(BQ) Part 2 book Tips and tricks of bedside cardiology presents the following contents: Exertional dyspnea, cyanosis and fainting, fever with chills and petechial spots; exertional dyspnea and sudden hemiparesis; retrosternal discomfort upon climbing stairs; recent increase in angina frequency;...
30 Case Exertional Dyspnea, Cyanosis and Fainting Patient Profile Age: 32 Sex: Female Built: Lean Chief Complaints • Progressively increasing dyspnea on exertion for the last year • Coldness of hands and blueness of fingers since months • Fainting on occasions in the preceding month Relevant History • There was no history of breath-holding spells or squatting episodes during her early life • There was no history of recurrent sore throat, joint pains or prolonged fever during childhood or adolescence • There was no history of fever, productive cough, chest pain or hemoptysis preceding her recent worsening of symptoms • There was no history of palpitation and skipped beats or of orthopnea and paroxysmal nocturnal dyspnea Physical Examination • • • • • No pallor or jaundice or ankle edema Cyanosis and clubbing of the finger-nails Pulse: 88 BP: 104/ 70 Temp.: 98 Resp.: 24 Pulse: regular, low in volume and feeble JVP: cm above angle of Louis at 45 degrees Prominent ‘a’ wave observed • CVS: Normal apex beat, sustained left parasternal heave Systolic pulsations visible in the pulmonary area S1 normal, P2 loud and audible upto the apex No S3 or S4 gallop sound heard Gr II /VI soft systolic murmur adjacent to the sternum • Chest: clear on auscultation, no rhonchi or crepts 118 Tips and Tricks of Bedside Cardiology An ECG was obtained ECG Findings: • Tall R wave in leads V1 to V3 • Deep S wave in leads V4 to V6 • Peaked P wave; P pulmonale An X-RAY was also ordered X-RAY Findings: • Right ventricular enlargement Exertional Dyspnea, Cyanosis and Fainting 119 • Prominent pulmonary artery • Normal pulmonary vasculature Diagnosis PRIMARY PULMONARY HYPERTENSION Discussion • A history of progressively increasing dyspnea on exertion raises the possibilities of chronic pulmonary disease, congenital or valvular heart disease, cardiomyopathy or pulmonary hypertension If there is additional history of syncopal episodes, outflow obstruction due to mitral stenosis, aortic stenosis, hypertrophic subaortic stenosis or pulmonary arterial hypertension should be considered • Causes of pulmonary hypertension are: – Increased pulmonary flow lt to rt shunt; ASD, VSD, PDA – Raised left atrial pressure mitral valve disease, LV dysfunction – Chronic pulmonary disease bronchitis, emphysema, fibrosis – Obstruction to pulmonary flow thromboembolic, veno occlusive – Primary pulmonary hypertension • In pulmonary hypertension due to Eisenmenger complex with left- toright shunt, chest X-ray features are RV hypertrophy, prominent pulmonary artery and increased pulmonary blood flow (pulmonary plethora) In mitral valve disease, there is straightening of the left heart 120 Tips and Tricks of Bedside Cardiology border due to prominent left atrial appendage In chronic pulmonary disease the bronchovascular markings are accentuated and there is pulmonary emphysema Clinical Pearls • The presence of cyanosis indicates the presence of chronic lung disease or a right-to-left cardiac shunt In primary pulmonary hypertension, cyanosis is caused by right-to-left shunt across a patent foramen ovale • A prominent ‘a’ wave in the jugular venous pulse indicates right atrial contraction against a noncompliant hypertrophic right ventricle It is observed in both pulmonary stenosis as well as in pulmonary hypertension • A sustained heave on palpation in the left parasternal area indicates the presence of right ventricular hypertrophy It is also observed in pulmonary stenosis • A loud pulmonary component (P2) of the second heart sound (S2) is a classical indicator of pulmonary hypertension In pulmonary stenosis, the P2 is muffled The fact that the P2 is heard even at the cardiac apex is in itself indicative of pulmonary hypertension • Prominent systolic pulsations felt with a soft systolic murmur heard in the second left intercostal space