Physical Examination

of the Heart
Clinical Practicum
Fall 2002
Ronnie B. Martin, D.O, FACOFP
Professor & Chairman, Department
of 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

mellitus
Obesity: dietary habits and an excessively
fatty diet
Sedentary life-style without exercise
Personality 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 Pain
Palpations
Dyspnea
Syncope
Fatigue
Edema
Hemoptysis
Cyanosis

Description of
Symptoms to be Elected
Location
Quality
Quantity
Chronology
Setting
Aggravating Factors
Alleviating Factors
Associated Manifestations

Chest Pain
 The

rule is:

 Chest

pain is cardiac until you have ruled

it out by history, physical or clinical
evaluation in all patients
Other

causes include somatic dysfunction,

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

Chest Pain
 Medically

described by:

Location
Intensity
Character
Duration
Radiation
Precipitation

events and relieving activities

Associated Symptoms
diaphoresis,

nausea, weakness et al

Angina: Cardiac
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 al
z

Generally described as skipped beats,

stopping, butter-flies, pounding
z

May be associated with shortness of breath, dyspnea,

chest pain, fatigue, anxiety, weakness, dizziness, light
headiness, skin flush, sweats, weight loss, swelling
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 air
Patient may or not be tachypnic or hypoxic
Common Causes:
z
z
z
z
z

Cardiac Function abnormalities or arrhythmias

Pulmonary Disease
Anemia's
Neurological Disease
Emotional States

Sub-Types of Dyspnea
Paroxysmal 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.
Important to distinguish dizziness or lightheadiness 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 Syncope
Autonomic Instability Syncope
Micturition Syncope
Vasovegal Syncope
Carotid Sinus Syncope
Post-Tussive Syncope
Metabolic Syncope

The Sinking History:

Determining Cause of
Syncope
What 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?

Edema
Accumulation 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.

Edema
Timing and pattern is critical to determine
etiology of edema.
Examples of questions that will give clues to
cause and lead toward treatment:
z
z
z
z
z
z
z
z

unilateral vs. bilateral edema

present while standing or lying
worse in the am or the pm
associated with leg pain or cramps
associated with SOB
associated with leg lesions or weeping
associated with trauma
associated with cyanosis or cold extremities etc.

Fatigue
A 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 al
Petachiae and
ecchymosis-indicative
of platelet dysfunction
or coagulopathy
History 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
HEART
Inspection
Palpation
Percussion
Auscultation

DO NOT SKIP IMMEDIATELY TO

AUSCULTATION. You will miss pathology
and clinical clues to disease and pathology

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.

INSPECTION


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.

PALPATION
 Hands

need to be warm

fingertip

and pads are the most

sensitive
BE 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 causes

Timing location
Probable cause
Systole

Diastole

Suprasternal notch
And/or second and third
Right intercostal spaces

aortic stenosis

Suprasternal notch
And/or second and third
Left intercostal spaces

pulmonic stenosis

Fourth left intercostal space

ventricular septal defect

Apex

mitral regurgitation

Left lower sternal border

Tetralogy of Fallot

Left upper sternal border

Often with extensive radiation

patient ductus arteriosus

right sternal border

Apex

aortic regurgitation
Aneurysm of ascending
Aorta
mitral stenosis

PERCUSSION


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.

AUSCULTATION
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
Valves (A-V) Closure
Produce the First Heart
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

Closure Produce the
Second Heart Sound:
 The

pulmonic and the aortic values

which allow the flow of blood to the
lungs and the body respectively.

The Cardiac
Cycle

Action with Contraction of

the 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.


S- 1


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.

S-2

The 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.

S- 3


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 hyperdynamic-activity.


Causes of hypertrophy of the atria include;

pulmonary hypertension.
congestive heart failure.
myocardial ischema.

S- 4
 The

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.

AUSCULTATION


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
 Pulmonic Valve
 2nd Pulmonic
 Tricuspid


Mitral

Right 2nd ICS @ RSB

Left 2nd ICS @ LSB
Left 3rd ICS @ LSB
Left 4th ICS @ LSB
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 MURMURS
Murmurs

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

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

Descriptive
Patterns

Mitral Stenosis
Low

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 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 Stenosis

Mid 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 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 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 Stenosis
 Diastolic

murmur, low and rumbling

 Louder with inspiration
 Frequently has a palatable thrill over
Right Ventricle associated
 Jugular venous pulse promanide
 Arterial pulse decreased

Tricuspid 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 Stenosis

 Heard

along RSB and at Apex

 Holosystolic-diamond shaped murmur
 Heard with diaphragm
 Palatable thrill along RSB
 Frequently have S3 and S4 gallop
 Bifid Carotid pulse is present
 Jugular Venous Pulse prominent

Mitral 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
Pathological States
of the Heart

Left Ventricular
Hypertrophy
 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
Hypertrophy
 See

LSB lift and thrill

 Evidence of pulmonary
hypertension with increased S2 and
distended jugular veins

Clinical Sign and

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
Associated with
Cardiac Tamponade:
 Muffled

hearts sounds and

diminished/absent PMI
 Decreased pulse pressure and systolic
pressure
 Paradoxic pulses

Cor Pulmonale Physical

Findings:

Loud S2, wide split in pulmonic areas

LSB lift and thrill in 2nd and 3rd ICS

 Associated

and RVH

with pulmonary hypertension

Myocardial Infarction
Associated Clinical
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 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

Symptoms:


Associated with fever, palpations, chest

pain, fatigue, dysrhythmia, summination
gallops, murmurs and pulses alternans

Clinical Examination
Findings Associated with
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

outcome.

early surgical intervention to maximize

Ventricular Septal DefectVSD

 Holosystolic

murmur-harsh, loud,
machine like, especially along LSB
 Lift and thrill prominent alone LSB
 VSD

doesnt radiate to neck, sub aortic

stenosis does, helps separate

Coarctation 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
Arteriosus
 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 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 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.