heart failure, and symptomatic P wave P wave aortic stenosis. The most common method of investigation is the Bruce protocol. The patient walks on the treadmill at an initial speed of 1.7 mph and an incline of 10 degrees; every Blood tests three minutes the speed and incline are increased, for example stage 2 is a speed of 2.5 mph and an incline of Electrocardiogram 12 degrees. The test continues until the target end point Diagnostic imaging a is reached (2 mm ST segment depression), until completion if no demonstrable ECG change suggestive of ischaemia Cardiac radionuclide occurs, or if a complication develops (ST segment elevation, imaging P wave P wave P wave hypotension, moderate angina, arrhythmia). Diagnostic imaging Chest X-ray (CXR) b The standard films for the evaluation of cardiac disease are the postero-anterior (PA) and the lateral plain chest X-ray (Fig. 1.5). In this section we focus on cardiac abnormalities. P wave P wave P wave P wave The right heart border consists of the superior vena cava and right atrium, whilst the left heart border consists of the aortic arch, pulmonary artery, left atrial appendage and the free wall of the left ventricle. Cardiomegaly is defined when the transverse diameter of the heart is more than 50% of the transverse diameter of the chest. This is an approximate definition; common c causes are congestive cardiac failure, mitral regurgitation, aortic valve disease and pericardial effusion (globular cardiac silhouette). P wave P wave P wave Other radiological features of congestive cardiac failure are bilateral patchy consolidation (pulmonary oedema), upper lobe venous diversion, Kerley B lines (linear shadows at the peripheral 2 cm of the lung fields) and bilateral pleural effusions (page 164). Isolated enlargement of the left atrium (mitral stenosis) d results in a double right heart shadow (the second shadow Fig. 1.4 Conduction blocks. (a) First-degree heart block. (b) Second-degree heart block (Mobitz type I (Wenckebach) block. (c) Second-degree heart block (Mobitz type II block). (d) Third-degree (complete) heart block. in V1 (or V2) and the R wave amplitude in V6 (or V5) is more than 35 mm, usually with accompanying left axis deviation. Right ventricular hypertrophy is less common and suggested by an R wave that is taller than the S wave in V1 and right axis deviation. Exercise electrocardiogram Exercise ECG is often used to determine the presence of coronary artery disease. The resting ECG is often normal in patients with stenotic coronary disease, therefore myocardial ischaemia is induced by stress (exercise or with pharmacological agents such as dobutamine) and the corresponding ST segment and T wave changes are screened to evaluate the presence of flow-limiting coronary disease. Exercise testing is contraindicated in patients Fig. 1.5 Plain chest film. 7
  8. 8. Ch01-F07260.qxd 5/9/07 10:57 AM Page 8 Diseases of the cardiovascular system RECENT ADVANCES Cardiac MRI (Fig. 1.6) has moved from research tool to mainstream imaging and is an important technique for three-dimensional assessment of cardiac structure, myocardial function, myocardial perfusion and myocardial viability.2 Cardiac gated CT is able to detect coronary calcification and is currently being evaluated as a tool for quantification and risk stratification of coronary artery disease.3 Fig. 1.7 Transthoracic echocardiogram—a four-chamber view. ization of the left atrium (situated immediately anterior to the oesophagus) and the mitral valve. The right heart struc- tures, situated furthest away from the probe, are better visualized by transthoracic echocardiography. Dobutamine stress echocardiogram Dobutamine stress echocardiography is a useful investi- gation for detecting inducible myocardial ischaemia. A Fig. 1.6 Cardiac MRI. In this scan of all four chambers of the resting echocardiogram is performed to assess wall motion heart, the cross-section is viewed as if looking from the feet up to the head. and is then repeated after exercise or pharmacologically induced stress. New regional wall motion abnormalities correspond to areas of ischaemia. The overall sensitivity is is the left atrial border, p. 1), tenting of the left heart border 82% and specificity is 84% for the detection of areas of (enlarged atrial appendage) and, in very large atria, significant coronary disease. splaying of the carina (due to pressure from the left atrium). Echocardiography Transthoracic echocardiography is a widely used non- invasive investigation that has the ability to visualize the INFORMATION ON ECHOCARDIOGRAPHY anatomy and function of the heart valves, myocardium and Cheitlin MD, Armstrong WF, Aurigemma GP, et al. pericardium. It is the investigation of choice for the ACC/AHA/ASE 2003 guideline update for the clinical evaluation of heart valve disease. application of echocardiography: summary article: a report The standard view on transthoracic echocardiography is of the American College of Cardiology/American