iii course biomedical applications of mathematics elements of cardiocirculatory physiology roberto...
TRANSCRIPT
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III CourseBiomedical Applications of Mathematics
Elements of cardiocirculatory physiology
Roberto BonmassariS.C. di Cardiologia
APSS-Ospedale Santa Chiara Trento
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Preamble
A Course of Biomedical Applications of Mathematics
……when the Hospital goes out and meet the University
I’m not a physiologyst I am a clinician, a cardiologist
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Agenda
Three lessons: 7-9-21 october 2015 (five hours)
• Aspects of cardiac anathomy
• The cardiac and circolatory function: phisiologic aspects
• Examples of clinical application of a phisiologic application in a pathologic condition: coronary stenosis and aortic stenosis
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The heart is costituted from 4
chambers:
2 atria (right and left)2 ventricles (right and
left)
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Atriarecive blood,Ventricleseject blood
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POLMONE
CUORE
ORGANI
Piccolo Circolo
Grande Circolo
Scambio Gassoso
Funzione di Pompa
Consumo di Ossigeno
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The Heart is a pump
• The cardiac pump is the ground of the circulation
• The are two circulation systems that works in series: systemic and pulmonary circulation
• The cardiac pump has the primary function of insurance an adeguate amount of blood flow through the systemic and the pulmonary vessel bed
• The cardiac pump works with two mechanisms : blood aspiration and pushing
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The Heart is a pump
• The cardiac pump produce a mechanical result (the circulation of the bood) due to the contraction and relaxation of the muscolar wall of the cardiac chambers (ventriculi and atria)
• But what is the primum movens of the cardiac function?
• Upstrem the mechanical function is necessary the electric function: the electric excitation
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Nodo del seno
Nodo atrio-ventricolare
Fascio di His
Branca destraBranca sinistra
Fibre di Purkinje
The conduction system: Physiology and pathology
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The Heart is a pump
• The cardiac electrical activity is an automatic activity
• Is only marginally influenced by nervous system
• These are the basis of the electro-mechanical coupling partneship
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The cardiac cycle
4040
Arterial Pressure Curve
IsovolumetricIsovolumetricContractionContraction
IsovolumetricIsovolumetricRelaxationRelaxation
00
120120
100100
6060
Electrocardiogram
Ventricular Pressure
Arterial Pressure
Approx. TimeApprox. Time 00 0.10.1 0.20.2 0.30.3 0.40.4 0.50.5 0.60.6 0.70.7 0.80.8
8080
1010AV ValveAV Valve
OpensOpens
AV ValveAV ValveClosesCloses
Semi-LunarSemi-LunarValve ClosesValve Closes
Semi-LunarSemi-LunarValve OpensValve Opens
Pre
ssu
re (
mm
Hg
)P
ress
ure
(m
m H
g)
VentricularVentricularSystoleSystole
AtrialAtrialSystoleSystole DiastoleDiastole
TTRR
PP
QQ SS
VentricularVentricularFillingFilling
VentricularVentricularEjectionEjectionPhasePhase
AtrialAtrialSystoleSystole
Ciclo di Wiggers 1915 Fasi1 contrazione Vs2 rilasciamento Vs3 riempimento Vs
12
33
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4040
Arterial Pressure Curve
IsovolumetricIsovolumetricContractionContraction
IsovolumetricIsovolumetricRelaxationRelaxation
00
120120
100100
6060
Electrocardiogram
Ventricular Pressure
Arterial Pressure
Approx. TimeApprox. Time 00 0.10.1 0.20.2 0.30.3 0.40.4 0.50.5 0.60.6 0.70.7 0.80.8
8080
1010AV ValveAV Valve
OpensOpens
AV ValveAV ValveClosesCloses
Semi-LunarSemi-LunarValve ClosesValve Closes
Semi-LunarSemi-LunarValve OpensValve Opens
Pre
ss
ure
(m
m H
g)
Pre
ss
ure
(m
m H
g)
VentricularVentricularSystoleSystole
AtrialAtrialSystoleSystole
DiastoleDiastole
TT
RR
PP
QQ SS
VentricularVentricularFillingFilling
VentricularVentricularEjectionEjectionPhasePhaseAtrialAtrial
SystoleSystole
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The cardiac cycle pressure/volume V sin
