General approach  Inspection  Palpation  Percussion  Auscultation

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.

Timing  1 systolic murmurs a- Mid-systolic ejection murmurs b- late systolic murmurs c- holosystolic murmurs

 2 Diastolic murmurs a- early diastolic murmurs b- mid-diastolic murmurs c- late diastolic murmurs  3 continuous murmurs  4- interventions that change murmur sounds

 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 :

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

 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

Pitch is determined by whether it can be auscultated best with the bell or diaphragm of a stethoscope.

Quality  Blowing  Harsh  Rumbling and musical

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

 Mitral prolapse :systolic murmur with midsystolic click, most frequent valvular lesion in young women  VSD : holosystolic murmur  PDA : continuous machine-like murmur

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

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.

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

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

Different types of dyspnea  Tachypnea  Orthopnea  Trepopnea  Platypnea  Paroxysmal nocturnal dyspnea

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.

    1)  3 types of Angina :stable , unstable and variant (Prinzmetal’s ).

Stable angina Most common type Brought on by exertion or emotion Pain increases over several minutes Relieved by rest or medication Follows a pattern

• • • • • Unstable Angina It is new It is accelerating Lasts longer Less responsive to medication Occurs at rest

• • • • • Prinzmetal’s 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

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

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.

Risk factors for CAD

Modifiables  Smokings  Hypercholesterol  Hypertension  Obesity  Diabetes mellitus  Physical inactivity Nonmodifiables  Age  Male  Family history

Differential  Tension pneumothorax  Aortic dissection  Pulmonary embolism  Unstable angina  Costochondritis  Intercostal neuritis  Pericarditis  pneumonia

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

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

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

• • • • • • • 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

Prinzmetal ‘s angina Calcium channel blockers 

are coronary vasodilators



Variable peripheral vasodilators



Negative inotropic activity



Negative chronotropic activity

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

• • 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 ( kawasaki’s disease)

• • • • • 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

• • • • 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.

iii.

iv.

v.

Anxiety Dyspnea Vomiting nausea

Diagnostic Evaluation ECG is important in the evaluation of possible AMI

 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.

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

• • • • • • Absolute contraindications to thrombolytic therapy Uncontrolled hypertension on iv vasodilators( systolic>180 Recent stroke Recent major surgery Active GI bleeding Concurrent trauma Intracranial mass

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)

• • • • • Major Risk Factiors Coronary artery disease Hypertension Valvular heart disease Pericardial disease cardiomyopathy

Left Heart failure

         Orthopnea Paroxysmal nocturnal dyspnea Rales Dyspnea on exertion Cough Nocturia S3 gallop Diaphoresis tachycardia

Right Heart failure

      RuQ pain due to hepatic congestion Hepatomegaly Hepatojugular reflex Ascites Cyanosis Peripheral edema

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

1.

Treatment ACE inhibitor ( decrease sx and mortality) 2.

3.

4.

5.

Diuretics Beta blockers(decrease sx and improve survival Digoxin ( for symtomatic relief only does not improve survival) Spironalactone ( decrease mortality by 34 %

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

Signs and Symptoms Beck’s Triad  Hypotension  Muffled heart sounds  Jugular vein distention Other symptoms/signs Dyspnea Tachycardia Pulsus paradoxus :decrease by >10 sBP with inspiration

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

Treatment  Immediate pericardiocentesis