The jugular venous pressure (JVP, sometimes referred to as jugular venous pulse) is the indirectly observed pressure over the venous system via visualization of the internal jugular vein. It can be useful in the differentiation of different forms of heart and lung disease.
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The jugular venous pressure (JVP, sometimes referred to as jugular venous pulse) is the indirectly observed pressure over the venous system via visualization of the internal jugular vein. It can be useful in the differentiation of different forms of heart and lung disease.
Kindly leave your comment if you found this helpful ;)
Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
Chronic Stable Angina- Diagnosis & management
By Dr Awadhesh Kumar Sharma
Dr. Awadhesh kumar sharma is a young, diligent and dynamic interventional cardiologist. He did his graduation from GSVM Medical College Kanpur and MD in Internal Medicine from MLB Medical college jhansi. Then he did his superspecilisation degree DM in Cardiology from PGIMER & DR Ram Manoher Lohia Hospital Delhi. He had excellent academic record with Gold medal in MBBS,MD and first class in DM.He was also awarded chief ministers medal in 2009 for his academic excellence by former chief minister of UP Smt Mayawati in 2009.He is also receiver of GEMS international award.He had many national & international publications.He is also in editorial board of international journal- Journal of clinical medicine & research(JCMR).He is also active member of reviewer board of many journals.He is also trainee fellow of American college of cardiology. He is currently working in NABH Approved Gracian Superspeciality Hospital Mohali as Consultant Cardiologist.
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
Chronic Stable Angina- Diagnosis & management
By Dr Awadhesh Kumar Sharma
Dr. Awadhesh kumar sharma is a young, diligent and dynamic interventional cardiologist. He did his graduation from GSVM Medical College Kanpur and MD in Internal Medicine from MLB Medical college jhansi. Then he did his superspecilisation degree DM in Cardiology from PGIMER & DR Ram Manoher Lohia Hospital Delhi. He had excellent academic record with Gold medal in MBBS,MD and first class in DM.He was also awarded chief ministers medal in 2009 for his academic excellence by former chief minister of UP Smt Mayawati in 2009.He is also receiver of GEMS international award.He had many national & international publications.He is also in editorial board of international journal- Journal of clinical medicine & research(JCMR).He is also active member of reviewer board of many journals.He is also trainee fellow of American college of cardiology. He is currently working in NABH Approved Gracian Superspeciality Hospital Mohali as Consultant Cardiologist.
The venous system contains about 70–80% of the circulating blood volume which is non-pulsatile. However, changes in flow and pressure caused by the right atrial and right ventricular filling produce pulsations in the central veins that are transmitted to the peripheral veins (e.g. jugular veins) and are opposite to the direction of the blood flow.
●
The arterial pulse and blood pressure reflects the dynamics of the left side of the heart, while the jugular veins provide the information about the hemodynamic events from the right side of the heart-right atrial pressure during systole and right ventricular filling pressure during diastole.
●
Hence, an accurate assessment of the venous pulse, the jugular venous pulse (JVP) reflects the dynamics of the right side of the heart.1
History ●
Lancis (1728) first described the cervical venous pulse of the external jugular vein in a patient with tricuspid regurgitation (see Table 16.1).
●
However, the classic graphic recordings of the JVP were done by Chauvea and Marey (1863).
●
But it was Potain (1869) who accurately described the wave pattern in the internal jugular vein.
Giant a Waves or Cannon Waves
These occur whenever the RA contracts against the closed TV during RV systole. Paul Wood described the giant a wave as ‘venous Corrigan’. Cannon waves may occur either regularly or irregularly and are most common in the presence of arrhythmias. ●
Regular cannon waves occur in – Junctional rhythm – Ventricular tachycardia (VT) 1:1 retrograde conduction – Isorhythmic AV dissociation
●
Irregular cannon waves occur in – Complete heart block (see Fig. 16.6) – Classic AV dissociation –VT – Ventricular pacing – Ventricular ectopics
This presentation is about normal wave patterns of JVP and their variations. It includes definition, mechanism, abnormalities and clinical significance of jugular venous pressure.
A case of missed diagnosis. Presentation can be in form of heart failure. Differentials can be of Constrictive pericarditis. Restrictive cardiomyopathy/Endomyocardial fibrosis, DCM. This presentation contains clinical presentation, differentials, hemodynamics of cath study, echocardiogrpahy in a case of CP
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
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Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
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2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
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2. Introduction
Oscillating top of the distended proximal portion of the
internal jugular vein (IJV).
