Physical ExaminationPhysical Examinationof the Heartof the HeartClinical Practicum Clinical Practicum Fall 2002Fall 2002

Ronnie B. Martin, D.O, FACOFPRonnie B. Martin, D.O, FACOFPProfessor & Chairman, Department Professor & Chairman, Department

of Family Medicineof Family Medicine

Risk Factors for Cardiac Disability

Gender (men more at risk than women; womens risk is increased in the postmenopausal years and with oral contraceptive/HRT use) #1 Cause of death in both men and women is still heart

disease!

Hyperlipidemia (both elevations in LDL and lowering of HDL independent risks)Hypertension (treated or untreated)

Smokingnumber one preventable, modifiable cause of heart disease!

Risk Factors for Cardiac Disability

Diabetes mellitusObesity: dietary habits and an excessively

fatty dietSedentary life-style without exercisePersonality type: intense, compulsive

behavior with feelings of hostility

Family history: cardiovascular disease, diabetes, hyperlipidemia, hypertension, or sudden death in young adults

Important History Questions

How long have you had the condition?How did/does it start?How long does it last?What makes it better?What makes it worse?What have you done to treat the condition?

Have you ever had this before?Family history of a similar condition?Describe the condition.What is the condition related to?What medications and drugs have been taken?Other medical.problems.

Review of Symptoms Significant in

Examination of the Heart

Chest PainPalpationsDyspneaSyncopeFatigueEdemaHemoptysisCyanosis

Description of Symptoms to be Elected

LocationQualityQuantityChronologySettingAggravating FactorsAlleviating FactorsAssociated Manifestations

Chest PainChest PainThe rule is:Chest pain is cardiac until you have ruled

it out by history, physical or clinical evaluation in all patientsOther causes include somatic dysfunction,

espohagitis, ulcer disease, gallbladder disease, emotional disorders, pleurisy and infections of the chest cavity etc.

Chest PainChest PainMedically described by:

Location IntensityCharacterDurationRadiationPrecipitation events and relieving activitiesAssociated Symptoms

diaphoresis, nausea, weakness et al

Angina: Cardiac Angina: Cardiac Mediated Chest Pain Mediated Chest Pain

Pain secondary to ischemia of the myocardial tissue and muscle.

Generally due to obstruction of the coronary arteries blood flow due to occlusion or spasm.

Can be due to increased nutrient and oxygen demand of the heart muscle secondary to arrhythmias, lack of oxygen supply to the muscle due to an ineffective pump and other causes.

Angina generally worsens with activity or stress, improves with rest, O2 supplementation or Nitrates.

Angina is classically :Left sided. Radiates to the neck, jaw or left arm.Associated with dyspnea, a heavy feeling

in the chest, diaphoresis, nausea &/or vomiting and weakness.Levines Sign is the clinched fist over the

sternum that is associated with angina.Generally, angina is relieved by rest, O-2

supplementation or nitroglycerine and increases with increased cardiac work load such as exercise, digestion of food, stress, etc.

After cardiac etiology has been ruled out, other causes of chest pain must be considered including cervical radiculopathy, pleurisy, pulmonary emboli, esophageal spasm, rib lesions, shingles, gall bladder disease, peptic ulcer disease et al. Cardiac enzymes like CPK- MB and Trophonins; Serial

EKGs, Stress Tests, Echocardiograms, Heart Catherizations et al are secondary in importance to history and physical to rule out heart disease!

Palpitations

Arrhythmias-PVCs, PAC, SVT, Fibrillation, Flutter et alz Generally described as skipped beats,

stopping, butter-flies, poundingz May be associated with shortness of breath, dyspnea,

chest pain, fatigue, anxiety, weakness, dizziness, light headiness, skin flush, sweats, weight loss, swelling

z Caused by coronary disease, pulmonary disease, psychological disease, hormonal and endocrine abnormalities, medications and drugs et al

Dyspnea

A subjective feeling of not getting enough airPatient may or not be tachypnic or hypoxicCommon Causes:z Cardiac Function abnormalities or arrhythmiasz Pulmonary Diseasez Anemia'sz Neurological Diseasez Emotional States

Sub-Types of DyspneaParoxysmal Nocturnal Dyspnea(PND)-sudden onset of dyspnea while asleep or when patient is supine:z associated with CHF and nocturnal

asthma/emphysema.Orthopneadyspnea when lying flat, improved by elevation of the head and thorax.z Trepopnea-dyspnea that is improved by lying on the

patients side.Dyspnea on Exertion (DOE)-shortness of breath brought on by activity such as stairs, sex, lifting, et al.z Associated with pulmonary and cardiac disease.

