Lecture notes Cardiology 5th edition

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Published Date:25-10-2017
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Euan A Ashley and Josef Niebauer Cardiology explained EXPLAINED SERIES One of the most time-consuming tasks in clinical medicine is seeking the opinion of specialist colleagues. There is a pressure not only to Cardiology make referrals appropriate, but also to summarize the case in the language of the specialist. Cardiology Explained is an essential tool in this task. It explains the basic physiology and pathophysiologic mechanisms of cardiovascular disease in a straightforward and explained diagrammatic manner, gives guidelines as to when referral is appropriate, and, uniquely, explains what the specialist is likely to do. Euan A Ashley and Josef Niebauer This facilitates an understanding of the specialty not available from standard textbooks. With wide appeal, this book is ideal for any hospital doctor, generalist, or even senior medical student who may need a cardiology opinion; or for that matter, anyone who simply wants some of cardiology – explained. Contents Cardiac arrest • Cardiovascular examination • Conquering the ECG • Understanding the echocardiogram • Coronary artery disease • Hypertension • Heart failure • Arrhythmia • Valve disease • Infective endocarditis • Cardiomyopathy • Aneurysm and dissection of the aorta • Pericardial disease • Adult congenital heart disease “Cardiology Explained is for the generalist who wants a no-nonsense, jargon-explaining, up-to-date overview of the latest developments in cardiology. It is not intimidating and is well-illustrated with clear diagrams and clinical data. The 14 chapters cover the whole range of modern cardiology in a thoroughly satisfactory manner.” Professor Peter Sleight Emeritus Professor of Cardiovascular Medicine, University of Oxford, UKCardiology explainedContents Chapter 1 Cardiac arrest 1 Chapter 2 Cardiovascular examination 5 Chapter 3 Conquering the ECG 15 Chapter 4 Understanding the echocardiogram 35 Chapter 5 Coronary artery disease 45 Chapter 6 Hypertension 77 Chapter 7 Heart failure 93 Chapter 8 Arrhythmia 111 Chapter 9 Valve disease 145 Chapter 10 Infective endocarditis 167 Chapter 11 Cardiomyopathy 181 Chapter 12 Aneurysm and dissection of the aorta 189 Chapter 13 Pericardial disease 197 Chapter 14 Adult congenital heart disease 203 Abbreviations 215 Index 219Chapter 1 Cardiac arrest Adult basic life-support algorithm Check responsiveness Shake and shout Open airway Head tilt/chin lift If breathing: Check breathing Look, listen, and feel recovery position Breathe Two effective breaths Assess Signs of a circulation 10 seconds only Circulation present No circulation Continue rescue breathing Compress chest Check circulation 100 per minute every minute 15:2 ratio Send or go for help as soon as possible according to guidelines 1Chapter 1 Advanced life-support algorithm for the management of cardiac arrest in adults (US version) Cardiac arrest Basic life-support algorithm Precordial thump Attach defibrillator/monitor Assess rhythm Check pulse +/– During CPR VF/VT Non-VF/VT  Check electrodes, paddle positions, and contact  Attempt to place, con firm, secure airway  Attempt/verify IV access Attempt  Patients with VF/VT refractory to initial shocks: defibrillation x3 – epinephrine 1 mg IV, every 3–5 minutes, or as necessary – vasopressin 40 U IV, single dose 1 time only  Patients with non-VF/VT rhythms: – epinephrine 1 mg IV, every 3–5 minutes  Consider: buffers, antiarrhythmics, pacing CPR CPR up to  Search for and correct reversible causes 1 minute 3 minutes Consider causes that are potentially reversible  Hypoxia  "Tablets" (drug OD, accidents)  Hypovolemia  Tamponade, cardiac  Hydrogen ion – acidosis  Tension pneumothorax  Hyper-/hypokalemia & metabolic disorders  Thrombosis, coronary (ACS)  Hypothermia  Thrombosis, pulmonary (embolism) ACS: acute coronary syndromes; CPR: cardiopulmonary resuscitation; IV: intravenous; OD: overdose; VF: ventricular fibrillation; VT: ventricular tachycardia. 2Cardiac arrest Advanced life-support algorithm for the management of cardiac arrest in adults (UK version) Cardiac arrest Precordial thump if appropriate Basic life-support algorithm if appropriate Attach defibrillator/monitor Assess rhythm Check pulse +/– During CPR VF/VT Non-VF/VT  Correct reversible causes If not already  Check electrodes, paddle positions, and contact Attempt  Attempt/verify airway and O2 IV access defibrillation x3 as necessary  Give epinephrine every 3 minutes  Consider: – amiodarone – atropine/pacing – buffers CPR CPR up to 1 minute 3 minutes Consider causes that are potentially reversible  Hypoxia  Tamponade  Hypovolemia  Tension pneumothorax  Hyper-/hypokalemia & metabolic disorders  Toxic/therapeutic disorders  Hypothermia  Thromboembolic & mechanical obstruction CPR: cardiopulmonary resuscitation; IV: intravenous; VF: ventricular fibrillation; VT: ventricular tachycardia. 