This document provides an overview of how to conduct a general physical examination, with a focus on examining the cardiovascular system. It describes examining general build and stature, posture, facial appearance, eyes, neck, spine, skin, and extremities. It also discusses common physical findings and their associations with various syndromes and diseases that can manifest cardiovascular issues, such as Marfan syndrome, Turner syndrome, and Cushing's syndrome. Examples of heart murmurs and their causes are also provided. The examination is designed to evaluate any signs, symptoms or physical clues that may indicate underlying cardiovascular conditions.

1. GENERAL PHYSICAL
EXAMINATION OF CVS
By : SUBODH KR. MAHTO
PGIMER, DR. RML
HOSPITAL,NEW DELHI

2. • General build and stature
• Posture or attitude
• Gestures and signs
• Facial appearance
• Eyes, Nose, Ear
• Oral cavity
• Neck
• Spine, skin
• Extremities

3. • GENERAL BUILD AND STATURE
– Height: upper segment-top of head to pubic ramus
Lower segment-pubic ramus to floor
– Upper segment to lower segment ratio, equal after 10yrs
– Arm span: distance b/w tips of middle fingers of one hand
to others
– Arm span to height ratio normally equal or <1.05
– BMI: 18.5-24.9 kg/m2( in indian, 18.5- 23kg/m2)

4. I. Tall stature : Height excess of average normal for the age
and race(>2 SD of mean height)
India usually >6 ft
• Causes :
– tall stature with equal upper and lower segment or equal arm
span to height ratio: constitutional and pituitary gaints.
– Tall stature with upper to lower segment ratio of ≤0.8 or arm
span to height ratio >1.05: Marfan syndrome, homocystinuria,
klinefelters syndrome

6. SYNDROME CVS MANIFESTATION CLINICAL FEATURE
Marfan
syndrome
1. Ascending aorta- dilatation(AR)
and dissection
2. MVP± valvular MR
3. Calcification of mitral annulus < 40
yrs
4. Dilatation of MPA in absence of
valvular or peripheral PS
5. Dilatation or dissection of
descending thoracic or abdominal
aorta < 50yr
1. S1 –audible and S2 – muffled
2. Ejection systolic murmur and
austin flint murmur .
3. In MR , soft S1 , S2widely split
,S3 over apex and pansystolic
murmer
Homocystinuria 1. Aortic and pulmonary dilatation
2. Intravascular thrombosis.
1. S1 –audible and S2 – muffled
2. Ejection systolic murmur and
austin flint murmur .
Klinefelters 1. Venous thromboembolism 1 .widely, fixed split of S2

7. Marfan syndrome

9. • SHORT STATURE:
– Indian < 4 Ft of height considered as short stature
– Causes:
• Constitutional(hereditary)
• Endocrine- Cretin, pituitary dwarf, Cushing syndrome
• Genetic – Turner syndrome, Noonan Syndrome, Hurler
syndrome, etc
• Skeletal – Ellis van creveld syndrome, achondroplasia
• Acquired skeletal- rickets

11. SYNDRO
ME
CVS MANIFESTATION CLINICAL S FEATURE
Turner
syndrome
1. Coarctation of aorta
2. Bicuspid aortic valve
3. PAVC(partial anomalous venous
connection)
1. Systolic thrill
2. Ejection systolic murmur
3. Contineous murmur
Noonan
syndrome
1. Dysplastic PS
2. HCM
1. S2 widely split
2. Pulmonary ejetion click
3. Ejection systolic murmur.
Ellis- Van
Creveld
syndrome
1. Single atrium
2. ASD
1 .widely, fixed split of S2
2.flow ESM across PV
3.flow MDM across TV

13. • BUILT:
– Obesity predisposes or aggravates hypertension, dyslipidemia,
diabetes mellitus, atherosclerosis, etc
– BMI- 30-39.9 kg/m2
– Waist circumference: males >102cms, females > 88cms
– Causes:
• Metabolic syndrome
• Cushing’s syndrome
• Pickwickian syndrome
• Laurence-Moon- Biedl syndrome

14. SYNDROME
S
CVS MANIFESTATIONS CLINCALS FEATURE
Pickwickian
syndrome
1. Increased pulmonary vascular
resistance
2. Pulmonary hypertension
1. Loud P2
Laurence-
Moon- Biedl
syndrome
1. Congential heart disease , dilated
cardiomyopathy
1.S3,S4 and late systolic murmur
Cushing
syndrome
1. Hypertension
2. Accelerated atherosclerosis(MI,
CHF)
1. Tachycardia
2. gallop

16. • POSTURE / ATTITUDE :
– Patient is in pain
• Sitting quietly- angina pectoris
• Moving restlessly- MI
• Sitting up posture- heart failure
• Kneeling forward- pericarditis
– Squatting posture to get relief from dyspnoea in cyanotic
congenital heart disease

