Post Operative Management
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Transcript of Post Operative Management
PULMONARY ENDARTERECTOMY:
POST-OPERATIVE MANAGEMENT
F. MOJOLICattedra di Anestesiologia e Rianimazione
Università degli Studi di PaviaServizio di Anestesia e Rianimazione IIRCCS Policlinico San Matteo - Pavia
POSTOPERATIVE MANAGEMENT
- Weaning from Mechanical Ventilation
- Weaning from Inotropes, Vasopressors
and Pulmonary Vasodilators
- Effective Anticoagulation
- Management of Complications
RESPIRATORY CHANGES AFTER PEA
Anesthesia Sternotomy CPB Bed Rest
Hypoventilation of DEPENDENT
pulmonary regions
Hyperperfusion of DEPENDENT
pulmonary regionsPulmonary Artery StealPEA
V’ / Q mismatchPostoperative Hypoxemia
Functional Residual Capacity decreaseAtelectasis formationExtraVascular Lung Water increasePulmonary Compliance decrease
Post PEA Mechanical Ventilation
To mantain adequate ventilation of dependent pulmonary parenchyma, two different STRATEGIES:
A protective approach limits pulmonary STRESS (transpulmonary pressure), STRAIN (pulmonary overdistention) and ATELECT TRAUMA (opening and closing of alveoli), therefore also VILI (Ventilation induced Lung Injury)
HIGH VOLUMES
VENTILATION
PEEP 5 cmH20
TV 12 -15 ml/Kg
PROTECTIVE
VENTILATION
PEEP 10 cmH20
TV ≈ 8 ml/Kg
WEANING FROM MECHANICAL VENTILATION
• PEEP, “normal” TV
• Forced diuresis, negative fluid balance
• Rapid switch from controlled to assisted modes
• Rapid extubation, irrespective of moderate-severe hypoxemia
• Eventually, post-extubation C-PAP (helmet) and respiratory physiotherapy
RATIONALE FORACCELERATED WEANING FROM
INVASIVE MECHANICAL VENTILATION
• CTEPH are “used” to severe hypoxemia
• A gradual improvement of gas exchange is expected
CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: SURGICAL TREATMENT
ARTERIAL BLOOD GASES
• Gas exchanges returned to normal values in the majority of pts already at the 3-month control
Pa O2
50
60
70
80
90
100
Before PEA 3 months 1 year 2 years 3 years 5 years
mm
Hg
Before PEA vs 3m, 1y, 2y, 3y and 5y p < 0.01
Pa CO2
25
30
35
40
45
Before PEA 3 months 1 year 2 years 3 years 5 years
mm
Hg
Before PEA vs 3m, 1y, 2y, 3y and 5y p < 0.02
O2-Sat
90
92
94
96
98
100
Before PEA 3 months 1 year 2 years 3 years 5 years
%
Before PEA vs 3m, 1y, 2y, 3y and 5y p < 0.02
RATIONALE FORACCELERATED WEANING FROM
INVASIVE MECHANICAL VENTILATION
• CTEPH are “used” to severe hypoxemia
• A gradual improvement of gas exchange is expected
RATIONALE FORACCELERATED WEANING FROM
INVASIVE MECHANICAL VENTILATION
• CTEPH are “used” to severe hypoxemia
• A gradual improvement of gas exchange is expected
• Prolonged Invasive MV increases ICU stay and infections
WEANING FROM MV:The accelerated approach
0
2
4
6
8
10
12
14
MV lenght (days) ICU stay (days)
before 03
03-05
P = 0.02P = 0.07
R2 = 0,9436
0
10
20
30
40
50
60
70
80
0 10 20 30 40 50 60
MV lenght (days)
ICU
sta
y (d
ays)
0
5
10
15
20
25
30
VAP (%) Infections (%)
before 03
03-05
P = 0.03P = 0.04
WEANING FROM MV:The accelerated approach
0
100
200
300
400
PaO
2 / F
iO2
(mm
Hg
)
PRE-EXTUBPRE-OP
POST-EXTUB
PRE-DISC
POST-OP
PRE-EXTUBATION PARAMETERS
PaO2/FiO2 246 ± 110 mmHg (113–491)
PEEP 7.5 ± 2 cmH2O (4–10)
FiO2 0.5 ± 0.1 (0.3–0.7)
POST-EXTUBATION C-PAP
2 / 3 patients
PEEP 9 ± 1 cmH2O (8 – 10)
Lenght 2.2 ± 1.4 days
INITIAL MVPARAMETERS
TV 666 ± 168 ml
TV / Kg 8.5 ± 2.2 ml/Kg
PEEP 9.7 ± 2.9 cmH2O
(5–14)
FiO2 0.7 ± 0.2
(0.4–1)
HEMODYNAMIC MANAGEMENT AFTER PEA
Weaning from CPB
Eventual SUPPORT to
RV
function
InotropesDobutamine
Ph 3 Inhibitors
Epinephrine
Systemic
circulation
Systemic
VasopressorsNorepinephrine
Pulmonary
VasodilatorsiNO
Prostanoids
Nitroprusside
HEMODYNAMIC MANAGEMENT
• Rapid weaning from Inotropes and iNO
• Diuretics• Gradual weaning
from vasopressors
• No persistent PH• Good RV function• CO increase limit.