Represents volumetric changes that faithfully reflect the
pressure changes in the right side of heart.
Useful in the differentiation of different forms
of heart and lung disease.
Classically three upward deflections and two downward
deflections:
Upward deflections: a, c and v.
Downward deflections: x and y.
3. Pulsations and pressure waves in jugular veins:
Right atrial pressure during systole.
Right ventricular filling pressure during diastole.
Evaluation of JVP offers a window into the right heart, providing
critical information regarding its hemodynamics.
6. Lateral to
carotid artery &
deep to SCM.
External jugular
is superficial to
SCM.
7. Examination of JVP
Done bedside to assess CVP and waveform.
Right IJV – for waveform and estimation of
venous pressure.
Unlike EJV pulsations, it is not possible to see IJV
pulsations directly as it is deep within the neck and
covered by SCM.
Actually seen are the transmitted pulsations to
overlying skin and soft tissues.
8.
9. IJV preferred to EJV
Anatomically, IJVs are closer to RA.
Take a direct course (‘straight line’) to SVC
and RA.
More accurately reflect the dynamics of the
Right Heart.
Transmission of RA pulsations prevented by
prominent valves at the proximal EJV.
Other structures of neck and upper thorax
causes extrinsic compression of EJV.
Sympathetic activity (as in CCF)
vasoconstriction of EJV Pulsations are
barely visible.
10. Right IJV Preferred to Left IJV
Rt. IJV
Straight line course through innominate vein to the SCV
and RA.
Less likely extrinsic compression from other structures
in neck.
Lt. IJV
Left innominate vein may be compressed by dilated
aorta or an aneurysm.
Drains into left innominate vein, which is not in straight
line from SVC and RA.
11. Differences between JVP and Carotid pulsations
JVP Carotid Pulsations
Superficial and lateral in the neck. Deeper and medial in neck.
Better seen than felt. Better felt than seen.
Two peaks and troughs per cardiac
cycle.
Single upstroke.
Descents more prominent than crests. Upstroke brisker and visible than
descent.
x and y more prominent during
inspiration.
No effect.
a and v transiently during
expiration.
No effect.
JVP falls during inspiration. No effect.
Digital compression at the root of neck
abolishes JVP.
No effect.
12. multiphasic - the JVP "beats" twice (in quick
succession) in the cardiac cycle
There are two waves in the JVP for each contraction-
relaxation cycle by the heart.
The first beat represents that atrial contraction
(termed a).
The second beat represents venous filling of the right
atrium against a closed tricuspid valve (termed v).
The carotid artery only has one beat in the cardiac cycle.
13. 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.
14. Level of sternal angle is about 5 cm above the level of
mid right atrium IN ANY POSITION.
Examined in ANY position in which top of the column is
seen easily.
<30⁰ in most normal subjects.
Most patients with heart disease - 45⁰.
In patients with high venous pressure, a greater (60-90⁰)
inclination is required to obtain visible venous
pulsations.
Usually JVP is less than 8 cm water
< 3 cm column above level of sternal angle.
15. Visualization
Patient should lie comfortably.
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, shine a beam of light
tangentially across the skin overlying the IJV to see its
pulsations.
Simultaneous palpations of the left carotid artery or cardiac
ausculation aids in timing of the JVP in cardiac cycle.
16.
17.
18. Measurement of JVP
Commonly used - two scale method.
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 = 7mmHg.
Elevated JVP: >4 cm above sternal angle.
19.
20.
21. JVP waveform
The JVP has a biphasic waveform.
The "a" wave: First positive presystolic wave.
Right Atrial contraction.
Precedes the upstroke of carotid pulse, synchronously with S1,
follows P wave of ECG.
Peak of the 'a' wave demarcates
the end of atrial systole.
Dominant wave in JVP during
inspiration.
Larger than “v” wave.
22. The "x" descent: (Systolic collapse)
Follows the 'a' wave
Corresponds to atrial relaXation and rapid atrial filling due to low
pressure.
Most prominent motion of normal JVP.
Begins during systole and ends just before S2.
Larger than “y” descent.
23. The " x' " (x prime) descent
Follows the 'c' wave
Occurs as a result of the right ventricle pulling the tricuspid
valve downward during ventricular systole.
As stroke volume is ejected, the ventricle takes up less space
in pericardium, allowing relaXed atrium to enlarge.
Can be used as a measure of right ventricle contractility.
The "c" wave
2nd positive venous wave.