17. • GESTURES AND SIGNS :
GESTURES/ SIGNS CAUSE
Levine’s sign Ischemic chest pain
Gower’s sign Muscular dystrophy(cardiomyopathy)
Localized chest discomfort Psychogenic chest discomfort
Sighing respiration with sweating Neurocirculatory asthenia
Dyspneic Heart failure, pericardial effusion

19. • FACIAL APPEARANCE :
• Facial dysmorphism
– May be due to hypertelorism, epicanthic folds, broad flat nose, low set
ears, thick lips, abnormal teeth, short and webbed neck, low hair line
and mid facial hypoplasia
– Down syndrome, Turner syndrome, Noonan syndrome and william
syndrome
– Characteristic facies can be seen in syndromes

20. Facial expression Syndromes/ cause
Hypertelorism, epicanthic folds, broad flat
nose, low set ears and short neck
Turner and Noonan syndrome
Moon face Cushing‘s syndrome
Ape like face Acromegaly
Senile face Werner’s syndrome
Mongoloid facies Down syndrome
Elfin facies William syndrome
Dull expression face Myxedema; myotonic dystrophy
Frightened and staring Thyrotoxicosis

21. • Facial edema :
– Present in patients with
• tricuspid valve disease
• constrictive pericarditis
• SVC obstruction syndrome
• Dull expressionless face
– With periorbital puffiness – Myxedema (pericardial effusion, risk of
atherosclerosis)
– With ptosis – Myotonic dystrophy (conduction defects, arrhythmias)

22. • Butterfly rash on face
– Associated with malar depigmentation seen in SLE
– SLE may be associated with CVS manifestations in 57%
• pericarditis
• Myocarditis
• Libman- Sacks endocarditis ( AR and MR., less freq to AS, MS, TS
and TR)
• Congential heart blocks in offsprings of affected mother
• Malar flush
– Seen on face, cheeks, nose and ears – Chronic MS

23. Butterfly rash
Myxedema
MOON FACE

24. • Facial expression of fright and anxiety
– Seen in thyrotoxicosis
– Associated with arrhythmias, wide pulse pressure, high output failure,
Means- Lerman scratch (high pitched sound in pulmonary area)
• Ape like appearance
– Acromegaly
– Associated with hypertension, cardiomyopathy , arrhythmias(PVC, AF,
interventricular conduction defects) and atherosclerosis
• Mongoloid facies
– Down syndrome
– Endocardial cushion defects, less frequently with TOF, ASD, PDA.

25. • Elfin facies
– Seen in williams syndrome
– Associated with
• supravalvular AS
• peripheral PS

26. • EYES :
• Hypertelorism :
– Wide set eyes – distance b/w two eyes more than size of one eye
– Observed in
• Noonan syndrome - associated pulmonary stenosis
• Turner syndrome – coarctation of aorta
• LEOPARD (multiple lentigines) synd –PS and HCM
• Hurler syndrome – arrhytmias and valvular regurgitaion
• William syndrome – supravalvular AS and PS
• Klippel – Feil syndrome - VSD

27. • Exophthalmos : Thyrotoxicosis
• Nystagmus
– Noted in Friedrich’s ataxia –HCM, SA node artery occlusion and
arrhytmias
• Eye lids
– Lid lag – hyperthyroidism
– Ptosis
• Kearns – Sayre syndrome – complete heart block, cardiomyopathy
• Klippel- Feil syndrome
– Xanthelasma –
• Present near inner canthus in dyslipidemia
• Leads to atheroscleosis

28. • Conjuctiva :
– examine for pallor,
– petechial hemorrhages : infective endocarditis
• Sclera
– Jaundice – CHF, large pulmonary infract, hemolysis
– Blue sclera –
• osteogenesis imperfecta – AR, aortic root dilatation, MR
• Ehlers –Danlos syndrome – arterial dilatation and rupture, AR and
MVP

29. • Cornea :
– Corneal arcus –sign of dyslipidemia, yellowish white ring in outer
margin
– Arcus senilis – ill defined greyish white
• Iris :
– Brushfield’s spots – grayish white spot in periphery of iris,
(Down syndrome)
– Congenital coloboma –
• Cat eye syndrome –TAPVC, VSD TOF
• CHARGE syndrome – TOF and conotruncal anomalies

30. • Lens :
– Premature cataracts : Myotonic muscular dystrophy, Refsum syndrome
congenital rubella infection
– Subluxation :
upward dislocation – Marfans syndrome
downward dislocation – Homocystinuria
( arterial and venous thrombosis )
• Retina :
– Helpful for diagnosis (COA, IE) and prognosis