Heart the apical four-chamber view (Fig. 1.7), where the probe Association Task Force on Practice Guidelines (ACC/AHA/ASE is positioned over the apex and the structure and function Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation 2003; 108: of all four cardiac chambers can be visualized. Additional 1146–1162. views are the parasternal short and long axis views. In addition, continuous wave and colour flow Doppler modal- ities can quantitate the presence and severity of valve stenosis and regurgitation. Transoesophageal echocardiography can be performed Cardiac radionuclide as a day case procedure or intraoperatively. The echo- cardiogram probe is introduced into the oesophagus and imaging visualizes the heart along the length of the oesophagus A cardiac radionuclide image (cardiac scintigraphy) is and from within the stomach. In contrast to transthoracic obtained by injecting a radionuclide into the peripheral echocardiography, the probe visualizes cardiac structures circulation and imaging with a gamma camera. The emitted from deep to superficial. The standard views are the gamma rays are focused using a collimator, and the midoesophageal four-chamber view and the transgastric anatomical origin and time of isotope decay is transformed short axis view. In addition, numerous other views are into an image. able to visualize the structures of the heart. The advantage The radiopharmaceuticals used for single photon 8 of transoesophageal echocardiography lies in the visual- myocardial perfusion imaging include thallium-201 (201Tl, a
  9. 9. Ch01-F07260.qxd 5/9/07 10:57 AM Page 9 Investigations for cardiac disease SECTION 1.2 potassium analogue) and technetium-99m (99mTc). The In some departments, the 99mTc MIBI injection is tracers used for positron emission tomography (PET) repeated the next day at rest, and rest scans are compared include oxygen-15, carbon-11 and fluorine-18, which may for discordant or concordant areas of activity (Fig. 1.8). A be coupled to physiologically active molecules such as discordant deficit indicates a region of ischaemia, whilst a fatty acids (11C labelled fatty acids), and deoxyglucose concordant deficit (no isotope visible on the stress or Blood tests (18F-labelled deoxyglucose). exercise study) is due to the presence of an infarct or scarred non-viable myocardium. It is possible to use Electrocardiogram Myocardial perfusion imaging different isotopes and perform the two phases of the same Diagnostic imaging Planar and single photon emission computed tomography study on the same day. (SPECT) images are widely acquired for the assessment of Cardiac radionuclide the presence and severity of coronary disease, detection of Analysis of ventricular function imaging myocardial viability, myocardial wall mass and global In addition to areas of regional ischaemia or infarction, it is ventricular function. possible to analyze the ventricular function. Gated SPECT The presence of coronary disease and myocardial myocardial perfusion images that are synchronized with viability can be assessed on rest and stress images that are the ECG (to determine the onset of systole and diastole) are induced by exercise or pharmacological agents such as used to estimate the area of the ventricle in systole and dobutamine. Typically, 99mTc is the myocardial perfusion diastole. The cross-sectional areas are used to calculate the agent of choice. The patient is usually subjected to three-dimensional ventricular volume and hence the pharmacological or exercise stress. Just before termination ejection fraction. An alternative method is to use a first-pass of the protocol, the isotope is injected and its myocardial radionuclide angiogram, where the ejection fraction is fixation represents blood flow in the stressed state. The estimated based on the change in radioactivity over time. 99m Tc MIBI (2-methoxy isobutyl isonitrile) attaches to the myocardium in proportion to the instantaneous regional Myocardial infarct avid imaging perfusion. Approximately 60 minutes later, images are Radionuclide imaging can also be used to assess the obtained using SPECT and reformatted to represent images presence of myocardial necrosis using tracers such as 99mTc perpendicular to the long and short axis of the heart. pyrophosphate that localize to infarcted myocardium. The Fig. 1.8 Cardiac SPECT scan. The presence of reversible ischaemia is indicated by the orange-lighted cardiac segments at rest. 9
