Prepared by:

Dr. Mohammad Shaikhani.

Sulaimani University,College of Medicine.
Sulaimani center for GE & Hepatology.
Sulaimanya-Iraqi Kurdistan.
 General exam: related to CVS
 1. FACIES
Apprehensive facies: from pain, anxiety&respiratory distress (MI,
angina, PE, P edema, arrhythmias as VT, fast AF)
A. Skin Color / Texture:
 Malar flush: long-standing MS.
Butter-fly rash across the nose/cheeks in SLE(HT,RF).
 Brick red color of polycethemia ( cause HTN,thrombosis, MI)
 Bronze skin in hemochromatosis (Cardiomyopathy)
 Brown + buccal pigmentation in Addison’s disease (hypotension)
 Flushing & telangiectasia in carcinoid sydrome (tricuspid & pulm
valve disease)
 Moon face in cushing’s disease (HTN)
 Coarseness & dryness in myxedema (bradycardia, HF, PE)
Central cyanosis (right-left intracardiac shunt or lung disease).
 General exam: related to CVS
B. Eyes/ Lids:
 Jaundice: CHF causing congested liver.
 Pallor: anemia of BE, Precipitating HF.
 Xanthelasma (hypercholesterolemia, DM)
 Lid edema/Puffy face (myxedema, nephrotic, SVC obst)
 Exophthalmos, lid retraction in thyrotoxicosis (A.F, high CO)
 Corneal arcus in youngs indicates severe hypercholesterolemia.
 Blue sclera in marfan/ Ehlers-Danlos syndrome (AR,MVP, ASD)
Lenses (subluxation in Marfan; superior, homocystenuria inferior)
 Pupils (Argyll Robertson sign) react to accommodation not to
light seen in neurosyphilis (AR, calcification in the ascending aorta)
 General exam: related to CVS
C. Bony developmental Abnormality:
 Large head (Paget’s disease): High-out failure
 Acromegaly (HTN, CHF)
 Marfan syndrome (with long narrow face, lens sublaxation,
 long arm, arachnodactyly)(AR, aortic dissection, MVP)
 Williams syndrome (small elf-like forehead, turned up nose, egg
shaped teeth, low set ears) associated with supravalvular AS.
 Noonan’s sydrome (widely set eyes, web neck) with PS
 General exam: related to CVS
D. Hands
 Tremor in thyrotoxicosis (AF, CHF)
 Clubbing (cardiac cause: cong HD, bacterial endocarditis)
 Capillary pulsation (AR, thyrotoxicosis, pregnancy)
 Splinter hemorrhage (SBE, acute glomeruloniphritis)
 Osler’s nodes (0.5-1 cm painful reddish-brown subcutaneous
papules occur on the tip of the fingers or toes, palm of the hand,
planter aspect of the feet (bacterial endocarditis)
 Arachnodactyly (long slender hand/ fingers) marfan sydnrome.
 Peripheral cyanosis: Cardiogenic shock, PVD.
 E: Feet:
 Pitting leg edema bilaterally.
 Cold legs & feet, Any gangrene: PVD.
 Unilateral swelling: DVT.
General exam: related to CVS
 General exam: related to CVS
BREATHING PATTERNS:
 1. Using accessory muscles of respiration? (P edema,asthma,
COPD, fulminant pneumonia)
 2. Breathlesness + wheezing (asthma, COPD, LV failure)
 3. Stridor (indicating upper airway obstruction) life-threatening
 4. Chyne-stokes respiration (CHF, strokes, oversedation, uremia)
 General exam: related to CVS
CYANOSIS
 1. Appears when deoxygenated Hb> 5 gms.
 1. Is not apparent when Hb < 5g/dl (central).
 2. In CHD cyanosis is observed if R-L shunt is > 25% of CO& not
improved by 100% of O2.
