PULMONARY HYPERTENSION

and its implications for anaesthesia

Dr Leong Siaw May

A/Prof Koay CK
2 May 2011
 Physiology of Pulmonary Circulation
 High-flow, low pressure and low resistance
circulation system
 Pulmonary vessels constrict with hypoxia,
relax in presence of hyperoxia
 Increases in CO decrease PVR with little effect
on PAP as vessels distend and previously
closed vessels are recruited
 Physiology of Pulmonary Circulation
 Contribution of intra- & extraalveolar vessels accounts for
the U-shaped relationship between lung volume and PVR
 Physiology of Pulmonary Circulation
 Blood flow & ventilation increases in the
dependent areas of the lung
 High PEEP narrows the capillaries in well-
ventilated lung areas and divert flow to less
ventilated or nonventilated areas
 Changing hemodynamics, mechanical forces and
hormonal environment influence the vascular
endothelium & underlying SMCs
 Pathophysiology of PHT
 Endothelial dysfunction is promoted by hypoxia,
acidosis, FR, inflammatory mediators, shear stress
caused by increased pulmonary blood flow from
LR intracardiac shunt and fibrin from
thromboembolism
 mPAP>25mmHg (normal 15mmHg) at rest of
>30mmHg with exercise is generally accepted as
indicative for PHT
 Pathophysiology of PHT
 Enhanced pressure in pulm circulation is a/w
an increase in PVR, resulting in progressive
inability of the RV to sustain its output leading
to RVH & RV failure
 Determination of PVR is difficult clinically
 Indirect estimations use the equation:
• PVR = [mPAP – LAP / pulmonary artery flow]
 Normal PVR ~ 90-120 dynes.s.cm-5
• PVR > 300 dynes.s.cm-5 is indicative of PHT
 Vascular Remodeling
 Chronic PHT leads to structural alterations of the
pulm vasculature and to a progression of
histological changes
• Increase in SMCs in already muscularized arteries
• Extension of SMCs into vessels that are normally thin and
nonmuscular
• Thickening of the adventitial layer from proliferation of
fibroblasts, collagen synthesis and deposition
• Vasomotor function may be altered in these remodeled
vessels
 Vascular Remodeling
 Major stimulus for remodeling is hypoxia
• Increase in PVR is predominantly caused by HPV
 HPV is inhibited by substance P, ANP, PGI 2, NO, increased
LAP, increased alveolar pressure & alkalosis
 Enhanced HPV with acidosis, epidural anaesthesia, inhibition
of COX or NOS
 Subsequent increases in PAP are due to
vascular remodeling and secondary
polycythaemia
 Vascular Remodeling
 Remodeling also happens in inflammation
secondary to sepsis, chronic lung disease and
ARDS
• Due to endothelial cell damage and disturbance of
pulmonary vessel tone
 WHO Diagnostic Classification of
Pulmonary Hypertension (1998)
1. Pulmonary arterial hypertension
2. Pulmonary venous hypertension
3. Pulmonary hypertension with disorders of the
respiratory systems and/or hypoxaemia
4. Pulmonary hypertension caused by chronic
thrombotic and/or embolic disease
5. Pulmonary hypertension caused by disoders affecting
the pulmonry vaculature directly
 1. Pulmonary Arterial Hypertension
1.1 Primary pulmonary 1.2 Related to
hypertension (a) Collagen vascular disease
(b) Congenital systemic-to-
(a) Sporadic
pulmonary shunts
(b) Familial (c) HIV infection
(d) Portal hypertension
(e) Drugs/toxins - anorexigens,
others
(f) Persistent PH of newborn
(g) Other
 2. Pulmonary Venous Hypertension
2.1 Left-sided atrial or ventricular heart disease
2.2 Left-sided valvular heart disease
2.3 Extrinsic compression of cantral pulmonary veins
(a) Fibrosing mediastinitis
(b) Adenopathy / tumours
2.4 Pulmonary venoocclusive disease
2.5 Other
 3. Pulmonary hypertension with disorders of
the respiratory system and/or hypoxaemia
3.1 COPD
3.2 Interstitial lung disease
3.3 Sleep disordered breathing
3.4 Alveolar hypoventilation disorders
3.5 Chronic exposure to high altitude
3.6 Neonatal lung disease
3.7 Alveolar-capillary dysplasia
3.8 Other
4. Pulmonary hypertension caused by 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, etc)
(b) In situ thrombosis
(c) Sickle cell disease
 5. Pulmonary hypertension caused by disorders
affecting the pulmonary vasculature directly
5.1 Inflammatory
(a) Schistosomiasis
(b) Sarcoidosis
(c) Other
5.2 Pulmonary capillary hemangiomatosis
 Primary PHT
 Rare, female:male (1.7:1), familial link in 6%
of all cases, dx of exclusion
 PAP usually > 60 mmHg
 Hypoxaemia & increased PVR and PAP can
lead to RV failure and death
 Poor prognosis
• median survival 2-3 yrs after dx