  10. 10. Ch01-F07260.qxd 5/9/07 10:57 AM Page 10 Diseases of the cardiovascular system most intense localization usually occurs 48–72 hours after REFERENCES infarction. However, serum troponin has largely superseded this radionuclide technique to detect myocardial infarction. (1) Wu AHB, Apple FS, Gibler WB, Jesse RL, Warshaw MM, Valdes R Jr. National Academy of Clinical Biochemistry Standards of Laboratory Practice: recommendations for the use of cardiac markers in coronary artery diseases. Clinical Chemistry 1999; 45: 1104–1121. INFORMATION ON RADIONUCLIDE (2) Constantine G, Shan K, Flamm SD, Sivananthan MU. Role of MRI in clinical cardiology. Lancet 2004; 363: 2162–2171. IMAGING (3) Schoepf UJ, Becker CR, Ohnesorge BM, Yucel EK. CT of coronary artery disease. Radiology 2004; 232: 18–37. Klocke FJ, Baird MG, Lorell BH, et al. ACC/AHA/ASNC guidelines for the clinical use of cardiac radionuclide imaging—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to Revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). Circulation 2003; 108: 1404–1418. SECTION 1.3 Diagnostic procedures Diagnostic cardiac For right heart catheterization, the cardiac catheter is introduced into the sheath and advanced to the right catheterization atrium, right ventricle and pulmonary artery where haemo- Cardiac catheterization is a technique that can be used to dynamic measurements or the injection of contrast media measure intracardiac pressures and perform coronary or can be performed. ventricular angiography. Percutaneous coronary inter- For left heart catheterization, the catheter is advanced vention and radiofrequency ablation are extensions to this to the ascending aorta, through the aortic valve and into technique in which angioplasty, stenting or the treatment the left ventricle (Fig. 1.9). Haemodynamic measurements of arrhythmia is performed through the same approach. can be performed and contrast media injected into the ventricle to obtain a ventriculogram or into the left main Indications The main indication for diagnostic cardiac catheterization is the identification and assessment of the severity of coronary artery disease. It may also be a complementary investigation to assess cardiac haemodynamic measure- ments and the severity of heart valve disease. Patient preparation Cardiac catheterization is usually performed as a day case. Informed consent is required and patients are admitted preoperatively to screen for relative contraindications such as coagulopathy and extensive femoral arterial disease. Procedure The patient is positioned supine in the cardiac catheter- ization suite, and an X-ray image intensifier is used. Right or left heart catheterization can be performed. The approach to the right heart is via the jugular, subclavian or femoral vein. The left heart is usually approached via the femoral artery. A needle is used to puncture the vessel and a guidewire is introduced. The original needle is removed and a sheath is introduced into the vessel using the guidewire. Once the sheath is securely in the vessel, the Fig. 1.9 A left ventricular angiogram illustrating reflux of contrast 10 guidewire is removed. into the left atrium due to mitral regurgitation.
  11. 11. Ch01-F07260.qxd 5/9/07 10:57 AM Page 11 Therapeutic procedures SECTION 1.4 and right coronary arteries for coronary angiography. An femoral artery has been punctured. Patients are monitored arch aortogram can also be performed if necessary to for femoral arterial bleeding and complications such as visualize the aortic arch. myocardial infarction and stroke. Complications Diagnostic cardiac REFERENCE There is a 0.11% risk of mortality, 0.05% risk of myocardial catheterization infarction and 0.07% risk of stroke with coronary (1) Scanlon PJ, Faxon DP, Audet A-M, et al. ACC/AHA guidelines angiography.1 for coronary angiography: executive summary and recommendations: Permanent pacing and a report of the American College of Cardiology/American Heart implantable cardioverter Association Task Force on Practice Guidelines (Committee on Coronary defibrillators Post procedure care Angiography) Developed in collaboration with the Society for Cardiac After the procedure, sustained pressure over the groin is Angiography and Interventions. Circulation 1999; 99: 2345–2357. usually required for left heart catheterization where the SECTION 1.4 Therapeutic procedures Permanent pacing and bifascicular) heart block, acute myocardial infarction, sinus node dysfunction or neurocardiogenic syncope. The disease implantable cardioverter specific indications are listed in Table 1.4. defibrillators An implantable cardioverter defibrillator looks like and can function as a pacemaker; however, it can also deliver Indications low-energy synchronized cardioversion and high-energy The main indications for a permanent pacemaker are defibrillation shocks that are successful in terminating 99% symptomatic bradycardia associated with (complete and of ventricular fibrillation attacks. The implantation proce- Table 1.4 Indications for a permanent pacemaker* Acquired atrioventricular block Third degree or advanced second-degree heart block with any of the following features: • Symptomatic bradycardia • Arrhythmia or other medical condition that requires medications that cause symptomatic bradycardia • Documented asystole of more than 3 seconds, or any escape beat less than 40 bpm • After catheter ablation of the atrioventricular junction • Atrioventricular block after cardiac