acute respiratory failure. - esc | congresses | esc congress 2013
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Acute Respiratory failure
of the critically ill cardiac
patient
Marco Maggiorini
Medical Intensive Care Unit
University Hospital Zürich
PathophysiologyDiastolic dysfunction
Pulmonary venous hypertension
Decreased left ventricular elastance following left ventricular systolic and diastolic dysfunction lead to pulmonary venous hypertension (PVH).
0
10
20
30
40
50
60
70
Pre
ssu
re (
mm
Hg
)
Time (sec)
Ppao 32 mmHg
mPpa 44 mmHg
TPP : mPpa – Ppao ≤ 12 mmHg
“Hydrostatic Capillary Leak”
Pc < 16 mmHg
Pc 16-19 mmHg
Pc > 19 mmHg
Pulmonary hemodynamics assessed by PAC
Drake R.E. et al, Am J Physiol 1987, 238:H430-H438
Pulmonary capillary filtration pressure
Critical pulmonary capillary pressure
Pc crit = 19.7 ± 5.4 mmHg
Zeit (Min.)
Ge
wic
htz
un
ah
me
(g
/10
0g
)
20.415.4
24.6
BMBM
CAVE: Remodeling
of the pulmonary
vessels ⇑ Pc crit.
Systemic / local Inflammation
INFLAMMATPRY RESPONCE
Decrease Pc Crit
&
Impairs alveolar fluid clearance
Hochman JS Circ 2003, 107:2998
iNOS
Systemic inflammation
Inflammatory cytokines
NOONOO
Vasodilation Permeability
Systemic perfusion
Coronary perfusion pressure
Permeability type of Pulmonary edema
LVEDPPulmonary congestion
Myocardial Infarction
Myocardial Dysfunction
Systolic Diastolic
Death
Infection on ICU admission
Rudiger et al SMW 2010
Infection during ICU stay
Rudiger et al SMW 2010
Conditions associated with
cardiogenic pulmonary edema
Acute heart failure with hypertension (Hypertensive crisis)
Acute heart failure with with normal blood pressure
Acute decompensated congestive heart failure
Severe cardiogenic shock
Acute heart failure with valvular dysfunction
High output failure
Adapted from ESC Guidelines 2005
Determinants of AHF patients
survival admitted to the ICU
Adamopoulos et al., Eur. J. Heart Fail., 2007, 9:935
355 patients admitted to the CCU/ICU for acutely decompensate heart failure
Is a pulmonary artery catheter (PAC) needed?
Hemodynamic monitoring of
cardiogenic pulmonary edema
Treatment goals:
Cardiac index > 2.2 l/min/m2
Mixed-venous oxygen saturation > 55%
Pulmonary artery occluded pressure < 20 mmHg)
0
10
20
30
40
50
Pre
ssure
(m
mH
g)
Pra Ppa Ppao
Targeting PAOP < 15 mmHg doesn't affect
time to clinical resolution of congestion
ESCAPE Trial, Binanay et al. JAMA 2005, 294:1695
Days alive and out of hospital Impact of intervention across subgroups
Fluid removal by targeting a PAOP < 15 mmHg
improves relative mitral regurgitation
ESCAPE Trial, Paladry et al. Circ Heart Failure 2009, 2:181
Assessment of fluid removal Improvement of mitral regurgitation
Median improvement relative to baseline
MR = mitral regurgitation; MR/LAA = MR in proportion of left atrium area
from
BL
mmHg
5 (12)
8 (9)
Monitoring changes in EVLW after ICU
admission and alternative to PAC?
Paop EVLW
CVP ITBV
BL 24h BL 24h
Bin
dels
et
al A
m J
Card
iol1999, 84:1
158
Resolution of cardiogenic pulmonary edema after intubation and MV
Monitoring changes in EVLW after ICU admission and alternative to PAC?