ratio
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Ventricular FillingVentricular Filling
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Arterial Pressure Curve
IsovolumetricIsovolumetricContractionContraction
IsovolumetricIsovolumetricRelaxationRelaxation
00
120120
100100
6060
Electrocardiogram
Ventricular Pressure
Arterial Pressure
Approx. TimeApprox. Time 00 0.10.1 0.20.20.30.3 0.40.40.50.5 0.60.60.70.70.80.8
8080
1010AV Valve
Opens
AV ValveAV ValveClosesCloses
Semi-LunarSemi-LunarValve ClosesValve Closes
Semi-LunarSemi-LunarValve OpensValve Opens
Pre
ss
ure
(m
m H
g)
Pre
ss
ure
(m
m H
g)
VentricularVentricularSystoleSystole
AtrialAtrialSystoleSystole
DiastoleDiastole
TT
RR
PP
QQ SS
VentricularVentricularFillingFilling
VentricularVentricularEjectionEjectionPhasePhaseAtrialAtrial
SystoleSystole
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4040
Arterial Pressure Curve
IsovolumetricIsovolumetricContractionContraction
IsovolumetricIsovolumetricRelaxationRelaxation
00
120120
100100
6060
Electrocardiogram
Ventricular Pressure
Arterial Pressure
Approx. TimeApprox. Time 00 0.10.1 0.20.20.30.3 0.40.40.50.5 0.60.60.70.70.80.8
8080
1010AV Valve
Opens
AV ValveAV ValveClosesCloses
Semi-LunarSemi-LunarValve ClosesValve Closes
Semi-LunarSemi-LunarValve OpensValve Opens
Pre
ss
ure
(m
m H
g)
Pre
ss
ure
(m
m H
g)
VentricularVentricularSystoleSystole
AtrialAtrialSystoleSystole
DiastoleDiastole
TT
RR
PP
QQ SS
VentricularVentricularFillingFilling
VentricularVentricularEjectionEjectionPhasePhaseAtrialAtrial
SystoleSystole
Atrial SystoleAtrial Systole
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4040
Arterial Pressure Curve
IsovolumetricIsovolumetricContractionContraction
IsovolumetricIsovolumetricRelaxationRelaxation
00
120120
100100
6060
Electrocardiogram
Ventricular Pressure
Arterial Pressure
Approx. TimeApprox. Time 00 0.10.1 0.20.20.30.3 0.40.40.50.5 0.60.60.70.70.80.8
8080
1010AV Valve
Opens
AV ValveAV ValveClosesCloses
Semi-LunarSemi-LunarValve ClosesValve Closes
Semi-LunarSemi-LunarValve OpensValve Opens
Pre
ss
ure
(m
m H
g)
Pre
ss
ure
(m
m H
g)
VentricularVentricularSystoleSystole
AtrialAtrialSystoleSystole
DiastoleDiastole
TT
RR
PP
QQ SS
VentricularVentricularFillingFilling
VentricularVentricularEjectionEjectionPhasePhaseAtrialAtrial
SystoleSystole
Isovolumetric ContractionIsovolumetric Contraction
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4040
Arterial Pressure Curve
IsovolumetricIsovolumetricContractionContraction
IsovolumetricIsovolumetricRelaxationRelaxation
00
120120
100100
6060
Electrocardiogram
Ventricular Pressure
Arterial Pressure
Approx. TimeApprox. Time 00 0.10.1 0.20.20.30.3 0.40.40.50.5 0.60.60.70.70.80.8
8080
1010AV Valve
Opens
AV ValveAV ValveClosesCloses
Semi-LunarSemi-LunarValve ClosesValve Closes
Semi-LunarSemi-LunarValve OpensValve Opens
Pre
ss
ure
(m
m H
g)
Pre
ss
ure
(m
m H
g)
VentricularVentricularSystoleSystole
AtrialAtrialSystoleSystole
DiastoleDiastole
TT
RR
PP
QQ SS
VentricularVentricularFillingFilling
VentricularVentricularEjectionEjectionPhasePhaseAtrialAtrial
SystoleSystole
Ventricular EjectionVentricular Ejection
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4040
Arterial Pressure Curve
IsovolumetricIsovolumetricContractionContraction
IsovolumetricIsovolumetricRelaxationRelaxation
00
120120
100100
6060
Electrocardiogram
Ventricular Pressure
Arterial Pressure
Approx. TimeApprox. Time 00 0.10.1 0.20.20.30.3 0.40.40.50.5 0.60.60.70.70.80.8
8080
1010AV Valve
Opens
AV ValveAV ValveClosesCloses
Semi-LunarSemi-LunarValve ClosesValve Closes
Semi-LunarSemi-LunarValve OpensValve Opens
Pre
ss
ure
(m
m H
g)
Pre
ss
ure
(m
m H
g)
VentricularVentricularSystoleSystole
AtrialAtrialSystoleSystole
DiastoleDiastole
TT
RR
PP
QQ SS
VentricularVentricularFillingFilling
VentricularVentricularEjectionEjectionPhasePhaseAtrialAtrial
SystoleSystole
Isovolumetric RelaxationIsovolumetric Relaxation
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300300
200200
100100
00
SystoleSystole DiastoleDiastole
Left Left
Right Right
Coronary Coronary Blood Blood Flow Flow
(ml/min(ml/min))
Slide courtesy of A.C. Guyton, MD, Slide courtesy of A.C. Guyton, MD, Textbook of Medical Textbook of Medical Physiology, Physiology, Sixth Edition, 1981 W.B. Saunders CompanySixth Edition, 1981 W.B. Saunders Company