surgery that is not expected to recover • Neuromuscular diseases with atrioventricular block Second-degree heart block with associated symptomatic bradycardia Chronic bifascicular and trifascicular blocks Intermittent third-degree atrioventricular block Type II second-degree atrioventricular block Alternating bundle branch block After myocardial infarction Persistent second-degree atrioventricular block with bilateral bundle branch block or third-degree atrioventricular block below the His–Purkinje system Transient advanced (second- or third-degree) infranodal atrioventricular block and associated bundle branch block Persistent and symptomatic second- or third-degree atrioventricular block Sinus node dysfunction Sinus node dysfunction with documented symptomatic bradycardia, including frequent sinus pauses that produce symptoms Symptomatic chronotropic incompetence Carotid sinus syndrome and neurocardiogenic syncope Recurrent syncope caused by carotid sinus stimulation * Selected class I indications from Gregoratos G, Abrams J, Epstein AE, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). Circulation 2002; 106: 2145–2161. 11
  12. 12. Ch01-F07260.qxd 5/9/07 10:57 AM Page 12 Diseases of the cardiovascular system dure is similar to that of a pacemaker but the indications Table 1.5 Indications for an implantable cardioverter differ and are listed in Table 1.5. defibrillator Patient preparation Cardiac arrest due to ventricular fibrillation or ventricular Informed consent is required and patients are required to tachycardia not due to a transient or reversible cause starve from midnight in case general anaesthesia is required. Spontaneous sustained ventricular tachycardia in association with structural heart disease Procedure Syncope of undetermined origin with clinically relevant, Under local anaesthesia, a small incision is sited below the haemodynamically significant sustained ventricular tachycardia or ventricular fibrillation induced at clavicle and a subcutaneous pocket is created. Access to electrophysiological study when drug therapy is ineffective, the subclavian vein is obtained and the pacemaker leads not tolerated, or not preferred are advanced under fluoroscopic (X-ray) control from the Non-sustained ventricular tachycardia in patients with subclavian vein to the brachiocephalic vein, superior vena coronary disease, prior myocardial infarction, left ventricular cava and into the right atrium and right ventricle. Dual dysfunction, and inducible ventricular fibrillation or sustained chambered pacemakers require the implantation of a ventricular tachycardia at electrophysiological study that is pacemaker lead in the right atrium and right ventricle. The not suppressible by a class I antiarrhythmic drug leads are tested to ensure good electrical contact and then Spontaneous sustained ventricular tachycardia in patients connected to the pacemaker, which is then placed into the without structural heart disease not amenable to other treatments subcutaneous pocket. The defect is closed in layers. Complications Complications that can arise include bleeding and infec- Post procedure care tion. Rarely, perforation of the heart can occur. Pacemaker- After the pacemaker has been implanted, a CXR is performed related complications include fracture and dislodgement of to screen for pneumothorax. Post procedure ECG is required the pacing leads. and a pacemaker check is performed prior to discharge. SECTION 1.5 Manifestations of heart disease Acute heart failure Table 1.6 Causes of acute heart failure Acute heart failure is defined as the rapid onset of Acute decompensation of existing heart failure symptoms or signs due to abnormal cardiac function. Acute coronary syndromes Acute heart valve disease Epidemiology Arrhythmia The overall incidence is not precisely known, but acute Hypertensive crises heart failure is associated with 13% of patients admitted Myocarditis to hospital with acute coronary syndrome.1 Cardiac tamponade High-output cardiac failure Pathology The causes of acute heart failure are listed in Table 1.6, the most common being coronary artery disease. The Scope of disease pathophysiological changes associated with acute heart failure are reduced cardiac output with poor tissue Reduced organ perfusion from acute heart failure results in perfusion and increased pulmonary capillary wedge a multisystem disorder as detailed below. pressure (a surrogate marker of increased left atrial pressure from reduced forward blood flow). In patients Clinical features without pre-existing chronic heart failure, the JVP may not be elevated (acute left ventricular failure), the heart size Acute heart failure can result in a number of clinical presen- is normal (cardiomegaly is a chronic process), and the tations. Acute decompensated heart failure is associated sudden increased back pressure leads to severe pulmonary with mild dyspnoea without evidence of pulmonary oedema 12 oedema. or cardiogenic shock.