Syncope

The most common cause of syncope in adults is cardiac arrhythmias. z Seizure, TIA, stroke, hypoglycemia all less

common.z Important to distinguish dizziness or light-

headiness from actual loss of consequence.z Clue to actual syncope include: Did they fall down or

injury themselves? Was it witnessed? How long were they unconsequence? Were they amnesic? Were they incontinent?

Types of Syncope

Orthostatic SyncopeAutonomic Instability SyncopeMicturition SyncopeVasovegal SyncopeCarotid Sinus SyncopePost-Tussive SyncopeMetabolic Syncope

The Sinking History: Determining Cause of

SyncopeWhat was the patient doing prior to the event?What medications is the patient taking?What medical conditions do they have?When did the patient eat/drink last and any changes in appetite or bowel habits noted?Were their any other symptoms such as palpations, blurred vision, or SOB?Any mental status changes noted?Any previous history of dizziness or syncope?

EdemaAccumulation of fluid in the tissue.Generally in dependent areas.Caused by increased intravascular volume, loss of autonomic tone or decreased onacotic pressure intravascularly.z Cardiac causes associated with ventricular

pump dysfunction secondary to ischemic heart disease, cardiomyopathy, post MI loss of muscle, etc.z Also associated with hepatic, GI, renal, lymphatic

and vascular disease.

EdemaTiming and pattern is critical to determine etiology of edema. Examples of questions that will give clues to cause and lead toward treatment:z unilateral vs. bilateral edema z present while standing or lying z worse in the am or the pm z associated with leg pain or crampsz associated with SOB z associated with leg lesions or weepingz associated with traumaz associated with cyanosis or cold extremities etc.

FatigueA non specific symptom that is often an early sign of ventricular dysfunction or ischemic heart disease.z Most common cause of chronic fatigue is

anxiety/depression syndrome!Cardiac fatigue tends to be brought on with activity or eating.z Patient complains,I just cant do what I used to be able to

do a few weeks/months ago. z May also be present due to LVD occurring during the night, lack

of sleeping well due to orthopnea etc.

Fatigue associated with other more specific symptoms such as leg cramps, dizziness, light headiness, SOB, etc. more likely cardiac.

Other Cardiac Historical Findings of Significance

Cyanosisindicative of anemia, blood dyscrasias, hypoxemia, et alPetachiae and ecchymosis-indicative of platelet dysfunction or coagulopathyHistory of anemia or blood loss

Leg Cramps or Claudication-indicative of ASCAD.History/Findings Symptoms Consistent with Metabolic Syndrome.Hemoptysisindicative of pulmonary edema from CHF, PE, mitral valve disease, et al.

EXAMINATION OF THE EXAMINATION OF THE HEARTHEART

InspectionPalpationPercussionAuscultationDO NOT SKIP IMMEDIATELY TO AUSCULTATION. You will miss pathology and clinical clues to disease and pathology

EXAMINE EXAMINE The peripheral pulses as well as the central pulses

and venous system. Examine the eyes including the fundascopic

examination. The only place you can directly look at the vessels without the

skin or muscle on top is in the retina of the eye where you can see the vessels directly.

Examine Jugular Veins for distension, Carotid pulses for complexion and bruits.

Measure the blood pressure in all extremities in 3 positions if the condition warrants but at least in the left arm with the arm at heart level. Note the pulse pressure.

INSPECTIONINSPECTION The chest wall should be symmetrical and

move freely. Look for pectus excavatum, pectus carinatum, a

barrel chest, severe scoliosis, extreme kyphosis, rib restriction or splinting among other abnormal findings.

The PMI may be visible in the left chest in the young and thin, or if the heart is enlarged. Normally, it should be in the 4 to 5th Intercostal

Space (ICS) at the Mid-Clavicular Line (MCL).

The nail beds should be pink with good capillary refill (blanche and flush) and not have splintering or hemorrhage.

Clubbing should not be present.Cyanosis or edema should not be present

peripherally or centrally.

