Mortality Conference– FESS and Pulmonary Hypertension

Mortality Conference– FESS and Pulmonary Hyperten

sion

R1 陳建宇 / VS 李宗勳

Brief History (1)

81/3/6: BOD 81/6(3m/o): s/p Kasai operation 86/6/24 (5y/o): RV: 66/6 mmHg/ MPA: 63/

17mmHg 87/4/27 (6y/o): Living related liver transpla

ntation( Prednisolone, FK506)

Brief History (2)

89/5(8y/o): MgSO4, PGE1 for pulmonary HTN

89/8/24: RV: 123/21 mmHg/ MPA: 120/75 mmHg, start i.v. use of PGI2 7 ng/kg/min

89/10/13: Timentin and Vancomycin for Pseudomonas and MRSA

89/10/17: FESS

EKG

89/8/24

CXR

89/10/7 89/10/17

Anesthesia Course(1)

Induction drugs:

Fentanyl 1ml

Pentothal 125mg

Atracurium 15mg

Droperidol 0.5mg Gas:

Isoflurane

ETT: 5.5mm with cuff (17cm)

A-line: L’t pedal a. I/O: 300/300ml

Anesthesia Course(2)

Brief History(3)

89/10/17 3:50pm: Transferred to PICU-- bradycardia, desat

uration; CPR; ABG revealed metabolic acidosis. Pupil was dilated.

7:05pm: Another episode of bradycardia followed by asystole happened

8:00pm: ECMO 89/10/19 12:10am: expired

Pulmonary Hypertension

Primary (Idiopathic)Pulmonary Hypertension

Secondary Pulmonary Hypertension Postoperative Pulmonary Artery

Hypertension

Primary Pulmonary Hypertension

A progressive, fatal d’x PAP↑PVR↑ Mean pressure>25mmHg Young population, F>M Median survival from time of diagnosis is

2-3 years

Secondary Pul. HTN

Causes:

L’t heart dysfunction, Hypoxic lung d’x,

L’t to R’t shunt, Liver d’x Same treatment as PPH

Postoperative Pul. Artery HTN

Especially perioperative Rapidly fatal

Treatment of Pul. HTN

Conventional Mamagement• General support care• Hyperventilation• Pharmacologic vasodilator

General Support Care

CO2:

O2 with mechanical positive-pressure ventilation(PPV)

PH Blood Pressure Narcotics and muscle relaxants can

decrease the morbidity and mortality

Hyperventilation

To produce respiratory alkalosis:• Pulmonary circulation is sensitive to hydro

gen ion than CO2 • Respiratory alkalosis promotes PGI2 relea

se High intrathoracic pressure may compromi

se CV function and exacerbate the hypoxemia

Vasodilator Therapy

Alpha-adrenergic antagonists Nitrovasodilators Beta-adrenergic agonists Prostaglandins Calcium channel blockers

Alpha-adrenergic Antagonists

Tolazoline Neonate PVR↓ Systemic hypotension

Nitrovasodilators

Sodium nitroprusside• Direct vascular smooth m. relaxant• Both arterial and venous smooth m. Nitroglycerin• Venous vasodilator• Reduction in PVR and PAP• Systemic hypotension

Beta-Adrenergic Agonists

Increase intracellular cAMP Isoproterenol Dobutamine

Prostaglandins

PGE1 PGI2

PGI2(Epoprostenol)(1)

Potent vasodilator and inhibitor of platelet aggregation

Adult: 5.5ng/kg/min( 5-20ng/kg/min) Effects: increase cardiac index, exercise

tolerance, subjective improvements Decrease PVR( 46+/-5%) and SVR( 50+/-

4%) Children greater than adults

PGI2(2)

Unstable at room temporature in solution and must be shielded from light, thus limiting its use to the acute setting

Iloprost is a stable synthetic analogue of PGI2

Delay the need of transplantation

PGI2(3)

Complications:

bradycardia, arrhythmia, hypotension,

prolonged bleeding time, severe

hypoxemia Abrupt withdrawal may results in rebound

pulmonary hypertension Expensive: £45,000/yr

Calcium Channel Blockers

Calcium: regulation of smooth muscle contraction

Nifedipine PAP and PVR↓ Side effects:

sinus arrest, systemic hypotension,

decreased myocardial contractility

Nonconventional Management

-- Fail to respond to conventional medical t’x

-- Only experimental and no routinely practice Mechanical ventilation Anticoagulants Experimental vasodilators Inhaled nitric oxide Extracorporeal support Transplantation

Mechanical Ventilation

Maintain gas exchange while decreasing adverse effort on CV function

High frequency ventilation( HFV) -poor outcome

Airway pressure release ventilation( APRV) -only one case

Anticoagulants

Warfarin Combined with a vasodilator Prostacyclin

Experimental Vasodilators

MgSO4:

activate adenylate cyclase which

suppress the release of catacholamine Adenosine and ATP:

rapid clearance and is relatively

selective pulmonary vasodilator

Inhaled Nitric Oxide

Most promise as a routine therapeutic tool Selective pulmonary vasodilator Both infants and adults Unknown potential toxicities

Extracorporeal Support

Extracorporeal membrane oxygenation (ECMO)

Mortality rate: 100% decrease to 40-60% Complications:

bleeding, neurologic injury and multiple

organ system failure

Transplantations

Heart/ lung or lung transplantation Three year survival rate: 50-60%

(prognosis similar to the results of i.v. prostacyclin)

Decision-making algorithm for postoperative pulmonary HTN

I. Ventilatory Strategy

1. Increase Alveolar and Arterial Oxygen

a. FiO2

b. Positive pressure ventilation

2. Alkalinization

a. Bicarbonate administration

3. Decrease PaCO2

a. Positive pressure ventilation

b. High tidal volume( 15-20 ml/kg)

c. Low ventilation rate( 15-20bpm)

d. Short inspiratory time( ,0.75sec)

4. Decrease Mean Airway Pressure

a. Low PEEP<4cmH2O

b. Low ventilatory rate

↓

If no improvement

↓

II. High Frequent Jet Ventilation

↓

If no improvement

↓

III.Pharmacologic Manipulation

1. Nitrovasodilators

2. Isoproterenol

3. PGE1, PGI2

4. Nitric oxide

↓

If no improvement

↓

IV. ECMO

Epinephrine(1)

Powerful alpha- and beta-adrenergic agonist Alpha-- Pulmonary vasoconstrction Beta-- Pulmonary vasodilation Low and medium doses-- PVR↓ Higher dose-- PVR↑ Increase of SVR> increase of PVR

Epinephrine(2)

In preinfusion high PVR p’t, high dose epinephrine may predominantly beta-adrenergic stimulation inducing pulmonary vasodilation

Side effects:

hypokalemia, hypercapnia( most common

metabolic side effects)

Discussing

Pre-evaluation: risk? 此刀非開不可嗎 ? Monitoring: CVP? Swan-Ganz? ETCO2 為何會上升 ? Anesthetic management:

對於麻醉用藥有否其他選擇 ? Drug’s effects: Bosmin, PGI2….. Why pupil dilated and bradycardia?