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