Look for jugular venous engorgement/distension when lying at 45 degree angle as well as recumbent.

Palpate intensity of the carotid pulses and their character.

Examine eye lids and dorsal surfaces for xanthomatas.

Examine for jaundice and enlargement of the liver or spleen.

PALPATIONPALPATION

Hands need to be warm fingertip and pads are the most

sensitiveBE METHODICAL AND

CONSISTENT

Begin at the apex, move up the sternal border to the base of the heart near the second intercostal space on the right and across to the left sternal border as well.

The size and position of the Point of Maxamine Impact (PMI) should be noted. Normal, this is less than 2cm and is located in

the 4 to 5 ICS in the MCL.

Enlargement, deviation or increased intensity of the PMI is generally associated with left ventricular hypertrophy (LVH). Obesity or breast material in the male or female

may occlude it. Notation of a parasternal lift should be made

if found along the left or right sternal border. Since the right ventricle is structurally anterior, a

lift is most due to enlargement of the right ventricle.

A palatable thrill or pre-cordial kick in these areas is associated with increased size of the heart or increased intensity of contraction of the heart muscle. A thrill is described as a palatable murmur and

is more commonly noted over valves.Thrills are seen with conditions such as

pulmonary hypertension, aortic stenosis, and pulmonic stenosis, atrial septal defect (ASD).

Thrill locations and causesTiming location Probable causeSystole Suprasternal notch aortic stenosis

And/or second and thirdRight intercostal spaces

Suprasternal notch pulmonic stenosisAnd/or second and third Left intercostal spaces

Fourth left intercostal space ventricular septal defect

Apex mitral regurgitation

Left lower sternal border Tetralogy of Fallot

Left upper sternal border patient ductus arteriosusOften with extensive radiation

Diastole right sternal border aortic regurgitationAneurysm of ascending Aorta

Apex mitral stenosis

PERCUSSIONPERCUSSION

Percussion of the heart is of limited benefit in determining the size or capacity of the heart due to the chest cage and the position the heart lies inside the thoracic cavity. It is used more in determining pathology of the

lung and thoracic cavity.

AUSCULTATIONAUSCULTATION

The worse place to listen to a patients heart is in the ER or hospital ICU!

The worse place to learn to listen to a heart is in the lab! Both are places you will learn initially, be patient,

take your time and practice at home.

The sounds the values produce as they open and close, as well as the ebbs and currents of blood flow through the heart and vessels produce MOST of the classic cardiac sounds that we describe during physical examination.

The Atrioventricular The Atrioventricular Valves (AValves (A--V) Closure V) Closure Produce the First Heart Produce the First Heart Sound:Sound:

tricuspid valves, which separates the R. atria and R. ventricle

&mitral valves, which separates the L. atria and

the L. ventricle.

The Semilunar Valves The Semilunar Valves Closure Produce the Closure Produce the Second Heart Sound:Second Heart Sound:

The pulmonic and the aortic valueswhich allow the flow of blood to the lungs and the body respectively.

The Cardiac The Cardiac CycleCycle

Action with Contraction of Action with Contraction of the Ventriclethe Ventricle

The atrioventricular (A-V) valves snap shut and prevents back flow of blood into the atria with ventricular contraction.

The semilunar (S-L) valves open with contraction of the ventricles to allow the flow of blood to the body and lungs then close with relaxation of the ventricles to prevent back flow and regurgiation.

SS--11 The sound produced by the closure of the

MITRAL AND TRICUSPID VALVES.Occurs when the pressure produced by the

contraction of the ventricle is sufficient to overcome the resistance of inflow from atria.S-1 is rarely split even thought the function of the

right side of the heart is slightly behind the left due to pressure, strength of contraction and electrical differences.

SS--22The sound produced by the closure of the AORTIC AND PULMONIC VALVES.

A2 is the closure of the aortic value and occurs first.

P2 is the closure of the pulmonic valve and is slightly delayed.

During diastole, when ventricular pressure is less than atrial pressure due to emptying of the ventricles and contracture of the atria, the mitral and tricuspid valves open.

The sounds of ventricular filling and atrial function account for the third and forth heart sounds (S3 and S4) heard in the young and athletic as well as in multiple pathological conditions.

SS--33

The sound produced by the filling of the ventricle, partially produced by the atrial kick at the end of diastole.

