Comprehensive presentation on intra arterial blood pressure with a good insight into the the basic physics and brief look into the risks and complications.
The CVP catheter is an important tool used to assess right ventricular function and systemic fluid status. Normal CVP is 2-6 mm Hg. CVP is elevated by : overhydration which increases venous return.
Comprehensive presentation on intra arterial blood pressure with a good insight into the the basic physics and brief look into the risks and complications.
The CVP catheter is an important tool used to assess right ventricular function and systemic fluid status. Normal CVP is 2-6 mm Hg. CVP is elevated by : overhydration which increases venous return.
Hemodynamic monitoring- Hemodynamic monitoring refers to the measurement of pressure, flow and oxygenation within the cardiovascular system. Hemodynamic monitoring is amandatory process in all the critical care units to assess the patients progress. This presentation is aimed to create an insight on Hemodynamic monitoring.
central venous pressure and intra-arterial blood pressure monitoring. invasiv...prateek gupta
central venous pressure and intra-arterial blood pressure monitoring. various sites for cvp and Ibp insertion. working principle for cvp and ibp. indication and complication. various waveform of cvp and ibp
Hemodynamic monitoring- Hemodynamic monitoring refers to the measurement of pressure, flow and oxygenation within the cardiovascular system. Hemodynamic monitoring is amandatory process in all the critical care units to assess the patients progress. This presentation is aimed to create an insight on Hemodynamic monitoring.
central venous pressure and intra-arterial blood pressure monitoring. invasiv...prateek gupta
central venous pressure and intra-arterial blood pressure monitoring. various sites for cvp and Ibp insertion. working principle for cvp and ibp. indication and complication. various waveform of cvp and ibp
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
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.
Acyanotic Congenital Heart Diseases;
1. Left-to-right shunts
a. Ventricular Septal Defect(VSD)
b. Atrial Septal Defect(ASD)
c. Patent Ductus Arteriosus(PDA)
d. Atrioventricular Septal Defect(AVSD)
e. Aortopulmonary window
* Eisenmenger Syndrome – The shunt becomes right-to-left
2. Left-sided obstructive lesions
a. Coarctation of the Aorta(COA)
b. Congenital Aortic Stenosis
c. Mitral Stenosis
d. Interrupted Aortic Arch
Cyanotic Congenital Heart Diseases;
1. Right-to-left shunts
a. Tetralogy of Fallot
b. Pulmonary stenosis
c. Pulmonary atresia
d. Tricuspid atresia
e. Ebstein’s anomaly
2. Complete mixed lesions
a. Transposition of the great vessels
b. Double outlet right ventricle(DORV)
c. Total anomalous pulmonary venous return
d. Truncus arteriosus
e. Hypoplastic left heart syndrome
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
1. Central Line
Interpretation of waveform & Clinical
application in Cardiac Surgeries and ICU
Dr. Harshil Joshi DM
Chief - Cardiac Anesthesia
Century Super speciality Hospital
Prerna Anesthesia &Critical Care Services
01/02/2018
2. What is CVP
• The central venous pressure (CVP) is the pressure measured in the
central veins close to the heart.
• It is the pressure measured at the junction of the superior vena cava
and the right atrium. And No valve in between.
• It indicates mean right atrial pressure and is frequently used as an
estimate of right ventricular preload.
01/02/2018
3. • It reflects the driving force for filling of the right atrium & ventricle
• It indicates the relationship of blood volume to the capacity of the
venous system.
