This document discusses various hemodynamic parameters and waveforms seen in different cardiac conditions:
- It compares pressures, waveforms and compliance in conditions like constrictive pericarditis, right ventricular failure, cardiac tamponade and pulmonary hypertension.
- Key waveforms and pressures are described for valvular lesions like mitral stenosis, aortic stenosis, mitral regurgitation and aortic regurgitation.
- Equations for calculating cardiac output, shunt fractions and valvular areas are provided.
- Diagnostic criteria for pseudosevere versus true severe aortic stenosis on stress echocardiography are outlined.
- A case example is presented of a patient evaluated for pulmonary
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
Our concepts of heart disease are based on the enormous reservoir of physiologic and anatomic knowledge derived from the past 70 years' of experience in the cardiac catheterization laboratory.
As Andre Cournand remarked in his Nobel lecture of December 11, 1956, the cardiac catheter was the key in the lock.
By turning this key, Cournand and his colleagues led us into a new era in the understanding of normal and disordered cardiac function in huma
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
Our concepts of heart disease are based on the enormous reservoir of physiologic and anatomic knowledge derived from the past 70 years' of experience in the cardiac catheterization laboratory.
As Andre Cournand remarked in his Nobel lecture of December 11, 1956, the cardiac catheter was the key in the lock.
By turning this key, Cournand and his colleagues led us into a new era in the understanding of normal and disordered cardiac function in huma
Hemodynamics in echo lab by Dr. Ranjeet S.PalkarRanjeet Palkar
ECHO LAB AND CARDIOVASCULAR HEAMODYNAMICS. A simple cost effective,non invasive approach which when used appropriately can be boon for physicians and cardiologists in diagnosis and prognostication.
Guytonian approach to shock - mean systemic filling pressure centeredCosmin Balan
In a world of binary decision there remains little room for applied maths and physiology. Or maybe not...
Parkin's approach brings out a forgotten tool-the volume state. Although reductionistic as well as Guyton's entire view, it might be a better language for us, for clinicians and for all those lost in translation when they've stumbled across loose binary decisions such as SVV,PPV,SPV etc.
Mean systemic filling pressure has been resurrected.
Parkin, Maas, Pinsky and Geerts have come a long way from Versprille.
Paradigms have been shifting.
Flow-centered ideas, ventriculo-arterial coupling and redistributions between compartments with different time constants.
A lecture highlighting the role of Echocardiography as a major hemodynamic monitoring tool in the Intensive Care settings and the assessment of loading conditions.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
9. PA systolic pressure = RV systolic pressure
mean PCWP = PA diastolic pressure (+5)
Mean PCWP = LVEDP
RVEDP = RA pressure
PCWP>RA pressure
LVEDP>RVEDP
Pressure
equalize in
CP, RVF, RCMP9
Atrial Ventricular Arterial
10. TP
V A
Two peaks/ QRS
v=T; a=P
PCWP: v>a; CVP: a>v (ASD a=v)
rises in diastole
falls in systole
end expiration (on ventillation: substract half of PEEP) 10
12. 12
LA
LV
RA
RV
PA
TR: ventricularization
RAP = RVEDP
13. 13
LA
LV
RA
RV
PA
MR: tall v
Severe PAH mPCWP = dPAP
14. Tall V
V>mean PCWP+10
decompensated LVF
Severe MR (early diastole slow downslope)
Severe MS (early diastole sharp downslope)
A=P, V=T (PA peaks before T)
V-V horizontal (downsloping)
No dicrotic notch
PV sat >95%, PA sat 75%
Mean PCWP = diast PA pr (+5) < PASP
PC-PA hybrid pressure