adjacent to the sternum (pulmonary area), indicates dilatation of the main pulmonary artery 31 Case Fever with Chills & Petechial Spots Patient Profile Age: 48 Sex: Male Built: Lean Chief Complaints • High grade fever with chills for the past 10 days • Malaise, arthralgias, anorexia and weight loss Relevant History • Patient underwent aortic valve replacement for a stenotic aortic valve with a St Jude’s prosthesis, months back • He recently underwent extraction of a carious tooth but failed to comply with the antibiotic regimen prescribed by his dentist • There was no history of sore throat, joint swelling, productive cough, burning micturition, pain abdomen or loose stools • There was also no past history of intravenous drug abuse, heavy alcoholic intake or having undergone a genitourinary procedure Physical Examination • • • • • • • Ill-looking, toxic, restless and tachypneic Petechiae under finger-nails (Splinter hemorrhages) Painful nodules on the finger-tips (Osler nodes) Hemorrhages on thenar eminences (Janeway lesions) Subconjunctival petechiae in both eyes (Roth spots) Pulse: 104 BP: 110/ 60 Temp.: 100.8 Resp.: 24 CVS: Normal precordium, heaving apex beat S1 loud, ejection click +, high pitched S2, no S3 sound Gr II /VI ejection systolic murmur, left sternal border • Chest: normal sounds; no rhonchi or crepts • Abdo.: no hepatosplenomegaly or ascites An ECHO was performed 122 Tips and Tricks of Bedside Cardiology ECHO Finding: • Nodular echo-reflective masses, attached to the aortic leaflets Lab Investigations • Blood counts: • Urinalysis: • Biochemistry: • Bacteriology: Hb 8.8, TLC 13800, N83 L15, ESR 52 Albumin +, WBCs 2-3, RBCs ++ Glucose 78, Urea 32, Creatinine 1.1, ASLO titer 220 IU, CRP level 80 mg/ L Bilirubin 2.2, SGOT 42, SGPT 48 Cholesterol 178, LDL 110, TSH 2.2 Throat swab culture: no growth Blood culture grew Streptococcus viridans Fever with Chills & Petechial Spots 123 Diagnosis AORTIC VALVE ENDOCARDITIS Discussion • Endocarditis is inflammation of the inner surface of the heart, including the lining of heart valves Inflammatory and infected material accumulates to cause discrete lesions called vegetations Vegetations are made up of tissue debris fibrin, platelets and leukocytes • Endocarditis may be caused by an infective pathogen or due to a noninfective disease: Infective causes: – Bacterial : Streptococcus, Staphylococcus – Fungal : Aspergillus, Candida – Others : Coxiella, Chlamydia Noninfective causes – Malignant disease : Marantic endocarditis – Collagen disorder : Libman-Sacks endocarditis – Rheumatic fever : Rheumatic pancarditis • On echo, vegetations appear as mobile, irregular echoreflective masses attached to a valve cusp or a cardiac shunt The valve may be native or prosthetic and is usually a left- sided mitral or aortic valve • Vegetations vary in size from few mm to several cm Those less than mm in size are difficult to visualize Large vegetations are associated with fungal or tricuspid endocarditis They shrink as they heal although rapid shrinkage is indicative of embolization • Vegetations move in concert with the leaflet, and not impair its excursion They may be sessile (nodular) or pedunculated and irregular or smooth Fresh vegetations are lumpy but they smoothen as they heal Fresh vegetations are isoechoic with the leaflet but they get brighter as they heal 124 Tips and Tricks of Bedside Cardiology Clinical Pearls • In the clinical setting of rapid onset of dyspnea and palpitation with a febrile illness, an infectious process must be considered Acute rheumatic fever and subacute bacterial endocarditis are the main possibilities An acute viral pericarditis or myocarditis or pneumonitis must also be excluded • The indications for performing serial echoes in endocarditis are: – diagnosis of vegetations – looking for complications – detecting predisposing lesion – evaluating response to treatment – timing of surgical intervention • Endocarditis can lead to valve destruction, valvular regurgitation, appearance of a new murmur or change in a preexisting murmur This occurs due to prolapse, perforation or rupture of a valve leaflet There