3Chapter 1 The adult basic life-support algorithm (UK version) is reprinted with permission from the Resuscitation Council (UK) website and is available at: www.resus.org.uk The advanced life-support algorithm for the management of cardiac arrest in adults (US version) is reprinted with permission from the American Heart Association (Circulation 2000;102:I-143). The advanced life-support algorithm for the management of cardiac arrest in adults (UK version) is reprinted with permission from the Resuscitation Council (UK) website and is available at: www.resus.org.uk 4Chapter 2 Cardiovascular examination Although technology has a high profile in cardiology, clinical examination remains a central tool, especially for the generalist. General inspection Many clues to the cardiac condition can be detected with a simple visual inspection. In the acutely unwell patient, cyanosis, pallor, and sweatiness can all be signs of impending danger – does the patient “look” ill? In nonacute patients, cachexia is perhaps the most important feature to note on general inspection since it is an important prognostic sign in heart failure. Palpation is essential to confirm that girth is excess fluid (pitting edema). Certain physical appearances should always prompt an awareness of cardiac abnormalities (see Table 1). Facial signs for which there is evidence of an association with cardiac conditions are shown in Table 2. Finally, it is important to document the condition of a potential cardiac patient’s teeth. Genetic disorder Associated cardiac manifestation Marfan’s syndrome Aortic regurgitation (aortic dissection) Down’s syndrome ASD, VSD Turner’s syndrome Coarctation of the aorta Spondyloarthritides, Aortic regurgitation eg, ankylosing spondylitis Table 1. Cardiac manifestations of genetic disorders. ASD: atrial septal defect; VSD: ventricular septal defect. Taking the pulse Taking the pulse is one of the simplest, oldest, and yet most informative of all clinical tests. As you pick up the patient’s hand, you should check for clubbing and any peripheral signs of endocarditis (see Table 3). Note the rate and document the rhythm of the pulse. The character and volume of the pulse can also be useful signs and traditionally it is believed that these are easier to detect in larger arteries such as the brachial and the carotid (see Table 4). 5Chapter 2 Facial sign Description Possible cardiac association Malar flush Redness around the cheeks Mitral stenosis Xanthomata Yellowish deposits of lipid around the Hyperlipidemia eyes, palms, or tendons Corneal arcus A ring around the cornea Age, hyperlipidemia Proptosis Forward projection or displacement of Atrial fibrillation the eyeball; occurs in patients with Graves’ disease Table 2. Facial signs associated with cardiac conditions. Peripheral Description Cardiac sign association Clubbing Broadening or thickening of the tips of Infective endocarditis, the fingers (and toes) with increased cyanotic congenital lengthwise curvature of the nail and a heart disease decrease in the angle normally seen between the cuticle and the fingernail Splinter Streak hemorrhages in nailbeds Infective endocarditis hemorrhages Janeway lesions Macules on the back of the hand Infective endocarditis Osler’s nodes Tender nodules in fingertips Infective endocarditis Table 3. Peripheral signs associated with infective endocarditis. Checking both radials simultaneously is important in all cases of chest pain as a gross screening test for aortic dissection. Adding radiofemoral delay (or radiofemoral difference in volume) may alert you to coarctation as a rare cause of hypertension. Peripheral pulses should also be documented, as peripheral vascular disease is an important predictor of coronary artery disease: • femoral – feel at the midinguinal point (midway between the symphysis pubis and the anterior superior iliac spine, just inferior to the inguinal ligament) • popliteal – feel deep in the center of the popliteal fossa with the patient lying on their back with their knees bent • posterior tibial – feel behind the medial malleolus • dorsalis pedis – feel over the second metatarsal bone just lateral to the extensor hallucis tendon 6Cardiovascular examination Type of pulse Pulse characteristics Most likely cause Regularly irregular – 