14
16. LVEDP
A bump
Diastolic slope
LVEDP normal/ low in MS
LVEDP high in CP, AR, LVDD
Absent A bump in MS, AF
Prominent in HOCM, LVDD
LVEDP = mPCWP
Except
1. MS
2. MR
3. PAH
16
Flat slope in chronic ARSharp slope in acute AR
17. LA 95% RA 75%
LV 95% RV 75%
AO 95% PA 75%
SVO2/ MVO2
SVC 74%
SCVO2
IVC 78%
PV 98%
Normal: SVO2> SCVO2
In shock relation reverses
MVO2 sat< 65%
Low CO 17
18. Chambers Step up D/D
SVC/IVC to RA >= 7% OS ASD, TAPVC, RSOV, CMF to RA
RA to RV >= 5% VSD, OP ASD, CMF to RV
RV to PA >= 5% PDA, APW
SVC to PA >= 8% L-R shunt
RA to PA >= 6% L-R shunt
PV to arterial SO2 >5% R-L shunt
MVO2
= O2 saturation in chamber proximal to shunt
= ASD: 3SVC+1IVC/4 (=SVC O2)
= VSD: RA SO2
= PDA: RV SO2
18
20. Fick
Gold standard
True Fick
O2 challenge
Not accurate in
- Low output state
- Shunt
- Regurgitation lesion
Thermodilution
SV = CO/ HR CI = CO/ BSA SVI = SV/ BSA = CI/ HR 20
21. SVR
N: 0.5-1 woods unit
High in PAH
- <3: passive PAH
- 3-5: mixed PAH
- >5: reactive PAH
• In shunt: Qp
PVR
MAP = 1SBP+2DBP/3
N: <700 dyn cm /sec5
Low SVR in septic shock
High SVR in ionotrps
W (mmHg/ L/min) = 80 dyn cm /sec5 21
26. MVA in MS
AF: 10 sec…X6 (avg over 10 beats)
Hakki area = CO/√PG
Mean grad in MS, peak instantaneous grad in AS
not validated for tachycardia or bradycardia
AVA in AS
Peak to
peak PG
= mean PG
mean PG
= 70% of Peak
instantaneous
PG
26
Area α Q
Gradient α Q2
A = Q/ √PG
Area α 1/ √PG
28. AS HOCM
Always rule out error in zeroing
Peripheral artery
-Pressure elevated
-No dicrotic notch
- delayed
28
29. Vena Contracta
(Ao pr lesser)
Aortic root<3cm
Pressure reco ery
Echo gradient
Higher
AVA less
In aortic root<3cm
catheter gradient accurate
Downstream to valve
(Ao pr higher)
HTN, LVDD
catheter gradient
Lower
AVA high
HTN, LVDD
Echo gradient accurate
29
Area
= Q/ √PG
LV load
SBP+PG/ SVI
= SBP+PG/ CI (ml) X HR
(> 4.5 abnormal)
30. 30
EF 55% CO4 CI 2 HR 80 SBP 178 mPG22
EF 55% CO4 CI 2 HR 80 SBP 138 mPG42
total LV load 8
total LV load 4.51 week
True severe AS
32. 32
Gradient α Q2
EF <40%EF >40%
low volume status
RAP, LVEDP low
fluid load - gradient rises
uncontrolled HTN
total LV load>4.5
control HTN- gradient rises
severe MS or MR
low forward flow
PCWP>15
Pseudosevere AS
True severe AS
DCM+ AS
Dobutamine
stress test
fluid load
RAP, LVEDP low
33. 33
True severe
AS
Pseudosevere
AS
DCM+AS
SV increase >20% >20% <20%
PG increase >50% (>40) <50% (<40) <50% (<40)
AVA increase <0.3 (<1.2) >0.3 (>1.2) >0.3 (>1.2)
PG ++++
Area +
PG +
Area ++++
True
severe AS
Pseudo
severe AS
43. Acute AR Chronic
compensated AR
Chronic
decompensated AR
LV vol Normal Increased Increased
EF (SV) Normal Very high Falls
LVEDP Steep Rise Normal to high Flat rise
LV-LA gradient
(end of diastole)
Present
(Austin Flint murmer)
No No
Pulse pressure Normal Wide Wide
Q = 2 X CO (severe AR)
Area= Q/ √PG= 2CO/ √PG
Otherwise Gorlin AVA falsely low
43
Severe AR
- L/O dicrotic notch
- LVEDP = DBP
- Q = 2CO
- LVEDP elevated
- Flat rise of LVEDP
44. 44
EF 15%
LVEDD 75
CO 3.6
mPG 31
AVA 0.65
Area
= Q/ √PG
= 2CO/ √PG
= 1.3 cm2
chronic severe decompensated AR
L/O dicrotic notch
45. 45
Acute severe AR
chronic compensated AR
chronic decompensated AR
46. -Severe PAH
- large V wave
-High PCWP (>25)
- mitral prosthesis
Mild MS + Stress test (2/3)
- Gradient >15
- mPAP>60
- PCWP>25
Low PG
Low MVA
High PG
High MVA
MVA = 220/ PHT
-Impaired LV compliance
- severe AR
High gradient
Low MVA
46
50. Acute MR Chronic
compensated MR
Chronic decompensated
MR
v 3 x mPCWP Normal High
PCWP High Normal High (>10 + mean PCWP)
LV vol Normal High High
EF High High Lower
50
Q = 2 X CO (severe MR)
Q = 1.5 X CO (moderate MR)
Gorlin MVA false low
53. Chamber pressures are high & equalises in early diastole