3. Good exam of tongue, lip, ear lobes, fingers, toes recommended.
 General exam: related to CVS
FOUR TYPE OF CYANOSIS
Central cyanosis: blue tongue, lips, extremities with warm
peripheries (CHD, lung disease as emphysema, pneumonia,ARDS,
chronic bronchitis, sometimes CHF)
Peripheral cyanosis: ( from sluggish circulation in capillaries
(extremities are blue & cold): low CO, hypovolemic shock,PVD)
Differential cyanosis (lower limb cyanosed, upper limb pink) in
PDA with revered shunt due to PHTN.
Reversed differential cyanosis. The cyanosis of the fingers exceeds
that of the toes; in transposition of the great vessels (blood from RV
ejected into the AO reaches the upper limbs/head, blood from LV
ejected into PA reaches the lower limb via PDA)
 Pulse:
1. PULSE:
Rate/Rhythm/Volume/Character/RF delay.
Rate at rest > 100/min (tachycardia):anxiety, pain, CHF, PE,
hyperthyroidism, anemia, fever, medications
 Rate < 60/min (bradycardia) due to (medications, MI,
hypothyroidism, hypothermia, SSS,…)
Rhythm (regular or irregular indicating AF, frequent PAC’s,
PVC’s, …etc.)
 Pulse:
Character
1. Collapsing pulse (water hammer pulse) jerky pulse with full
expansion followed by sudden collapse (AR, PDA, A-V fistulas,
pregnancy, paget’s disease, thyrotoxicosis, anemia)
2. Alternating pulse or pulses alternans (regular rate, amplitude
varies from beat to beat) seen in LVF
3. Pulses bisferiens (two strong systolic peaks separated by a
midsystolic dip) seen in HOCM, AS/AI
4. Anacrotic pulse slow rising pulse in A.S. (Parvus et tardus)
5. Diacrotic pulse, two systolic/ diastolic peaks (sepsis,
hypovolemic, cardiogenic shock)
6. Paradoxic pulse (amplitude decreases with inspiration &
increases during expiration) seen in cardiac tamponade, COPD,
massive P.E.
 Peripheral pulses:
 Symmetry: Exam both radial, carotid, femoral, tibial, dorsalis
pedis.
JVP:
JVP:
JVP:
 JVP:

Don’t worry too much about the wave form, just try to see it first!
 JVP:
Normal JVP waves:
H Period of slow filling of atria before atrial contraction
a Atrial systole
X Atrial relaxation
C Bulging of TV into RA during V systole
X´ RA pressure falls because of pulling of RA floor during V
systole. Some authors refer to this as X wave
V filling of RA while TV is closed
Y Decline in RA pressure when TV opens
X´ descent: systolic
Y descent: diastolic
 JVP: Abnormal waves
1. Giant “A” wave seen in RA contraction against an obstructed
TV (TS, atresia, myxoma) high resistance to RA emptying (RVH,
PHTN, PS, PE, …)
2. Cannon “A” wave: (RA contracts against closed TV) seen in
CHB.
3. Prominent “V” wave (V wave caused by RA filling against TV
closure coincide with S2 & T wave on the ECG) seen in significant
TR, VSD, ASD causing distolic RA overloading
4. Kussmaul’s sign: paradoxical rise with inspiration (constrictive
pericarditis, severe RHF)
 Precordial exam: inspection
Any deformities.
 Pulsations.
 Scars.
 Asymetry.
 Precordial exam: Palpation
 APEX BEAT localization.
 Character of apex beat.
 Any thrils in all precordial areas; mitral, pulm, aortic & tricuspid
areas.
Thril is a palpable murmur, has localizing benefit.
 Left parasternal heave.
 Precordial exam: Palpation
1. APEX BEAT:
Patient should be examined in the supine, sitting, left lateral
decubitus position.
Normal apical impulse occurs during early systole with an
outward motion imparted to the chest wall.
Apex beat: is outermost lowermost palpable cardiac pulsation.
Normal apex beat is palpable as brief outward impulse
(intersection of left MCL & 5th intercostal space by the fingers.
Apex beat > 2cm indicate LV enlargement.