01/02/2018
4. Indication
• Major operative procedures involving large fluid shifts or blood loss
• Intravascular volume assessment when urine output is not reliable or unavailable
• Temporary Hemodialysis
• Surgical procedures with a high risk for air embolism, CVP catheter may be used to aspirate
intracardiac air
• Frequent venous blood sampling, Inadequate peripheral intravenous access
• Temporary pacing
• Venous access for vasoactive or irritating drugs & Chronic drug administration
• Rapid infusion of intravenous fluids (using large cannulae)
• Total parenteral nutrition
01/02/2018
5. Common Insertion Site
• Internal Jugular
• Subclavian
• Femoral
• External Jugular
• Basilic
• Axillary
01/02/2018
6. Right IJV is Preferred
• Consistent, predictable anatomy
• Alignment with RA
• Palpable landmark and high success rate
• No thoracic duct injury
01/02/2018
7. Complication
Complications of Central Venous
Access and Cannulation
• Arterial puncture with hematoma
• Arteriovenous fistula
• Hemothorax, Chylothorax or Pneumothorax
• Nerve injury
• Air embolus
• Catheter or wire shearing
• Right atrial or right ventricular perforation
Complications of Catheter
Presence
• Thrombosis, thromboembolism
• Infection, sepsis, endocarditis
• Arrhythmias
• Hydrothorax
01/02/2018
8. Factors Affecting CVP
• Cardiac Function
• Blood Volume
• Capacitance of vessel
• Intrathoracic & Intraperitoneal pressure
01/02/2018
9. Interpretation from Numbers
• CVP is recorded in centimetres of water (cm H2O) or millimetres of
mercury (mm Hg) read from manometer markings.
• Normal CVP ranges from 5 to 10 cm H2O or 2 to 6 mm Hg.
• Single value has no value. Trend is important.
• CVP is surrogate marker.
01/02/2018
10. Series Circulation
• Right Atrium Right Ventricle Pulmonary Circulation
TV PV
Left Ventricle Left Atrium
MV
01/02/2018
12. Physiology…
• It would be ideal to monitor cardiac chamber volumes continuously in
critically ill patients, this goal remains elusive in clinical practice.
• The relationship between ventricular volume and filling pressure
depends on the portion of the pressure-volume curve over which the
patient's heart is operating and the shape or slope of the curve.
Commonly termed ventricular compliance
01/02/2018
13. Transmural Pressure
• The cardiac chambers are all contained within the pericardium and
thorax. Changes in pressure in the structures surrounding the heart
will influence pressures recorded within the heart.
• Transmural pressure is the difference between chamber pressure and
juxtacardiac or pericardial pressure.
01/02/2018
14. Measurement
• The phlebostatic axis is the reference point for zeroing the
hemodynamic monitoring device.
• 4th intercostal space, mid-axillary line
• 1 mmHg = 1.36 cm H2O.
• the first step in pressure transducer setup is to zero the transducer by
exposing it to atmospheric pressure
• Thus, a cardiac filling pressure of 10 mm Hg is 10 mm Hg higher than
ambient atmospheric pressure.
01/02/2018
15. Respiratory Effect
A, During spontaneous ventilation, the onset of
inspiration (arrows) causes a reduction in
intrathoracic pressure, which is transmitted to
both the CVP and pulmonary artery pressure
(PAP) waveforms. CVP should be recorded at
end-expiration.
B, During positive-pressure ventilation, the
onset of inspiration (arrows) causes an increase
in intrathoracic pressure. CVP is still recorded at
end-expiration.
01/02/2018
16. • Kussmaul sign is a paradoxical rise in jugular venous pressure (JVP) on
inspiration, or a failure in the appropriate fall of the JVP with
inspiration. It can be seen in some forms of heart disease and is
usually indicative of limited right ventricular filling due to right heart
dysfunction.
• Hepatojugular Reflex: A positive result is variously defined as either a
sustained rise in the JVP of at least 3 cm or more or a fall of 4 cm or
more after the examiner releases pressure.
01/02/2018
18. • Fluid Responsiveness: inspiratory fall of CVP > 1 mmHg is high
predictive of fluid responders
• Keeping CVP > 5 mmHg in renal transplant surgery is associated with
good graft function In first 3 post op days
• Post cardiac surgery CVP > 15 mmHg is associated with poor outcome
01/02/2018
19. • Decrease in CVP is relatively late sign of depletion of intravascular
volume
• CVP is better measurement of volume status in anesthetised patient
whose autonomic reflexes are abolished
• Goal directed fluid therapy has not shown good results in critically ill
patients.
