Heart and Peripheral Vasculature

Anatomy and Physiology: Heart Base @ top Apex @ bottom Pericardium Parietal layer Visceral layer

Anatomy and Physiology: Heart 4 Chambers of the heart Right and left atria Right and left ventricles Heart valves Atrioventricular (AV) valves Tricuspid Mitral (bicuspid) Semilunar valves Pulmonic Aortic

Direction of Blood Flow Inferior & Superior Vena Cava to Right Atrium (RA), then into Right Ventricle (RV) Venous blood flows to Pulmonic Valve to Pulmonary Artery (unoxygenated) to the lungs. Lungs oxygenate blood. Pulmonary veins (oxygenated) to Left Atrium (LA). Into LA through Mitral Valve to Left Ventricle (LV) and ejected through Aortic Valve into Aorta. Aorta delivers oxygenated blood to body.

Neck Vessels

Coronary Circulation Left main coronary artery Right coronary artery Left circumflex artery Left anterior descending artery Right coronary artery

Cardiac Cycle Systole Isovolumic contraction Early systole Late systole Diastole Isovolumic relaxation phase Early and mid-diastolic filling periods Atrial systole (atrial kick)

Cardiac Cycle Diastole Systole Ventricles relax and fill with blood The AV valves(tricuspid & mitral) are open During the first rapid filling phase, blood pours rapidly from the atria into the ventricles (early diastolic filling). At the end, the atria contract & push the last amount of blood into the ventricles (presystole = atrial kick). Systole After this, the AV valves close and we hear the first heart sound “S1”. This is the beginning of Systole. AV valves close to prevent regurgitation into the atria during contraction. Then, the aortic and pulmonic valves (semilunar valves) open & blood is ejected rapidly into the arteries. After all the contents are ejected, the semilunar valves close. This causes the second heart sound, “S2”. This is the end of systole.

Excitation of the Heart Sinoatrial (SA) node Atrioventricular node Bundle of His Right and left bundle branches Purkinje fibers

Conduction Pathway and EKG Sinoatrial node (SA Node) initiates an electrical impulse It is the “pacemaker” of the heart. Travels to the Atrioventricular node (AV Node) Then it travels to the “Bundle of His” Through the left and right bundle branches. And lastly, through the ventricles.

Electrocardiogram (EKG) P Q R S T Isoelectric line

Peripheral Vasculature Arterial system Three layers of arterial walls: tunica intima, media, externa Arteries Arterioles Capillaries pulsating flow, no valves Venous system Veins Venules steady flow, 1 way valves,thinner walls , less elastic

Peripheral Vasculature

Health History Race Age Gender Childhood onset: rheumatic fever Adult onset: HTN, CAD, MI, CVA, AAA Gender Female Male Race May predispose to higher risk for CVA, CAD, HTN, diabetes mellitus

Common Chief Complaints Chest pain Syncope Palpitations Peripheral edema Extremity pain Characteristics of Chief Complaints Quality Associated manifestations Aggravating factors Alleviating factors Setting Timing

Past Health History Medical Surgical Common medications Cardiac specific: AAA, angina, cardiogenic shock, chest trauma Noncardiac specific Surgical Previous cardiovascular procedures Common medications Antianginals or vasodilators Antidysrhythmics Anticoagulants Antihypertensives Antilipemics Diuretics Inotropics Thrombolytics

Past Health History Communicable diseases Childhood illnesses Allergies Aspirin IVP dye Seafood Injuries and accidents

Family Health History Assess for Aneurysm CVA CAD HTN MI or sudden cardiac death MVP

Social History Alcohol, drug, or tobacco use Sexual practices Travel history Work and home environment Hobbies and leisure activities Stress

Health Maintenance Activities Sleep Diet Exercise Stress management Use of safety devices Health check-ups

Risk Factors Fixed Modifiable Age, gender, race, family history HTN, hyperlipidemia, tobacco use, glucose intolerance, physical inactivity, diet, stress, sedentary lifestyle, obesity

