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Slide 2 General approach Inspection Palpation Percussion Auscultation Slide 3 Slide 4 Heart murmurs Abnormal heart sounds produced as a result of turbulent blood flow sufficient to produce audible noise. Characteristics: timing, shape, location, radiation, intensity, pitch and quality. Slide 5 Timing 1 systolic murmurs a- Mid-systolic ejection murmurs b- late systolic murmurs c- holosystolic murmurs Slide 6 2 Diastolic murmurs a- early diastolic murmurs b- mid-diastolic murmurs c- late diastolic murmurs 3 continuous murmurs 4- interventions that change murmur sounds Slide 7 Slide 8 Location 5 places on the anterior sternum Radiation Refers where the sound radiates Regle of thumb : sound radiates in the direction of the blood flow : Slide 9 Intensity Grade 1 Very faint,heard only after listener has tuned in,may not be heard in all positions Grade 2 Quiet,but heard immediately after placing the stethoscope on the chest Grade 3 Moderately loud Slide 10 Grade 5 Very loud, with thrill.May he heard when stethoscope is partly off the chest Grade 6 Very loud,with thrill.May be heard with stethoscope entirely off the chest Slide 11 Pitch is determined by whether it can be auscultated best with the bell or diaphragm of a stethoscope. Quality Blowing Harsh Rumbling and musical Slide 12 Heart murmurs Aortic stenosis : crescendo-decrescendo systolic murmur Aortic regurgitation : high-pitched blowing diastolic murmur Mitral stenosis :rumbling late diastolic murmurs, opening snap Mitral regurgitation : high pitched holosystolic murmur Slide 13 Mitral prolapse :systolic murmur with midsystolic click, most frequent valvular lesion in young women VSD : holosystolic murmur PDA : continuous machine-like murmur Slide 14 Respiration Right-sided murmurs typically increase with inspiration, while left-sided murmurs generally are louder during expiration. Valsalva maneuver Most murmurs decrease in length and intensity during the Valsalva maneuver. Two exceptions are the systolic murmur of hypertrophic cardiomyopathy (HCM), which usually becomes much louder, and the systolic murmur of mitral valve prolapse (MVP), which becomes longer and often louder. Following release of the Valsalva, right-sided murmurs tend to return to baseline intensity earlier than left-sided murmurs Slide 15 Exercise Murmurs caused by blood flow across normal or obstructed valves (eg, mitral or pulmonic stenosis) become louder with both isotonic and submaximal isometric (handgrip) exercise. Murmurs of mitral (MR) and aortic regurgitation (AR) and ventricular septal defect (VSD) also increase with handgrip exercise. Slide 16 Positional changes Most murmurs diminish with standing due to reduced preload. However, the murmur of HCM becomes louder, and the murmur of MVP lengthens and often is intensified. Similarly, most murmurs become louder with prompt squatting (or usually passive leg raising), while the murmurs of HCM and MVP typically soften and may disappear Slide 17 Slide 18 Slide 19 Slide 20 Sounds S1 mitral and tricuspid valve closure S2 aortic and pulmonary valve closure S3 end of rapid ventricular filling S4 high atrial pressure/stiff ventricle Slide 21 Different types of dyspnea Tachypnea Orthopnea Trepopnea Platypnea Paroxysmal nocturnal dyspnea Slide 22 Coronary artery disease ANGINA Refer to substernal chest pain that originates from myocardial ischemia( increased oxyxen demand or decreased oxygen suppy).Pain described as a substernal pressure,heaviness radiating to the jaw,shoulder and arm. Slide 23 Slide 24 3 types of Angina :stable, unstable and variant (Prinzmetals ). 1) Stable angina Most common type Brought on by exertion or emotion Pain increases over several minutes Relieved by rest or medication Follows a pattern Slide 25 Unstable Angina It is new It is accelerating Lasts longer Less responsive to medication Occurs at rest Slide 26 Prinzmetals angina Due to coronary vasospasm Not linked to exertion Chronic, intermittent nature Occurs at a specific hour early in the morning Coronary vessels angiographically normal Slide 27 Typical scenario A 62 year old smoker presents complaining of three episodes of severe heavy chest pain this morning.Each episode lasted 3 or 5 minutes, but he has no pain now. He has never had this type of pain Slide 28 Scenario II A 43 y/o woman presents with frequent episodes of dull chest chest pain on and off for 8 months.He says the pain wakes him from sleep. Slide 29 Risk factors for CAD Modifiables Smokings Hypercholesterol Hypertension Obesity Diabetes mellitus Physical inactivity Nonmodifiables Age Male Family history Slide 30 Differential Tension pneumothorax Aortic dissection Pulmonary embolism Unstable angina Costochondritis Intercostal neuritis Pericarditis pneumonia Slide 31 Work-up Resting ECG is normal in half of patient with angina pectoris ECG may show ST-segment depression or T-wave