General Examination

Pulse-The arterial pulse is the abrupt expansion of an artery

resulting from the sudden ejection of blood into the aorta
and its transmission throughout the arterial system.
Hypokinetic pulse-low volume and amplitude
low cardiac output in shock or myocardial infarction,
Idiopathic dilated cardiomyopathy, valvular stenosis,
pericardial tamponade, or constrictive pericarditis.
Pulsus parvus et tardus
Severe aortic stenosis .It is a low-amplitude pulse with a
delayed upstroke best palpated on the carotid artery.
Hyperkinetic
large-amplitude and strong pulses that are normal. If these
become bounding, they are called hyperkinetic. Anxiety,
exercise, fever, hyperthyroidism, anemia, pregnancy,
beriberi, AVF
Water-hammer and collapsing-AR
Rapid peripheral runoff of blood in addition to a large stroke
volume from the left ventricle
Bisferiens pulse double systolic pulse .
two waves
the percussion wave followed by a tidal wave—both in
systole
AS + AR
AR
Idiopathic hypertrophic subaortic stenosis.
Twice-beating or bifid pulses where one impulse occurs in
systole and one occurs in diastole. These can be seen when
the peripheral resistance or the diastolic blood pressure is
low. Low cardiac output states
Pulsus alternans. This is a regular pulse with alternation of
beat amplitude every other beat. It is associated with severe
left ventricular failure of any cause, easiest to detect in the
femoral pulse
Pulsus paradoxus
If the pulse decreases dramatically in amplitude with
inspiration and increases with expiration, it is called pulsus
paradoxus.
Pericardial tamponade restricts right heart filling, superior
vena cava syndrome.
Asthma, emphysema, or airway obstruction can cause
changes in intrathoracic pressure and effect wide swings in
pulmonary blood volume and thus left ventricular venous
return
Palpable delay from the radial to the femoral pulse, it
suggests coarctation of the aorta or at least an aortic
obstruction below the takeoff of the left subclavian artery.
Apex Pulse Deficit
>10 Afib
<10 ectopics
Clubbing
Clubbing was first described by Hippocrates in the 5th
century BC
Clubbing of the nails is soft tissue swelling of the terminal
phalanx resulting in straightening of the angle that exists
between the nail bed and the nail
The phalangeal depth ratio, which is the ratio of digit’s depth
measured at the nail and the distal interphalangeal joint, is
another objective criterion used to assess clubbing.
The depth at the DIP joint is normally greater than that of the
nail. A ratio of greater than 1, therefore, supports clubbing.
Theories of clubbing
Increased capillary density.
PDGF
Increased release of platelet-derived growth factor (PDGF)
and vascular endothelial growth factor (VEGF) from
peripheral megakaryocytes leads to increased vascularity,
permeability, and ultimately connective tissue changes. The
release of both PDGF and VEGF is thought to be enhanced by
hypoxia.
Hypoxia
Humoural
Prostaglandins, bradykinin, ferritin, adenosine nucleotides,
interleukin-6, von Willebrand factor, serum transforming
growth factor-beta1 (TGF-beta1), tumor necrosis factor-a,
growth hormone, epidermal growth factor.
Neurogenic

Grades of clubbing
I Angle obliteration
II Parrot beak
III Drum stick
IV HPOA

Lovibond Angle
Nail and Nail bed angle 160 degrees

Schamroth sign
In 1976, Schamroth reported a clinical sign associated with
clubbing demonstrating obliteration in clubbed fingers of the
diamond-shaped window normally produced when the dorsal
surfaces of the corresponding finger of each hand are
opposed and now called Schamroth sign.
HPOA
Bamberger–Marie syndrome
Hypertrophic pulmonary osteoarthropathy (HPOA) is a
syndrome characterized by the triad of periostitis, digital
clubbing and painful arthropathy of the large joints,
especially involving the lower limbs
RS causes of clubbing –
Chronic suppurative lung infections – Suppurative
intrathoracic disease associated with clubbing includes lung
abscess, bronchiectasis, cystic fibrosis, empyema, and
chronic lung cavitary mycobacterial or fungal infection.
Diffuse pulmonary disease associated with clubbing includes
idiopathic pulmonary fibrosis, asbestosis, Langerhans cell
histiocytosis, lipoid pneumonia, and pulmonary
arteriovenous malformations.
Malignancy -Neoplastic intrathoracic disease associated with
clubbing includes bronchogenic carcinoma, malignant and
benign pleural tumors, metastatic cancers, Hodgkin
lymphoma, thymoma, pulmonary artery sarcoma,
nasopharyngeal carcinoma, rhabdomyosarcoma, primary
lymphosarcoma of the lung, and esophageal cancer.
COPD Doesn’t cause clubbing unless associated with
malignancy .