 Secondary PHT
 Mostly due to cardiac or pulmonary disease
and may be reversible in some cases
 Reich et al’s study showed that in patients
undergoing CABG, the development of PHT
was a significant predictor of increased
mortality and periop MI
 Secondary PHT
 Intraop injury & postop endothelial
dysfunction of pulm endothelium is promoted
by
• Preop status of pulm vascular bed: PHT, COPD,
valvular pathology, L-R intracardiac shunt
• Intraop vasospastic stimuli: hypoxia, hypercarbia,
acidosis, total duration of CPB, ischaemic-reperfusion
injury, inflammatory mediators, microemboli
• Postop factors: adrenergic tone, atelectasis, HPV
PHT During Anaesthesia
Symptoms & Signs of PHT
 Treatment of Pulmonary Hypertension
 Basic Considerations:
• Priority is to treat the underlying disease
 anti-obstructive therapy in COPD
 corticosteroids for interstitial lung disease
 systemic anti-coagulation for chronic lung embolism
 antibiotics for pneumonia
 early definitive repair of congenital heart disease
 immediate revascularisation in cases of right heart infarction
 Treatment of Pulmonary Hypertension
 Symptomatic Therapy
• Supports causal treatment & reduce PVR
 Improving oxygenation with 100% oxygen
 Avoidance of respiratory acidosis, moderate hyperventilation (PaCO 2
30-35mmHg)
 Correction of a metabolic acidosis (aim: pH >7.4)
 Recruitment maneuvers, avoid V/Q mismatch
 Adaptation of respiratory therapy, avoiding over-inflation of the lung
alveolae
 Avoidance of catecholamine release caused by stress situations:
adequate analgesia and sedation
 Avoidance of shivering: body temp 37°C
 Treatment of Pulmonary Hypertension
 Specific Treatment
• Vasodilative drugs for RV dysfunction with increased
PVR
• Positive inotropic drugs in RV dysfunction with normal
PVR
• Optimisation of RV preload
• Reduction of RV afterload (without significant decrease
in SVR)
 Magnesium, adenosine, ACEi, calcium antagonists,
milrinone/amrinone, PGI2, PGE1, INO
 Treatment of Pulmonary Hypertension
 Specific Treatment
• Enhancement of R coronary perfusion pressure
 Enoximone, combination of dobutamine & GTN
 Noradrenaline, phenylephrine
• Improvement of RV contractility
• Assist Devices
• Respiratory Mx of Increased PVR
 Hyperventilation (PaCO2<30) with increase in pH (>7.6)
decreases PVR and improves oxygenation
 In pts with OSA, CPAP decreased daytime PAP & PVR
 Treatment of Pulmonary Hypertension
 Implications of treating PHT must be carefully
evaluated
• Physiological changes from treatment have major
impact on systemic hemodynamic status and gas
exchange
• No current therapeutical options is ideal
• Factors that increase PVR can also extend into the
postop period. Hypoxaemia, acidosis, hypercapnia,
hypothermia & increased sympathetic stimulation can
worsen PHT
 Influence of Anaesthetic Drugs
 Anaesthetic mx cannot change the component
of PVR increases related to structure but they
can produce changes in PVR, RV afterload and
intracardiac shunting
 IV Anaesthetics
 Propofol for sedation after CPB decreases
mPAP, PVR and MAP
 During OLV for oesophageal surgery,
anaesthesia with propofol was a/w a higher
PaO2 and lower shunt fraction values
compared with anaesthesia with isoflurane and
sevoflurane
 IV Anaesthetics
 OLV with ketamine resulted in a more stable
PaO2 and pulmonary shunt when compared
with volatile anaesthetics
 Ketamine increased PVR in adults during
spontaneous respiration but in normocarbic
infants PVR index was little changed by
ketamine administration during spontaneous
breathing
 Thiopentone decreases PVR
 Volatile Anaesthetics
 In OLV, 1-1.2 MAC levels of isoflurane did not
affect HPV and PaO2
 Halothane decreased pulmonary blood flow and
left PVR unchanged
 During OLV, PaO2 with 1 MAC isoflurane was
higher than with enflurane
 Comparing desflurane and isoflurane before
OLV, desflurane increases PAP & PVR with
unchanged SVR. Isoflurane increased PAP but
did not alter PVR & CO
 Volatile Anaesthetics
 After CPB for valve surgery, FiN2O 50%
increased PVR & RAP
 In patients with PHT before elective MV
replacement, N20 increased PVR
• However this increase was not a/w alterations in other
hemodynamic variables
 Summary
 Endothelial dysfunction & vascular remodeling
are 2 important processes explaining the
development of PHT
 Therapeutic mx has progressed but there is still
no ideal treatment for this condition
 Most anaesthetics have little effects on the
pulmonary circulation with the exception of
ketamine and N2O