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How is the Cardiac function?
Cardiac output and pressure
CO= Pr / R= SV x HR
Legenda
1.Pr = systemic pressure2.R = systemic resistance3.SV = stroke volume (amount of blood eject every beat)4.HR = number of beats per minute
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Cardiac function = CODeterminants
• Cardiac rate
• Inotropic condition = contractility
• Venus return (RV): influenced from neuroumoral factors (Frank-Starling law)
• Peripheric resistance
=CARDIAC OUTPUT 4-6 l/min
CARDIAC INDEX 1.6-2.5 l/min/m²
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Cardiac output = CO
CO= Pr / R= SV x HRexamples :
1. Increase of FC -> does not increase GC, decrease of the VOLUME SYSTOLE-SV (if Rv does not increase)2. Increase of RV -> increases GC 10-20% (increase of Pa A dx 10 mmHg)3. Increase of FC + increase of RV -> increases GC with = SV4. Stirring adrenergethic -> increases RV + increase of the function of the pump (HR, contract?) = INCREASES GC 5. Important reduction of FC or alteration of V dx -> increase of Pa A dx = barrier for the venous comeback
Organs are able to change their flow working on the oppositions; they are able to regulate the distribution of the CARDIAC RANGE.
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Cardiac function: Frank-Starling mechanism
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Cardiac function:CO-CI & R ; Conduttance= 1/R
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Vascular resistance
The vascular regulation is a local methabolic process in all organs, a part in kidney and skin. In fact even if in a denervation condition these organs are able to matain a adequate vascular tone modificated by methabolic influences. Flow depend closely by the radius
R = L x h8/ x r4
10% in reduction diameter vessel = 50% in increase resistance
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sistolica
diastolica
sistolica
Difetto di riempimento
Difetto di espulsione
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Cardiac power outputVentricular function index
Cardiac Power output
=MAP x CO
= SW X HR
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Cardiac power output
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Function of blood circulation
TRANSPORT• substrates and cathabolism products to and from organs and tissues• in a changeable measure and in proportion of her requirements and necessities
GOAL• to maintain an optimal composition of the interstitial fluid necessary for the cellular function
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PLACCA ATEROSCLEROTICA
VASO ARTERIOSO
TONACA MEDIA
TONACA INTIMA = ENDOTELIO
TONACA AVVENTIZIA
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Distribution of blood flow
• It is necessary to give at any time to organs and tissues
a blood flow distribution based on requirements
• There are two control mechanisms in a close correlation
• Central Autoregulation
• Local Autoregulation
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Distribuzion of blood flow
Central Autoregulation GOAL: TO MAINTAIN COSTANT
perfusion pressure of the organs (independently from the flow: Fl= P/R)
Mechanism: neuro-ormonal central control on R e Fl
Local Autoregulation GOAL: TO MAINTAIN ADEQUATE
flow for each organ for the metabolic erquirements
(independently from systemic pressure)Mechanism: regulation of local vascular resistance
due to metabolism activity
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Circulation modelling
• • ORGANS in parallelo if we consider AORTA with different metabolic, vascular, anathomic characteristics (f.e. heart, abdominal argans, muscols, brain…)
• VASCULAR SYSTEM: determinate from a segments sequence in serie similar in each organ
Arterie – arteriole – capillari – venule – vene
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The Vascular System: segments
1) Aorta e great proximal arteries
• Elastic matrix tessue prevalent HISTOLOGY
• Improve distention of vascular wall during sistole PHISIOLOGY
• cinetic energy of stroke volume (during systole ) is storaged as elastic
energy released during diastole (partecipate at the diastolic value of BP)