31. FINDINGS DISEASE
Hypertensive retinopathy hypertension
Arteriosclerotic retinopathy Atherosclerosis
Wreathlike AV anastomosis Takayasu ‘s disease
Corkscrew tortuous retinal arteries Coarctation of aorta
Roth spots Infective endocarditis
papilledema Malignant hypertension
Angiod streaks Pseudoxanthoma elasticum

32. • NOSE :
– Broad , flat nose as a part of facial dysmorphism observed in Down
syndrome, Cornelia de Lange syndrome, William syndrome, Hurler’s
syndrome
• EARS :
– Ear lobe crease (Frank sign) – frequently have CAD
– Low set ears : <1/3rd of ear lobe present above line drawn from outer
canthus of eye
• Noonan syndrome
• Turner syndrome
• Klippel – Feil Syndrome
• Down syndrome
• Cornelia de Lange’s syndrome

33. • ORAL CAVITY :
 LIPS :
– Pallor
– Cyanosis
– Thick lips – Hurler’s syndrome, Acromegaly, Myxedema
– Absent Philtrum –fetal alcohol syndrome
– Capillary pulsations
– Rhagades – congenital syphilis
 Mucous membranes :
– Examine for petechiae and telangiectasia

34.  Teeth
– Malformed and premature dentition at birth along with gum
hypertrophy , lip tie, observed in Ellisvan Crevald syndrome
– Peg shaped teeth
• Hurler’s syndrome
• Willam’s syndrome
• Hutchinson’s teeth(congenital syphills)
– Widely spaced teeth
• Acromegaly
• William’s syndrome
 TONGUE : colour and size

35.  PALATE
– High arched : Marfan’s syndrome, Pierre Robin syndrome
– Cleft/perforated palate : tertiary syphilis, TB

36. • NECK :
– examine for short neck, webbed neck, low hair line, lymphadenopathy,
thyromegaly
 Short neck : bird’s index – ratio of height to distance between
occipital protuberence and C7 spinous process
• Normal ≤ 12.8, ≥13.6 indicates short neck
 Low hair line :
• Posterior hair line extends below C5 spinous process OR
• Ratio of distance from external occipital protuberence to hair line
and distance from hair line to C7 spinous process is > 1/6 in males
and >1/4 in females.

37. SHORT NECK WEBBED NECK LOW HAIR LINE
Klippel- Feil syndrome Noonan syndrome Noonan syndrome
Morquio’s syndrome Turner syndrome Turner syndrome
Edward’s syndrome Klippel- Feil syndrome
Cornelia de Lange
syndrome

38. • SPINE :
– Marfan syndrome –kyphoscoliosis, pectus excavatum , pectus
carnitum
– Ankylosing spondylitis – AR, MR and comlete heart block
– Straight back syndrome
• SKIN :
– Skin lesions are alphabets of systemic disease
 Pigmentation

39. SKIN LESION SYSTEMIC DISEASE CV MANIFESTATIONS
Bronze pigmentaion Hemochromatosis Cardiomyopathy
Café au luit spots Von Recklinghausen’s disease Pheochromocytoma
Myocarditis
Multiple Lentigines LEOPARD syndrome HCM
Angiofibromas Tuberous sclerosis Rhabdomyoma and
arrhythmias
Erythema marginatum Rheumatic fever Carditis
Janeway lesions Infective endocarditis Valvular lesion and embolism

40.  Skin texture
• Coarse , thick , dry with brittle , sparse and coarse hair –
Myxedema
• Moist – Hyperthyroidism
• Hyperextensible and rubber like skin with cigarette paper scar –
Ehlers Danlos syndrome
 Xanthomas
Xanthomas Hyperlipoproteinemia type
Palmar xanthomas Type III
Tendinous xanthomas Type II
Eruptive Xanthomas Type I and V

41.  Nodules :
• SC nodule : nontender, freely mobile , 0.5-2 cm
located over extensor surface of joints, occipital protuberance ,
spinous process over thoracolumbar vertebrae
• Osler’s nodes : small , tender subcutaneous nodules on pads of fingers or
toes and palms and soles
 Cyanosis, pallor and Icterus.
NODULES DISEASE
Waxy flat nodules Amyloidosis restrictive cardiomyopathy
SC nodules Rheumatic fever, SLE and Rheumatoid
arthritis
Osler’s nodes Infective endocarditis

42. • EXTREMITIES :
 DIGITS :
DIGIT DESCRIPTION DISEASE
Arachnodactyly Marfan syndrome
Polydactyly Ellis-Van Crevald syndrome
Laurence Moon Biedl syndrome
Syndactyly Ellis-Van Crevald syndrome
Laurence Moon Biedl syndrome
Clindactyly Down syndrone
Ellis-Van Crevald syndrome
Hurler’s syndrome
Brachydactyly Down syndrome
Turner syndrome
Sclerodactyly Scleroderma

43. • In Marfan syndrome patients have positive thumb sign
(Steinberg sign) and wrist sign(Walker- Murdock).

