Fig. 2B.25: Examination of height of JVP.
Fig. 2B.26: Image showing engorged neck veins.
Causes of Raised JVP
Engorged (Fig. 2B.26) and pulsatile neck vein Engorged and nonpulsatile neck vein
Cardiac causes Superior mediastinal syndrome
Valsalva maneuver
Chronic constrictive pericarditis (advanced stage) Right heart failure
Congestive cardiac failure
Chronic constrictive pericarditis
Cardiac tamponade
Complete heart block
Restrictive cardiomyopathy
Superior vena cava (SVC) obstruction
Tricuspid stenosis
Noncardiac causes
Pulmonary thromboembolism
Pulmonary hypertension
Acute nephritis
Pregnancy
Fluid overload status
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Waveforms of JVP:
Component Cardiac event responsible
A wave Atrial contraction/systole
X wave (initial x descent) Atrial relaxation
C wave Closure of the tricuspid valve (some consider c wave is due to the impact of carotid pulsation)
X’ wave (X descent following
“C” wave)
Downward movement of the floor of the right atrium while the right ventricle contracts (called
the ‘descent of the base’)
V wave Atrial filling during ventricular systole
Y wave RA emptying during ventricular diastole
H wave (Hirschfelder wave) Seen in diastasis
“a” wave (most prominent of JVP)
Absent Atrial fibrillation
Large/giant “a” wave
Tricuspid stenosis (TS)
Tricuspid atresia (TA)
Right atrium (RA) myxomas
Right ventricular (RV) infarct
RV cardiomyopathy
Pulmonary hypertension (PH)
Pulmonary stenosis (PS)
Pulmonary embolism (PE)
Aortic stenosis (AS)*
Hypertrophic cardiomyopathy (HCM)* (Bernheim effect*)
Cannon “A” waves
Regular Junctional rhythm
Ventricular tachycardia (VT) (1:1 retrograde conduction)
Irregular Complete heart block (CHB)
Atrioventricular (AV) dissociation
Ventricular ectopics
Ventricular tachycardia
V pacing
*Bernheim effect: Left-sided diseases causing prominent a wave, (ie) severe LVH with septal
thickening interfere with RV filling resulting in prominent a wave.
“v” wave
Diminished Cause of diminished v wave is hypovolemia
Prominent Tricuspid regurgitation (TR)*
Atrial septal defect (ASD)
Ventricular septal defect (VSD), Gerbode defect—abnormal shunting between the left ventricle and the right
atrium due to either a congenital defect or prior cardiac insults
Congestive heart failure (CHF)
Atrial fibrillation
Cor pulmonale
*In TR due to absent X and prominent V wave merging with C wave, it results in large positive systolic
and regurgitant waves (CV wave) followed by a rapid deep ‘y’ descent. This may cause subtle motion of
earlobe with each heart beat (The LANCISI’s sign)
Fig. 2B.27: Jugular venous pulse demonstration.
Fig. 2B.28: Jugular venous wave pattern JVP components and waveforms (Fig. 2B.27).
‘X’ descent (systolic collapse)
Absent Tricuspid regurgitation
Prominent Tamponade
Atrial septal defect (ASD)
Pericarditis—constrictive
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‘Y’ descent (diastolic collapse)
Slow descent Tamponade
Tricuspid stenosis (TS)
Right atrial (RA) myxoma
Rapid descent Constrictive pericarditis
Severe tricuspid regurgitation (TR)
Severe right ventricular (RV) failure
Differences between Constrictive Pericarditis and Cardiac Tamponade (Fig. 2B.29)
X wave Y wave
Pericarditis—constrictive + ++ (prominent Y)
Tamponade ++ (prominent X) --
TR -- ++
(Mnemonic: Prominent Y and X waves can be remembered with mnemonic PaY TaX)
Fig. 2B.29: Waveforms of JVP in tamponade versus constrictive pericarditis.
OTHER SITES OF JVP ESTIMATION
Gaertner’s Method
Normally, the superficial veins of dorsum of hand collapse when raised above the sternal angle.
Persistent prominence is suggestive of raised central venous pressure (anthem sign—when the same
is tested by asking the patient to make a fist and raise the arm like an anthem pledge).
May’s Sign
Visible engorged vein on the undersurface of tongue in sitting posture.
ABDOMINOJUGULAR (AJR) REFLUX OF RUNDOTT (PREVIOUSLY KNOWN
AS HEPATOJUGULAR REFLUX)
Demonstration (Fig. 2B.30)
The patient is placed in a 45° semirecumbent position and firm, consistent abdominal pressure 40 mm
Hg is applied, preferably over the right hypochondrium (an inflated BP cuff may be used).