  13. 13. Ch01-F07260.qxd 5/9/07 10:57 AM Page 13 Manifestations of heart disease SECTION 1.5 Patients with pulmonary oedema (as confirmed by chest X-ray) usually present with severe dyspnoea and on examination may be cyanosed with diffuse pulmonary crepitations. Patients with cardiogenic shock usually have hypoten- Acute heart failure sion and a low urine output associated with a pulse rate of more than 60 bpm. Chronic heart failure Less common manifestations of acute heart failure include hypertensive acute heart failure (symptoms and signs of heart failure with elevated blood pressure and pulmonary oedema) and high-output heart failure. Initial investigations Fig. 1.10 Acute pulmonary oedema. The CXR shows bilateral patchy consolidation, Kerley B lines, and pleural effusions with a Full blood count relatively normal heart size. Anaemia is associated with reduced oxygen carriage and may be a precipitating cause. Urea and electrolytes Reduced organ perfusion can lead to renal impairment. Initial management Liver profile Oxygen Reduced organ perfusion can lead to a deranged liver Maintaining oxygen saturations above 95% is important profile. to improve tissue oxygenation and reduce pulmonary artery pressure (improve right ventricular forward flow). Serum cardiac markers If adequate oxygenation cannot be achieved by supple- Elevated troponin levels would suggest myocardial mentary oxygen, continuous positive airway pressure infarction (p. 28) as the underlying cause for acute heart (CPAP) can be employed. With severe heart failure, intuba- failure. tion and ventilation may be required. Monitoring of oxygen levels can be undertaken by Arterial blood gases peripheral saturations, or by repeated measurements from An estimation of PO2 is useful to guide management. an indwelling arterial line. Patients with pulmonary oedema may have type I respi- ratory failure (low PO2 and low PCO2). Morphine Morphine is indicated in the early stages to induce vasodi- Electrocardiogram latation and alleviate symptoms of dyspnoea. An ECG is useful to screen for myocardial ischaemia (p. 8) and arrhythmia. Nitrates Intravenous nitrates are administered to relieve pulmonary Chest X-ray congestion and improve coronary flow. However, tolerance A plain chest film will reveal pulmonary oedema in patients to treatment usually develops after 24 hours. with severe heart failure (Fig. 1.10). Identify and address any precipitating cause Echocardiogram Any precipitating cause such as myocardial infarction, A transthoracic echocardiogram is an essential inves- arrhythmia or infection should be addressed. Drugs tigation to assess ventricular function, heart valve disease, that are associated with hypotension (ACE inhibitors, pericardial disease and mechanical complications of β-blockers) should be stopped in the presence of acute myocardial infarction. heart failure. Further investigations Medical management Haemodynamic measurements Diuretics Measurements of cardiac output and other haemodynamic Loop diuretics are administered to patients with acute indices (pulmonary capillary wedge pressure) can be heart failure and fluid overload. Volume status is usually obtained with a pulmonary artery flotation catheter assessed using central venous or pulmonary capillary (Swan–Ganz) and are usually reserved for patients with wedge pressure. More rapid removal of fluid can be severe heart failure requiring inotropic support. undertaken using haemofiltration. 13
  14. 14. Ch01-F07260.qxd 5/9/07 10:57 AM Page 14 Diseases of the cardiovascular system Inotropic agents setting of temporary assistance for acute cardiac failure in Inotropic agents may be required to augment cardiac anticipation of full recovery in conditions such as acute output. Usually pulmonary artery flotation catheter myocarditis (bridge to recovery) or as a holding measure measurements of cardiac output, pulmonary capillary prior to heart transplantation (bridge to transplantation). wedge pressure and systemic vascular resistance are More recently, the scope for ventricular assist devices has performed to guide selection of an appropriate inotropic been extended to prolong the quality of life in end stage agent. Adrenaline is a commonly used inotropic agent, heart failure (destination therapy). and phosphodiesterase inhibitors (enoximone) are also a useful alternative when increased