Echocardiography Primer
for Intensivists
Bucharest 2014
But first…
A Glimpse of Hemodynamics
“New” conceptual approach?
Currently, BF and vT can be effectively assessed at the bedside Quantitative measures of capillary leak (vB) would be useful in guiding fluid therapy The objective measures for vC are cumbersome Bedside measures of vC are not yet available
REDUCTIONIST DIDACTICISM
How close are we of anything?
SVR - centered view
Critical closing pressure - centered view
Dynamic tone assess-
ment
Radioiodinated albumin
- DAXOR
Hb – dilution technique
MSFP–centered approach
ECHOCARDIOGRAPHY
PICCO
VIGILEO
SWAN
Biomarker panel
Radioiodinated albumin - DAXOR
EVLWi/PVPI - PICCO
NIRS
OPS/SDF SL tonometry
NADH fluorescence
Delayed fluorescence
mitoPO2
Miscellaneous
Paradigms have been shifting for some
time now…
SHIFTING THE PARADIGM -flow centered era-
SHIFTING THE PARADIGM -flow centered era-
α
β
SHIFTING THE PARADIGM -flow centered era-
SHIFTING THE PARADIGM -flow centered era-
TONE SDF
OPS
SHIFTING THE PARADIGM -flow centered era-
“EFFECTS OF PERFUSION PRESSURE ON TISSUE PERFUSION IN SEPTIS SHOCK”
SHIFTING THE PARADIGM -flow centered era-
The effects of dobutamine on microcirculatory alterations in patients
with septic shock are independent of its systemic effects
SHIFTING THE PARADIGM -flow centered era-
SHIFTING THE PARADIGM -flow centered era-
NITROGLYCERIN ?
SHIFTING THE PARADIGM -flow centered era-
NITROGLYCERIN ?
μVESSELS TONE
SHIFTING THE PARADIGM -flow centered era-
FLOW
SHIFTING THE PARADIGM -μvessels centered era-
RECRUIT THE μCIRCULATION AND KEEP IT OPEN
“Run the circulation at the lowest possible pressures?” -flow centered ideas-
Monitoring the right vessels
μvessels
FLOW
MAP TONE
MAP
μvessels
FLOW
The Break-up
Open up the μcirculation and keep it open -resuscitation-
De-stress the distressed heart -contextual innuendo-
SIADH
CRITICALLY ILL CM
IMMUNO SUPR.
POST CA SYNDROME
SIRS/ALI ARDS CATECHOL
ADM.
PHEOCHR.
CSW/RSW RENAL STUNNING
SAH
HYPER CATAB.
SEPSIS
TBI
Takotsubo -like CM
DISTRESS
TL
R
RAAS
PAMP/DAMP
SU
RG
E
βblockers
Alpha7n
AChR
HMGCoA
HOLISTIC APPROACH
SIADH
CRITICALLY ILL CMP
IMMUNO SUPR.
POST CA SYNDROME
SIRS/ALI ARDS CATECHOL
ADM.
PHEOCHR.
CSW/RSW RENAL STUNNING
SAH
HYPER CATAB.
SEPSIS
TBI
Stunning
Band contraction
Uncoupling of biological oscillators
Reversibility potential
Hysteresis
HRV “fingerprint”
Tone related paradigms
How should one quantify tone state? How is tone related to ΔMAP responsiveness? Is tone a prognostic factor?
I = V / R (Ohm’s law)
Q = (P1- P2) / R
CO = (MAP - PRA) / SVR
SVR -mathematical counterfeit-
α
ctgα =(MAP-Pc)/Q Pc=critical closing pressure ctgα = Ra
Why a critical closing pressure? -intuitive image-
What if it exists a critical closing pressure? -intuitive image-
Raynaud Arteriovenous
malformation
Measuring CCP
ctgα = (MAP-Pc)/Q Pc = critical closing pressure ctgα = Ra
α
On the edge of waterfalls
Is there any purpose in waterfalls?
Organ specific PCC reflecting organ
specific vascular control
Vital organ perfusion is more efficiently
maintained
Arterial flow stability during short
lasting Pcv changes
A Pcc-Pmsf gradient means transient
heart/brain flow during stop-flow
conditions
Rsys vs Ra
Ra=0.52•Rsys-0.55
Pearson correlation 0.945
If it were that easy!