• Increasing availability of non-invasive and apparently better
measurement of preload and circulatory filling will decrease
dependence on CVP.
01/02/2018
22. • Role of CVP monitoring for stabilizing critically ill patient in ICU will be
secondary… because we put central line not to monitor cvp but for
other reasons.
• So monitoring CVP become risk free.
01/02/2018
23. Interpretation from Waveform
The CVP waveform consists of five phasic events,
three peaks (a, c, v) and two descents (x, y)
01/02/2018
24. Mechanical Events
Waveform Component Phase of Cardiac Cycle Mechanical Events
‘a’ wave End Diastole Atrial Contraction(after P wave)
‘c’ wave Early Systole Isovolumic right ventricle
contraction, TV bow in RA(after
QRS)
‘x’ descent Mid Systole Atrial Relaxation, Descent of RV
base(TV annulus)
‘v’ wave Late Systole Filing of RA with venous blood(just
after T wave)
‘y’ descent Early Diastole Early ventricular filling, opening of
TV
‘h’ wave Mid to Late Diastole Diastole plateau
01/02/2018
25. ‘a’ wave
• Atrial Contraction(after P wave)
• End Diastole
• Prominent a wave: resistance in RV filling- RVH, TS, Temponade,
PS, Pulmonary hypertension
• Absent a wave: Atrial fibrillation or
• flutter
Cannon A waves occur as the RA
contracts against a closed TV: junctional
rhythm, CHB,ventricular arrhythmias
01/02/2018
26. ‘c’ wave
• Isovolumic right ventricle contraction, TV bow in RA(after QRS)
• Early Systole
• TR: Tall Systolic c-v wave
• It is call holosystolic cannon v waves
01/02/2018
27. ‘x’ descent
• Atrial Relaxation, Descent of RV base(TV annulus)
• Mid Systole
• Dominant x descent –good RV function and vice versa
• Cardiac Tamponade-
• X descent is steep & Y descent is diminished
• Early diastolic runoff is impaired by the pericardial fluid collection.
01/02/2018
28. ‘v’ wave
• Filing of RA with venous blood(just after T wave)
• Late Systole
• Prominent v wave with increase venous return. ASD, PAPVC or TAPVC,
A-V malformation
• Large V waves may also appear later in systole if the ventricle becomes
noncompliant because of ischemia or RV failure.
• Decrease in RA emptying. TS
01/02/2018
29. ‘y’ descent
• Early ventricular filling, opening of TV
• Early Diastole
• Attentuation of y descent: TS, Tachycardia, RVF, Tamponade,PS
01/02/2018
30. Constrictive Pericarditis
• This causes prominent A and V waves and steep X and Y descents
(creating an M configuration) like decreased RV compliance.
• Blood from the RA to the right ventricle is initially rapid during
early diastolic filling of the right ventricle (creating a steep Y
descent) but is short-lived and abruptly halted by the restrictive,
noncompliant right ventricle.
• The right atrial pressure then increases rapidly and reaches a
plateau until the end of the A wave, at the end of diastole.
• This portion of the waveform is analogous to the ventricular
diastolic dip-and-plateau sign.
01/02/2018
31. Heart Block
• two-to-one heart block is recognized by A waves, that occur with
twice the frequency of the artery pulse.
• PR interval prolongation is recognized by an increase in the interval
between the jugular A wave and the arterial pulse
01/02/2018
32. LVH(AS,Coarctation,LVOTO)
• Directing attention to the amplitude of the jugular venous A wave in
subjects with isolated obstruction to left ventricular outflow is
seemingly paradoxical.
• However, left ventricular hypertrophy serves to decrease right
ventricular distensibility, so the right atrium contracts with greater
force and the amplitude of the jugular venous A wave increases in the
absence of pulmonary hypertension
01/02/2018
33. Pulmonary Stenosis
• The jugular venous A wave is distinctive and increases progressively as
the stenosis increases, culminating in a giant A wave.
• Attenuates y descent
• Powerful right atrial contraction generates a giant A wave via the
superior vena cava and a presystolic liver pulse via the inferior cava.