44. • Digits also examined for Raynaud’s phenomenon and sclerodactyly
 NAILS : examine nails for cyanosis, splinter hemorrhage , capillary
pulsations(quinke’s sign), abnormal nails like
Abnormal nails Disease
Nail stripes Chronic constrictive pericarditis
Dysplastic nails Ellis-Van Crevald syndrome
Plummer nails Hyperthyroidism
Square/ broad nails Acromegaly, cretin
Koilonychias Iron deficiency anemia
clubbing Cyanotic congenital heart disease
Infective endocarditis
Myxoid tumour

45. MURMUR:- due to when that arises when blood velocity
increases due to increased flow
TYPES OF MURMUR :-
1. SYTOLIC MURMUR :- pccurs during any part or the whole of
systolic .
A) Early systolic murmur:-
a)VSD
b) acute severe TR
c) acute severe MR

46. • B)Mid systolic murmurs :
a) AS
b) PS
C) HOCM
Late systolic murmur
1.MVPS
2.TVPS
Pansytolic murmur
1. MR and TR
2. VSD

47. 2.DIASTOLIC MURMURS:- occur during any part of diastrole.
early diastolic murmur:-
1. AR
2. PR
Mid Diastolic murmur
1.MS
2.TS

48. • Dyspnoea-
abnormally uncomfortable awareness of braething.
Grading(NYHA )-
Class1- no symptoms
Class2-symptoms with ordinary activity, slight limitation of physical work.
Class3-symptoms with less than ordinary activity,maked limitation of activity.
Class4- symptoms with any physical work.
Cause of dyspnoea-
1.cardiac-a.LHF
b.valvular heart ds
c.coronary heart ds
d. cardiomyopathies.

49. • 2. Respiratory-
a.brochial asthama
b.Emphysema
c.Chronic bronchitis
d.Interstitial lung ds
e.Pneumonia
f.Pulmonary embolism

50. • PULSE :
– “Arterial pulse is a wave produced by cardiac systole traversing in the
peripheral direction in arterial tree at a rate faster than the column of blood
”
– Two positive deflection during systole and one during diastole
• Systole : percussion wave
tidal wave
• Diastole : dicrotic or diastolic wave
– Pulse wave transimitted peripherally
• Carotid - 30ms
• Brachial - 60 ms
• Radial - 80ms
• Femoral -75 ms

51. • Examination of arterial pulse :
– Rate,
– Rhythm,
– Character ,
– Volume ,
– Condition of arterial wall ,
– Radioradial delay ,
– Radiofemoral delay,
– peripheral pulses.

52. • RATE :
– 60- 100 bpm , Normal sinus rhythm in adult
– 7 days =140/min , 1 yr = 120/min, 6 yr = 100 / min , puberty = 80/ min
– Tachycardia , bradycardia , pulse deficit
– Tachycardia :
 Sinus tachycardia : sinus rate > 100 bpm
CAUSES
Physiological Infancy, childhood, anxiety , exercise , emotional stress
Pharmacological Amyl nitrate, epinephrine, isoproterenol, atropine,
Alcohol, nicotine
Pathological CHF, MI , Pulmonary embolism , myocarditis
Non cardiac- fever, anemia , thyrotoxicosis, hemorrage ,
hypotension , hypoxemia

53.  Tachyarrhythmias :
• Most tachycardia associated with regular pulse are of supraventricular
origin
• Tachycardia with irregular pulse
– Ventricular tachycardia and AV dissociation
• Bradycardia
– Sinus bradycardia : < 60 bpm
– Bradyarrhythmias : usually due to AV conduction abnormalities
especially with second degree heart AV block and complete heart
block

54. SINUS BRADYCARDIA CAUSES
Physiological Athletes , sleep
Pharamacological Beta- blockers , amiodorone , propafane , lithium ,
parasympathomimetic drugs
pathological Inferior wall MI , SA block , vasovagal syncope
Myxedema , increased ICT, hypothermia , obstrutive
jaundice, enteric fever

55. • Pulse deficit : difference b/w radial pulse rate and heart rate
– Occurs in tachyarrhythmias
– > 6 / min is diagnostic of atrial fibrillation
– < 6 / min can occur in PVCs

56. • RHYTHM :
– Normal pulse is regular in rhythm
– Irregular pulse can be regularly irregular, irregularly irregular
REGULARLY IRREGULAR IRREGULARLY IRREGULAR
Sinus arrhythmia Atrial fibrillation
Pulsus bigeminus Multifocal atrial tachycardia
Pulsus alternans Frequent PVCs
Partial 1st and 2nd degree heart block