GI causes of Clubbing
Primary biliary cirrhosis
Inflammatory bowel disease

Cardiac causes Clubbing – CHD , IE

Reversible causes of clubbing

IE Empyema
JVP-
Hepatojugular reflux
Hepatojugular reflux is the distension of the neck veins
precipitated by the maneuver of firm pressure over the liver.
The HJR maneuver may be performed as follows:
The patient is positioned supine with elevation of the head at
45 degrees. Look at jugular pulsations during quiet
respirations (baseline JVP). Apply gentle pressure (30-40 mm
Hg) over the right upper quadrant or middle abdomen for at
least 10 seconds (some suggest to 1 minute). Repeat the
JVP.An increase in JVP of >3 cm is a positive HJR test.
Normal subjects will have a decrease in JVP with this
maneuver since venous return to the heart will be reduced.
The jugular venous pressure may transiently rise and then
return to normal or decrease within 10 seconds.
Negative in BCS

Cyanosis
Bluish discoloration of the skin or mucous membrane
cyan, a blue-green color.
Central cyanosis occurs when the level of deoxygenated
hemoglobin in the arteries is more 5g/dL with oxygen
saturation below 85%.
When looking for cyanosis, one should inspect those body
sites that contain minimal melanotic pigment, that have a
capillary bed close to the skin surface, and that are well
perfused. Lips, ears, trunk, nailbed, hands, conjunctiva, and
circumoral areas have been compared in detecting cyanosis
due to arterial hypoxemia; the tongue is the most sensitive
area, but the lips are more specific.
Respiratory Causes
 Impaired gas exchange secondary to pneumonia
 Embolism and ventilation perfusion mismatch
 Impaired gas diffusion via the alveoli
 Arteriovenous malformation
 Intrapulmonary shunt

Cardiac causes Cyanosis-CHD , Eisenmengarisation

The reason for the differential cyanosis and clubbing is that

due to the right-to-left shunt across the PDA, deoxygenated
blood from the right ventricle is preferentially directed into
the aorta distal to the left subclavian artery and into the
lower extremities.
If the patent ductus enters the aorta below the left
subclavian artery, the left arm is pink; if it enters above the
left subclavian artery, the left arm is blue.
In reverse differential cyanosis, the arms are more cyanotic
than the legs. This occurs in children with transposition of the
great arteries (TGA) when oxygenated blood from the
pulmonary circulation enters the descending aorta through a
patent ductus arteriosus.
Reverse differential cyanosis is seen in TGA with coarctation
of the aorta or interrupted aortic arch, and TGA with
suprasystemic pulmonary vascular resistance. In this
circumstance, the descending aorta is filled with oxygenated
blood from the pulmonary circulation and the lower
extremities have higher oxygen saturation than the upper
extremities