Double apical impulse caused by LVH &forceful LA contraction.
2. LEFT PARASTERNAL LIFT,Best appreciated by the distal
palm or with the finger tip, Palpable anterior systolic movement
sustained up to S2,indicate RVH.
Giant presystolic lift seen in HCM.
 Auscultation:
AREAS TO AUSCULTATES
1. Apex (mitral area) murmur from the MV are best heard.
2. Right Lower sternal edge (tricuspid area)
3. Lower left parasternal (4th ICS) murmur of AR is best heard
4. Upper left parasternal (pulmonary area, 2nd left ICS)
5. Upper right parasternal (aortic area, 2nd right ICS, murmurs
arising from aortic valve area best heard)
6. Below the left clavicule: continuous murmur of PDA is best
heard
7. Posterior chest for bruits caused by bronchial collaterals in case
of coarctation of the aorta
8. Other areas: (abdominal aorta, renal arteries, carotide, femoral
arteries)
Auscultation:
 Auscultation: S1
Produced by M&T valve closure
 Best heard at the apex.
 Occurs just before the palpable upstroke of the carotide pulse.
 Factors influencing intensity of S1:
1. PR interval : - short PR-loud S1,long PR-soft S1
2. Mitral Valve Disease: MS typically causes loud S1,but later in
the course of the disease, when the valve becomes calcified/immobile,
S1 intensity decreases.
Soft S1 occur also in AR due to premature closure of MV.
 Intensity of S1 increase in (MS, TS, myxoma, short PR)
 Intensity of S1 decrease in (fibrosis or cacification of MV, prolong
PR, HF, MR, AR)
 Variable intensity of S1 in A.F., CHF, VT.
 Auscultation: S2
Closure of AV & PV,normally AV closes before PV.
Inspiration splitting of S2 is due to delay in P2 due to:
1. Increase capacitance of pulmonary vascular bed
2. Increase-RV volume.
Normally intensity of A2 exceeds that of P2.
A) Loudness of A2 or P2 is proportional to the respective
pressures in Ao or PA at onset of diastole, i.e., higher pressure –
louder A2 or P2
 A2 is louder with HTN, dilated aorta.
 P2 is louder with pulmonary HTN, dilated PA
B) Decrease intensity of A2 or P2 is due to decrease pressure
beyond the valve, stiff semilunar valves (A.S, P.S.), chest wall or lung
deformity (emphysema)
 Auscultation: S2
Wide but not fixed splitting of S2:
1. Delayed electrical activation of RV (RBBB, PVC from LV)
2. Prolonged RV mechanical systole (massive PE, Pulm HTN,P.S.)
3. Early aortic closure (MR).
Reversed Splitting:
1. Delay electrical activation of LV (LBBB, PVC from RV)
2. Prolonged LV mechanical systole (HTN, A.S., severe LV dysfun)
3. Early pulmonic closure (TR), early electrical activation of RV
(WPW)
 Auscultation: S2
Fixed Splitting: A.S.D., severe RV failure
 Auscultation: S3
Normal findings in younger patients
Due to passive diastolic filling of ventricle (0.14 to 0.22s after S2)
Best heard at the apex patient on the LLP
 Causes of S3 include
Abnormal ventricular relaxation
Ventricular failure
Dilated and hypertrophic cardiomyopathy
Severe TR, MR
LV dyskenesia or aneurysm
Hyperdynamic states (AV fistula, thyrotoxicosis)
 Auscultation: S4
Due to vigorous atrial contraction to propel blood into a stiff
ventricle (absent in AF)
Best heard at the apex, patient on LL decubitus
 S4 is heard in:
LVH
Acute MI
HOCM, DCM
Severe AS, PS
 S4 occurs just before the S1 (# diagnosis with split S1: firm
ressure by the diaphragm eliminates S4 but not split S1)
 Auscultation: Ejection clicks
Three mechanisms:
1. Intrinsic abnormality of AV or PV (congenital bicuspid AV,
congenital P.S.)