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Historically pressure was applied for 15 seconds; however, recent studies suggest 10 seconds is
adequate
Fig. 2B.30: Demonstration of abdominojugular reflux.
Normal response:
Transient rise of around 4 cm for about 4–5 cardiac cycles (approximately 5 sec)
Sustained response/positive response:
Earliest sign of right heart failure (RHF), also seen in tricuspid regurgitation (TR)
Absent response/negative response:
Obstruction/thrombosis of inferior vena cava (IVC) or hepatic veins as seen in Budd-Chiari
syndrome.
Friederick’s Sign of Constrictive Pericarditis
Friederick’s sign describes a rapid fall and rise in the JVP. It occurs when stiff ventricles are unable to
accommodate the rapid ventricular filling that should follow opening of the tricuspid valve in the
presence of elevated atrial pressure.
Square Root Sign of JVP
Dip and plateau pattern of JVP seen in constrictive pericarditis.
Kussmaul Sign of JVP
Normally when the patient inspires there is fall in the height of JVP due to increased negative
intrathoracic pressure.
Kussmaul sign is the paradoxical elevation of JVP during inspiration.
Seen in:
Constrictive pericarditis
Severe heart failure
Right ventricular infarction
Restrictive cardiomyopathy.
M pattern in JVP
Constrictive pericarditis Due to prominent x and y waves
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ASD Due to prominent A and V waves
Raised jugular venous pressure with shock
Congestive heart failure
Cardiac tamponade
Right ventricular infarction
Tension pneumothorax
Massive pulmonary embolism
BODY TEMPERATURE
Core Body Temperature
It usually refers to the temperature of the internal body core, measured under the tongue, in the ear
canal or in the rectum.
Normal range (oral): 36.8 ± 0.4°C (98.2 ± 0.7°F)
Regulation of temperature: Under the control of neurons of preoptic anterior hypothalamus and
posterior hypothalamus.
Site of Examination of Temperature
Oral temperature Probe placed under the tongue into the sublingual pockets and the lips closed around the
instrument
The patient should not have recently smoked or ingested cold or hot food or drink
Usually tested for about 3 minutes
Oral temperature reflects changes in core body temperature through the branch of the external
carotid artery which perfuses the posterior sublingual pockets
Rectal readings are 0.4–0.6°C
higher than oral recordings
Measured with a lubricated blunt-tipped glass thermometer inserted 4– 5 cm (2.5 cm in
children) into the anal canal at an angle 20° from the horizontal with the patient lying prone
Usually tested for about 3 minute
Lags behind changes at other core sites as it is located far from the central nervous system
as well as from the pulmonary artery
Indicates the deep visceral temperature. Can be affected by the temperature of the skin of the
buttocks, the iliac artery and iliac vein
Tympanic temperature The scanning tip should be gently placed in the ear canal and then slowly inserted against
the tympanic membrane snugly
Measures the infrared heat waves from the tympanic membrane
Close to hypothalamus and rapid measurement of core body temperature
Axillary readings lag behind
oral temperature by 0.1–0.2°C
Thermometer placed in the axilla and shoulder adducted
Convenient for patient
Core temperature cannot be assessed directly
Lags behind the changes in core body temperature
Temporal (forehead) measurement
Placed on the skin of the forehead
An electronic thermometer that is fast and accurate
Less invasive than the tympanic thermometer and more reliable when used correctly
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Thermometers (Fig. 2B.31)
Glass thermometer and electric digital thermometer
Glass thermometer bulbs contain an alloy called galinstan.
Electric digital thermometers are more convenient than glass instruments because the probe cover is
disposable, response time is quicker (allowing accurate measurements within 10–20 seconds), and
there is a signal when the rate of change in temperature becomes insignificant.
The most common methods of temperature assessment that carry the least amount of risk for patient
injury are the use of glass or electronic digital thermometers to measure oral, rectal, axillary, or vaginal
temperatures; basal thermometers; temporal artery thermometers; tympanic thermometers; and liquid
crystal forehead temperature strips. These methods can be utilized in healthcare settings and also
within the patient’s home.
Although the more invasive methods are more accurate, they carry a higher risk of potential
complications, so they are not routinely utilized in areas outside of a critical care or surgical setting.
Examples of invasive methods of temperature assessment are esophageal and rectal temperature
probes, temperature-sensing indwelling urinary catheters, temperature-sensing pulmonary artery (PA)
catheters, a cardiopulmonary bypass (CPB) machine, and extracorporeal membrane oxygenation
(ECMO).
Fig. 2B.31: Thermometer showing marking in both Celsius and Fahrenheit.
Circadian Variation of Temperature
Circadian rhythm is governed by suprachiasmatic nuclei in anterior hypothalamus.
