Download Chronic thromboembolic pulmonary hypertension

Chronic
thromboembolic
pulmonary
hypertension
Epidemiology and Pathophysiology
• Present late in the course of the disease.
• Early natural history of the condition is
not completely known.
• Can occur without symptoms.
• May remain asymptomatic for months or
years.
• May involve recurrent
thromboembolism.
• May involve in situ pulmonary-artery
thrombosis.
• Vascular remodeling.
• Hypertensive pulmonary arteriopathy.
• Inadequate anticoagulation.
Predisposing factors
• Defective fibrinolytic systems
• Presence of lupus-like anticoagulant
• Deficiency of protein C, protein S, and
antithrombin III
• Malignancy
• Atrial septal defects
• Indwelling venous catheters
Several lines of evidence
• Low correlation between the extent of
central anatomical obstruction and the
degree of pulmonary hypertension.
• Documented hemodynamic progression in
the absence of recurrent embolic events.
• Evidence of in situ pulmonary-artery
thrombosis.
• Histopathological evidence of arteriopathic
changes in the resistance vessels
Selected etiologic conditions giving
rise to pulmonary hypertension
1. Pulmonary Arterial hypertension
2. Pulmonary Venous hypertension
3. Pulmonary hypertension associated with disorders of the
respiratory system and/or hypoxaemia
4. Pulmonary hypertension due to chronic thrombotic and/or
embolic disease
4.1. Thromboembolic obstruction of proximal pulmonary arteries.
4.2. Obstruction of distal pulmonary arteries
a). Pulmonary embolism (thrombus, tumour, ova and/or
parasites, foreign material)
b). In-situ thrombosis
c). Sickle cell disease
5.Pulmonary hypertension due to disorders directly affecting the
pulmonary vasculature.
Clinical Manifestation
• Progressive exertional dyspnea
• Exercise intolerance
• Pulmonic component of the second heart
sound
• Chest pain on exertion
• Presyncope
• Syncope
• Inability of a compromised right ventricle
to meet the body’s demands for CO
Clinical Manifestation
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Loud second heart sound,
Tricuspid regurgitation murmurs
Engorged liver and neck veins
Elevated jugular pressure with a
positive hepatojugular reflex
• The presence of peripheral oedema
• Peripheral and central cyanosis
• Prominent right ventricular impulse
“honeymoon period”
The existence of a “honeymoon
period” during which time pulmonary
hypertension is present but the subject
exhibits few symptoms, if any. It is
during this time that compensatory
hypertrophy of the right ventricle
occurs in an effort to maintain cardiac
output in the presence of increased
pulmonary vascular resistance (PVR).
The pathophysiological
events in the progression of
pulmonary hypertension
during this period have not
been well defined.
Diagnostic Approach
• To establish the presence and extent of
pulmonary hypertension.
• PASP > 35 mmHg, PADP > 15 mmHg
• PVR > 300 dynes/s/cm*
• To determine its cause
• To determine whether it is amenable to
surgical correction
Laboratory Tests
• Standard laboratory tests are
nonspecific.
• Transthoracic echocardiography
is usually the first study to
suggest that a abnormality of the
pulmonary vasculature is
present.
TEE
•Abnormal right ventricular systolic
function
•Tricuspid regurgitation
•Leftward displacement of the
interventricular septum
•Decreased left ventricular size
•Abnormal left ventricular systolic and
diastolic function
•Right atrial and right ventricular
enlargement
Patients with PVR greater than
300/dynes/s/cm5
are good candidates for PTE
The procedure
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Median sternotomy
Cardiopulmonary bypass
Periods of cardioplegia
Hypothermia
Circulatory arrest
Post bypass
Surgical success depends on
having a bloodless field so
cardiopulmonary bypass with
periods of circulatory arrest is
essential to prevent bronchial
arterial flow flooding the
surgical field.
Probable Complications
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Arrhythmias
Haemodynamic instability
Electrolyte imbalance
Pericardial effusion
Pericarditis
Infection
Persistence of pulmonary hypertension
Reperfusion pulmonary oedema
Primary Objectives
• Preserve adequate hemodynamic function
• Preserve RV function
• Maintain of adequate coronary perfusion
pressure
• Avoid excessive ischemia during By pass
• Prevention of pulmonary oedema
reperfusion injury
• Cerebral protection
• Preserve of the main functions of the
organism
Premedication
• Anxyolithyc or sedative night
before PTE
• Morphine 10 mg SC 1hr before
transporting the patient unto the
operating block.
Mortality Risk Factors
• PVR > 1100 dynes/s/cm5
• PAP > 50 mmHg
Monitoring
• Pulse Oximetry
• ECG (5 leads)
• NIBP (when arrive
into OR)
• IBP
• Capnography
• TEE (if severe
deterioration of VD)
• PA catheter
• Thermometers
Induction of the Anaesthesia
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Good preoxygenation
Sufentanyl 25γ bolus
Midazolam 0.5 mg bolus
Etomidate 0.2 – 0.3 mg/kg
Pancuronium bromide 0.3 – 0.4mg/kg
Maintenance
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Ventilation VT 10 ml/kg
FR 12 c/min
FiO2 0.6 ( air/oxygène)
PEEP 5 mmHg ( At the and of by pass)
Sufentanyl 7.5 γ/kg
Midazolam 0.1mg/kg/hr
Objectives of the Anaesthetist
• Respect hemodynamic stability (CO,CI)
• Prevention of the factor which
aggravate CTEPH (hypoxia, acidosis,
hypercania, hypothermia, pulmonary
hyperinflation, PEEP, α adrenergetic
stimulation, histamine liberation)
• Participation in cerebral protection
Pharmacological agents that
diminish CMRO2
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Halogen compounds anesthetics
Pentothal
Propofol
BZD
Etomidate
Conclusion
• Long term of survival 85% in 3 years
80% in 5 years
• Continuing anticoagulant treatment
• Relative complications:
hemorrhages < 5%
neurologicals < 3%
Eugene Yevstratov MD
Phone: 0054111540682712 (ARG)
Private: 0030372236344 /
0030372231698(UKr)
Fax: 001 775 796 2780 (USA)
Email: [email protected] /
[email protected]
Link: http://myprofile.cos.com/eugenefox
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