chronic thromboembolic pulmonary hypertension l.
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Chronic thromboembolic pulmonary hypertension. Epidemiology and Pathophysiology. P resent late in the course of the disease. E arly natural history of the condition is not completely known. C an occur without symptoms . M ay remain asymptomatic for months or years.

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epidemiology and pathophysiology
Epidemiology and Pathophysiology
  • Present late in the course ofthe disease.
  • Early natural historyof the condition is not completely known.
  • Can occur withoutsymptoms.
  • May remainasymptomatic for months or years.
  • May involve recurrent thromboembolism.
  • May involvein situ pulmonary-artery thrombosis.
  • Vascular remodeling.
  • Hypertensive pulmonary arteriopathy.
  • Inadequate anticoagulation.
predisposing factors
Predisposing factors
  • Defective fibrinolytic systems
  • Presence of lupus-like anticoagulant
  • Deficiency of protein C, protein S, andantithrombin III
  • Malignancy
  • Atrial septal defects
  • Indwelling venous catheters
s everal lines of evidence
Several lines of evidence
  • Low correlation between the extent of central anatomicalobstruction and the degree of pulmonary hypertension.
  • Documented hemodynamic progression inthe 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
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
Clinical Manifestation
  • Progressive exertional dyspnea
  • Exercise intolerance
  • Pulmoniccomponent of the second heart sound
  • Chest pain on exertion
  • Presyncope
  • Syncope
  • Inabilityof a compromised right ventricle to meet the body’sdemands for CO
clinical manifestation7
Clinical Manifestation
  • Loud second heart sound,
  • Tricuspid regurgitation murmurs
  • Engorged liver and neck veins
  • Elevated jugular pressurewith a positive hepatojugular reflex
  • The presence of peripheral oedema
  • Peripheraland central cyanosis
  • Prominent right ventricular impulse
honeymoon period
“honeymoon period”

The existence of a “honeymoon period” during which time pulmonaryhypertension is present but the subject exhibits few symptoms, if any. It is during thistime that compensatory hypertrophy of the right ventricle occurs in an effort to maintaincardiac output in the presence of increased pulmonary vascular resistance (PVR).

slide9

The pathophysiologicalevents in the progression of pulmonary hypertensionduring this period have not been well defined.

diagnostic approach
Diagnostic Approach
  • To establish thepresence and extent of pulmonary hypertension.
  • PASP > 35 mmHg, PADP > 15 mmHg
  • PVR > 300 dynes/s/cm*
  • Todetermine its cause
  • To determine whether itis amenable to surgical correction
l aboratory t ests
Laboratory Tests
  • Standard laboratory tests are nonspecific.
  • Transthoracic echocardiography is usually the firststudy to suggest that aabnormality of the pulmonaryvasculature is present.
slide13
TEE
  • Abnormal right ventricularsystolic function
  • Tricuspid regurgitation
  • Leftwarddisplacement of the interventricular septum
  • Decreasedleft ventricular size
  • Abnormal left ventricular systolicand diastolic function
  • Right atrial and rightventricular enlargement
the procedure
The procedure
  • Mediansternotomy
  • Cardiopulmonary bypass
  • Periods of cardioplegia
  • Hypothermia
  • Circulatory arrest
  • Post bypass
slide18

Surgical success depends on having a bloodless field socardiopulmonary bypass with periods of circulatory arrest is essential to preventbronchial arterial flow flooding the surgical field.

probable complications
Probable Complications
  • Arrhythmias
  • Haemodynamic instability
  • Electrolyte imbalance
  • Pericardial effusion
  • Pericarditis
  • Infection
  • Persistence of pulmonary hypertension
  • Reperfusionpulmonary oedema
primary objectives
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
Premedication
  • Anxyolithyc or sedative night before PTE
  • Morphine 10 mg SC 1hr before transporting the patient unto the operating block.
mortality risk factors
Mortality Risk Factors
  • PVR > 1100 dynes/s/cm5
  • PAP > 50 mmHg
monitoring
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
Induction of the Anaesthesia
  • 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
Maintenance
  • 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
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
Pharmacological agents that diminish CMRO2
  • Halogen compounds anesthetics
  • Pentothal
  • Propofol
  • BZD
  • Etomidate
conclusion
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
Eugene Yevstratov MD

Phone: 0054111540682712 (ARG)

Private: 0030372236344 / 0030372231698(UKr)

Fax: 001 775 796 2780 (USA)

Email: ostlandfox@yahoo.de / ostlandfox@medscape.com

Link: http://myprofile.cos.com/eugenefox

Thanks