2. Pulsatile distension of dilated great artery (HTN, PHTN, dilated
PA,aortic aneurysm)
3. Increase flow states (ASD, pulmonic EC) (truncus arteriosus
aortic EC)
Mid to Late Systolic Clicks:
Commonly heard in MVP
Sharp high pitched sound
Maneuvers that decrease LV volume move the click earlier.
Maneuvers that increase LV volume move the click later.
 Auscultation: Opening snap
 Caused by the opening of the stenoic but pliable MV or TV
(disappears in severe calcified MS or TS).
 Higher LA pressure leads to short S2-OS
Occurs 0.08 s after S2
Best heard between apex and left sternal border
DD: Split S2. However, having the patient stands help to
differentiate the two.
The S2 – OS internal widens, while split S2 does the change or
narrow.
 Auscultation: Murmurs
Grading:
Grade I - So faint and heard only with special effort
Grade II - Soft but readily detected
Grade III - Prominent but not loud
Grade IV - Loud usually with palpable thrill
Grade V - Very loud with thrill
Grade VI - Heard without stethoscope on the chest wall
High pitch sounds (use diaphragm of stethoscope)
 S1, S2, murmurs of valvular regurgitation
 OS, clicks, obstruction of semilunar valves (AV, PV)
 Pericardial knock
 Low pitch sound (use of bell of stethoscope)
 S3, S4 obstruction of AV valve (MV, TV)
 Auscultation: Murmurs
Classification of Murmurs: (Systolic, Diastolic, Continuous)
I. Systolic Murmurs (SM)
Stenosis of semilunar valve causes delay in peaking of SM related
to prolongation of ejection.
The duration not the intensity is proportional to severity of
obstruction.
 Commonly encountered clinic problem is the differentiation of AS
Vs benign aortic sclerosis.
 With aortic sclerosis there should be no clinical, ECG, or
radiological evidence of heart disease.
The carotid upstroke is normal.
 Auscultation: Murmurs
The SM peaks early with normal S2.
MR murmur is usually pansystolic, It can be late systolic in timing
(suspect MVP, papillary muscle dysfunction).
It can also be early systolic in acute severe MR with markedly
increased LA pressure reducing late systolic LV-LA gradient.
The SM of TR is best heard at LLSB or over xyphisternum &
associated with large V-wave.
 The murmur of VSD parallels the pressure difference between the
two ventricles.
The murmur is typically pansystolic and associated with thrill.
With significant pulmonary HTN, the murmur duration shortens.
 SM heard in the back may be caused by coarctation, aortic
dissection, peripheral PA stenosis or pulmonary AV fistula.
 Auscultation: Murmurs
II. Diastolic Murmurs: Early diastolic murmurs:
Aortic regurgitation: configuration of the murmur reflects volume
& rate of regurgitation flow,therefore, with chronic AR, the aortic
diastolic pressure consistently exceeds the LV diastolic pressure and
the murmur is heard throughout diastole.
However, with acute AR, the LV diastolic pressure is very high
(because the LV is not dilated and unprepared), so the murmur tend
to short.
Pulmonary regurgitation murmurs secondary to pulmonary HTN
(Graham-steel murmur) is high velocity blowing murmur that can
last throughout diastole.
While PR without elevation of PA pressure results in mid diastole
murmur because the diastolic pressure exerted on PV is minimal in
early diastole.
 Auscultation: Murmurs
Mid diastole murmurs
Majority originates across mitral or tricuspid valves.
Murmur is easily appreciated with increase flow through the
valves.
Duration of the murmur correlates with severity.
Mid diastolic murmurs occur with:
(1) obstruction of AV valves (MS, TS, Austin flint) &
 (2) Increase flow across AV valves (functional obstruction), e.g.,
ASD, VSD.
 Auscultation: Murmurs
Late diastolic murmur (presystolic)
Represented by increased flow through obstructed mitral or
tricuspid valves during atrial contraction
Can be heard (opposite to common belief) in MS or TS in patients
with atrial contraction (AF).