57. • CHARACTER OF PULSE :
– Best evaluated by palpating carotid pulse
– Pulsus Tardus (slow rising pulse ) :
• Slow rising pulse with delayed systolic peak and upstroke
• Frequently associated with thrill in carotids is characterstic of AS
• Often occurs with pulsus parvus (pulsus parvus et tardus)
• Indicates 70 mmhg of pressure gradient in AS

58. • Water- hammer (collapsing) pulse or Corrigan pulse or pulsus
celer :
– Rapid upstroke (percussion wave) followed by rapid descent (collapse)
of pulse without dicrotic notch (low systemic vascular resistance)
– best appreciated at radial pulse
– Patient’s wrist held in examiner’s hand and with the patient’s arm
suddenly elevated above shoulder

60. • Causes :
– With aortic run off : AR, PDA, AP window rupture of sinus of
valsalva into right chambers , AV fistulas
– Cyanotic congenital heart disease : truncus arteriosis with truncal
insufficiency , pulmonary atersia with bronchopulmonary
collaterals
– Hperkinetic circulatory states : pregnancy , anamia ,
thyrotoxicosis, beriberi, fever

61. • Pulsus bisferiens (Bis= two, ferise= to beat) :
– Characterised by two systolic peaks sepearted
by distinct midsystolic dip
– Causes :
• Severe AR, PDA, Hyperkinetic circulatory states
• AS with AR
• HOCM
• Normal (rare)
– Detection : palpating carotids
• Carotid systolic thrill may mask
• Apply graduated pressure or completely obliterate the pulse and
gradually release it to appreciate two waves

62. • Dicrotic pulse
– Two peaks , one in systole and other in diastole
immediately after S2
– Commonly seen in low output states :
• Enteric fever
• Cardiomyopathy
• Myocarditis
• Cardiac tamponade
– Detection : can felt in carotids , but better appreciated in radial artey ,
in inspiration , inhaltion of amylnitrate

63. • Irregularly regular pulse :
– Consists of pulsus bigeminus and pulsus alternans
– Pulsus bigeminus :
• Caused by PVCs
• Weak beat always follows the short interval and long compensatory
pause following premature beat is followed by a stronger than
normal pulse
• May also seen in AV blocks and atrial flutter with block

65. • Pulsus alternans :
– Strong beat alternates with a weak beat
– Frequently precipitated by PVCs
– Sign of severe LV dysfunction
– Causes : Severe AS , Daileted cardiomyopathy , myocarditis , acute
pulmonary embolism , severe pulmonary stenosis
– Detection : better appreciated in the peripheral pulses (radial and
femoral)
– Exaggerated by upright position , infusion of nitroglycerine

66. • Pulsus paradoxus :
– Exaggerated decrease in strength of arterial pulse during normal quit
inspiration due to the exaggerated of normal inspiratory decline in
systolic arterial pressure of > 10 mmhg
– Apparent paradox of disappearance of pulse during inspiration despite
presence of heart beat
– Causes :
• Physiological : pregnancy, obesity
• CVS : cardiac tamponade, constrictive pericarditis (50%),
pulmonary embolism
• COPD, acute severe asthma,

67. • VOLUME OF PULSE :
– Gives idea about pulse pressure
– Depends on stroke volume and compliance of arteries
– Normal , low or high volume
– Pulsus parvus : low volume small amplitude pulse
• Decreased stroke volume
• Observed in severe heart failure
• Carotids
– Pulsus magnus : high volume large amplitude
• Increased stroke volume , characteristically in AR
– Hyperkinetic or bounding pulse :
• Increased stroke volume and rapid ejection from left ventricle

68. • CONDITION OF VESSEL WALL :
– Examined by flattening of artery by digital pressure and sliding it
sideways
• Atherosclrotic vessel is thickened, rigid and tube like
• Hard and calcified in Monckeberg’s degeneration

69. • RADIAL PULSE SYNCHRONICITY :
– Radial pulse on one side may be diminished or absent in patients with:
• Takayasu arteritis
• Thoracic outlet syndrome
• Subclavian steal syndrome
• Chronic atherosclerosis
• Coarctation of aorta
• Dissection of aorta

70. • ABSENT OR DELAYED FEMORAL PULSATION :
– while palpating radial pulse, place finger of ther hand over femoral
pulse
– Noticeable delay in femoral is suggestive of :
• COA –delay is due to delay in its rate of rise .
• Occlusive disease of bifurcation of aorta, common iliac or external
iliac arteries

72. • Peripheral signs of AR :
– Water hammer pulse , pulsus bisferiens, pulsus magnus
– Hill’s sign
– Landolf’s sign , Becker’s sign
– De Musset’s sign
– Corrigan’s sign
– Muller’s sign
– Locomotor brachialis
– Quincke’s pulse
– Traube’s sign
– Duroziez’s sin(murmur)
– Rosen Bach’s sign, Gerhardt’s sign