• modulation of suddenly variations of BP : dynamic sistolic reserve • pressure wave downstream is delayed
• Riduction of elastic properties PATHOLOGY
• reduction of dynamic sistolic reserve• increase differential blood pressure even if a costant stroke volume• increase of afterload of left ventricle• increase of the rate of propagation of the pressure wave
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The Vascular System: segments
2) Muscolar small arteries• Arteries with a thick muscolar medium tonaca: are the junction betweengreat arteries and organs and tessues
– Thick medium muscolar tonaca ( high thickness/lumen ratio )– COSTANT STRESS of the wall (PR x radius/ thickness)– COSTANT DIAMETER with variations due to neuro-horrmonal control– Regulatory mechanims : metabolics production and myogenic control
• Play a central role in the vascular resistance control = control and persistance of an adequate flow to organs and tessues FL= P / R
– Is the principal location of the flow resistance (aortic pressure 100 mmHg, small arteries pressure 30 mmHg, vein pressure 15 mmHg)
• The pressure gradient between small arteries and veins (about 15 mmHg) permits
– The capillar filtration – The distal reabsorbtion
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The Vascular System: segments 3) Capillars
• In this segments is present the most importanti function of circulation = SUBSTRATES AND OXIGEN EXCHANGE BETWEEN BLOOD/TESSUES WIT H AN FOUDAMENTAL ROLE IN OMEOSTASIS OF THE INTERSTITIAL FLUID
– The walls are very smooth , sometimes in certein organs fenestrates – Little diameter = little transmural stress (Stress= D x P/spessore) with a better tolerance of the transmural pressure – There is a significant flow resistance with a fall of pressure (from 30 mmHg to 15 mmHg)– At the arteriolar portion happen THE FILTRATION at the venular portion THE REABSORBTION– In any time not in all THE CAPILLARS there is perfusion: the density of the perfused capillars is important in terms of exchange between the tessues– The exchange happen due to:
•Pressure gradients (FLUIDS): hydrostatic pressure (proximal side) and colloido osmotic pressure (distal side)•Diffusion: liposoluble gas and yhdrosoluble substances
– The amount of not reabsorbed fluids returns to the systemic circulation through an alternative circulation : THE LINFATIC SYSTEM = 4-5/L in a day-> 1/4 -1/2 TOTAL PLASMATIC ALBUMIN
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The Vascular System: segments 3) Capillars
CAUSES OF INCREASE OF FILTRATION
1.Increase of the exchanges surface (due to the increase of number of the perfused capillars)
2.Increase of the pre-capillar pressure (more diffusion)
3.Increase of the postcapillar pressure (less reabsorbtion))
4.Increase of the permeability per surface unit (increase of holes)
INTERCAPILLAR DISTANCE =
less distance = more opend capillars = more fast the exchange
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The Vascular System: segments
4) Venule and veins
• EMODYNAMIC: – Pressure = 15 mmHg in orizzontal position– Prefusion pressure for the veins heart return
• HISTOLOGY: –Thin wall– Very strechable–Muscolar portion very thin
•FUNCTION: – Return of blood from tissue sto the heart– Storage of blood able to control the return to the heart– Influence to the capillar pressure
• LEGS: superficial and deep veins– Muscolar wall more thick– Unidirectional valves (distribution of the Hydrostatic pressure in orthostatisms)
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Vascular resistance
• Not uniform distribution a long the segments of circulation1. Arteries 5%2. Small arteries 60%3. Capillars 20%4. Veins 15%
• Medium vascular resistence-> integrated values of organs and tissues in parallelo respect the aorta
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Vascular resistance
The vascular regulation is a local methabolic process in all organs, a part in kidney and skin. In fact even if in a denervation condition these organs are able to matain a adequate vascular tone modificated by methabolic influences. Flow depend closely by the radius
R = L x h8/ x r4
10% reduction diameter vessel = 50% increase resistance