cardiac output is required in addition to lowering of the systemic vascular RECENT ADVANCES resistance. The first totally implantable artificial heart was implanted at the Jewish Hospital in Kentucky in 2001.2 The recipient survived 151 days, and at least 4 recipients have now Surgical management survived past 60 days. Definitive surgical management is directed to correcting any underlying cause such as acute heart valve regurgi- tation, correcting any mechanical complication of myocar- dial infarction, and relief of cardiac tamponade. Mechanical circulatory assistance can be provided whilst the under- FURTHER INFORMATION lying cause is being addressed, or if the underlying cause Nieminen MS, Bohm M, Cowie MR, et al. ESC Committee for is reversible, or whilst awaiting definitive treatment (e.g. Practice Guideline (CPG). Executive summary of the guidelines heart transplantation). on the diagnosis and treatment of acute heart failure: The Task Force on Acute Heart Failure of the European Society Intra-aortic balloon pump support of Cardiology. European Heart Journal 2005; 26: 384–416. The intra-aortic balloon is a 25–50 mL elongated balloon (17–27 cm) that is designed to rest in the aorta, distal to the subclavian artery and proximal to the renal arteries (Fig. 1.11). It is introduced percutaneously (via the femoral artery) and controlled by timed helium inflation during REFERENCES diastole and deflation during systole. The effect of the (1) Steg PG, Dabbous OH, Feldman LJ, et al. for the Global Registry balloon is to increase aortic pressure during diastole of Acute Coronary Events (GRACE) Investigators. Determinants and (improving coronary perfusion) and decrease aortic prognostic impact of heart failure complicating acute coronary syndromes: Observations from the Global Registry of Acute Coronary pressure during systole (reducing workload and myocardial Events (GRACE). Circulation 2004; 109: 494–499. oxygen consumption). (2) SoRelle R. Cardiovascular news. Totally contained AbioCor The indications of intra-aortic balloon usage are tem- artificial heart implanted July 3, 2001. Circulation 2001; 104: porary cardiac support during acute ventricular failure/ E9005–9006. cardiogenic shock or mechanical complications of myocar- dial infarction (p. 28). In view of the favourable effects on coronary perfusion it is also used in refractory unstable angina (p. 23) and intractable ischaemic ventricular arrhythmia. Contraindications are aortic regurgitation, Chronic heart failure aortic aneurysm and severe aorto-iliac disease. Compli- The most encompassing description of heart failure is a cations of usage include lower limb ischaemia, aortic state in which the heart fails to maintain an adequate dissection and haemolysis. circulation for the needs of the body despite a satisfactory filling pressure. The latter part of the definition excludes all Ventricular assist devices conditions that cause poor venous return such as hypo- Ventricular assist devices are designed to provide a longer volaemia. Congestive heart failure refers to concomitant period of cardiac support and require surgical implantation symptoms or signs of fluid overload. with the use of cardiopulmonary bypass. Ventricular assist devices can augment or take over the role of the heart by Epidemiology diverting the flow of blood from the ventricles into the Fig. 1.11 An intra-aortic assist device and back into the aorta (or pulmonary artery The epidemiology of heart failure is variable due to the balloon pump. for right ventricular assist devices). They can be implanted lack of agreement in definition and diagnostic criteria. Image courtesy of Datascope on the left, right, or both sides of the heart. A multitude of The overall prevalence is up to 2%, and this increases with Medical, Huntingdon, devices are currently employed and differ with respect to age (13% in individuals over 65 years).1 The overall sex United Kingdom. construction from pulsatile (pump assisted) to continuous distribution is equal. However, after adjustment for age, flow (axial and centrifugal flow pumps). heart failure is approximately 1.5 times more common in Candidate selection is paramount as this is currently a men (reflecting the epidemiology of myocardial infarc- 14 very expensive treatment option. It is usually used in the tion).2 It is more common in developed countries.