can be abscess formation around a valve ring or in the interventricular septum which can cause conduction block • Healed vegetations differ from fresh ones by being smaller, smoother and hyperechoic Shrinkage of vegetations alone does not indicate cure while rapid shrinkage suggests embolization Increase in vegetation size indicates persistence of infection and ineffective antimicrobial therapy The risk of embolization persists for as long as months even after bacteriological cure • How often serial echos should be done while the patient is receiving antibiotics is a matter of debate It is difficult to justify frequent echos unless this will clearly alter clinical decisions in management However, repeat echo should be definitely carried out if there is deterioration in the patient’s clinical condition 32 Case Fever with Chills & Illicit Drug Abuse Patient Profile Age: 28 Sex: Male Built: Lean Chief Complaints • High-grade fever with chills and night sweats for weeks • Malaise, easy fatigability, anorexia and kg unintentional weight loss • Mild breathlessness on physical exertion for the same duration Relevant History • • • • No history of cough, hemoptysis or chest pain No urinary complaints or altered bowel habits No history of orthopnea, nocturnal dyspnea or palpitation He was a college drop-out who was presently not engaged in any gainful employment • He admitted to be a smoker and alcoholic on a regular basis • On further questioning he confessed having taken drug-snorts and intravenous injections of illicit drugs, once in a while Physical Examination • • • • • • Drowsy, confused and slightly dyspneic Multiple needle-prick marks on forearms Neck veins distended; mild pedal edema Moderate anemia, mild jaundice, no cyanosis Pulse: 106 BP: 104/ 70 Temp.: 101.6 Resp.: 24 CVS: Pansystolic murmur in parasternal area No gallop sound or pericardial rub heard • Chest: normal breathing, few rhonchi/crepts • Abdo.: hepatomegaly with jugular reflux; no ascites or splenomegaly An ECHO was performed 126 Tips and Tricks of Bedside Cardiology ECHO Finding: • Rounded mass in the right atrium, prolapsing into tricuspid valve Lab Investigations • Blood counts: • Urinalysis: • Biochemistry: • Bacteriology: Hb 9.2, TLC 14600, N78L21, ESR 48 Albumin +1, WBCs 2-3, RBCs nil Glucose 86, Urea 38, Creatinine 1.2, Cholesterol 158, SGOT 24, SGPT 28 ASLO titer 180 IU, CRP level 79 mg Staph epidermidis grown in out of blood culture bottles Throat swab culture: no growth Systemic Hypertension, Dizziness & Confusion 207 Diagnosis SICK SINUS SYNDROME (SSS) Discussion • The ECG features of sick sinus syndrome are: – Sinus bradycardia – Sinoatrial exit block – Slow atrial fibrillation – Junctional escape rhythm • Other clinical features of this syndrome are : – Inadequate tachycardia with stimuli – Atropine resistant bradyarrhythmias – Excessive beta-blocker sensitivity – Alternating fast and slow rhythms (the “brady- tachy” syndrome) • Symptoms of sick sinus syndrome are: – Dizziness, syncope or fainting attacks – Fatigue and dyspnea from heart failure – Palpitation and angina pectoris – Mental confusion and memory defects • Symptoms of sick sinus syndrome are often caused by high-grade sino atrial exit block At times, there may be atrial fibrillation with slow ventricular response or a junctional rhythm The coexistence of fast and slow heart rhythm constitutes the ‘ brady- tachy’ syndrome • In sinoatrial exit block, dropped beats result in pauses In a pause, the entire P-QRS-T complex is missing since neither atrial nor ventricular activation occurs If alternate beats are dropped (2: S-A block), the rhythm resembles sinus bradycardia 208 Tips and Tricks of Bedside Cardiology Clinical Pearls • The “sick sinus syndrome” (SSS) is a clinical condition caused by a diseased sinus node which fails to produce or successfully conduct a sufficient number of impulses It is observed in elderly patients and is believed to be caused by a degenerative condition (amyloidosis) or infiltration of the atria by a fibrocalcareous process • Certain cardiovascular drugs notably beta-blockers (atenolol, metoprolol), calcium- blockers (verapamil, diltiazem) and digoxin may also cause SA node dysfunction which is reversible after discontinuation of therapy • Spells of dizziness and syncope in sick sinus syndrome are due to transient ventricular asystole causing a precipitous decline in stroke volume and cerebral perfusion Such episodes are known as StokesAdams attacks Besides SSS, other causes of Stokes-Adams attacks are: – Advanced atrio-ventricular block – Malignant ventricular arrhythmias – Carotid sinus hypersensitivity – Subclavian steal syndrome • Quite often, sinus node dysfunction is suspected clinically but difficult to prove because the ECG is normal and Holter monitoring does not show up the arrhythmia during the period of observation A prolonged sinus node recovery time (SNRT) and sino-atrial conduction time (SACT) on electrophysiological studies (EPS) is diagnostic of sick sinus syndrome (SSS) 53 Case Athletic Youth & Alarming ECG Patient Profile Age: 25 Sex: Male Built: Athletic Relevant History • This 35-year-old athletic male of African-American descent, presented to the cardiologist for opinion on an abnormal ECG, obtained during routine pre employment medical check-up • He had been actively involved in competitive sports during his college days and denied any present or past history of chest pain, breathlessness, fatigue, palpitation or syncope • The patient did not smoke or take alcohol but was fond of fast-food He did not suffer from diabetes mellitus or systemic hypertension and never had a serum lipid analysis • One of his paternal uncles had expired at the age of 52 years due to sudden cardiac death but there was no parental history of premature coronary artery disease or cerebrovascular accident Physical Examination • • • • • Well-built, well-nourished, muscular physique Conscious, cooperative and comfortable No anemia, cyanosis, jaundice or edema Pulse: 64, BP: 120/ 80, Temp.: 98.2, Resp.: 18 CVS: Normal precordium and apex beat location S1 and S2 normal; no S3 , S4 or pericardial rub • Chest: vescicular breathing; no rhonchi or crepts An ECG was obtained 210 Tips and Tricks of Bedside Cardiology ECG Findings: • Tall R waves in leads V4 to V6 • Deep and narrow initial Q waves • Concave-upward ST segment elevation • Initial slur on ST segment, the J wave • Tall and upright symmetrical T waves Athletic Youth & Alarming ECG 211 Diagnosis EARLY REPOLARIZATION VARIANT Discussion • Common causes of S-T segment elevation are: – Coronary artery disease - Myocardial infarction - Prinzmetal’s angina - Dressler’s syndrome – Acute pericarditis – Ventricular aneurysm – Pulmonary embolism – Early repolarization – Brugada syndrome • The “early repolarization” variant is an alarming electrocardiographic entity that presents with S-T segment elevation and an entirely normal clinical profile It represents early repolarization of a portion of the ventricle before the entire myocardium has been depolarized There is an early uptake of the S-T segment before the descending limb of the R-wave has reached the baseline This causes an initial slur on the S-T segment known as the J-wave • The S-T segment is elevated and concave upward There is an associated increased amplitude of the R-wave The T-wave is also tall but the ratio of S-T segment elevation to T- wave height is less than 0.25 Interestingly, the degree of S-T elevation and T-wave height may vary on a day-to-day basis and the S-T segment may normalize after exercise 212 Tips and Tricks of Bedside Cardiology Clinical Pearls • Early repolarization is a normal ECG variant of unknown etiology that is frequently observed in young athletic males of African-American descent The clinical features of early repolarization are: – Subject is a young black male – He is healthy and of athletic built – He is active and free from symptoms – The clinical evaluation is entirely normal – S-T segment is elevated concave upward • The S-T segment elevation of early repolarization can simulate the injury pattern of acute myocardial infarction The differentiating features are: – S-T segment elevation in concave upwards in lead V6 – Ratio of S-T elevation