Found with atria hypertrophy and hyper-dynamic-activity. Causes of hypertrophy of the atria include; pulmonary hypertension. congestive heart failure. myocardial ischema.

SS--44The sound of the blood flowing into a

non-compliant (stiff) chamber of the heart and meeting resistance.

Due to stiffness of the ventricle walls, the chorda tenne, valves and other structures from ischemia, infiltration,inflammation, etc.

All sounds produced by the right side of the heart are slightly behind those produced by the left side of the heart.

AUSCULTATIONAUSCULTATION The key is to listen to each site and take the time to

identify each heart sound at each sight. Do not try to digest the total symphony, listen to each

component until you are comfortable with what you are hearing and can describe it accurately, then move to the next.

Develop a pattern of how you will listen to the heart, starting at the apex and going up the LSB to the base of the heart OR starting at the 2nd ICS near the RSB and progressing toward the apex. Be consistent.

You must listen to each area with both the diaphragm and the bell or you will miss pathology and sounds.The bell hears lowed pitched, rumbling,

soft sounds not heard with the diaphragm.You need to apply the diaphragm firmly

against the chest wall but the bell should be help loosely to prevent stretching the skin tight and creating a pseudo-diaphragm during auscultation.

Remember that sound travels in the direction of the blood flow so some structural sounds will be heard down stream and radiate, I.e. The murmur of aortic stenosis is also

heard in the carotids.The murmur of mitral regurgiation is

heard by referral in the axilla.

You need to know the location of the auscultatory areas and the heart sounds associated with them!

Aortic Valve Right 2nd ICS @ RSBPulmonic Valve Left 2nd ICS @ LSB2nd Pulmonic Left 3rd ICS @ LSBTricuspid Left 4th ICS @ LSBMitral APEX, generally 5th

ICS in MCL

Complete cardiac examination consists of listening to all 5 sites with both the bell and the diaphragm with the patient upright, supine and lying in the left lateral decubi position.

Listen in a systematic manner. Identify the S1, S2, as well as any extra heart

sounds, murmurs, rubs etc. at each site before moving on to the next.

Be sure that you can identify the phase of the cardiac cycle to determine if sounds are occurring in systole or diastole. You can coordinate with palpation of the carotid

or radial pulse to help with timing. Deep inspiration will exaggerate the S2 and

holding the breath in expiration will increase the S1 sounds.

S1 should be louder that S2 at the apex, in mitral and tricuspid areasnear the PMI and lower left sternal border.

S2 should be louder that S1 in Pulmonic and Aortic areas, the base of the heart-near the 2nd and 3rd intercostal areas and along the upper sternal border.Use of maneuvers like handgrip, squatting, Val

Salva, amyl nitrate, leg lift can help alter murmurs by increasing or decreasing return to the heart and stroke volume.

S2 is higher pitched and shorter in duration that S1.A2, the aortic component of the S2

sound, is loudest in the aortic area, the right 2nd ICS RSB. P2, the pulmonic component of S2, is

heard best in the 2nd pulmonic area at 3rd ICS.

Conversely, S1 is lower pitched and longer in duration than S2.

Remember that S2 is physiologically split with inspiration. Delay is due to increased venous return

to the heart and the delayed closure of the pulmonic valve.

Split S2 is heard best in the pulmonic areas.

A split S1 is rarely heard! May be heard in the tricuspid valve area with

tachycardic conditions such as elevated body temperature, strenuous exercise or hyperdynamic states such as hyperthyroidism or uremia.

The S1 volume may be diminished with calcific valves or in cases of pulmonary hypertension.

Abnormal Heart Sounds

Fixed splitting of S-2 (unaffected by respiration), Seen when the output of the right ventricle is

greater than the output of the left ventricle. As in ASD, VSD with Left to Right shunting or in

cases of MI, Heart Failure with Left Ventricular dysfunction, etc.

Reverse splitting of S-2 can be seen with severe cases of LBBB.

S3 and S4 are generally heard best at the apex with the bell. They are associated with pathological

conditions of the heart after age 35 except in the extremely athletic heart. They are low intensity and pitched, rumbling sounds.

S3 sounds are secondary to the filling of the ventricles early in diastole and the vibration of the ventricular walls. A protodiastolic gallop rhythm can be seen

in severe CHF if S-3 intensity is enough.