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Peripheric distribution ofCO and oxygen consumption
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Myocardial ischemiaFractional Flow Reserve –
FFR
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Coronary circulation:anatomic aspects
• Coronary tree = vascular system with dicotomyc regular ramification with a diameter progressively smaller
• 2 distinct section in term of anatomic and functional characteristics
- 1 Epicardic portion - 2 Microcirculation section
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Epicardial segment
Microcirculation)
Coronary Circulation: segments
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Coronary circulation:anatomic aspects
• Epicardic portion (diameter 4-5 - 0.5 mm) - “Conduttance” vessel : not able to influence the
vascular resistance - are visible using contrast media
• Microcirculation (diameter < 0.5 mm) - “ Resistance” vessel site of autoregulation
process - Are able to modify vascular resistance up to 6
times - Incompletely visible with contrast media (cause of
“myocardial blush”)
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Coronary Circulationphysiologyc aspects
• Coronary Flow = Pressure/Resistance = 300-600 ml/min
• 5-10% of cardiac output (4-6 l/m)• Can increase up to 5-6 times (Resistance can change
up to 6 times)• Pulsed flow (not continue) with a prevalent diastolic
component• Cardiac methabolism: exclusively aerobic - O2
dependent with a very high O2 extraction from the arterial blood (10 ml/100gr/min vs 0.5 ml/100gr/min in the skelectric muscle) and with 30% O2 saturation the blood of coronary sinus
= more oxigen demand request more oxigen supply
it is mandatory an increase of coronary flow it is not possible more oxigen extraction
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300300
200200
100100
00
SystoleSystole DiastoleDiastole
Left Left
Right Right
Coronary Coronary Blood Blood Flow Flow (ml/min(ml/min))
Slide courtesy of A.C. Guyton, MD, Slide courtesy of A.C. Guyton, MD, Textbook of Medical Textbook of Medical Physiology, Physiology, Sixth Edition, 1981 W.B. Saunders CompanySixth Edition, 1981 W.B. Saunders Company
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PLACCA ATEROSCLEROTICA
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Physiopathology ischemia
MVO2
SupplySupply Demand Demand
Supply: stenosi spasmo riserva coronaricaDemand: FC PAO e contrattilità, ipertrofia
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Coronary stenosis: physiopathology
concept of coronary flow reserve
• A coronary stenosis (> 40%) determine a reduction in perfusion pressure without a concomitant flow reduction due to contemporary microcirculation resistance reduction FL= P/R, if decrease P and R contemporary = FL remain stable
• Stenosis upper a limit level (80-85% diameter) run out the dilatation possibilities of the microcirculation: in this condition every other reduction of pressure means reduction of flow because the incapacity of reduction of resistance = ischemia
RUN OUT OF THE CORONARY FLOW RESERVE
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IVUS - INTERMEDIATE LESION RCAIVUS - INTERMEDIATE LESION RCA
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FFR
CFR (E TEST NON INVASIVI)
FFR and CFR: What Do They Investigate?
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Fractional Flow Reserve (FFR)
FFR = Qmax
Qmax
S
N
Pd
Pa
=
During maximal hyperemia
Pa
Pd
FFR = the ratio of maximal myocardial flow in the stenotic territory to maximal myocardial flow in that same territory
if the stenosis were absent
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FFR = Q Pd
Q Pa
=
sten
N
FFR: a Flow Index Derived from Pressures
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Normal Value of Myocardial Fractional Flow Reserve
Normal FFR = 1
Pa Pd
FFR = Pa
Pd
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Myocardial Fractional Flow Reserve: Definition
Qmax
S
Qmax
N= FFR
FFR =Pd / R myo
Pa / R myo
=Pd
Pa
Pa Pd Pv
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Pa
100 Pd
70 Pv
0
Pa
100 Pv
0
During Maximal Vasodilatation
FFR = Pd
Pa = 0.70
Q
P10070
Q100
Q70
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R.E. 50-y-old man. Aborted sudden death.