2nd-degree heart block, ventricular bigeminy Irregularly irregular – Atrial fibrillation, frequent ventricular ectopics Slow rising Low gradient upstroke Aortic stenosis Waterhammer, Steep up and down stroke Aortic regurgitation, collapsing (lift arm so that wrist is patent ductus arteriosus above heart height) Bisferiens A double-peaked pulse – the Aortic regurgitation, second peak can be smaller, hypertrophic cardiomyopathy larger, or the same size as the first Pulsus paradoxus An exaggerated fall in pulse Cardiac tamponade, volume on inspiration acute asthma (10 mm Hg on sphygmomanometry) Bounding Large volume Anemia, hepatic failure, type 2 respiratory failure (high CO ) 2 Pulsus alternans Alternating large and small Bigeminy volume pulses Table 4. Abnormal pulses. Blood pressure This is described in Chapter 6, Hypertension. Jugular venous pressure Of all the elements of clinical examination, the jugular venous pressure (JVP) is the most mysterious. It is highly esoteric, and whilst some people wax lyrical about the steepness of the “y” descent, others will feel grateful to be convinced they see it at all. Two things are very clear: (1) the JVP is a very useful clinical marker in many situations, and (2) the exact height of the JVP is a poor guide to central venous pressure. Taken together, this suggests that noting whether the JVP is “up” or “down” is good practice in every cardiac patient. In particular, it can be very useful in diagnosing right-sided heart failure and in differentiating a cardiovascular cause of acute shortness of breath (right ventricular failure, pulmonary embolism) from an intrinsic pulmonary cause (asthma, chronic obstructive pulmonary disease). For the general physician, the waveform of the JVP (see Figure 1) is, for most purposes, only of academic significance. 7Chapter 2 a a v c y x Diastole Ventricular Diastole systole a wave x descent v wave y descent Atrium contracting Atrium relaxing then Atrium tense, full; Atrium emptying, tricuspid valve open filling, tricuspid tricuspid closed tricuspid open closed Figure 1. Waveforms of the jugular venous pressure (including a brief explanation for each wave). The “c” wave represents right ventricular contraction “pushing” the tricuspid valve back into the right atrium. Reproduced with permission from Oxford University Press (Longmore JM et al. The Oxford Handbook of Clinical Medicine, 5th Edn, p. 79). The JVP should be assessed with the patient reclined at a 45º angle (see Figure 2). Accepted practice is that only the internal jugular vein should be used, as only this vessel joins the superior vena cava at a 180º angle. The JVP is defined as the height of the waveform in centimeters above the sternal angle (4 cm is normal). Abnormalities of the JVP are described in Table 5. 8Cardiovascular examination Internal External jugular jugular vein vein Sternocleidomastoid muscle Figure 2. The jugular veins. The patient is lying at a 45° angle, thus revealing the surface markings of the neck. JVP abnormalities Probable cause Large “a” wave Tricuspid stenosis, pulmonary hypertension, pulmonary stenosis Cannon wave Atrial fibrillation, complete heart block, VVI pacing, ventricular tachycardia (a cannon wave occurs when the right atrium contracts against a closed tricuspid valve) Steep “x”, “y” descent Constrictive pericarditis, cardiac tamponade Large “v” wave, “cv” wave Tricuspid regurgitation Kussmaul’s sign Rise of JVP on inspiration, constrictive pericarditis, cardiac tamponade Table 5. Abnormalities of the jugular venous pressure (JVP). Palpation Before auscultation, inspection of the precordium can be a useful indicator of previous surgery – eg, midline sternotomy suggests previous bypass, lateral thoracotomy suggests previous mitral valve or minimally invasive bypass surgery (left internal mammary artery to left anterior descending coronary artery). Locate the apex beat – the furthest point laterally and inferioraly where you can clearly feel the apex (usually the fifth intercostal space in the midclavicular line). There are many different descriptions for abnormal apex beats. One scheme distinguishes heaving (high afterload, eg, aortic stenosis) from thrusting (high preload, 9Chapter 2 eg, aortic regurgitation). The apex may also be “tapping”, but this reflects a loud first heart sound. In addition, you should place your left hand over the sternum and feel for any significant ventricular heave (right ventricular hypertrophy) or thrill (tight aortic stenosis, ventricular septal defect). Auscultation Held by many as the key to physical examination, the importance of auscultation remains, but is diminished in