• Intraop. Overload• Hypoxemia• Rapid MV weaning
• Need for negative fluid balance
• Effective surgery• Cardiac protection
HEMODYNAMIC MANAGEMENTRESULTS
Dobut.5.9 ± 2.7
(2-12)
1.3 ± 0.8
(1 – 4)
Norep.0.2 ± 0.1
(0.01-0.5)
4.1 ± 3.7
(1 – 13)
2
3
4
5
6
7
8
CO
(l/m
in)
0
250
500
750
1000
1250
1500
PV
R (
dy
ne
s/s
*cm
-5)
Dosemcg/Kg/min
Lenghtdays
1 2 3 4 5
0
20
40
60
80
100
% p
ati
en
ts
postoperative days
Dobutamine
Norepinephrine
PRE-OP
POST-OP
POST-OP
PRE-OP
Mean ∆PVR -68 %
Mean ∆CO +37 %
ANTICOAGULATION
• Prevention of local re-thrombosis:- Early start of SC heparin- Early resumption of Vit. K antagonism• PLT count daily monitoring (high risk HIT)
In our experience:1° dose SC Heparin: 15 ± 9 hours (6 – 36)
1° dose VKA: 2.4 ± 1.3 days (1 – 6)after ICU admission
POSTOPERATIVE COMPLICATIONS OF PEA
• Persistent PH and RH failure
• Reperfusion pulmonary edema
• Pulmonary hemorrhage
• Neurologic disturbances
• Infections
• Heparin induced thrombocytopenia
• Arrhythmyas
CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: SURGICAL TREATMENTOPERATIVE MORTALITY
Survivors 95.6 %
Deaths 4.4 %500 patients
Low postoperative PVR
Deaths 0.9 %
High residual PVR
Deaths 30,1 %
90 % 10 %
CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: SURGICAL TREATMENT
Patients at risk for PPH?
- Distal disease
- Inhomogeneous disease (unilateral!)
Pervious branches
Obstructedbranches
normal
plexiformlesions
muscularthickening
CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: SURGICAL TREATMENT
Secondary Small Vessel Disease
PREOPERATIVE EVALUATION
PAC
Prediction of responsiveness to
surgery
Outcome
Pulm.Angiography
Treatment of PPH
• Pulmonary vasodilators
PULMONARY VASODILATORS
Which agent?To decrease right ventricle afterload without
systemic vasodilation and arterial oxygen desaturation, use a
SUPER-SELECTIVE AGENT:Inhaled Nitric Oxide
- Effective decrease of Pulmonary Vascular resistance- No effect on systemic circulation (pulmonary selective)- Vasodilates only ventilated lung areas (super-selective)- Decrease of V’/Q mismatch- Blunted reperfusion injury?
Ghofrani et al,JACC 2004; 44 (7): 1488-96
Treatment of PPH
• Pulmonary vasodilators
Treatment of PPH
• Pulmonary vasodilators
• Inotropic support
• Systemic vasopressors
• Preload optimization
Treatment of PPH
• Pulmonary vasodilators
• Inotropic support
• Systemic vasopressors
• Preload optimization
• Control of O2 consumption
• Gas exchange optimization
• Acidosis treatment
• (ECMO)
PVR (last)
< 500 dynes*s*cm-5 > 500 dynes*s*cm-5 Functional group Persistent group
35 % 65 %
PVR (114 ICU admission)
< 500 dynes*s*cm-5 > 500 dynes*s*cm-5
Control Group Study group
77 % 23 %
High residual PVR after PEA:outcome in the Pavia experience
High residual PVR after PEA:
Postoperative
management
Control Group(n = 88)
Study group(n = 26)
p
ICU stay (days) 7.7 ± 9.1 18.2 ± 16.9 < 0.0005
Dobutamine (mcg/Kg/min) 5.9 ± 2.5 7.6 ± 2.9 < 0.01
Norepinephrine (days) 2.7 ± 2.6 4.8 ± 6.1 < 0.05
Fluid balance (ml) -1772 ± 2253 -875 ± 1231 < 0.05
Inhaled NO (n, %) 10 (16.1 %) 10 (41.7 %) < 0.05
Mech. Ventilation (days) 4.2 ± 6.0 11.5 ± 11.7 < 0.0001
PEEP (cmH2O) 7.7 ± 1.9 8.9 ± 2.1 < 0.01
FiO2 (%) 58.6 ± 14.3 68.5 ± 14.9 < 0.005
CPAP (days) 1.8 ± 1.2 3.8 ± 4.7 < 0.02
Tracheotomy (n, %) 2 (3.2 %) 5 (20.8 %) < 0.02
Sedation (days) 3.0 ± 3.5 4.8 ± 5.2 < 0.05