LV angiogram: mild hypokinesia of the anterior wall.
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Pa Pd
FFR = Pd /Pa = 56/80 = 0.70
HYPEREMIA
Coronary Pressure Measurements 1979 2001
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Coronary Pressure Measurements: Prerequisits
1. Pressure Measuring Guide Wire
2. Maximal Hyperemia
3. FFR instead of P
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0.014”
3 cm
Pressure Monitoring Guide Wires
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0
100
50
Pa = Guiding Catheter
Pd = Pressure Wire
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Coronary Pressure Measurements: Prerequisits
1. Pressure Measuring Guide Wire
2. Maximal Hyperemia
3. FFR instead of P
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Hyperemia - administration• Hyperemic stimuli
– Intravenous Adenosine 140-160 g/kg/min
– Intracoronary Adenosine LCA: 20-40 g
RCA:15-30 g
– Intracoronary Papaverine LCA: 15 mg
RCA: 10 mg
– Adenosine Triphosphate (ATP) (ic. or iv) (same dosages as for Adenosine)
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0
100
50
ADENOSINE
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200
100
0
200
100
0
Aortic Pressure = 122 mm Hg Aortic Pressure = 89 mm Hg
Coronary Pressure = 52 mm Hg Coronary Pressure = 40 mm Hg
P = 70 mmHG P = 49 mmHG
FFR = 52/122 = 0.43 FFR = 40/89 = 0.45
Influence of Systemic Pressure on Transstenotic Gradient
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Coronary Pressure Measurements: Prerequisits
1. Pressure Measuring Guide Wire
2. Maximal Hyperemia
3. FFR instead of P
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Pa
Pd
FFR = Pd /Pa (during hyperemia) = 58/79 = 0.730
Pa
Pd
Baseline HyperemiaAdenosine IC
100
80
60
40
20
Fractional Flow Reserve in Clinical Practice
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REST HYPEREMIA
FFR=58/112=0.52
150
50
0
100
Proximal to the lesion
Distal to the lesion
Crossing the lesion
58
112
Fractional Flow Reserve in Clinical Practice
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Coronary Pressure Measurements
Clinical Applications1. Diagnostic Setting:
Is this lesion responsible for patient’s complaints?
Should this lesion be revascularized?
2. Interventional Setting:
Is a stent needed after balloon angioplasty?
Is the stent well deployed?
BDB 98/029
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Clinical Applications of FFR
1. Before PTCA:
when FFR > 0.75 the prognosis is at
least as good without than with an angioplasty.
when FFR < 0.75 an angioplasty is
justified by a marked symptomatic
improvement following
revascularization.
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Clinical Applications of FFR
2. After balloon:
when FFR > 0.90 and angio is OK, the long-term outcome after POBA is similar than
what can be expected after additional stent implantation.
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Clinical Applications of FFR
3. After stent:
pullback maneuver : No pressure drop during hyperemia.
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A B C D
FFR = 91 / 107 = 0.85FFR = 75 / 101 = 0.74 FFR = 90 / 106 = 0.85 FFR = 98 / 100 = 0.98
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represents the true fraction of maximum flowwhich can still be maintained in spite of the
presence of a stenosis.
FFRmyo Myocardial Fractional Flow Reserve
Myocardial Fractional Flow Reserve
It is exactly that index which tells to what extent a patient is limited by his coronary disease.
FFRmyo
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FFRmyo
=Max. myocardial blood flow in the presence of a stenosis
normal maximum blood flow
FFRmyo Myocardial Fractional Flow Reserve
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is a lesion specific index
is independent of hemodynamic parameters
has a normal value of 1.0
takes into account collateral flow
has no need for a normal control artery
can be easily obtained: FFRmyo = Pd / Pa
In summary
FFRmyo ...
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Courtesy of Charles Chan, M.D.
National Heart Center, Singapore
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Courtesy of Charles Chan, M.D.