Naeije’s pressure/flow diagram -CCP in pulmonary vessels-
PcPpa
PlaPpaPVRaPVR
Inflow
pressure
Outflow
pressure
Pla Pc
Ppa PVR = (Ppa – Pla) / Q ->A PVRa = (Ppa – Pc) / Q ->B
A: Pla>Pc B: Pc>Pla
1►2: no change
1►3: VD
A
B’
B
PVR=tgα
1►2: VC 1►3: no change
A
B
PVR when Pla>Pc
PVR as seen through PVR = (Ppa – Pla) / Q
Q or Ppa
PVR
PVR when Pla<Pc
Ppa
Pla
Pc
P’c
α
α PVRa=tgα
PVR→∞
1
2
3
PVR→∞
PVR→tgα
PVR→tgα tgα
cb
cx
bxaPVR
x→∞=>PVR=PVRa=tgα
x→Pc=>(x-c)→0=> =>PVR→∞ Q
Naeije’s tone diagram -solving Versprille’s conundrum-
C
VASOCONSTRICTION
VASODILATATION
Q
Ppa
PVRa=0
Pla
Ppa-Pc=PVR→•Q
Pc
0
Magder’s view -didacticism with a taste of mathematical compromise-
Should the flow begin to go down, then Pv will go upwards (in this picture it appears to stand still). This Pv’s rise will dampen the resistance’s (SVR’s) rise but it will not abrogate it (Pv’s rise is less than Part’s fall due to Cart<Cven). So… SVR will appear as rising with falling flow. Should you consider Pcrit as the outflow pressure, only then you shall grasp the real picture: the tone stands still.
MAP’s preload dependence
MAP’s preload dependence
MAP’s preload dependence -ventriculo-arterial coupling diagram-
Ees=tgα=Pes/(EDV-SV-Vo)
Ea=tgβ=Pes/SV
Pes=a•(Ved-Vo) unde
a=1/(1/Ea+1/Ees)
High baseline Ea, Ees(ESPVR)
Diastolic dysfunction(EDPVR)
High sympathetic overdrive/panic
Great redistribution potential
Active inflammation capable of
modulating Ea,EDPVR
Little to no involvement of Ees
ΔEes=0
keyw
ord
s
MAP’s preload dependence
PPV SVV
PPV/SVV=
Eadyn
0.89
Eadyn echivaleaza cu tonus vasomotor.
MAP’s preload dependence
Pentru Eadyn>0.89 cresterile tensionale pentru
acelasi SVV sunt mai pronuntate si denota un tonus
vasomotor mai accentuat.
Tone and prognosis -cardiogenic shock focus-
T
O
N
E
F
O
C
U
S
T
O
N
E
F
O
C
U
S
Weaning failure-another paradigm shift
Weaning failure
Redistribution Lusitropism Inotropism
Weaning failure
Redistribution
Why does pulmonary venous pressure rise after
onset of LV dysfunction: a theoretical analysis
Gelm→n’s two comp→rtment model
The decrease in intrathoracic pressure favours redistribution
Weaning failure
Lusitropism
Myocardial ischemia
► WOB
► tachycardia
► hypoxemia
RV dilation: RV/LV interdependence
► increase in venous return
► increase in PVR
LV afterload induced fall in relaxation
r→te filling pressure hypoxemi→, panic, sympathetic surge, myocardial
ischemia
Weaning failure
Inotropism
Effect of intrathoracic pressure on left ventricular performance, Buda NEJM 1979
Left ventricular function during weaning of patients with chronic Obstructive pulmonary disease, Richard ICM 1994
LUSITROPISM
-shift in focus-
Right ventricular protective ventilation -echo era-
Right ventricular protective ventilation -echo era-
Right ventricular protective ventilation -echo era-
Fluid responsiveness -echo era-
• Is the patient unaffected by serious valvular disease?
• Is the patient unaffected by right ventricle dysfunction or severe left ventricle dysfunction?
• Is the patient ventilated without spontaneous efforts?
• Is the patient ventilated in nonprotective ventilation (TV at least 8ml/kg)?
• Is the patient in sinus rhythm( or other regulated
rhythm)?
• How is Ecw versus El?
• How is the patient’s IAP ?
• Have you established that the patient’s heart
rate/respiratory rate ratio is > 3.6? • Which treshhold will you use for your binary
decision?
• Have you established your patient’s compliance in order to standardize the VE?
2%
F
L
U
I
D
R
E
S
P
O
N
S
I
V
E
N
E
S
S
Welcome
to
the echo era !
Oct 2014
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