73. • BLOOD PRESSURE :
– Lateral force exerted by blooorotd column per unit area of vascular
wall , expressed in mm of hg
– Korotkoff sounds – examined preferably with bell
• Five phases
• I- Appearence of clear , tapping sound
• II – tapping sounds replaced by soft murmurs
• III - Murmurs become louder
• IV – Muffling of sounds
• V – disappearance of sounds

74. • CUFF SIZE :
– Length of bladder is twice that of width , average length is 25cm ,
width of 12.5 cm (thigh = 20-25 cm )
– Air bag within cuff should extend 2/3rd of arm length and
circumference
• Midportion of the rubberbag within the cuff should lie over brachial artery
• Cuff should be deflated at a rate of 2-3mm of hg
• BP difference :
– Of >10 mm hg in both arms is significant
– Of > 20 mm hg in in lower limb as compared to upper limb

75. • Orthostatic / postural hypotension :
– BP recorded in lying , sitting and standing position especially when
postural hypotension is suspected
– Fall in systolic pressure of > 20mm hg after standing for 3 min , from
lying posture
• Pulse pressure :difference between systolic and diastolic pressure
– Normal pulse pressure is 30-60 mm hg
– Wide pulse pressure : hyperkinetic circulatory states, AR, PDA ,
complete heart block
– Narrow pulse pressure : heart failure , severe AS , DKA

76. JUGULAR VENOUS PRESSURE
• JVP is the oscillating top of distended proximal portion of the
internal jugular vein and represents volumetric changes that
reflect the pressure changes in the right heart

77. 1. Anatomy
2. JVP measurement
3. Causes of elevated JVP
4. Normal wave pattern
5. Abnormal wave pattern
6. Kussmaul’ s sign and hepatojugular reflux
7. Specific conditions

78. • Jugular veins
– Internal jugular vein
– External jugular vein

79. • Lateral to carotid artery & deep to
sternomastoid muscle.
• External jugular is superficial to
sternomastoid

81. Examination of JVP
• Right IJV is usually assessed both for waveform and
estimation of venous pressure
• Transmitted pulsations to overlying skin between two heads
of sternocleidomastoid

82. Right IJV Preferred : Why?
• Straight line course through innominate vein to the
svc and right atrium
• Less likely extrinsic compression from other
structures in neck
Why not EJV
• No or less numbers of valves in IJV than EJV

83. INTERNAL JUGULAR VEIN CAROTID
Superficial and lateral in the neck Deeper and medial in the neck
Better seen than felt Better felt than seen
Digital compression abolishes venous
pulse
Digital compression has no effect
Jugular venous pressure falls during
inspiration
Do not change with respiration
Abdominal compression elevates jugular
pressure
Abdominal compression has no effect on
carotid pulse
Has two peaks and two troughs Has single upstroke only

84. • Measurement of JV Pressure
– Sternal angle or angle of Louis - reference point
– Found approximately 5 cm above the center of the right
atrium
– Sternal angle – RA Fixed relationship

85. • Position of Patient :
– Patient should lie comfortably and trunk is inclined by an angle
– Elevate chin and slightly rotate head to the left
– Neck and trunk should be in same line
– When neck muscles are relaxed , look tangentially over the skin
and see pulsations
– Simultaneous palpation of the left carotid artery or apical
impulse aids in timing of the venous pulsations in cardiac cycle .

87. • Measurement of JVP
– Two scale method is commonly used
– Normally JV pressure does not exceed 3- 4 cm above the
sternal angle
– Since RA is approximately 5 cm below the sternal angle ,
the jugular venous pressure corresponds to 9 cm
– Elevated JVP : JVP of >4 cm above sternal angle

88. • Elevated JVP
– Increased RVP and reduced compliance:
Pulmonary stenosis
Pulmonary hypertension
Right ventricular failure
RV infarction
– RV inflow impedance:
Tricuspid stenosis / atresia
RA myxoma
Constrictive pericarditis

89. • Circulatory overload :
Renal failure
Cirrhosis liver
Excessive fluid administration
• SVC obstruction

90. • Kussmaul's sign
– jugular venous pressure increases during inspiration
– Seen in
• Constrictive pericarditis
• Severe right heart failure
• RV infarction
• Restrictive cardiomyopathy
• Impaired RV compliance.

91. • Abdominal -Jugular Reflux
– Hepatojugular reflux – Rondot (1898)
– Apply firm pressure to periumbilical region 30- 60 sec
– Normally JV pressure rises transiently to < 1cm while
abdominal pressure is continued
– If JV pressure remains elevated >1cm until abdominal
pressure is continued: Positive AJR.

