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PRINCIPLES

Do your auscultation in a quiet room, forpractical reasons that you can hear the heart

sounds better.

Use the bell for the low-pitched sound. (e.g. S3,S4)

Bell with an L is for low-pitchedsound;Diaphragm with an H is for high-pitched

sound

Examine the patient in 3 positions. Left lateral decubitus

- S3, if you cant find the apex beat, ifyou turn the patient in this position

then you can maximize the contact

between the left ventricle and the chest

wall

- When palpating the patient, what youfeel is the vibration of the heart to the

chest wall- Exaggerates the apex beat and the

heart sounds

Supine Sitting

- Exaggerates the murmurs found in thebase >referring to the pulmonic area,

aortic area and the S2

Use the inching technique Move the stethoscope inch by inch and not

too fast from different auscultatory areas sothat you wont miss any sound in between

(from the apex or mitral to the tricuspid

area)

Listen to one event at a time. At first, try to listen the heart sound in the

apex then listen to thefirst heart sound

because it is maximal at theapex

Concentrate on one heart sound at a time Listen to whatever there is between the 1st

and 2nd heart sound Listen to interval between 1st and 2nd sounds,

listen to any extra heart sounds (e.g.

murmur).

AUSCULTATORY AREAS

- Pulmonic Area: left side, 2nd

ICS, swallow

- Aortic Area: right side, 2nd

ICS; radiation of the

sound towards the ascending aorta

- Mitral Area: Apex, below the nipple; 5th

ICS

bisected by the midclavicular line

- Tricuspid: left side, 4th ICS; shallow

FIRST HEART SOUNDS (S1)

Caused by closure of mitral and tricuspidvalve. There will be motion of blood,

chordae tendinae and papillary muscles.

This coincides with beginning of systole(contraction of ventricles, closure of MV

and TV, 1st heart sound)

First heart sound heard, S1 This is best heard over the apex (intensity

at the base is decreased). Intensity is affected by strength and

contractility of the ventricle and position

of valves prior to closure.

E.g TachycardiaS1 is louder in:

Tachycardia because the valves arewidely open and tends to close again

Short PR interval Fever because the px tends to betachycardic Thyrotoxicosis increased metabolism;

a.k.a. hyperthyroidism

Mitral Stenosis increased metabolism,faster HR; increased pressure in left

atrium

Subject: Physical DiagnosisTopic: Physical Examination for CVS 2Lecturer: Dr. Jaime Pacifico

Date of Lecture: 09.09.11Transcriptionist: Mating Cats =^.^=

Pages: 4SY

2011-2012

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S1 is soft in:

Bradycardia slow cycle of systole anddiastole, valves are practically closed

prior to closure, so long diastolic filling

time.

Prolonged PR interval (exceeding 0.2second) **semi closure of the mitralvalve occurs following atrial systole and

before ventricular systole begins

Mitral regurgitation most commoncause is rheumatic heart disease

Acute MI dead myocardium; reducedleft ventricle pumps

SECOND HEART SOUNDS

This is due to the closure of the aortic and pulmonic

valve during inspiration. Beginning of diastole, indicates end of

systole

This is best heard at the base. (+) splitting you can hear separately the

aortic and pulmonic components of the 2nd

heart sound.

During inspiration, there is low intrathoracic

pressure->more blood returning to the right side of

the heart->prolonging systole->causing delayed

closure of pulmonic valve->splitting

Types of splitting:

Normal/Physiologic splitting single soundduring expiration, 2 sounds upon

inspiration.

Wide splitting splitting is prominent butvariable with respiration. (ex. RBBB)

Wide splitting, Fixed there is 2 heartsounds heard regardless if its inspiratory or

expiratory. (most common cause is atrial

septal defect)

Reversed splitting - this is the paradoxicalbranch block (LBBB), there is a single sound

inspiration and split on expiration.

Hubbard THIRD AND FOURTH HEART SOUNDS

S3 This is associated with early diastole in

rapid ventricular filling.