Right ventricular (isovolumic) Contraction triCuspid valve to bulge
towards the right atrium.
24. The "v" wave
3rd positive wave.
Begins in late systole and ends in early diastole.
Corresponds to Venous filling when the tricuspid valve is closed and
venous pressure increases from venous return.
Occurs during and following the carotid pulse and peaks after S2.
The "y" descent:
Downslope of v wave.
Decline in RA pressure –
rapid emptYing of the RA into
the RV following the opening of
the tricuspid valve in early diastole.
25.
26.
27.
28. Quantification
A classical method for quantifying the JVP was
described by Borst & Molhuysen in 1952.
It has since been modified in various ways. A venous
arch may be used to measure the JVP more accurately.
Moodley's Sign - Determine which waveform you are
viewing.
Feel the radial pulse while simultaneously watching the
JVP.
Waveform seen immediately after the arterial pulsation
is felt is the 'v wave' of the JVP.
29.
30.
31. a wave abnormalities
Prominent or Large a waves
Increased resistance to RA emptying Increased RA
contraction. (e.g. TS, RA myxomas, Tricuspid atresia).
Increased RVedp RVH Decreased RV
compliance. (e.g. PS, PAH as in MS, Acute PE, RV
infarction.)
32. Giant a Waves or Cannon Waves
RA contracts against closed TV during RV systole.
Paul Wood – Venous Corrigan.
Most prominent during arrhythmias.
Regular seen in:
Junctional rhythm
VT 1:1 retrograde conduction
Irregular seen in:
CHB
Classic AV dissociation
VT
VPCs
33. Absent a Waves
Seen when there is no effective atrial contraction.
AF
Sinus tachycardia – a wave may fuse with preceding v
wave.
34. Abnormalities of x descent
Absent x descent
TR
Blunting of x descent – early sign of TR.
Prominent x descent
Vigorous RV contraction.
Cardiac tamponade.
Constrictive pericarditis.
RV overload – ASD.
35. Abnormalities of v wave
Prominent v wave
Increased RA blood volume during ventricular systole
when normally TV is closed in TR.
It can sometimes cause:
Systolic movement of earlobe.
R L head throbbing with each ventricular systole.
Pistol shots heard over IJV.
Pulsatile exophthalmos.
36. Prominent v wave in absence of TR
Large ASD.
VSD of LV to RA shunt (Gerbode’s defect).
Severe CHF.
AF.
Cor Pulmonale.
37. Prominent a and v wave
Non restricted ASD with normal venous pressure.
CP with increased venous pressure.
38. Abnormalities of y descent
Rapid (Diastolic Collapse) y descent
Elevated venous pressure, myocardial dysfunction or
severe ventricular dilatation.
Severe TR.
CP. (Friedrich’s sign) Usually accompanied by
pericardial knock.
Severe RVF.
ASD with MR.
39. Slow y descent
Impeded RA emptying and RV filling.
TS.
RA myxoma.
Cardiac tamponade (y descent may even be absent).
40.
41. Hepatojugular reflux (HJR)
Rondot (1898) coined the term ‘hepatojugular reflux’.
Useful diagnostic maneuver when –
1. JVP is borderline elevated
2. Latent RVF
3. Silent TR is suspected
42. Maneuver:-
Gently apply firm pressure to the periumblical region
for 10 – 30 sec with patient lying comfortably and
breathing quietly.
JVP is observed.
Pressure shouldn’t applied over the Liver in Rt.
hypochondrium region, as it may be painful in
presence of hepatic congestion.
43.
44. Observations:
Normal subjects:
JV pressure rises transiently (<15 sec.) to <3cm while
abdominal pressure is continued.
Normal RV is able to receive the augmented venous
return to Rt. heart without a rise in mean venous
pressure.
Positive HJR:
Elevated CVP or PAWP.
Acute RVF.
LVF with hypervolemia or fluid overload.
TR
COPD (false positive AJR).
45. Positive Response
A Sustained rise of >3cm in venous pressure for at least
15 sec after resumption of spontaneous respiration is a
positive response.
A positive test result indicates the inability of the right
heart to handle an increased venous return.
46. Mechanism
Displacing splanchnic venous blood towards the heart.
In CCF systemic venous hypertension makes the
venous system inelastic, tight, and non-compliant.
In any such hydraulic system, pressure exerted upon
smaller vessels (e.g. splanchnic) will be transmitted to
larger vessels (e.g. cervical veins).