The S4 sound is associated with the late filling of the ventricle and is produced by vibration of non-compliant, stiff structures like the valves, papillae, and walls of the ventricle to name a few. It is increased in intensity with increased non-compliance

of these structures, such as ischemia, inflammatory diseases of the myocardium, after MI or in amyloidosis to name a few.

It is seen also in cases of anemia, thyroid toxicosis and Pregnancy.

Increased intensity of S-4 may develop to a presystolic gallop sound.

Extra Heart Sounds are generally due to pathology associated with the abnormal closure of the valves of the heart or muscle rigidity.

Examples: Snaps and Clicks. Mitral stenosis can led to opening snaps in mid to late

systole due to stiffness of the leaflets. Mid too late systolic none-ejection clicks are seen in

mitral prolapse where the leaflets initially close then prolapse into the chamber. This can easily be missed unless the patient is sitting

upright and leaning forward or in the left lateral position! Pulmonic ejection clicks are heard best in expiration. Aortic clicks due to stenotic valves frequently radiate to

the carotids and across the sternum.

Friction rubs are associated with inflammation of the pericardium and can be of varying intensity.

Loudest and most promenade are Three Phase Rubs, which may drown out other heart sounds. These can usually be heard in the back as well

as the precordium. They can be confused for a murmur due to

machine like grating nature. They are generally loudest at the apex of the

heart.

HEART MURMURSHEART MURMURSMurmurs are produced by alteration of normal flow of blood into or out of the chambers of the heart, or across the valves of the heart.Murmurs are described by:

Frequency.Intensity.Duration.Timing.Pattern.Location.Radiation.Characterization of Murmurs.

Classification and Description of Murmurs are important to know for clinical practice.

Clinical Pearls about Clinical Pearls about murmurs:murmurs: Innocent murmurs: generally heard best

with the diaphragm, they are mid systolic in timing, generally soft, never > grade II, most often at the 2nd ICS LSB location, are accompanied by a physiologically split S2 and do not radiate. The change with activity and exercise as well.

Diastolic murmurs are never innocent!

Right sided murmurs, Pulmonic and Tricuspid murmurs, increase with inspiration and decrease with expiration.

Grade IV and higher murmurs are generally associated with a palatable thrill at the location over the valve involved.

Radiation of the murmur generally occurs in the direction of the flow of blood. aortic stenosis radiates up the carotid while

aortic regurgiation does not. Mitral regurgiation mummers refer to the axilla, et al.

Mitral regurgiation murmurs are increased in intensity by the increased return of blood to the heart produced by maneuvers such as handgrip and elevation of the leg.

Murmurs of Hypertrophic Cardiomyopathy are increased with decreased return to the heart.Maneuvers such as Valsalva will decrease flow

into the heart due to increased thoracic pressure.

Amyl nitrate will also decreased return secondary to peripheral pooling of blood.

Heart Murmurs and Heart Murmurs and Descriptive Descriptive PatternsPatterns

Mitral StenosisMitral StenosisLow and rumbling murmur, heard in early diastole.Associated with an increased S1.Heard best with Bell.Non radiating.Associated with LSB kick or thrill.Best heard in Left Lateral Decubitus position (LLD).Often seen accompanied by mitral regurgitation.Commonly caused by rheumatic fever.

Mitral RegurgiationMitral Regurgiation High pitched, holosystolic murmur. Heard best at apex and radiates to axilla. S2 may be covered by murmur.May have thrill at apex. PMI enlarged and deviated down and to left. S3 usually present and S3-S4 summation

gallop common. Common causes are MI, rheumatic fever,

ruptures chordae, myxoma.

Aortic StenosisAortic StenosisMid to late systolic murmur that is diamond

shaped (crescendo-decrescendo appearance). Tighter stenosis may produce murmur later in cycle.

Radiates along left sternal border and to carotids.

Loudest at 2nd ICS RSB. S1>S2 in 2nd ICS RSB. Palatable S4 common at apex and LSB.May not have split S2. Frequently has ejection click. PMI enlarged, diverted down and to left.

Aortic RegurgiationAortic Regurgiation Early diastolic murmur, high pitched and blowing,

heard with diaphragm. Often co-existent with aortic stenosis. Enlarged, deviated PMI down & to left common. Intense S2, often tambour like quality, soft S1. Wide pulse pressure with bisferiens pulse.