High residual PVR after PEA:Postoperative complications
Study group(n = 26)
Control group(n = 88)
p
Hemorrhage (n, %) 2 (8.3 %) 7 (11.3 %) ns
RPE (n, %) 10 (41.7 %) 10 (16.1 %) < 0.05
Arrhythmia (n, %) 9 (37.5 %) 16 (25.8 %) ns
Pneumonia (n, %) 12 (50.0 %) 11 (17.7 %) < 0.01
Extubation failure (n, %) 10 (41.7 %) 7 (11.3 %) < 0.01
Pneumothorax (n, %) 2 (8.3 %) 7 (11.3 %) ns
Neurologic disturbances (n, %) 5 (20.8 %) 7 (11.3 %) ns
HIT (n, %) 1 (4.2 %) 3 (4.8 %) ns
Mortality (n, %) 3 (11.5%) 5 (5.7%) ns
RAMI PERVI
RAMI OCCLUSI
REPERFUSION PULMONARY EDEMACHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: SURGICAL TREATMENT
Massive blood flow diversion from “remodeled” areas to those cleared by surgery
• First described by Utley and Moser in 1982
• 5-25 % incidence• Rarely life-treatening
REPERFUSION PULMONARY EDEMA
0
5
10
15
20
25
MV lenght (days) ICU stay (days)
RPE
no RPE• Lenghten Invasive Mechanical Ventilation and ICU stay
p<0.001 p<0.001
Reperfusion Pulmonary Edema
• Prevention:
CO increase limitation? Protective MV?
Negative Fluid Balance?
• Treatment:
- iNO
- aggressive diuretic therapy
- PEEP, post-extubation C-PAP
- postural changes
- (ECMO)
PULMONARY HEMORRHAGE
• O.5 – 5 % incidence• 3° cause of perioperative mortality• Soon after CPB weaning• Experience and skill of the surgeon• Advanced age• Residual PH
Main Goals of Treatment
Hemodynamic
Stability
Adequate
Gas Exchange
Massive Pulmonary Hemorrhage After Pulmonary Thromboendarterectomy
Gerard R. Manecke et al.Anesth Analg 2004;99:672-5
Treatment of pulmonary hemorrhage
• PEEP
• Topical vasoconstrictors
• Treatment of coagulopathy
• Control of Pulmonary Artery Pressure
• Bronchial blockade
• Surgical repair
• Lung resection or embolization
INFECTION• In our series, the most frequent
complication of postoperative period• Blood Stream, Urinary tract, Wound
infections, but especially
(Ventilator Associated) Pneumonia• Risk factor: prolonged MV
Management:
Distal and protected pulmonary specimens
Empiric antibiotic therapy
Eventual down escalation
Pulmonary Samples
BronchoAlveolarLavage
PluggedTelescopicCatheter
TrachealAspirate
NEUROLOGIC DISTURBANCES
Typical manifestations:- Prolonged Drowsiness- Temporary Delirium- Hallucinations- Agitation •Lower cardiac arrest times
•Effective local cooling
•Cerebral continuous monitoring
Post-operative neurologic disorders rarely prevent extubation, maintenance of spontaneous breathing and
normal patient recovery
HEPARIN INDUCED THROMBOCYTOPENIA
Antibodies vs Heparin-PF4 complexes
Platelet activation
Thrombocytopenia Venous and ArterialThrombosis
Typical features
• Seroconversion and initial PLT count fall
(5-10 days after Heparin exposure)
• PLT < 50% or < 150 109/L
(7-14 days after Heparin exposure)
•25% pts: Rapid Onset HIT
(Heparin exposure within the previous 100 days and residual circulating antibodies)
HIT in cardiac surgery patients
Teatment of HIT• Alternative, Non-Heparin
Anticoagulation:- Direct Thrombin Inhibitors
- Factor Xa Inhibitors• Routine ultrasonography• VKA after PLT recovery
(PLT > 100-150 109/L)
• Vit K Antagonism reversal (pts receiving VKA at HIT diagnosis)
• PLT transfusion (High bleeding risk or overt bleeding)
• 1-5 % incidence• DD with po PLT decrease:- secondary to CPB, hemodilution- nadir day 2 after surgery