M or W pattern RA pr = mPCWP LVEDP = RVEDP
Square root
(dip & plateu)
D/D
RVF
RCMP
RVEDP > LVEDP +5
PA pressure high
Better seen
in volume loading 53
54. Ventricular interdependance
Discordant systolic peak
CP
Concordant systolic peak
RCMP , RVF
Better seen in low
volume status
Also in COPD
RVEDP rises in inspiration
but not >LVEDP
RVEDP rises in inspiration
>LVEDP
54
55. Dissociation of intracardiac / intrathorasic pressure
>5
RAP does not decrease in
inspiration (kussmaul’s sign)
D/D COPD
Inspiration
Lack of transmission of
-ve intrathorasic pressure to LV
RV is sucked by LV
55
58. Tamponade Constriction
Early diastole
Later part of diastole
Compressed
Compressed (no Y)
Expands
Constrained (y)
Elevation & equalization of pressure + +
Dissociation of
intracardiac / intrathorasic pressure
- +
RAP Deep x flat y Deep x deep y
Early diastolic dip Abesnt Present
RAP decreases in inspiration Yes No
Kussmaul’s sign in JVP - +
Ventricular interdependance + (RV pushes LV) + (RV sucked by LV)
CO Low Maintained
Pulsus paradoxus
(Inspiratory decrease of SBP> 10 mmHg)
Present Absent usually
58
Pulsus paradoxus absent in
1. ASD
2. AR
59. Post capillary Pre capillary
Prevalence Common Less common
Mechanism Passive Reactive
Causes Mitral valve disease
LVF
Vascular dis (ASD, SSC)
Chr thromboembolism
Lung disease
Eisenmengers
PCWP >15 <15 (may be high)
Diast PA pr <5+ PCWP >5+ PCWP
PVR <3 >5
Transpulmonary gradient <12 >12
Chronic PAH
-PAP may be normal
-PVR>5
- >50 mmHg
59
Rule out shunt
Vasoreactivity
61. Positive when
- mean PAP drops by >10 (to a value<40)
- PVR drops by >20% (to a value <5)
- PCWP <15
-Role of CCB
- safety of CCB
- long term prognosis
- shunt reversibility
61
62. 62
CO 4
CI 1.9
mPCWP= 15
PVR = 55 – 15/ 4 = 10
mPAP – PCWP = 40
dPAP> mPCWP+5
SVC/IVC/PA 58/62/58 (5%): no o2 step up: no L-R shunt
Vasoreactivity test negative
63. Pulmonary embolism Cardiac tamponade
CVP High (>PCWP) High (=PCWP)
PAP High N
<700
Fluid response: leg rising
-CO increase by >10%
- IVC diameter >12mm
- pulse pressure >9%
Fluid challenge
Risky if PCWP>15
63
Mean BP<80
Dicrotic pulse
high PCWP (A)
High RAP
SVR >700
CI<2.2
PA sat <65%
SVO2< SCVO2
Septic
64. 64
CO 8; CI 3.3
PA o2sat 53%
SPO2 93%
Hb 11
High filling pressure
Dicrotic pulse
Normal CI
Low SVR
SVO2 53%
SVC SO2 63%
Cardiogenic shock on ionotrops
Septic shock
65. Normal and abnormals
Traces & relations
Shunt / o2 challenge/ resistance
Grdaient –area mismatch of severe AS
AS/ HOCM/ CoA
Severe MS/ stress test
Compensated/ decompensated AR/MR
RVF/ LVF
Contriction/ RVF/ tamponade
Passive/ reactive PAH/ vasoreactivity
Shock
65
Objective findings
Hemodynamics in paper
Decision making
At the cost of invasive procedure
Swan ganj cathter was first to be introduced for hemodynamic monitoring
Transducers transforms pressure signas to electrical signals
Importance of equalization of pressure to atmosphere to get a proper curve
Wiggers diagram
Once thought to be the best way to decipher hemodynamics
Understanding science is easier than understanding philosophy
Abnormal is more attractive and romantic than the naïve normal
Abnormal values
Normal relations
Equality
Inequals get equal (eisenmenger/ CP)// equal get inequal is a problem
Inequality
Pericardial pressure is measured by RAP
In CP, LVEDP is elevated..but if RAP is substacted..true transmural pressure will be obtained..and that wl be low due to low filling
Hakki area lesser than gorlin area
Hakki area: not validated for tachycardia or bradycardia
Hakki area: angel’s correction: <75 in MS, >90 in AS, multiply with 1.35
Hakki area: Mean grad in MS, peak instantaneous grad in AS
But not free of fallacies
Exams/ quiz
Mathemetical
Composite data f clin findings/ echo/ ecg