• With the advent of right ventricular failure and tricuspid regurgitation,
the large A wave is accompanied by an increase in the V wave.
01/02/2018
34. Ebstein’s Anomaly
• Prominent C wave that coincides with mobility of the anterior tricuspid leaflet.
• The interval between the jugular A wave and the carotid pulse is often prolonged,
reflecting prolongation of the PR interval.
• Prominent A waves are seldom seen in the jugular pulse.
• A stenotic or imperforate tricuspid orifice is accompanied by A waves that may be giant.
• An attenuated X descent and a systolic venous V wave of tricuspid regurgitation seldom
appear in the jugular pulse despite severe regurgitant flow because of the damping effect
of the commodious right atrium and the thin-walled toneless atrialized right ventricle and
because tricuspid regurgitation is low-pressure and hypokinetic.
01/02/2018
35. ASD
• Most important is left atrialization of the jugular venous wave form.
• The crests of the A and V waves tend to be equal as they are in the left
atrium because the two atria are in common communication through
a nonrestrictive atrial septal defect.
• The A wave amplitude varies with heart rate and compliance of
ventricle as in healthy subjects.
• Pulmonary vascular disease results in an increased force of right atrial
contraction and a dominant, if not giant, A wave
01/02/2018
36. Lutembacher’s syndrome
• The right and left atrium function as a common chamber when the
atrial septal defect is nonrestrictive, so the height and contour of the
left atrial pressure pulse are transmitted into the right atrium and into
the internal jugular vein.
• Elevated mean jugular venous pressure in the absence of right
ventricular failure and for an elevated jugular venous A wave in the
absence of pulmonary hypertension.
• Post ASD closure-- Don’t Target CVP
01/02/2018
37. AVCD
• The V wave is dominant in the jugular venous pulse because the right
atrium receives left ventricular systolic flow across an incompetent left
AV valve directly through the atrioventricular septal defect or indirectly
through an ostium primum atrial septal
01/02/2018
38. VSD
• Moderately restrictive and nonrestrictive ventricular septal defects
with congestive heart failure are accompanied by an elevated mean
jugular venous pressure and an increase in A and V waves.
• However, the jugular venous pulse in Eisenmenger’s syndrome(PDA,
AP window) is normal or nearly so, with a small dominant A wave
01/02/2018
39. TOF
• Normal- RV will offload in to LV
• Restrictive VSD - RV pressure will increase more then systemic: large a
wave in CVP
• Absent PV: initially large a wave, and after development of TR large v
wave
01/02/2018
40. Univentricular physiology
• The right atrial A wave, V wave, and mean pressure are elevated
• Post BDG: IJV attached to PA and IVC attached to RA which is affected
by common ventricle pressure.
• Post Fontan: no longer CVP, only PA pressure.
01/02/2018
41. Case Scenario 1
• Post OP CABG, extubated
• Breathlessness, hypotension, tachycardia
• BP responding to fluid bolus
• Drain- 400 ml
• Lungs – clear
• Swing in arterial trace
• Prominent x descent
01/02/2018
42. Case Scenario 2
• Post MVR, Female patient
• Breathlessness, hypotension, tachycardia
• Bilateral crepitation
• A wave disappear
• C wave more prominent
01/02/2018
43. Case Scenario 3
• Young male patient with weakness, jaundice, fatigue and dependant
odema
• Systolic thrill and murmur in neck
• Tender hepatomegaly
• Prominet c & v wave
01/02/2018
44. Summary
• Individual CVP waveforms provide unique diagnostic clues about the
circulation.
• Trends in CVP over time may also be useful in estimating fluid or
blood loss and guiding replacement therapy.
• It is important to remember that there is a significant range of normal
values and that a small change in CVP may reflect a significant
alteration in circulating blood volume and right ventricular preload.
• Additional useful information may be derived from examining how a
fluid bolus simultaneously alters CVP and other variables of clinical
interest, such as blood pressure, urine output, and so forth.
01/02/2018