47. Abdominal compression forces venous blood into
thorax.
A failing/dilated RV is not able to receive venous
return without rise in mean venous pressure.
A challenging alternative view is that in a normal
patient the IVC is a flaccid tube, which is compressed
by abdominal pressure, thereby reducing venous
return to the heart.
48. As with all tests of physical signs there is inevitable
inter-observer variability.
Nonetheless this test – performed correctly – has a
66% sensitivity and up to 100% specificity for
distinguishing tricuspid from mitral incompetence.
It has again a high specificity for diagnosing heart
failure.
49. When done in a standardized fashion, correlates
best with the PAWP.
Reflection of an increased central blood volume.
In the absence of isolated RVF, seen in some
patients with RV infarction, a positive
abdominojugular test suggests a PAWP of
≥15 mm Hg.
51. Kussmaul’s sign and Pulsus Paradoxus
Increase in jugular venous pressure with inspiration is
commonly referred to as Kussmaul’s sign.
Disappearance of the radial pulse or a drop in systolic
blood pressure of 10 mmHg or greater with inspiration
is recognized as pulsus paradoxus.
Both Kussmaul’s sign and pulsus paradoxus are
commonly attributed to the discoveries of Dr. Adolf
Kussmaul.
52. Kussmaul’s sign
Normally, JVP decreases with inspiration.
Kussmaul’s sign – Increase in venous pressure during
inspiration.
53. Inspiration negative intrathoracic pressure
Enhances the pressure gradient between the positive
abdominal pressure and negative intrathoracic
pressure within the thorax and superior vena cavae.
Translocation of blood volume.
Increasing right ventricular pressure and volume, and
decreasing right atrial pressure.
54. Increase in negative
intrathoracic pressure.
Increased pulmonary pooling of
blood volume.
Decreased LA and LV filling from
the pulmonary venous system.
Slight drop in systolic blood
pressure.
55. Pathophysiological mechanisms
Kussmaul’s sign explained by conditions which cause RV
dysfunction, impair RV filling, and raise atrial pressure .
The inability for cardiac chambers to expand due to-
(1) hypoelasticity or inelasticity of the myocardium:
infection and fibrosis (RCM)
2) mechanical compartmentalization by constrictive
pericardial diseases (constrictive pericarditis)
(3) impaired RV function resulting from RVMI, impede
effective RV filling and cause a paradoxical increase in JVP
during inspiration.
57. Thus, Kussmaul’s sign is seen in conditions that
restrict RV filling such as
Constrictive pericarditis
RVF
RVMI
Tricuspid stenosis
Therefore, conditions that raise right atrial and venous
pressure are a prerequisite to cause Kussmaul’s sign.
58. Kussmaul’sign not seen in Cardiac Temponade
Increase in pericardial pressure inward force
compressing the entire heart during inspiration.
Increase in negative intra-thoracic pressure is still able
to be transmitted to the right side of the heart and
subsequent increase in blood flow to the RA ensues.
59. JVP DCM RCM EMF Cardiac
Tamponade
CP
JV pressure May be
elevated
May be
elevated
Usually
elevated
Elevated Elevated
a waves Normal Prominent Prominent Never
prominent
Normal or
may be
prominent
v waves May be
prominent
Normal Prominent
due to TR
Normal Usually
equal to a
waves
x descent Normal Normal Obliterated
with TR
Normal Prominent
y descent May be
rapid
descent
Normal Rapid
descent due
to TR
or absent Rapid
Kussmaul’s
sign
Negative May be
positive
Negative Negative.
May be
positive
Usually
positive
60. JVP Cardiac Tamponade Constricitve Pericarditis
JV pressure Elevated Eleavted
a waves Never prominent. Normal, may be prominent
v waves Normal Usually equal to a waves
x descent Normal Prominent
y descent or absent Rapid
Kussmaul’s sign Negative, may be positive Usually positive
JVP in Pericardial Diseases
61. ASD with R L shunt VSD with R L PDA with R L shunt
JV pressure may be
elevated.
Usually normal. May be elevated.
Normal a waves, but
absent with AF
Normal a waves a waves may be
prominent
Prominent v waves with
CHF or TR
Normal v waves.
CHF and TR rare
Prominent v waves with
CHF or TR
JVP in Eisenmenger complex and syndrome
62. Take message
An accurate assessment of the venous pulse, JVP reflects the dynamics
of the right side of the heart.
Therefore, a careful examination of the neck veins in various
conditions is helpful.