an age of increasingly portable echocardiography. Listen over the aortic (second right intercostal space) and pulmonary (second left intercostal space) areas and at the left lower sternal edge with the diaphragm of your stethoscope (better for higher pitches), then use the bell for the apex (better for lower pitches). If in doubt, use both. Press lightly with the bell. If you hear an abnormality over the aortic or pulmonary areas, you should listen over the carotids. If you hear an abnormality at the apex, listen in the axilla. Listen systematically. Start with the heart sounds – ignore everything else. Heart sound variations When listening to heart sounds, note their volume (normal, diminished, loud) and whether physiological splitting is present (see Figure 3). Physiological splitting of the second heart sound is when the sound of aortic valve closure (A2) occurs earlier than that of pulmonary valve closure (P2). It occurs in inspiration and is more common in the young. It is caused by increased venous return and negative intrathoracic pressure. This delays right ventricular emptying and pulmonary valve closure, at the same time that pooling of blood in the pulmonary capillary bed hastens left ventricular emptying and aortic valve closure. Reverse splitting of the second heart sound can occur in conditions where aortic valve closure is delayed, such as left bundle branch block or paced right ventricle, or where pulmonary valve closure occurs early, such as in the B form of Wolff–Parkinson–White syndrome. Wide fixed splitting of the second heart sound occurs in atrial septal defect. A third heart sound may be heard soon after the second heart sound. It is thought to be due to rapid, high-volume filling of the left ventricle. As such, it is found in pathological (left ventricular failure) as well as physiological (athletic heart, pregnancy) states. A fourth heart sound may be heard just before the first sound. This is caused by atrial contraction filling a stiff left ventricle, eg, hypertensive heart or diastolic heart failure. 10Cardiovascular examination Systole S4 S1 EC MSC A2 P2 S3 OS S2 Figure 3. Relative positions of heart sounds and added sounds in auscultation. Sounds in red are high pitched. A2: aortic component of second heart sound; EC: ejection click; MSC: mid systolic click; OS: opening snap; P2: pulmonary component of second heart sound; S1–S4: heart sounds 1–4. Murmurs When you have considered these heart sound variations, move on to consider the gaps between the heart sounds. If you hear a murmur, first establish whether it occurs in systole or diastole (time against the carotid pulse if necessary). Then determine its length and, if short, its exact position (early, mid, or late; systole or diastole) (see Figure 3). Added sounds An opening snap occurring after the second heart sound represents a diseased mitral valve opening to a stenotic position. An ejection click soon after the first heart sound occurs in aortic stenosis and pulmonary stenosis. A mid systolic click is heard in mitral valve prolapse. After listening to the heart Listen to the base of the lungs for the fine inspiratory crackles of pulmonary edema. If you suspect right-sided cardiac pathology, palpate the liver, which will be enlarged, congested, and possibly pulsatile in cases of right ventricular failure or tricuspid valve disease. Also, check the patient’s ankles for swelling. Table 6 outlines common associations in cardiovascular clinical examination. 11Chapter 2 AS Aortic Aortic Mitral Mitral Tricuspid Pulmonary sclerosis/ regurgitation stenosis regurgitation regurgitation regurgitation minimal AS Pulse Low Normal ↑ volume, Low Normal/AF Normal/AF Normal volume, collapsingvolume, slow normal/AF rising Pulse – – ––– ↓ ↑ pressure JVP –– – – – ↑, prominent – systolic wave (“cv” wave) Apex Heaving, Just Thrusting, Tapping, Thrusting,–– not palpable, displaced not displaced displaced not displaced displaced First –– – Loud Soft –– sound Second Soft A2 A2 – – ––– sound not soft Added Ejection–– No third Third –– sounds click can sound sound occur with opening bicuspid snap valve MurmurLoud, Ejection Blowing, Low, Pansystolic Pansystolic Early diastolic harsh, systolic high-pitched rumbling, mid- neither early diastolic mid-diastolic systolic harsh nor ejection loud Heard Second Second LLSE Apex with Apex LLSE in Second left best right right (patient patient inspiration ICS ICS ICS forward in turned expiration) to left Radiates Into Faintly to–– To axilla –– carotids carotids Table 6. Common associations in cardiovascular clinical examination. AF: atrial fibrillation; AS: aortic stenosis; ASD: atrial septal defect; ICS: intercostal space; JVP: jugular venous pressure; LLSE: left lower sternal edge; PDA: patent ductus arteriosus; PR: pulmonary regurgitation; VSD: ventricular septal defect. See Chapter 9, Valve disease, for more on columns 1–9 and Chapter 14, Adult congenital heart disease, for columns 10–13. 