Normal variation is 0.5–1.0°C over the day
Lowest temperature is noted at 6:00 am and peaks at 4:00–6:00 pm.
Variation of Temperature during Menstrual Cycles
An abrupt increase of 0.3–0.5 °C accompanies ovulation and may be useful as a fertility guide.
Fever
Fever is an elevation of body temperature that exceeds the normal daily variation and occurs in
conjunction with an increase in the hypothalamic set point.
It can be defined as temperature of >37.2°C (98.9°F) at 6 am or >37.7°C (99.9°F) at 4–6 pm. When the hypothalamic set point is raised, the body is perceived to be cooler than the new set point.
Shivering is initiated to generate heat. Blood is shunted from the periphery to the core to conserve heat
and sweating is diminished. The generated heat will raise the body temperature to match the elevated
set point. When the hypothalamic set point is lowered, either as part of the normal diurnal fluctuations
that occur during an infection or in response to antipyretic agents, heat is lost by evaporation (sweating)
and radiation (cutaneous vasodilation).
Types of fever based on duration
Acute fevers <7 days Infectious diseases such as malaria and viral-related upper respiratory tract
infections
Subacute
fevers
Usually not more than
2 weeks in duration
Typhoid fever and intra-abdominal abscess
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2.
Chronic or
persistent
fevers
>2 weeks duration Chronic bacterial infections such as tuberculosis, viral infections like human
immunodeficiency virus (HIV), cancers and connective tissue diseases
Grading of Fever based on Body Temperature
Body temperature °C °F
Normal 37–38 98.6–100.4
Mild/low grade fever 38.1–39 100.5–102.2
Moderate grade fever 39.1–40 102.2–104.0
High grade fever 40.1–41.1 104.1–106.0
Hyperpyrexia >41.1 >106.0
The conversion formula is:
T°F = 9/5 (T°C) + 32
T°C = 5/9 (T°F) – 32
Patterns of fever (Fig. 2B.32)
Type of
fever
Description Seen in
Continuous
or
sustained
fever
Defined as fever that does not fluctuate more than about
1°C (1.5°F) during 24 hours, but does not touch the
baseline
Lobar and gram-negative pneumonia, typhoid, and
acute bacterial meningitis
Remittent
fever
Defined as fever with daily fluctuations exceeding 2°C
but does not touch the baseline
Remittent fevers are often associated with infectious
diseases such as infective endocarditis, rickettsia
infections, and brucellosis
Intermittent
fever
Defined as fever present only for several hours during
the day
Malaria, pyogenic infections, tuberculosis (TB),
schistosomiasis, lymphomas, leptospira, Borrelia, Kalaazar, or septicemia
Double quotidian fever (12 hours periodicity) Kala-azar, gonococcal endocarditis. Adult-onset Still’s
disease
Quotidian fever (periodicity of 24 hours) Mixed falciparum and vivax
Tertian fever (periodicity of 48 hours) Plasmodium falciparum, ovale and vivax
Quartan fever (periodicity of 72 hours) Plasmodium malariae
Pel-Ebstein’s fever (intermittent low-grade fever
characterized by 3–10 days of fever with subsequent
afebrile periods of 3–10 days)
It is thought to be a typical but rare manifestation of
Hodgkin’s lymphoma
Relapsing
fevers
Refer to those that are recurring and separated by
periods with low-grade fever or no fever
Seen in malaria, lymphoma, Borrelia, cyclic
neutropenia, and rat-bite fever
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Fig. 2B.32: Clinical pattern of fevers.
Fever with Night Sweats
It has been described in infectious diseases such as TB, Nocardia, brucellosis, liver or lung abscess,
and subacute infective endocarditis, as well as in noninfectious diseases such as polyarteritis nodosa
and cancers such as lymphomas.
Fever with Bradycardia
It is a feature of untreated typhoid, leishmaniasis, brucellosis, Legionnaire’s disease and psittacosis, and
yellow fever.
Fever with Unknown Origin
In 1961, pyrexia of unknown origin (PUO) was originally defined by Petersdorf and Beeson as an illness
of more than 3 weeks duration, fever higher than 38.3°C (101°F) on several occasions and diagnosis
uncertain after 1 week of study in hospital.
This definition has been modified, removing the requirement that the evaluation must take place in
the hospital and refined to include four different subgroups, each requiring different investigative
strategies: classical, nosocomial, neutropenic, and human immunodeficiency virus (HIV)-related.
Hyperpyrexia
(Body temperature >105°F)
Causes Include:
Pontine hemorrhage
Rheumatic fever
Meningococcal meningitis
Cerebral malaria
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