92. • Abdominal compression forces venous blood into
thorax.
• A failing/dilated RV not able to receive venous return
without rise in mean venous pressure.
• Positive AJR :
– Incipient and or compensated RVF
– Tricuspid regurgitation
– COPD

93. • Normal JVP reflects phasic pressure changes in RA
during systole and RV during diastole
• Two visible positive waves ( a and v) and two
negative troughs ( x and y)
• Two additional positive waves can be recorded C
wave interrupts x descent and h wave

94. Normal JVP Waveform
• Consists of 3
positive waves
– a, c & v
• 3 descents
–x, x'(x prime) and
y

95. • “a wave”
– First positive presystolic a wave is due to right atrial
contraction
– Effective RA contraction is needed for visible a wave
– It precedes upstroke of the carotid pulse and S1, but follow
the P wave in ECG

96. • “x descent”
– Systolic x descent is due to atrial relaxation during atrial
diastole
– X descent is most prominent motion of normal JVP which begins
during systole and ends just before S2
– It is larger than y descent
– X descent more prominent during inspiration

97. • “C Wave”
– Not usually visible
– Two different causes
- Transmitted carotid artery pulsations.
- Upward bulge of closed Tricuspid valve in isovolumic systole

98. “x` Descent” :
• x`descent is systolic trough after c wave
• Due to
 Fall of right atrial pressure during early RV systole
 Downward pulling of the TV by contracting right ventricle
 Descent of RA floor

99. • “v wave” :
– Begins in late systole
ends in early diastole
– Rise in RA pressure due to continued RA filling during
ventricular systole when tricuspid valve closed
– Roughly synchronous with carotid upstroke and
corresponds S2 .

100. • “y descent” :
• Diastolic collapse wave
(down slope v wave)
• It begins and ends during
diastole well after S2
• Decline of RA pressure due to RA emptying during early
diastole when tricuspid valve opens

101. • “h wave” :
– Small brief positive wave following y
descent just prior to a wave
– Described by Hieschfelder in 1907
– It usually seen when diastole is long
– With increasing heart rate, y descent
immediately followed by next a wave
.

102. • Prominent a wave :
– Forceful atrial contraction when there is resistance to RA emptying or
increased resistance to ventricular filling
– RV inflow obstruction:
Tricuspid stenosis or atresia
RA mxyoma
– Decreased ventricular compliance:
Pulmonary stenosis
Pulmonary hypertension of any cause
RV infarction
RV cardiomyopathy (HOCM)
Acute pulmonary embolism

103. • Cannon Waves :
– Whenever RA contracts against closed TV valve during RV systole
– Regular cannon waves:
Junctional rhythm
VT with 1:1 retrograde conduction
Isorhythmic AV dissociation
– Irregular cannon waves :
Complete heart block
Ventricular tachycardia
Ventricular pacing or ventricular ectopics .

104. • Absent a wave :
– When no effective atrial contraction as in atrial fibrillation
• Prominent x descent :
– Presence of atrial relaxation with intact tricuspid valve and good RV
contraction
– Causes :
Cardiac tamponade
Constrictive pericarditis

105. • Reduced x descent :
– Moderate to severe TR: early sign
– Atrial fibriillation
• Prominent v wave :
– Increased RA volume during ventricular systole produce prominent v wave
– Severe TR : giant v wave
– Giant v wave sometimes cause systolic movement of ear lobe, head bobbing with
each systole , systolic pulsation of liver , pulsatile exophthalmos .
– ASD with mitral regurgitation
– VSD of LV to RA shunt (Gerbode's defect)
– RV failure

106. cv wave

107. • Rapid y descent :
– Severe TR
– C .Pericarditis (Friedreich's sign):
Early rapid ventricular filling
– Severe RV failure
– ASD with mitral regurgitation

108. • Slow y Descent :
– When RA emptying and RV filling are impaired y descent
is slow and gradual
Tricuspid stenosis
Right atrial tumours
Pericardial tamponade( y descent may even be absent).

109. • Cardiac tamponade :
– JVP is usually elevated
– y descent is diminished or absent
– x wave is normal
– Kussmaul's sign
usually negative

110. • Constrictive pericarditis :
– JVP is elevated
– a wave is usually normal
– v wave is usually equal to a wave
– x descent –prominent
– y descent – rapid descent
– Kussmauls sign is usually positive

111. cyanosis-(kyanos-blue ,osis-condition)
bluish discoloration of skin and mucous
membrane .
a. increased quality of reduced HB(<4)
b. abnormal hemoglobin pigments in the blood.
TYPE OF CYANOSIS
1.Peripheral cynosis
2.Central cynosis
3.Differential cynosis

112. • Peripheral cynosis
stasis of blood flow in the periphery with normal
arterial O2 saturation
Etiology-
1.Low cardiac output-CHF,septicemia
2.Exposure to cold envirment
3.Raynauld phenomenon
4.Pheripheral vascular disease

113. • 2.central cynosis
apparent at capillary concentration of > 4g/dl
of reduced Hb or >o.5 g/dl of
methemoglobin.
Etiology-
A.Decreased arterial oxygen saturation
1. decreased atmospheric pressure- high
altitude

114. • 2. impaired pulmonary function
a. Alveolar hypoventilation
b. ventilation perfusion mismatch
3.Anatomic shunt
a. CHD
b. pulmonary arteriovenous fistula
4 Hemoglobin with low affinity for oxygen.