This is heard among young individuals age20 to 25, and it is still normal according to

doc.

In hearing this, your reference would be the2

ndheart sound (it comes shortly after the

2nd

sound) lab-ti-lab

Pathologic in 40 years old and above suggests heart failure

After the S2S4

Believed to be because of the flow of bloodwhich coincides with atrial systole (late

diastole)

Shortly before the S1 Common in ventricular hypertrophy or

fibrosis an exaggerated S4 because during

this condition, the atrium will contract more

to overcome the pressure due to

hypertrophy

Ventricular Hypertrophy : chronichypertension; Fibrosis : MI

EXTRA HEART SOUNDS

Diastole

Probably more important than systolic Opening snap

-pathognomonic ofmitral stenosis which is

commonly caused by rheumatic heart

disease among Filipinos

This is a high-pitched sound heardat the left lower parasternal

border.

Orienting at S2; shortly after S2 Closure of AV and PV

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Systole

Ejection sound/ Click Mid-systolic click

- it is an extra sound between S1 and S2.- Mitral Valve Prolapse

CARDIAC MURMURS

Extra heart sounds during systole anddiastole due to the turbulent flow of blood,

in addition this may be due to high output

states and structural defects.

Occur commonly in diseased valves (e.g.RHD)

Other causes: high output states anemia (most common);

thyrotoxicosis

structural defects ASD altered blood flow in the major

vessels patent ductus arteriosus

Characteristics of a murmur:

Intensity e.g. Grade 1/6 or 2/6 etc. Timing e.g. Systole, Diastole, or

continuous

Pitch / Frequency e.g. Low-pitched,High-pitched

Location where in the chest you bestheard the murmur (e.g. Apex, Base,

etc.)

Radiation common is mitralregurgitation; from apex to the axilla

Quality of sound e.g. Stabbing, heavy,etc machinery type of murmur ductus

arteriosus

Example on how to report: a probing

holosystolic 4/6 murmur at the apex

radiating to the axilla

Most likely diagnosis= mitral regurgitation

*Note: It is important to palpate the

carotids/branchial artery to serve as

reference point if youre listening for 1st

/2nd heart sound

Inspiration: increase blood flow increase

turbulence

exaggerating the murmur

Intensity/Grading of Murmurs (LEVINES GRADING

SYSTEM)

Grade 1 so faint, heard only withspecial effort; in optimal environment

Grade 2 faint but can be heard readilyby an experienced observer; quiet, can

be recognized readily after placing the

stet on the chest wall.

Grade 3 moderately loud Grade 4 loud murmurs, although the

stet must be in complete contact with

the chest wall to hear them; may/ may

not be associated with trill

Grade 5 very loud, with stethoscopelightly pressed on the skin; always

associated with thrill

Grade 6 exceptionally loud with thestethoscope slightly above the chest

wall; always assoc with thrill

*Note: Grade 1-3 lack thrills, Grade 4-6 have thrills

Thrill a palpable murmur; a sensation of running

water on the fingertips; comes in terms of intensity

Example of presentation:

o +systolic thrill (would be at least grade 4up to grade 6 murmur)

o 5/6 systolic murmur at 2nd ics parasternalarea without radiation

TIMING OF MURMUR Systolic occurs at anytime from S1 to S2 Diastolic occurs at anytime from S2 to S1 Continuous starts from S1 and continues

to S2

Mid-systolic starts after S1 before S2, seenin aortic stenosis ends

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Holosystolic starts at S1 and ends at S2,from the start the intensity doesnt change;

appreciate the murmur throughout the

systole

Systolic Murmur

If the murmur starts or coincides with thepulse of the carotid artery

Two causes: It is an abnormal flow over an

outflow tract or semilunar valve.

Eg. aortic stenosis

It can also be a regurgitant flowfrom a ventricle into a low pressure

chamber.

