Chronic thromboembolic pulmonary hypertension - PowerPoint PPT Presentation

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Chronic thromboembolic pulmonary hypertension

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Can occur without symptoms. May remain asymptomatic for months or years. ... pulmonary hypertension is present but the subject exhibits few symptoms, if any. ... – PowerPoint PPT presentation

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Title: Chronic thromboembolic pulmonary hypertension


1
Chronic thromboembolic pulmonary hypertension
2
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.

3
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

4
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

5
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.

6
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 bodys demands for CO

7
Clinical Manifestation
  • 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

8
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).
9
The pathophysiological events in the progression
of pulmonary hypertension during this period have
not been well defined.
10
Diagnostic Approach
  • To establish the presence and extent of pulmonary
    hypertension.
  • PASP gt 35 mmHg, PADP gt 15 mmHg
  • PVR gt 300 dynes/s/cm
  • To determine its cause
  • To determine whether it is amenable to surgical
    correction

11
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12
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.

13
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

14
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15
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16
Patients with PVR greater than
300/dynes/s/cm5 are good candidates for PTE
17
The procedure
  • Median sternotomy
  • Cardiopulmonary bypass
  • Periods of cardioplegia
  • Hypothermia
  • Circulatory arrest
  • Post bypass

18
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.
19
Probable Complications
  • Arrhythmias
  • Haemodynamic instability
  • Electrolyte imbalance
  • Pericardial effusion
  • Pericarditis
  • Infection
  • Persistence of pulmonary hypertension
  • Reperfusion pulmonary oedema

20
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

21
Premedication
  • Anxyolithyc or sedative night before PTE
  • Morphine 10 mg SC 1hr before transporting the
    patient unto the operating block.

22
Mortality Risk Factors
  • PVR gt 1100 dynes/s/cm5
  • PAP gt 50 mmHg

23
Monitoring
  • Pulse Oximetry
  • ECG (5 leads)
  • NIBP (when arrive into OR)
  • IBP
  • Capnography
  • TEE (if severe deterioration of VD)
  • PA catheter
  • Thermometers

24
Induction of the Anaesthesia
  • Good preoxygenation
  • Sufentanyl 25? bolus
  • Midazolam 0.5 mg bolus
  • Etomidate 0.2 0.3 mg/kg
  • Pancuronium bromide 0.3 0.4mg/kg

25
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 ?/kg
  • Midazolam 0.1mg/kg/hr

26
Objectives of the Anaesthetist
  • Respect hemodynamic stability (CO,CI)
  • Prevention of the factor which aggravate CTEPH
    (hypoxia, acidosis, hypercania, hypothermia,
    pulmonary hyperinflation, PEEP, a adrenergetic
    stimulation, histamine liberation)
  • Participation in cerebral protection

27
Pharmacological agents that diminish CMRO2
  • Halogen compounds anesthetics
  • Pentothal
  • Propofol
  • BZD
  • Etomidate
















































28
Conclusion
  • Long term of survival 85 in 3 years 80 in 5
    years
  • Continuing anticoagulant treatment
  • Relative complications
  • hemorrhages lt 5
  • neurologicals lt 3

29
Eugene Yevstratov MD
Phone 0054111540682712 (ARG) Private
0030372236344 / 0030372231698(UKr) Fax 001 775
796 2780 (USA) Email ostlandfox_at_yahoo.de /
ostlandfox_at_medscape.com Link http//myprofile.co
s.com/eugenefox
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