Approach To The Cardiac Patient Howard Sacher D.O. Chief, Division of Cardiology, New York College of Osteopathic Medicine. Adjunct Clinical Associate.

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Presentation transcript:

Approach To The Cardiac Patient Howard Sacher D.O. Chief, Division of Cardiology, New York College of Osteopathic Medicine. Adjunct Clinical Associate Professor of Medicine, New York College of Osteopathic Medicine

Signs and Symptoms Most Common are non-specific Dyspnea Chest Pain Palpations Presyncope/ Syncope Fatigue

Dyspnea More often than not is a results of either: Elevated left atrial pressure LV dysfunction valvular obstruction Elevated pulmonic venous pressures Pulmonary Edema secondary to acute LA HTN Hypoxemia Pulmonary Edema Intracardiac shunting

Paroxysmal Nocturnal Dyspnea Most specific for cardiac disease Occurs acutely with 30min to 2hrs of going to bed Relieved by sitting or standing up

Chest Pain Most commonly associated with angina pectoris Not always associated with acute myocardial infarction (AMI) Patients usually complain not of pain but rather Pressure Tightness Squeezing Gassy/Bloated feeling

Ischemic Chest Pain Usually subsides within 30min (depends) Precipitated by Cold Exertion Meals Stress

Usually pain > 30min is indicative of an AMI Usually associated with Anxiety and uneasiness SSCP that may radiate

Other causes of cardiac chest pain Ventricular hypertrophy Valvular heart disease Myocarditis Endocarditis Pericarditis Cardiomyopathies Aortic Dissection

Palpitations The “awareness of one’s heart beat” Usually normal Pathologies include: Cardiac abnormalities that increase Stroke Volume Regurgitant diseases Bradycardia Ventricular or Atrial Premature beats Supraventricular Tachycardia Ventricular Tachycardia

These pathologies can cause a significant decline in CO leading to impaired cerebral blood flow, causing Dizziness Blurring of vision Syncope

Cardiogenic Syncope Most commonly a result of Sinus node arrest Exit block Atrioventricular block Ventricular tachycardia Ventricular fibrillation Other significant causes: Aortic valve disease Idiopathic hypertrophic subaortic stenosis Hyperstimulation of the vagus nerve

Edema Right heart failure most commonly presents with dependent edema Other causes Pericardial diseases Tricuspid and pulmonic Valve diseases Cor Pulmonale Should also look for a “nutmeg liver” as a possible etiology

4 Functional Classes of Heart Disease (Very Important) Class I No limitation of physical activity Ordinary activity does not induce symptomology

Class II Slight limitation on physical activity in which the patient becomes symptomatic Class III Marked limitation on physical activity; comfortable only at rest. With ordinary activities the patient becomes symptomatic Class IV Pt is symptomatic at rest and is unable to engage in any limited activities without discomfort and pain

Look at your patient: Appearance: Diaphoretic? – Think hypotension, cardiac tamponade, tachyarrhythmias, or an acute MI Cachectic? – Think CHF, low cardiac output states Cyanotic? – Ask is it central or peripheral? Central – think arterial desaturation states Peripheral – think impaired tissue delivery Check Vital Signs: HR BP – check bilaterally as well as sitting and standing RR Temp

Pulses Peripheral Central Check carotid pulse for evidence of delayed carotid upstroke and/or a “bisferiens” pulse Pulsus Paradoxus – decrease in blood pressure > 10 mmHg with inspiration Pulsus Alternans – amplitude of the the pulse alternates with each beat during normal sinus rhythm (most commonly seen in patients with pericardial effussions) Jugular venous pulsations – helps in evaluating right atrial pressure Cannon A waves suggest 3 rd degree heart block

Pulmonary Exam Crackles (aka Rales) – CHF Wheezing – COPD (COLD) Rhonchi – COPD (COLD) Pleural effusion on CXR – CHF is cause most commonly Precordial Pulsations Parasternal lift – think RVH, LAH, PHTN Displaced or Exaggerated PMI – think LVH

Heart Sounds S 1 – First heart sound – closing of the MV and TV; occurs during isovolumetric systole E j – Second heart sound as the contraction begins to take place and the blood is ejected S 2 – Third heart sound as diastole begins with isovolumetric relaxation forcing the AoV and PV closed (on inspiration S 2 has a normal physiologic splitting)

OS - The fourth heart sound during the tailend of isovolumetric relaxation – a point in which the ventricular pressure falls below atrial pressure and one can hear the opening snap of the MV/TV (this usually silent but accentuated with MVS) S 3 – normal in young adults, peds and pregnancy. A Sound made by the deceleration of the blood as it hits the ventricular wall. Pathologic in all other patients – sign of a stiff ventricle S 4 – abnormal in all patients if heard, this last heart sound of the cardiac cycle is indicative of an atrium that is trying to pump blood into a very stiff ventricle Please review heart sounds in Harrison’s textbook

Murmurs Innocent murmurs – vary with inspiration most commonly in adolescence and diminishes in the upright position – located along the lower left sternal border Most murmurs are diagnostic for valvular disease Systolic Murmurs Holosystolic – start with S1 ending with S2 Ejection – start with S1 and end before S2 Diastolic Murmurs Associated with a palpable vibration - Thrills