flattening Obtain cardiac enzymes every 8 hrs for 24 hrs to r/o MI Exercise stress test can confirm suspected diagnosis of CAD Slide 32 Slide 33 Slide 34 Treatment Stable angina Nitrates : Cause systemic venodilation which relieves cardiac workload. Cause coronary arterial dilation Increase myocardial blood flow Used in sublingual form for relief of acute ischemia Side effects : hypotension, lightheadedness and headache Slide 35 2-Aspirin Limits platelet aggregation 3-Beta-adrenergic blocking agents Reduce myocardial workload by limiting adrenergic increases in heart rate and contractility Side effects :fatigue, impotence, bradycardia and worsening of heart failure Slide 36 Risk factors modification Smoking cessation Treatment of hyperlipidemia Treatment of hypertension Control diabetes Weight loss Reduction of physical and emotional stress Improvement in physical improvement Slide 37 Prinzmetal s angina Calcium channel blockers are coronary vasodilators Variable peripheral vasodilators Negative inotropic activity Negative chronotropic activity Slide 38 Acute myocardial infarction Epidemiology Common manifestation of CAD Each year 1 million suffer an AMI in USA Of these about 10% to 15% will die within within several days and another 10 to 15 % will die within 1 year Slide 39 Etiology /pathogenesis Most MI occur in the setting of underlying CAD. Rupture of an atherosclerotic with thrombus formation is reponsible for most AMIs. Other mechanisms can cause AMI: Coronary artery dissection Coronary vasospasm( cocaine) Vasculitis ( kawasakis disease) Slide 40 Early death from AMI can be due to a number of complications: Arrhythmia( ventricular fibrillation/tachycardia Cardiogenic shock Ventricular rupture (incidence 3 to 5 days Sudden arrhythmia Mitral papillary rupture Slide 41 Clinical manifestations Retrosternal chest pain, prolonged and persistent Radiate to the shoulder, jaw and left arm Nitrates provide some reliefs but resolution of the pain Associated symptoms include: i. Diaphoresis ii. Anxiety iii. Dyspnea iv. Vomiting v. nausea Slide 42 Diagnostic Evaluation ECG is important in the evaluation of possible AMI Slide 43 Serum Markers for MI Myoglobin : elevated within 1 hr but nonspecific CK MB specific marker for myocardial tissue damage Troponin T or I : very specific and sensitive markers for cardiac muscle injury.Elevated within 3 hrs and can stay elevated for more > a week. Slide 44 Treatment Relief of pain Reduction of myocardial oxygen demand Improvement /restoration of myocardial perfusion Recognition and treatment of complications Thrombolytic therapy with tissue plasminogen activator if pain persists after the administration: O2, aspirin, nitrates,opiates and beta-blockers Slide 45 Absolute contraindications to thrombolytic therapy Uncontrolled hypertension on iv vasodilators( systolic>180 Recent stroke Recent major surgery Active GI bleeding Concurrent trauma Intracranial mass Slide 46 Heart Failure Heart Failure defined as the inability of the heart to pump blood at a rate that meets metabolic demands. Heart failure can be classified according to: The hemodynamic state of the cardiovascular system (congestive versus high output) The predominance of the ventricle affected(left vs right) The predominant form of myocardial dysfunction( systolic or diastolic The time course (acute or chronic) Slide 47 Major Risk Factiors Coronary artery disease Hypertension Valvular heart disease Pericardial disease cardiomyopathy Slide 48 Left Heart failure Right Heart failure Orthopnea Paroxysmal nocturnal dyspnea Rales Dyspnea on exertion Cough Nocturia S3 gallop Diaphoresis tachycardia RuQ pain due to hepatic congestion Hepatomegaly Hepatojugular reflex Ascites Cyanosis Peripheral edema Slide 49 Diagnosis Chest film : enlargement of cardiac silhouette, pulmonary vascular congestion with redistribution to upper lobe. Echocardiogram :Assess left ventricular function (LVF) Basic natriuretic peptide(BNP):elevates in CHF Slide 50 Treatment 1. ACE inhibitor ( decrease sx and mortality) 2. Diuretics 3. Beta blockers(decrease sx and improve survival 4. Digoxin ( for symtomatic relief only does not improve survival) 5. Spironalactone ( decrease mortality by 34 % Slide 51 Pericardial tamponade Definition Tamponade is the physiologic result of rapid accumulation of fluid in the in-elastic pericardial sac.Pericardial tamponade impairs cardiac filling and reduces cardiac. Etiology Pericarditis Trauma Aortic dissection Slide 52 Signs and Symptoms Becks Triad Hypotension Muffled heart sounds Jugular vein distention Other symptoms/signs Dyspnea Tachycardia Pulsus paradoxus :decrease by >10 sBP with inspiration Slide 53 DIAGNOSIS Auscultation may demonstrate distant heart sounds ECG may show low voltage or electrical alternans CXR may show enlarged cardial silhouette Echocardiogram will show large pericardial effusion Slide 54 Treatment Immediate pericardiocentesis