115. B. Hemoglobin abnomalities
1.Methmoglobinemia(> 1.5 gm/dl)
a. Hereditary
b. drugs-nitrate ,nitrites,sulphonamide
2.sulfhemoglobinemia(>0.5gm/dl)
3.carboxyhemoglobinemia.

116. 3. Differential cynosis-
a.lower limbs- PDA with PHT, with right to left
shunt
b.Upper limb-limbs- PDA with PHT, with right to
left shunt,TGA.
Intermittent cynosis –Ebstein’s abnomaly.

117. feature Central cynosis Peripheral cynosis
mechanism Right to left shunt or lungs
disorders
Peripheral stasis
site Whole body Nail bed , nose tip,ear lobe
,extremities
extremities warm cold
Arterial blood gas Pao2 <85% normal
On warming the extremites No change disappears

118. • Clubbing-selective bulbous enlargement of
the distal portion of the digital due to
increased subungual soft tissue.
• 1st appears in the index fingers
Grading of clubbing-
Grade 1-obliteration of the angle between the
nail and nail bed and fluctuation test positive
Grade2-parrot beak apperance

119. • Grade 3-drumstick appearance
• Grade 4-Hypertrophic osteoarthropathy. Caus
• Cause of clubbing-
1.cardiovascular cause
a.CHD- TOF,TGA,TAPVC,Tricuspid atresia
b.infective endocardities
b.acyanotic CHD-myxoid tumor.

120. 2.Pulmonary disease with hypoxia-
a.bronchiectasis
b.Emphysema
c.Lung abcess
d.Pulmonary TB
e.Bronchogenic ca
3.GIT cause

121. • a.crohn’s ds
• b.ulcerative colitis
• C.biliary cirrhosis
Unilateral clubbing of fingers-
1. Arotic aneurysm
2. Pancoast tumours
3. Brachial arteriovenous fistula
4. Erythromelagia.

123. • Unidigital clubbing-
1.Local injury
2.Sarcoidosis
3.Gout
Differential clubbing- PDA with revesal.
Pseudo clubbing-
1.Hansen’s ds
2.Hyperparathyroidism

124. Jaundice –yellowish appearance of skin and mucous membrane
CHF, large pulmonary infract, hemolysis
1.Hepatocellular jaundice
a,.hepatitis. A,B,C,D,E
b.drugs-halothane, phenytoin,INH etc
2.Hemolytic jaundice
A. Intraerythrocytic.- spherocytosis,haemoglobinopathies
B. Extraerythrocytic-autoimmune,alloimmune chemical trauma

125. • 3.obstructive jaundice
a.viral hepatisis
b.cirrhosis.
c.Pregnancy
d.Lymphoma
e.Calculi
e.Ca of pancreas

126. • Peripheral oedema-
Excess accumulation of fluid in the subcutaneous
tissue due to increase in the intertitial volume.
Cause-
A.Increased capillary hydrostatic pressure- due to
increased blood volume or venous obstruction
a.increased blood volume –due to renal Na and
salt retention – CHF, renal failure and early
hepatic failure.

127. b.venous obstruction-
1. hepatic cirrhosis
2. local venous obstruction
B.Decreased plasma oncotic pressure
a.Nephrotic syndrome
b.Liver disease
c.Protein losing enteropathy.
d.Malnutrition
C.Increased interstitial oncotic pressure
a.Lymphatic obstruction
b.Hypothyroidism
c

128. Types and sites of peripheral edema-
1.localized- limited to one leg or one /both arm
-venous or lymphatic obstruction.
2.anasarca-generalised edema characterised by
periorbital edema.
- CHF , nephrotic syndrome
3.Leg edema- unilateral or bilateral; pitting or
nonpitting.

130. Bilateral pitting Unilateral pitting Bilateral non-
pitting
Unilateral non
pitting
1.CHF 1.trauma 1.myxedema 1.filariasis
2.Constrictive
pericarditis
2.vericoseveins 2Trauma
3.Nephrotic
syndrome
3.becker’scyst 3.milroy’s disease
4.Cirrhosis of liver 4.inflammation 4.malignancy
5.Protein losing
enteropathy
5.Congenital
venous
malformation
6.pregnancy
7. idiopathic