National Heart Center, Singapore
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Aortic stenosis
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AORTIC VALVE: tricuspid
Valvola normale Valvola stenotica
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Aortic stenosis: pathology
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AORTIC STENOSIS: imaging
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Aortic stenosis: pressure curves
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Acquiring Hemodynamic DataAcquiring Hemodynamic Data
• O2 consumption measured from metabolic hood or Douglas bag; it can also be estimated as 3 ml/min/kg or 125 ml/min/m2.
• AVo2 difference calculated from arterial – mixed venous (pulmonary artery) O2 content, where O2 content = saturation x 1.36 x Hg
• O2 consumption measured from metabolic hood or Douglas bag; it can also be estimated as 3 ml/min/kg or 125 ml/min/m2.
• AVo2 difference calculated from arterial – mixed venous (pulmonary artery) O2 content, where O2 content = saturation x 1.36 x Hg
*Accurate method of measuring CO, especially in patients with low cardiac output.
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CO/(SEP)(HR)Area in cm² = ---------------------------------------- 44.3(C)(sq rt of pressure gradient)
Where C = empirical constant For MV, C = 0.85 (Derived from comparative data)
For AV, TV, and PV, C = 1.0 (Not derived, is assumed based on MV data)
Aortic stenosis hemodynamic evaluation Gorlin equation
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Alternative to the Gorlin FormulaAlternative to the Gorlin Formula
*A simplified formula for the calculation of stenotic cardiac valves proposed by Hakki et al…Circulation 1981. Tested 100 patients with either AS or MS.
*Based on the observation that the product of HR, SEP or DFP, and the Gorlin equation constant was nearly the same for all patients measured in the resting
state (pt. not tachycardic). Values of this product were close to 1.0.
*Calculations somewhat comparable………
*A simplified formula for the calculation of stenotic cardiac valves proposed by Hakki et al…Circulation 1981. Tested 100 patients with either AS or MS.
*Based on the observation that the product of HR, SEP or DFP, and the Gorlin equation constant was nearly the same for all patients measured in the resting
state (pt. not tachycardic). Values of this product were close to 1.0.
*Calculations somewhat comparable………
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How measure stenosis severty?
Echocardiography
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Pressure gradients
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VTI LVOT
VTI AO
LV
LA
Ao
Continuity equation: equal istantaneal flow through left ventricular outflow tract (LVOT) and the aortic valve Flow LVOT = Flow Ao V
Aortic Stenosis: valvular area with continuity equation
Flow = area (3.14 x (D/2)² x Integral time velocity Doppler (ITV)
Area LVOT (3.14 x (D/2)² x Integral time velocity Doppler (ITV LVOT) = Area Ao V (3.14 x (D/2)² x Integral time velocity Doppler (ITV Ao V)
Aortic Valve area = 3.14 x (D/2)² x (ITV LVOT / ITV Ao V)
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Classification of severty of Valve Disease in Adults
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Prognostic Importance of Quantitative Ex DopplerEchocardiography in Asymptomatic Valvular
Aortic Stenosis
Prognostic Importance of Quantitative Ex DopplerEchocardiography in Asymptomatic Valvular
Aortic Stenosis
All patients who displayed hard events (D or HF) had an AVA 0.75 cm2, an abnormal exercisetest, and a significant exercise-induced increase in mean transaortic pressure
gradientLancellotti et al. Circulation, 2005; 112: I-377 Lancellotti et al. Circulation, 2005; 112: I-377
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Relationship between CO and Aortic Pressure Gradient over a range of values for AV area (Based on Gorlin formula)
A
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Discrepancies between Gorlin and continuity-calculated effective orifice areas
Discrepancies between Gorlin and continuity-calculated effective orifice areas
JACC 2006; 47: 1241JACC 2006; 47: 1241
Since recommended cut-off values for the severity of aortic stenosis are largely based on the clinical experience with Gorlin-calculated areas, the use of the inherently lower continuity calculated effective orifice areas will
lead to a systematic overestimation of stenosis severity.
Since recommended cut-off values for the severity of aortic stenosis are largely based on the clinical experience with Gorlin-calculated areas, the use of the inherently lower continuity calculated effective orifice areas will
lead to a systematic overestimation of stenosis severity.
PRESSURE RECOVERY PHENOMENON