Jaundice, or icterus, is yellowish discoloration of the skin,

mucous membranes, sclerae, and body fluids resulting from
excess accumulation and deposition of bilirubin in the body
in the presence of serum hyperbilirubinemia.
Bilirubin is a breakdown product of hemoglobin in RBCs
Approximately 80% of bilirubin is formed from the
breakdown of heme in reticuloendothelial cells, primarily the
spleen and liver. The remainder comes from heme molecules
in other proteins, such as myoglobin.
Heme is converted to biliverdin by heme oxygenase and then
to bilirubin by biliverdin reductase.
The bilirubin formed by these enzymatic reactions is
unconjugated or indirect and is highly insoluble in water. It is
transported in the blood tightly but reversibly bound to
albumin, escaping kidney filtration and readily taken up by
the liver for conjugation. Normally, 90% to 95% of circulating
bilirubin is unconjugated
Hepatic uptake of unconjugated bilirubin across the
sinusoidal membrane occurs, and within the hepatocyte,
bilirubin is conjugated by microsomal uridine
diphosphoglucuronyl transferase (UDPGT) to a direct, water-
soluble form facilitating its excretion into bile. Bilirubin that
spills into the urine therefore is conjugated bilirubin.
Conjugated bilirubin is excreted in bile into the duodenum
and then metabolized by gut bacteria into urobilinogen.
Some of this product is excreted in the feces as oxidized
stercobilin (which gives feces a brown color), and some is
reabsorbed, entering the portal venous circulation to be re-
excreted by the liver. A small amount escapes hepatic
uptake, passes into systemic circulation, and is excreted in
urine as urobilinogen (normal levels of urobilinogen in urine
are 0 to 0.2 mg/dL)
Normal serum values for total bilirubin are 0.2 to 1.0 mg/dL;
for conjugated bilirubin, 0.1 to 0.3 mg/dL; and for
unconjugated bilirubin, 0.2 to 0.8 mg/dL.
Jaundice is detectable when serum bilirubin levels are
greater than 2.5 to 3.0 mg/dL.

Types of jaundice
Prehepatic
Hepatic
Post hepatic

Unconjugated- Overproduction, impaired uptake, or

conjugation of bilirubin
Conjugated - Dysfunction of hepatocytes, impaired excretion
into the bile ducts, or backward leakage of the pigment with
reflux of conjugates into the plasma
Mixed
Lymphadenopathy
Normal size of lymph node upto 1 cm
Epitrochlear 0.5cm
Inguinal 1.5 cm
Children 2 cm ( 2-10yrs)
Generalised LNP – 3 or more than 3 non contiguous
area
Regional LNP history
Upper respiratory tract infection. HNF malignancy = cervical
group of LNP
Scalp infection= occipital
Conjuctival infection= preauricular LNP
Upper extremity infection , breast lump= Axillary
Inguinal LNP= Lower extremity infection, genital infection
STD( herpes simplex virus, gonococcal infection, syphilis,
chancroid, granuloma inguinale, and lymphogranuloma
venereum)
Examination
Cervical group
Axillary group
Inguinal group
Mediastinal LNP

> 8cm

Etiology
Infective
HIV
TB NTM
Infectious mononucleosis
EBV CMV
Syphilis( epitrochlear LNP)
Histoplasma

Malignancy
Lymphoma
Leukemia
Solid organ malignancy
Virchows nodes
Sister mary joseph nodule

Infiltrative
Lipid Storage disorders
Niemann pick
Tangiers
Gaucher
Fabry
Metabolic
Sarcoidosis
Hyperthyroidism
Kikuchi-Fujimoto disease (KFD), also known as histiocytic
necrotizing lymphadenitis, is a benign and self-limiting
disease typically characterized by the enlargement of
regional lymph nodes and accompanied by fever. KFD affects
predominantly young adult females of Asian origin

Kimura disease is a rare and benign chronic inflammatory soft

tissue disorder of unknown origin, characterized by a triad of
painless subcutaneous masses in the head or neck region
accompanied by regional lymphadenopathy, blood and tissue
eosinophilia, and markedly elevated serum immunoglobulin E
levels.

Castleman's disease is an uncommon clinicopathological

entity characterized by non-neoplastic lymph node
hypertrophy and histologically characterized by
angiofollicular lymph node hyperplasia. Castleman et al first
described it in 1956 in a group of patients with localized
benign lymphadenopathy