12Cardiovascular examination Tricuspid Pulmonary ASD VSD PDA Pulmonary stenosis stenosis hypertension Pulse Usually Low Normal/AF Normal Regular, Low volume, low volume, volume collapsing AF AF Pulse –– – – – ↑ pressure JVP Prominent Large “a” –– – ↑ (tricuspid “a” wave wave regurgitation) (if sinus with rhythm) prominent “a” wave (if sinus rhythm) Apex –– Just May be Thrusting, – palpable, displaced displaced not displaced First –– – – – – sound Second – Soft P2 Wide fixed P2 may – Loud P2 sound splitting be loud of S2 Added –– – – – – sounds Murmur Rumbling Harsh Ejection Pan-systolic Continuous – mid-diastolic mid-systolic systolic (↑ ± early machinery ejection flow across diastolic murmur with pulmonary (PR) systolic valve) ± accentuation harsh, explosive, brief early diastolic (PR) and ejection click Heard LLSE Second – LLSE ± 5–7 cm above – best (louder on left ICS second left and left of inspiration) (louder on ICS 2nd left ICS inspiration) beneath clavicle Radiates–– – Apex Posteriorly – Table 6. Continued. 13Chapter 2 Summary A careful clinical examination can reveal much about the condition of your patient’s heart. In addition, noting the findings of a full examination will greatly facilitate specialist referral. In an age of high technology, skilled clinical examination has yet to be surpassed in terms of convenience, safety, and value for money. Further reading Bickley LS, Hoekelman RA, editors. Bates’ Pocket Guide to Physical Examination and History Taking, 3rd edn. Lippincott Williams & Wilkins, 2000. Gleadle J. History and Examination at a Glance. Blackwell Science, 2003 Perloff JK. Physical Examination of the Heart and Circulation, 3rd edn. WB Saunders, 2000. Turner RC, Blackwood RA. Lecture Notes on Clinical Skills, 3rd edn. Blackwell Science, 1997. 14Chapter 3 Conquering the ECG Besides the stethoscope, the electrocardiogram (ECG) is the oldest and most enduring tool of the cardiologist. A basic knowledge of the ECG will enhance the understanding of cardiology (not to mention this book). Electrocardiography At every beat, the heart is depolarized to trigger its contraction. This electrical activity is transmitted throughout the body and can be picked up on the skin. This is the principle behind the ECG. An ECG machine records this activity via electrodes on the skin and displays it graphically. An ECG involves attaching 10 electrical cables to the body: one to each limb and six across the chest. ECG terminology has two meanings for the word “lead”: • the cable used to connect an electrode to the ECG recorder • the electrical view of the heart obtained from any one combination of electrodes Carrying out an ECG 1) Ask the patient to undress down to the waist and lie down 2) Remove excess hair where necessary 3) Attach limb leads (anywhere on the limb) 4) Attach the chest leads (see Figure 1) as follows: • V1 and V2: either side of the sternum on the fourth rib (count down from the sternal angle, the second rib insertion) • V4: on the apex of the heart (feel for it) • V3: halfway between V2 and V4 • V5 and V6: horizontally laterally from V4 (not up towards the axilla) 5) Ask the patient to relax 6) Press record 15Chapter 3 1 2 Angle of 3 Louis 4 5 6 V2 V1 V6 V3 V5 V4 Figure 1. Standard attachment sites for chest leads. The standard ECG uses 10 cables to obtain 12 electrical views of the heart. The different views reflect the angles at which electrodes “look” at the heart and the direction of the heart’s electrical depolarization. Limb leads Three bipolar leads and three unipolar leads are obtained from three electrodes attached to the left arm, the right arm, and the left leg, respectively. (An electrode is also attached to the right leg, but this is an earth electrode.) The bipolar limb leads reflect the potential difference between two of the three limb electrodes: • lead I: right arm–left arm • lead II: right arm–left leg • lead III: left leg–left arm The unipolar leads reflect the potential difference between one of the three limb electrodes and an estimate of zero potential – derived from the remaining two limb electrodes. These leads are known as augmented leads. The augmented leads and their respective limb electrodes are: • aVR lead: right arm • aVL lead: left arm • aVF lead: left leg 16

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