Heart and Peripheral Vasculature

N1037

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– 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 CycleDiastole• 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”. 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”.“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• Age

– 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

– 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– Age, gender, race, family history

• Modifiable– 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

AuscultationUse 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– 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 veinsAbnormal • 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