Associated Austin-Flint murmur heard with bell at apex. This is a low rumbling diastolic murmur.

Associated with Rheumatic fever, endocarditis, aortic disease like Marfan, syphilis, ankylosing spondylitis.

Pulmonic StenosisPulmonic Stenosis Diamond shaped, holosystolic murmur. Heard best in pulmonic areas and radiates to

neck and across chest. Ejection click common. Thrill palatable usually in 2nd ICS if grade IV or

greater. Diminished & wide split S2 seen. S4 commonly present due to RVH. Confused with VSD frequently due to prolonged

murmur duration. Generally congenital.

Tricuspid StenosisTricuspid StenosisDiastolic murmur, low and rumblingLouder with inspirationFrequently has a palatable thrill over

Right Ventricle associatedJugular venous pulse promanideArterial pulse decreased

Tricuspid RegurgitationTricuspid Regurgitation

Holosystolic murmur heard best with diaphragm at lower LSB.

Murmur increases with inspiration. Associated with prominent S3 and thrill at R 4th ICS. Jugular venous pulse has large V wave. Pulmonary artery may be palatable in 2nd ICS on

left secondary to associated pulmonary hypertension.

Seen with pulmonary hypertension, endocarditis especially that associated with IV drug usage and congenital defects.

Sub Aortic StenosisSub Aortic StenosisHeard along RSB and at ApexHolosystolic-diamond shaped murmurHeard with diaphragmPalatable thrill along RSBFrequently have S3 and S4 gallopBifid Carotid pulse is presentJugular Venous Pulse prominent

Mitral Valve ProlapseMitral Valve Prolapse Heard best with patient upright at apex and

along LSB in 4th to 5th ICS Late systolic murmur proceeded by mid

systolic click Prolapse can advance yielding a holosystolic

murmur and chest pain or Arrythmias See more frequently with pectus excavatum

Physical Findings in Physical Findings in Pathological States Pathological States of the Heartof the Heart

Left Ventricular Left Ventricular HypertrophyHypertrophy

The heart is enlarged with PMI deviated inferiority and to the left.Precordial kick at apex and LSB

lift noted usually.JVD, Cyanosis, Edema, Dyspnea

maybe present if 2nd to CHF.

Right Ventricular Right Ventricular HypertrophyHypertrophy

See LSB lift and thrillEvidence of pulmonary

hypertension with increased S2 and distended jugular veins

Clinical Sign and Clinical Sign and Symptoms of Pericarditis:Symptoms of Pericarditis:

Classic signs: chest pain, associated with tachycardia.

Improves if leans forward, worse lying down. Arrhythmias. Three Phase Friction Rub, generally loud

and grating in nature, noted at apex and along LSB.

Physical Findings Physical Findings Associated with Associated with

Cardiac Tamponade:Cardiac Tamponade:Muffled hearts sounds and

diminished/absent PMIDecreased pulse pressure and systolic

pressureParadoxic pulses

Cor Pulmonale Physical Cor Pulmonale Physical Findings:Findings:

Loud S2, wide split in pulmonic areas

LSB lift and thrill in 2nd and 3rd ICSAssociated with pulmonary hypertension

and RVH

Myocardial Infarction Myocardial Infarction Associated Clinical Associated Clinical

Signs: Signs:

Diminished S1 and S2 Positive S4 present Soft, blowing systolic murmur at apex common Dysarrhythmia common Diminished blood pressure common, especially

systolic pressure

Myocardial InfarctionMyocardial Infarction Classic symptoms

pain associated with activity, relieved by rest or NTG, associated with SOB or chest heaviness

diaphoresis, nausea and vomiting Classic symptoms may be absent in elderly The diabetic may not have pain Women commonly do not present with classic

chest pain Infarction of the posterior or inferior portion of the

heart or the right side of the heart may present without pain, only SOB, nausea, weakness et al

Myocarditis Signs and Myocarditis Signs and Symptoms:Symptoms:

Associated with fever, palpations, chest pain, fatigue, dysrhythmia, summination gallops, murmurs and pulses alternans

Clinical Examination Clinical Examination Findings Associated with Findings Associated with

Tetralogy of Fallot:Tetralogy of Fallot: Congenital defect marked by VSD, Pulmonic

Stenosis, and Dextroposition of Aorta and RVH.