Temperature
Normal body temperature is considered to be 37°C (98.6°F);
however, a wide variation is seen.
Among normal individuals, mean daily temperature can differ
by 0.5°C (0.9°F), and daily variations can be as much as 0.25
to 0.5°C.
The nadir in body temperature usually occurs at about
4 A.M. and the peak at about 6 P.M
Normal rectal temperature is typically 0.27° to 0.38°C (0.5° to
0.7°F) greater than oral temperature. Axillary temperature is
about 0.55°C (1.0°F) less than the oral temperature.
For practical clinical purposes, a patient is considered febrile
or pyrexial if the oral temperature exceeds 37.5°C (99.5°F) or
the rectal temperature exceeds 38°C (100.5°F).
Hyperpyrexia is the term applied to the febrile state when
the temperature exceeds 41.1°C (or 106°F).
Hypothermia is defined by a rectal temperature of 35°C
(95°F) or less.
The oral temperature is measured with the probe placed
under the tongue and the lips closed around the instrument.
The patient should not have recently smoked or ingested
cold or hot food or drink. Three minutes is the time
commonly quoted for accurate temperature measurement,
but it is wise to wait at least 5 minutes.
Rectal thermometers are indicated in children and in patients
who will not or cannot cooperate fully. Rectal temperature is
measured with a lubricated blunt-tipped glass thermometer
inserted 4 to 5 cm into the anal canal at an angle 20° from
the horizontal with the patient lying prone. Three minutes
dwell time is required.
Electric digital thermometers are more convenient than glass
instruments because the probe cover is disposable, response
time is quicker (allowing accurate measurements within 10 to
20 seconds), and there is a signal when the rate of change in
temperature becomes insignificant.
Palpation of the skin in the diagnosis of fever is highly
unreliable.

Blood Pressure
Various devices available for Bp measurements are
1-Mercury column sphygmomanometer
2-Aneroid manometer
3-Electronic semiautomatic devices
4-Automatic devices
4a) Upper arm devises
4b) Finger devices
4c) Wrist devices
5-ABPM-Ambulatory blood pressure measuring devices
6-Central aortic blood pressure measuring devices
According to BHS recommendations standard cuff sizes are as
below
Type of adult Bladder size
Standard cuff for majority of 12x26cm
adults
Large cuff for obese adults 12x40cm
Small cuff for lean adults and 12x18cm
children

Guidelines for cuff size from AHA are different and it depends
on arm circumference.
Type of Adult Arm Circumference Bladder size
Small adult 22-26cm 10x24cm
Average Adult 27-34cm 13x30cm
Large Adult 35-44cm 16x38cm
Adult Thigh Cuff 45-52cm 20x42cm

Palpatory method is ideal to start with followed by

ascultatory .While measuring SBP with palpatory method cuff
is inflated to pressure almost 30mm Hg above the point of
disappearance of radial pulse and then slow deflation of cuff
at 2-3 mm /sec is made to the point of return of radial pulse
which is documented as Systolic blood
pressure(SBP) .Palpatory method of Bp measurement is
important in view of ascultatory gap phenomenon where
phase I Korotkoff’s sounds may sometimes disappear and
reappear later at lower pressure when cuff is deflated further
and hence if ascultatory method is used at first go itself may
lead to false underestimation of SBP. After palpatory method
observer should go ahead with ascultatory method by
inflating cuff 30mm of Hg above SBP reading gained by
palpatory method and slowly deflation at 2-3 mm /sec to be
done so that the level at which first Korotkoff’s sounds are
heard are labeled as SBP and disappearance of Korotkoff’s
sound are labeled as Diastolic blood pressure (DBP). After
DBP reading rapid deflation should be done to avoid
unnecessary venous congestion and tingling sensation to
patient. AHA recommends use of bell of stethoscope for
auscultation of low pitched korotkoff’s sounds but diaphragm
is easier to hold and covers greater area .Try avoiding
touching clothing ,cuff ,tubings as it may give friction sounds .
Korotkoff’s Characteristics of sound
sounds phase
1 faint, repetitive clear tapping sounds
appear
2 short period where sounds soften, in
some patients they may disappear (silent
gap)
3 Sharper sounds are again heard which
may increase in intensity compared to
phase 1
4 Muffling of the sounds start abruptly and
distinctly
5 All sounds disappear

Due to diastolic dilemma of labeling stage 4 Vs stage 5 for

DBP it is recommended to take pressure at level 5 i.e.
disappearance of korotkoff’s sounds as DBP unless
korotkoff’s sounds persists down till 0 when muffling of
sounds at stage 4 can be considered as DBP