Assessment Equipment Equipment Stethoscope Sphygmomanometer Watch with second hand Tape measure

Inspection Ape To Man Aortic 2ICS Pulmonic 2ICS Midprecordial 3ICS Tricuspid 5ICS Mitral 5ICS N = no visible pulsations except for the PMI in the mitral area

Palpation Assess for pulsations, thrills, heaves Assess the following areas: aortic, pulmonic, midprecordial, tricuspid, and mitral N = No pulsations, thrills, or heaves palpated, except in the mitral area, where the apical impulse may be palpated

Auscultation Use diaphragm and bell of stethoscope N= Aortic: S2 is louder than S1 N= Pulmonic: S2 is louder than S1 N= Tricuspid: S1 is louder than S2 N=Mitral: S1 is louder than S2 Remember S1 = Apex, S2 = Base

Auscultation: Normal Findings Aortic and Pulmonic N= physiologoical split of S2 Mitral and tricuspid: N= S3 (gallop) may be heard in children, young adults, and pregnant women N= S4 may indicate cardiac decompensation

Auscultation Abnormal Murmurs Pericardial friction rub Use stethoscope diaphragm over aortic, pulmonic, mitral, and tricuspid areas Use stethoscope bell over mitral and tricuspid areas Possible causes Characteristics: location, radiation, timing, intensity, quality, pitch, configuration Pericardial friction rub Characteristics: location, radiation, timing, quality, pitch Possible cause

Assessment of Peripheral Vasculature Inspection of jugular venous pressure Place pt at 45°angle measure vertical distance from sternum to top of distended neck vein N= <4cm Abnormal > 4 cm indicates R ventricular pressure,  bld vol, or obstruction

Inspection of Hepatojugular Reflux Position pt at 30 ° in bed, press firmly on RUQ, observe neck for elevation of JVP N = no change in jugular veins Abnormal A rise of more than 1 cm = right-sided CHF or fluid overload

Assessment of Arterial Pulses Palpate temporal, carotid, brachial, radial, femoral, popliteal, posterior tibial, dorsalis pedis for rate, rhythm, amplitude, symmetry auscultate with bell carotids, temporal & femoral pulses N= equal bilaterally, no bruits auscultated at carotids, temporal & femoral Abnormal Presence of bruits = obstruction due to atherosclerotic plaques, high-output states such as anemia or thyrotoxicosis

Special Techniques Assessing for Pulsus paradoxus take BP while pt supine, note 1st systolic sound heard, note point where all systolic sounds are not heard N= paradox should be < or = 10 mmHg Abnormal cardiac tamponade, pericardial effusion, cardiomyopathy, obstructive lung disease dt blood return to the L ventricle

Assessment of Peripheral Perfusion Overall …..Evaluate peripheral pulses, color, clubbing, capillary refill, skin temperature, edema, ulcerations, hair distribution Assess Venous system Inspect fingers, legs, feet & toes bend pts knee slightly and dorsiflex each foot - monitor for Homan sign N= no c/o calf pain Abnormal + VE Homan sign indicates DVT or thrombophlebitis

Assessment of Peripheral Perfusion Assess Arterial system Pallor test Instruct pt to raise extremities note the time it takes for pallor or lack of color to devlop N= no pallor develops within 60 secs Allen test ask pt to make fist , occlude ulnar and radial artery open hand and release one artery while compressing the other, repeat with opposite artery N= + ve Allen test = good blood flow both arteries in palm of hand Abnormal no blood flow dt thrombus or atherosclerosis

Palpation of Epitrochlear Node Place pt in supine position support pt hand in your hand plappate behind elbow in btwn biceps & triceps for epitrochlear node for size, shape, consistency , tenderness, & mobility N= node not palpable Abnormal enlarged lymph node

Gerontological Variations Decreased size of heart muscle Atria and ventricles become fibrotic and sclerotic Decreased cardiac output Change in heart position Obesity Vessels become fibrotic and rigid