Patients present with dyspnea, central cyanosis, single S2, loud, machine like, holosystolic murmur. Requires early surgical intervention to maximize

outcome.

Ventricular Septal DefectVentricular Septal Defect--VSDVSD

Holosystolic murmur-harsh, loud, machine like, especially along LSB

Lift and thrill prominent alone LSBVSD doesnt radiate to neck, sub aortic

stenosis does, helps separate

Coarctation of AortaCoarctation of Aorta Congenital stenoses of the arch of aorta

generally near the origin of the left subclavian artery.

Patients have delayed and diminished femoral pulses.

Blood pressure elevated in arms. Lower extremity cyanosis may be seen. Holosystolic pan-precordial murmur noted,

grade IV + with thrill in aortic area common.

Patient Ductus Patient Ductus ArteriosusArteriosus

RVH and Pulmonary Hypertension associated.

Distended neck veins seen.Cyanosis, dyspnea common.Wide pulse pressure present.Harsh, machine like continuous systolic

and diastolic murmur 1st to 3rd ICS.

Atrial Septal DefectAtrial Septal Defect

Diamond shaped systolic murmur in pulmonic area and low rumbling diastolic murmur

Wide split S2 Parasternal lift on left

Children and Heart Disease

Poor eating & lack of growth & development are first manifestations of heart disease generally.

Children with heart disease are generally less active.

Patients exhibit more dyspnea & exhibit cyanosis. They generally have a weakened cry and complain

of leg pain and headaches.Children with heart disease generally do not

complain of chest pain.

Geriatric HeartGeriatric Heart Decreases in mass and strength of the

myocardium is seen. The valves calcify and lose compliance due to

fibrosis. The stroke volume decreases, cardiac output

declines, the myocardial muscles become less constrictive, less compliant and the endocardium thickens.

These changes all add to decreased strength, cardiac output, decreased compliance, decreased exercise tolerance and prolonged recovery from increased workloads.

Calcification and arteriosclerotic changes in the arteries and aorta led to high pressure, tortuosity, irregularity, rigidity and compromised ability of the vessels to dilate and constrict with demand shifts. The generally results in increased

peripheral vascular tone and elevated systolic and diastolic blood pressures.

Also increases risk for aneurismal changes.

Physical Examinationof the HeartClinical Practicum Fall 2002Risk Factors for Cardiac DisabilityRisk Factors for Cardiac DisabilityImportant History QuestionsReview of Symptoms Significant in Examination of the HeartDescription of Symptoms to be ElectedChest PainChest PainAngina: Cardiac Mediated Chest PainPalpitationsDyspneaSub-Types of DyspneaSyncopeTypes of SyncopeThe Sinking History: Determining Cause of SyncopeEdemaEdemaFatigueOther Cardiac Historical Findings of SignificanceEXAMINATION OF THE HEARTEXAMINEINSPECTIONPALPATIONPERCUSSIONAUSCULTATIONThe sounds the values produce as they open and close, as well as the ebbs and currents of blood flow through the heart and vesThe Atrioventricular Valves (A-V) Closure Produce the First Heart Sound:The Semilunar Valves Closure Produce the Second Heart Sound:The Cardiac CycleAction with Contraction of the VentricleS-1S-2S-3S-4All sounds produced by the right side of the heart are slightly behind those produced by the left side of the heart.AUSCULTATIONAbnormal Heart SoundsHEART MURMURSClinical Pearls about murmurs:Heart Murmurs and Descriptive PatternsMitral StenosisMitral RegurgiationAortic StenosisAortic RegurgiationPulmonic StenosisTricuspid StenosisTricuspid RegurgitationSub Aortic StenosisMitral Valve ProlapsePhysical Findings in Pathological States of the HeartLeft Ventricular HypertrophyRight Ventricular HypertrophyClinical Sign and Symptoms of Pericarditis:Physical Findings Associated with Cardiac Tamponade:Cor Pulmonale Physical Findings:Myocardial Infarction Associated Clinical Signs:Myocardial InfarctionMyocarditis Signs and Symptoms:Clinical Examination Findings Associated with Tetralogy of Fallot:Ventricular Septal Defect-VSDCoarctation of AortaPatient Ductus ArteriosusAtrial Septal DefectChildren and Heart DiseaseGeriatric Heart