to T wave height is less than 0.25 – There is no reciprocal ST depression in other leads – ECG changes not evolve as in case of infarction – Serial cardiac enzyme titers (e.g CPK) are not increased – Echo does not show regional wall motion abnormality • In case of acute pericarditis too, the S-T segment is elevated and concave upwards but sinus tachycardia is almost invariably present Acute pericarditis is practically always associated with fever, chest pain and a classical triphasic pericardial rub on auscultation 54 Case Healthy Man & Unique ECG Patient Profile Age: 38 Sex: Male Built: Average Relevant History • This apparently healthy gentleman visited a cardiologist for opinion on an abnormal ECG obtained during a routine health check-up • He was physically active and denied any history of breathlessness, chest pain, palpitation or fainting spells • His childhood had been normal without any history of recurrent sore throat, joint pains or prolonged illness • He neither smoked nor consumed alcohol and did not suffer from diabetes, hypertension or bronchial asthma • One of his cousin brothers had died suddenly due to cardiac arrest, at the age of 32 years Physical Examination • • • • • Well-built, well-nourished and healthy looking Conscious, cooperative and lying comfortably No anemia, cyanosis, jaundice or edema Pulse: 72, BP: 120/ 80, Temp.: 98.2, Resp.: 18 CVS: Normal precordium and apex beat location S1 and S2 normal; no S3 , S4 or pericardial rub • Chest: vescicular breathing; no rhonchi or crepts An ECG was obtained 214 Tips and Tricks of Bedside Cardiology ECG Findings: • rSR’ pattern in lead V1 • Normal rSR’ duration • Elevated S-T segment • Large, inverted T wave Healthy Man & Unique ECG 215 Diagnosis BRUGADA SYNDROME Discussion • Causes of S-T segment elevation in V1 are: – Septal infarction – Acute pericarditis – Ventricular aneurysm – Pulmonary embolism – Early repolarization – Brugada syndrome • The rSR’ pattern in lead V1 observed in case of Brugada syndrome superficially resembles a right bundle branch block (RBBB) But unlike in RBBB, the ventricular complex is not more than 0.12 sec wide and there are no broad S waves in leads L1 and V6 • The characteristic ECG abnormalities observed in Brugada syndrome may be transiently observed and not constant These may become exaggerated or unmasked after drug challenge with antiarrhythmic agents such as flecainide and procainamide 216 Tips and Tricks of Bedside Cardiology Clinical Pearls • The Brugada syndrome is a rare but striking electrocardiographic abnormality It is believed to be a genetic disorder of sodium transport across ion channels located in the right ventricle This produces an abnormal pattern of right ventricular repolarization • Patients who have this abnormality are prone to develop sudden collapse because of malignant ventricular arrhythmias These include syncope due to ventricular tachycardia or even cardiac arrest due to ventricular fibrillation • The genetic defect underlying Brugada syndrome may exist in more than one family member and form the basis of familial ventricular arrhythmias • There is no specific treatment of the underlying disorder However, insertion of a defibrillator device (automatic implantable cardioverter defibrillator—AICD) may be considered in those with recurrent syncope or after cardiac resuscitation from ventricular fibrillation Index A Abnormal ECG 173 Abrupt symptom termination 197 Accelerated hypertension 19 idioventricular rhythm 195 Acquired PS 75 Acute aortic dissection 24 regurgitation 51 mitral regurgitation 47 myocardial infarction 155 myocarditis 79 pericarditis 99, 100, 207 rheumatic fever 83 Advanced atrio-ventricular block 204 Alarming ECG 205 Alveolar edema 78 Amiodarone toxicity 183 Anemia 53 Aneurysm of aorta 15, 16 sinus of valsalva 12 Angina 93 Ankylosing spondylitis 43 Annulo-aortic ectasia 51 Anterior mitral leaflet 95 Antero-septal myocardial infarction 193 Antiarrhythmic drugs 183 Aortic coarctation 11 dissection 16, 47, 116 knuckle 26 regurgitation 16, 43, 64 root dilatation 16 stenosis 15, 39 valve endocarditis 51, 123 regurgitation 20 stenosis 