 Auscultation: Murmurs
III. Continuous Murmurs – due to
(1) Aortopulmonary connection (PDA)
(2) AV connection (AV fistula, anomalous origin of left coronary
from PA)
(3) Disturbance of flow in arteries or veins (mammary soufflé,
cervical venous hum)
 Auscultation: common valve lesions
MS:
Malor flush, small volume pulse, - S1, opening snap, middiastolic
murmur (MDM), presystolic accentuation
Signs of Severity:
1) duration of murmurs (longer is severe).
2) S1 ¾ OS interval (shorter is severe).
MR:
Soft S1, wide splitting of S2, S3 present, systolic murmur
(pansystolic, early, mid or late systolic).
Signs of Severity: Longer duration or confined to early systole
 Auscultation: common valve lesions
AS:
Slow-rising pulse, S1, (N or soft), S2 (single, paradoxicalsplitting),
S4 present, ejection click if valve is mobile, ejection systolic murmur
with late peaking.
Signs of Severity:
1. Single S2 or paradoxical splitting
2. Longer murmur
3. Late peaking of murmur.
 Auscultation: common valve lesions
AR:
 Peripheral signs with chronic not acute AR. S1 (soft), S2 (absent,
single),S3 present.
Early diastolic murmur – short in acute AR
Ejection systolic murmur due to increase flow across AV
Austin flint – MDM due to narrowed mitral valve due to rising
ventricular diastolic pressure
Signs of Severity:
1) Duration of murmur – longer is severe in chronic
2) Systolic ejection flow murmur
3) Austin flint
4) Reduced diastolic BP
 Auscultation: common valve lesions
T.S.:
Prominent A-wave, OS, MDM at LSB with presystolic
accentuation
Both the OS and the murmur are accentuated with inspiration,
leg raising, squatting and manoeuvres that increase transtricuspid
valve flow
Signs of Severity:
1) duration of murmurs (longer is severe)
3) S1 ¾ OS interval (shorter is severe)
 Auscultation: common valve lesions
TR:
Prominent V-wave, pulsatible liver, soft S1, S3 present,pansystolic
murmur at LSB increase in inspiration
Signs of Severity:
Peripheral signs with TR, longer duration of the murmur
 Auscultation: common valve lesions
PS:
Ejection click, S1 (N)
S2 (wide splitting), S4 present
Ejection systolic murmur increase with inspiration
 Auscultation: common valve lesions
PR:
S1 (soft), S2 wide splitting
S3 present, S4 present
Diastolic murmur increase in inspiration.
If secondary to PHTN it begins in very early diastole.
If secondary to organic valve lesion, it begins slightly later and
ends in mid diastole.
 Auscultation: common valve lesions
Pulmonary HTN:
 Prominent A-wave
Early systolic click (sudden opening of P.V. into high pressure
artery)
Prominent P2 (due to increase force of pulmonary valve closure)
Left parasternal left (RVH)
Mid systolic ejection murmur (turbulent transvalvular pulmonary
flow)
Signs of Severity:
 1. Murmur of PR
 2. Murmur and peripheral signs of TR
 3. If advanced pulmonary HTN – look for signs of RVF
 Maneuvers to differentiate
murmurs:
Valsalva: During active strain phase most murmurs decrease in
intensity except murmur of:
1) HOCM – typically get louder
 2) MVP – longer and louder
Respiration: Right sided sounds and murmurs get louder with
inspiration (except for pulmonary ejection click)
Handgrip: By increasing BP (afterload), augments murmur of
MR, AR but does not affect murmur of AS and tends to decrease
murmur of HOCM
Prompt Squatting:Causes a rapid increase in venous return and
increase in peripheral resistance. Because LV volume and peripheral
resistance increase, the murmur of HOCM gets softer. The murmurs
of MR/AR get louder because of increase resistance
Extrasystolic beats: Both HOCM/AS murmur get louder because
of increased post-extrasystolic contractility, while MR unaffected.