13Mitral prolapse :systolic murmur with midsystolic click, most frequent valvular lesion in young womenVSD : holosystolic murmurPDA : continuous machine-like murmur
14RespirationRight-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
15Exercise 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.
16Positional changesMost 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
20SoundsS1 mitral and tricuspid valve closureS2 aortic and pulmonary valve closureS3 end of rapid ventricular fillingS4 high atrial pressure/stiff ventricle
21Different types of dyspnea TachypneaOrthopneaTrepopneaPlatypneaParoxysmal nocturnal dyspnea
22Coronary artery disease ANGINARefer 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.
243 types of Angina :stable , unstable and variant (Prinzmetal’s ). Stable anginaMost common typeBrought on by exertion or emotionPain increases over several minutesRelieved by rest or medicationFollows a pattern
25Unstable AnginaIt is newIt is acceleratingLasts longerLess responsive to medicationOccurs at rest
26Prinzmetal’s anginaDue to coronary vasospasmNot linked to exertionChronic, intermittent natureOccurs at a specific hour early in the morningCoronary vessels angiographically normal
27Typical 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
28Scenario 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.
29Risk factors for CAD Modifiables Smokings Hypercholesterol HypertensionObesityDiabetes mellitusPhysical inactivityNonmodifiablesAgeMaleFamily history
31Work-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
34Treatment Stable angina Nitrates : Cause systemic venodilation which relieves cardiac workload.Cause coronary arterial dilationIncrease myocardial blood flowUsed in sublingual form for relief of acute ischemiaSide effects : hypotension, lightheadedness and headache
352-AspirinLimits platelet aggregation3-Beta-adrenergic blocking agentsReduce myocardial workload by limiting adrenergic increases in heart rate and contractilitySide effects :fatigue, impotence, bradycardia and worsening of heart failure
36Risk factors modification Smoking cessationTreatment of hyperlipidemiaTreatment of hypertensionControl diabetesWeight lossReduction of physical and emotional stressImprovement in physical improvement
38Acute myocardial infarction EpidemiologyCommon manifestation of CADEach year 1 million suffer an AMI in USAOf these about 10% to 15% will die within within several days and another 10 to 15 % will die within 1 year
39Etiology /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 dissectionCoronary vasospasm( cocaine)Vasculitis ( kawasaki’s disease)
40Early death from AMI can be due to a number of complications: Arrhythmia( ventricular fibrillation/tachycardiaCardiogenic shockVentricular rupture (incidence 3 to 5 daysSudden arrhythmiaMitral papillary rupture
41Clinical manifestations Retrosternal chest pain, prolonged and persistentRadiate to the shoulder, jaw and left armNitrates provide some reliefs but resolution of the painAssociated symptoms include:DiaphoresisAnxietyDyspneaVomitingnausea
42Diagnostic Evaluation ECG is important in the evaluation of possible AMI
43Serum Markers for MIMyoglobin : elevated within 1 hr but nonspecificCK –MB specific marker for myocardial tissue damageTroponin T or I : very specific and sensitive markers for cardiac muscle injury.Elevated within 3 hrs and can stay elevated for more > a week.
44TreatmentRelief of painReduction of myocardial oxygen demandImprovement /restoration of myocardial perfusionRecognition and treatment of complicationsThrombolytic therapy with tissue plasminogen activator if pain persists after the administration: O2, aspirin, nitrates,opiates and beta-blockers
45Absolute contraindications to thrombolytic therapy Uncontrolled hypertension on iv vasodilators( systolic>180Recent strokeRecent major surgeryActive GI bleedingConcurrent traumaIntracranial mass
46Heart FailureHeart 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 diastolicThe time course (acute or chronic)
48Left Heart failure Right Heart failure Orthopnea Paroxysmal nocturnal dyspneaRalesDyspnea on exertionCoughNocturiaS3 gallopDiaphoresistachycardiaRuQ pain due to hepatic congestionHepatomegalyHepatojugular reflexAscitesCyanosisPeripheral edema
49DiagnosisChest 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
50TreatmentACE inhibitor ( decrease sx and mortality)DiureticsBeta blockers(decrease sx and improve survivalDigoxin ( for symtomatic relief only does not improve survival)Spironalactone ( decrease mortality by 34 %
51Pericardial tamponade DefinitionTamponade is the physiologic result of rapid accumulation of fluid in the in-elastic pericardial sac .Pericardial tamponade impairs cardiac filling and reduces cardiac .EtiologyPericarditisTraumaAortic dissection
52Signs and SymptomsBeck’s TriadHypotensionMuffled heart soundsJugular vein distentionOther symptoms/signsDyspneaTachycardiaPulsus paradoxus :decrease by >10 sBP with inspiration
53DIAGNOSIS 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