75 Aortico-pulmonary window 24, 64 Arteriovenous fistula 52, 64 Atherosclerosis 16 Athletic youth 205 Atrial fibrillation 72, 115 thyrotoxicosis 191 septal defect 55, 56 Austin flint murmur 28 B Bacterial endocarditis 47 Bat-wing appearance 42 Beri-beri disease 64 heart disease 52 Berry aneurysm 12 Bicuspid aortic valve 11, 43 Blood counts 78 Blue hand 17 lips 65 Blunt chest-wall trauma 51 Body fluid loss 172 Bradyarrhythmias 183 Brady-Tachy syndrome 203 Bronchial asthma 13 105 cuffing 78, 86 Brugada syndrome 207, 211 C Calcific mitral annulus Calcified aortic valve Cardiac surgery 196 Cardiovascular drugs 171 Carey Coomb’s murmur 28 218 Tips and Tricks of Bedside Cardiology Carotid sinus hypersensitivity 204 Casualty medical officer 193 Cephalized blood vessels 78 vessels 86 Chest pain 101, 105, 113 on inspiration 97 wall trauma 47 Chronic effort angina 165 obstructive pulmonary disease 111 pulmonary disease 119 stable angina 143 Circle of Willis 12 Coarctation of aorta 11, 19, 39 Cold 17 Collagen disorder 123 Collapsing radial pulse 16 Commissural calcification 27 Confusion 201 Congenital mitral stenosis 27 PS 75 Conn’s syndrome 172 Connective tissue disorder 27, 43 Constitutional symptoms 129 Constrictive pericarditis 107 Continuous murmur 21 wave 59 Coronary arterio-venous fistula 24, 64 artery disease 13, 183, 207 care unit 153 insufficiency 175 Corrigan’s sign 44 Coxsackie B virus 79 Cushing’s disease 172 Cyanosis 117 D de Musset’s sign 44 Deep vein thrombosis 116 Diabetes mellitus 13, 105 Digitalis toxicity 179, 196 Digoxin 101 Dilated cardiomyopathy 31, 87, 167 main pulmonary artery 54 pulmonary artery 74 Displaced apex beat 16 Dissection of aorta 12, 19, 51 Distended abdomen 105 Dizziness 1, 201 Double apex beat 93 Dressler’s syndrome 207 Ductus arteriosus 11 Dynamic precordium 29 Dyspnea 25, 53, 109 after air travel 113 E Early diastolic murmur 13, 16, 49 repolarization 100, 207 Ebstein’s anomaly 71, 72 Edema 105 Ehlers-Danlos syndrome 15, 36 Ejection systolic murmur 73 Electrolyte deficiency 183 Electrophysiological studies 204 Emergency room 153 Endocarditis at site 12 Endomyocardial fibrosis 91 End-stage renal disease 173 Enlarged cardiac silhouette 78 left ventricle 42 right atrium 54 ventricle 54, 66, 74 Enlargement of heart Episodic machine-like fluttering in chest 185 palpitation 33 Exertional angina dyspnea 41, 117, 133 fatigue 9, 37 F Fainting 117 episodes Fallot tetralogy 67 Fatigue 77 Fever with chills 121, 125 Flu-like syndrome 77 Focal narrowing of aorta 10 Frusemide 101, 177 Furosemide 101, 177 G Global hypokinesia in cardiomyopathy 31 Glycogen storage disease 91 Index H Headache Hemochromatosis 91 Hemoptysis 105 High fever 81 Hilar congestion 86 vascular congestion 78 Hurler’s syndrome 27 Hyperacute infarction 175 Hyperdynamic precordium 16 Hyperkalemia 175 Hypertension 105 in pregnancy 19 Hypertensive heart disease Hypertrophic cardiomyopathy 39, 95 obstructive cardiomyopathy 95 Hypokalemia 171 I Idiopathic cardiomyopathy 31 dilatation of pulmonary artery 76 hypertrophic subaortic stenosis 95 Illicit drug abuse 125 Immobility of leaflet base 27 Incidentally detected pansystolic murmur 57 Increased pulmonary flow 54, 119 Inducible VT 181 Intensive coronary care unit 196 Inter-atrial septum 55 Interventricular septum 3, 59, 107, 155 Intracranial aneurysmal bleed 12 event 183 Ischemic cardiomyopathy 87, 167 Janeway lesions 121 Jerky JVP 69 Jervell-Lange -Neilsen syndrome 183 Joint pains 81 Kent bundle 200 Kerley B lines 78, 86 Kussmaul’s sign 92 Left thrombus 27 ventricle 26 ventricular aneurysm 163 dysfunction 20 end-diastolic pressure 47, 51 failure 12 hypertrophy outflow tract 43 posterior wall thrombus 139 Libman-Sacks endocarditis 123 Lisinopril 101 Loss of appetite 105 Low BP 101 fever with bodyache 97 grade fever 105 Lown-Ganong-Levine syndrome 200 LV dysfunction 177, 181 Lyme disease 79 M Malaise 105 Malignant disease 123 ventricular arrhythmias 204 Marantic endocarditis 123 Marfan syndrome 15, 16, 19, 43 Mid-diastolic murmur 25, 28 Mitral annular calcification 31 regurgitation 31 stenosis 27, 72 valve prolapse 16, 31, 35, 72 Mucopolysaccharidosis 