Ritter et al preliminary data
6.2%
22.4%
0
5
10
15
20
25
30
Survivors Non Survivors
Pe
rce
nt (%
)
Percent of cardiogenic pulmonary edema patients with a decrease in EVLW of <
10% during first 3 ICU Days
(17 Pts) (9 Pts)
p = 0.03
EVLW EVLW
Intra-thoracal blood volume (ITBV)
Assessment of extra-vascular lung water (EVLW)
using the trans-thoracal thermodilution method
Management of acute respiratory
failure of cardiac origine
Left-ventricular filling pressures
Str
oke v
olu
me
congestive and
low output
symptoms
congestive
symptoms
low output
symptoms
Inotropic + vasodilator
Vasodilator + diuretic
Vasodilator
normal
heart failure Diuretic
Pro
port
ion o
f P
atients
(%
)
Nitroglycerin
(N=143/143)
Nesiritide
(N=203/204)
Placebo
(N=142/142)
-40
-30
-20
-10
0
10
20
30
40
50
60
70
80
90
100
p=0.191p=0.034 Markedly
Better
ModeratelyBetter
MinimallyBetter
No Change
Minimally*Worse
* No patients mod-markedly worse
Dyspnoe at 3 hours after initiation of a
vasodilator therapy (VMAC-trial)
JAMA 2002, 287:1531
Randomized trial of high-dose isosorbide dinitrate plus
low-dose furosemide vs. high-dose furosemide plus low-
dose isosorbide dinitrate in severe pulmonary edema
(Cotter G et al. Lancet 1998; 351: 389-93)
Group A Group B p-value
(n = 52) (n = 52)
Required MV 7 (13%) 21 (21%) 0.0041
Myocardial Inf. 9 (17%) 19 (37%) 0.047
Any adv. event 12 (25%) 24 (46%) 0.041
p < 0.0063
Inotropics are indicated in servere
cardiogenic shock
Kivikko et al Circ 2003, 107:81
Time (h)
Stroke volume
Time (h)
Pulmonary artery occluded pressure
Levosimendan
Placebo
Levosimendan
Placebo
Non-invasive mechanical ventilation in
congestive heart failure
SaO
2%
PaO2:FiO2 (mmHg) PaCO2 (mmHg)
NIVPS Standart
Intubation 5% 33% .037
Resolution time (Min.) 30 105 .002
Masip et al
Lancet 2000,
356:2126
Pressure support
Vt > 400 ml
PEEP: 5 cmH2O
Trigger 0.5 cmH2O
n = 40
Gray AJ et al. NEJM 2008, 359:143
Non-invasive ventilation in cardiogenic pulmonary edema
Non-invasive ventilation vs. Standard
treatment in cardiogenic pulmonary edema
Gray AJ et al. NEJM 2008, 359:143
• NIV for at least 2 hours
CPAP: 5 – 15 cm H2O
NIPPV: EPAP 4-10 cmH2O, IPAP 8-20
cmH2O
• SaO2 at baseline (all): 90 ± 8 %
• PaO2 at baseline (all): 13.4 ± 8.6 kPa
• PaCO2 at baseline (all): 7.7 ± 2.3 kPa
NIV in
congestive
heart failure
Masip et al
JAMA 2005,
294:3124
Effects of NIV on
the need to intubate
in acute heart
failure
NIV in
congestive
heart failure
Masip et al
JAMA 2005,
294:3124
Effects on death
rate of NIV in acute
heart failure
Summary: management of acute
respiratory failure in cardiac patients
RESTORE OXYGEN DELIVERY TO THE TISSUE
To assure arterial oxygenation, improve physiology and
patient confort using NIV
Decrease cardiac afterload if appropriate using i.v.
Vasodilators
RESTORE MYOCARDIAL FUNCTION
PCI, ACBP, Valve repair
Convert to Sinus Rhythm is necessary
Intra-Aortic Balloon Pump (IABP)
INOTROPICS
Improve cardiac contractility: Dobutamine,
Levosimendan, Milrinone