Eg. mitral regurgitation

Early Systolic Murmur

Begins in S1 and ends in mid systole This can be heard in tricuspid regurgitation

in the absence of pulmonary hypertension

Mid Systolic Murmur

Also called systolic ejection which startsafter S1

Diamond shape-characteristic of intensity ofmurmur/ ascend-crescendo description- it

increases then decreases typical of aortic

stenosis

may be seen in aortic stenosis

Late Systolic Murmur

Starts after ejection, does not obliterate S1and S2

This is heard in mitral regurgitation due tomitral valve prolapse which is late systolic

timing

Holosystolic or Pansystolic Murmurs

Starts from S1 and ends within or extendsbeyond S2 occurring between chambers

that have widely different pressures. (e.g.

tricuspid regurgitation, ventricular septal

defects)

Turbulence is throughout the systoleDiastolic Murmur

Two causes:o May be due to an abnormal

backward flow across a leaking

semilunar valve. (e.g. aortic and

pulmonic regurgitation normally

during diastole aortic and pulmonic

should close to fill the RV and LV)

o May be also due to an abnormalforward flow across and

atrioventricular valve. (e.g. mitral

stenosis the hole is small which

causes a turbulent flow from LA to

LV which causes the loud noise)

Early Diastolic Murmur

Starts with 2nd heart sound, begins with orshortly after S2

E.g. Aortic RegurgitationMid Diastolic Murmur

Usually occurs across the MV and the TVduring early ventricular filling.

Severity of stenosis is proportional to theduration rather than the loudness of the

murmur

Pre Systolic MurmurLate Diastole

Usually this is due to atrioventricular valvestenosis

Continuous Murmur

Begins in systole, peaks near S2 This is due to the communication between

high and low pressure chambers. (e.g.

murmur that sounds like a machine due to a

patent ductus arteriosus)

Can be heard at the left supraclavicular areaPERICARDIAL FRICTION RUB

Not a heart sound perse Parietal/visceral pericardium This is due to an inflamed layer of the

pericardium sliding over one another

This is described as scratching, grating,crunching or creaking sounds which is

better heard during deep inspiration and

the patient leaning forward (to maximize

contact between pericardium)

Described always as to and fro, systolicplus one or two diastolic component

This is sometimes just transient so examineyour patient everyday to note for any

changes

Seen in patient with pericarditis-chestpainfever; an ECG will differ pericarditis from

myocardial infarction

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EFFECTS OF PHYSIOLOGICAL AND

PHARMACOLOGICAL INTERVENTIONS OF THE

INTENSITY TYPE OF MURMURS

Respiration right sided murmurs increasewith inspiration

To differentiate between mitral and

tricuspid regurgitation ask the patient to

inspire, if the intensity increases, it istricuspid = Carvallos Sign

Valsalva most murmurs decrease inintensity (due to decreased blood volume)

and duration except in hypertrophic

cardiomyopathy (HCOM; presents with

systolic murmur) and mitral valve prolapse

(MVP)

Positional Changes with standing(decrease cardiac output) most murmurs

decrease in intensity except HCOM and

MVP

Exercise with hand grip exercise, MR, VSD,and AR increase; Left-sided S3 and S4 also

increase (increase total peripheral

resistance> more blood will go back to left

side of the heart > increase intensity).

Pharmacologic Amyl nitrite decreasesmurmur of MR, VSD, AND AR. (Amyl nitrite

is a vasodilator> decreases TPR, therefore

blood in aorta will move forward rather

than go back to the left side of the >decrease intensity)

Transient arterial occlusion Compressionof both arms increases the murmur of MR,

VSD, AR.

Notice that in Hypertrophic CM, valsava

exaggerates the murmur; it is prolonged.

In other murmurs like in aortic stenosis there

is a decrease in intensity; in mitral

regurgitation there is a decrease in intensity

as well as a decrease in duration.

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Always listen to your heart, because even though it's

towards your left; it's always right.