27 Multifocal VPCs 177 Mycoplasma 79 Mycotic aneurysm 16 Myocardial infarction 20, 24, 47, 91, 100, 116, 139, 155, 157, 159, 175, 207 Myocarditis 183 Myxomatous degeneration 36 valuve 47 N L atrial appendage 26 myxoma 27, 131 219 New systolic murmur 45 Nocturnal dyspnea 101 Non ST-elevation myocardial infarction 147 220 Tips and Tricks of Bedside Cardiology O Obstruction to pulmonary flow 119 Occlusion of neck vessels 20 Opening snap 28 Orthopnea 13, 77, 101 Osler nodes 121 Ostium secundum atrial septal defect 36, 72 Overriding aorta 67 P Paget’s bone disease 64 Palpitation 25, 189 Pansystolic murmur 29, 69 Papillary muscle dysfunction 31, 155 rupture 155, 159 Parachute valve 27 Paroxysmal atrial tachycardia 188 nocturnal dyspnea 105 supraventricular tachycardia 72 Patent ductus arteriosus 24, 52, 63 foramen ovale 55 Pericardial effusion 20, 103 Petechial spots 121 Posterior mitral leaflet 159 Post-stenotic dilatation 75 Precordial bulge after myocardial infarction 161 Pre-systolic accentuation 28 Primary pulmonary hypertension 36, 119 Prinzmetal’s angina 100, 175, 207 Productive cough 109 Prominent aortic knuckle Psychotropic drugs 171 Pulmonary artery 26, 63 hypertension 75 congestion 42 edema 86 embolism 24, 47, 115, 116, 207 oligemia 67, 75 plethora 54 stenosis 67, 75 valve stenosis 75 Q Quincke’s sign 44 R Raised JVP 101 left atrial pressure 119 Recent heart failure 165 increase in angina frequency 145 Red eye 41 Reduced pulmonary flow 66, 75 Regional wall motion abnormalities 31, 87 Reiter’s syndrome 15 Restrictive cardiomyopathy 91 Retrosternal discomfort upon climbing stairs 141 Rheumatic mitral stenosis 75 Rheumatic carditis 196 Rheumatic fever 123 heart disease 31, 36, 43 pancarditis 123 Right atrial enlargement 71 bundle branch block 115, 211 sided aortic arch 66 ventricular conduction delay 71 ventricular hypertrophy 67 ventricular outflow tract 23, 67 Romano-Ward syndrome 183 Roth spots 121 Ruptured sinus of Valsalva 47 aneurysm 12, 64, 116 RV volume overload 76 S Sarcoidosis 91 Severe anemia 52, 64 chest pain 17, 149 dyspnea 13 Shelf-like luminal projection 11 Sick sinus syndrome 203, 204 Silent precordium 101 Sinking 149 Sino-atrial conduction time 204 Sinus node recovery time 204 Sinus of Valsalva 23 aneurysm 23 Sinus tachycardia 115 Skin rash 81 Small pulmonary artery 66 Soft systolic murmur 53 Sore throat 81 Index Splinter hemorrhages 121 Spontaneous pneumothorax 47, 116 Squatting attacks 65 ST-elevation myocardial infarction 151 Stiff back 41 Stokes-Adams attacks 204 Strong bounding pulse 61 collapsing pulse 49 Sub-aortic stenosis 75 Subclavian steal syndrome 204 Sudden breathlessness 45 chest pain 21 hand cyanosis 129 hemiparesis 133 Supravalvular ring 27 Supraventricular tachycardia 187 Sweating 149 Syncopal episodes 37 Syncope 93 Syphilitic aortitis 16 Systemic hypertension 1, 13, 39, 43, 201 Systolic anterior motion 95 Systolo-diastolic murmur 61 T T2DM-HTN-ESRD 173 Tetralogy of Fallot 67 Thickening of chordae 27 Thyrotoxicosis 52, 64 Torn myxomatous cusp 51 221 Torsade de pointes 183 Transesophageal echo 23, 27, 55, 135 Transurethral resection of prostrate 201 Traube’s sign 44 Tricuspid valve endocarditis 127 Tuberculosis 105 U Unique ECG 209 Urinalysis 78 Vague chest discomfort 33 Ventricular aneurysm 100, 207 premature complexes 177 septal defect 24, 59, 67, 155 rupture 155 V Visible carotid pulsations 16 W Weak pulse 85 Weight-loss 189 Wheeze 109 Wide pulse pressure 16 William’s syndrome 39 Wolff-Parkinson-White syndrome 72, 199 WPW syndrome 188 ... L15, ESR 52 Albumin +, WBCs 2- 3, RBCs ++ Glucose 78, Urea 32, Creatinine 1.1, ASLO titer 22 0 IU, CRP level 80 mg/ L Bilirubin 2. 2, SGOT 42, SGPT 48 Cholesterol 178, LDL 110, TSH 2. 2 Throat swab... leaflet but they get brighter as they heal 124 Tips and Tricks of Bedside Cardiology Clinical Pearls • In the clinical setting of rapid onset of dyspnea and palpitation with a febrile illness, an... antimicrobials and not anticoagulants 128 Tips and Tricks of Bedside Cardiology Clinical Pearls • Tricuspid valve involvement occurs in the majority of drug-abuse related endocarditis and is rare