  15. 15. Ch01-F07260.qxd 5/9/07 10:57 AM Page 15 Manifestations of heart disease SECTION 1.5 Pathology in poor peripheral tissue perfusion, confusion (poor cere- bral perfusion) and renal impairment. The combination Heart failure is not a diagnosis, it is a clinical syndrome of mucosal oedema impairing absorption, feeling of produced by a variety of cardiac and some circulatory fullness from ascites or general anorexia can result in disorders. Although classified into broad groupings, the cardiac cachexia. Acute heart failure pathophysiological effects of each disease often overlap. Chronic heart failure Cardiac disorders Clinical features Impairment of myocardial function A spectrum of disease is increasingly recognized, ranging Diseases of the myocardium (cardiomyopathies) make up from the risk of heart failure to asymptomatic ventricular the majority of the causes of impairment of myocardial dysfunction to clinically apparent congestive heart failure. function. Ischaemic cardiomyopathy is the most common The predominant symptoms of left ventricular failure cause and accounts for two-thirds of patients with heart are dyspnoea, orthopnoea and paroxysmal nocturnal failure. The non-ischaemic cardiomyopathies are caused dyspnoea. It is important to assess how far patients can by chronic hypertension, valvular heart disease and walk before breathlessness sets in and how many pillows myocarditis. In some cases the cause is unknown (idio- they require to sleep. Symptoms originating from right pathic dilated cardiomyopathy). heart failure are peripheral oedema, abdominal distension (hepatomegaly, ascites) and anorexia. In addition, patients Mechanical overload may have symptoms suggestive of an underlying cause, Acute mechanical overload due to aortic regurgitation (e.g. such as angina (ischaemic heart disease). A positive family aortic dissection) or mitral regurgitation (e.g. myocardial history of heart failure at an early age may indicate familial infarction) can cause heart failure despite normal heart cardiomyopathies, and a history of chronic alcohol abuse is function. Over a period of time, this usually results in hyper- associated with dilated cardiomyopathy. trophy, dilatation and scarring, leading to impaired On inspection, cyanosis, peripheral oedema and ascites myocardial function. may be visible. The JVP is usually raised. A sinus tachycardia may be present from increased sympathetic tone and the Impairment of ventricular filling blood pressure may be low (severe disease) or elevated Ventricular filling can be impaired by pericardial constric- (chronic hypertension as an underlying cause). The apex tion (pericardial effusion), increased passive stiffness beat may be displaced by cardiomegaly. On auscultation, a (restrictive cardiomyopathy) and impaired relaxation third heart sound is characteristic and murmurs can arise (consequence of ageing, chronic hypertension). These from underlying heart valve disease or functional mitral/ conditions give rise to diastolic dysfunction and, if suffi- tricuspid regurgitation (failure of valve coaptation due to ciently severe, result in diastolic heart failure (symptoms ventricular/valve annulus distension). Coarse crepitations and signs of heart failure and preserved ejection fraction). can arise from pulmonary oedema. Hepatomegaly and ascites can be confirmed on abdominal examination. Serial Circulatory disorders body weight estimation is a simple method to monitor fluid With any degree of impairment, the heart may not be able status and subsequent response to therapy. to maintain adequate circulation for the needs of the body A detailed clinical assessment should identify any in conditions such as severe anaemia (where oxygen carry- precipitating factors (Table 1.7) and underlying causes ing capacity is impaired), large arterio-venous fistulae (due (Table 1.8) and discriminate between other causes of to shunting of blood), thyrotoxicosis and Paget’s disease dyspnoea (p. 112). The severity of dyspnoea is graded (due to increased metabolic demands of peripheral tissue). according to the NYHA functional class (Table 1.9), and an estimation of volume status (body weight, JVP, pulmonary Scope of disease and peripheral oedema) directs the clinician to the need for subsequent diuretic therapy. Whilst heart failure is rarely confined to a single chamber, the pathophysiology, symptoms and signs are usually presented for the left and right sides of the heart to improve understanding. Table 1.7 Precipitating factors of heart failure As the left heart fails, filling pressures rise and the back pressure exerted by the left heart in turn increases Non-compliance with existing heart failure therapy pulmonary capillary pressure. The imbalance on Starling Inadequate existing heart failure therapy forces results in accumulation of fluid in the interstitium of Uncontrolled hypertension the lung; when the amount is greater than can be ordinarily Arrhythmia removed by lymphatic drainage, pulmonary oedema and Infection pleural effusions result. Drugs (NSAIDs) Increasing back pressure from failure of the right heart results in hepatic congestion, hepatomegaly, ascites and Myocardial infarction peripheral oedema. A low cardiac output state can result 15