pulmonary hypertension and it pathophysiology. pre operative, intraoperative and post operative complications and anesthetic management.
drugs that can be used in anesthetic management of pulmonary hypertensiom
2. • Pulmonary circulation is a high flow,
low resistance circuit capable of
accommodating the entire right
ventricular output at one-fifth the
pressure of the systemic circulation
3. DEFINITION
• Pulmonary hypertension can be defined by
echocardiography or by cardiac
catheterization.
• Pulmonary hypertension is suspected when
systolic pulmonary arterial pressure is >40
mmHg by echocardiography.
• It is confirmed by cardiac catheterization
when mPAP>25 mmHg at rest or >30
mmHg with exercise
• A mean pulmonary artery pressure of 8 to
20 mmHg at rest is considered normal,.
4. • Pulmonary arterial hypertension
(PAH) is defined as:
1 – Pulmonary hypertension.
2 – Pulmonary capillary wedge
pressure PCWP < 15 mmHg.
3 – Pulmonary vascular resistance
PVR > 3 woods units (240 dynes. sec.
cm-5).
5. CLASSIFICATION
• Pulmonary arterial Hypertension (PAH)
• Pulmonary hypertension owing to left heart
disease
• Pulmonary Hypertension owing to lung
disease
• Chronic thromboembolic pulmonary
hypertension (CTEPH)
• Pulmonary hypertension with unclear
multifactorial mechanisms
19. CXR
• Enlargement of the main, right and left
pulmonary arteries
• Main PA diameter > 29 mm, right PA > 16
mm and left PA > 15 mm
• Tapering of the pulmonary vasculature
(‘peripheral pruning’)
• Heart size - normal or enlarged e.g. right atrial
contour
• Underlying causes, e.g. COPD, cardiac disease
• Loss of aortico-pulmonary window
24. Echo Features of Pulmonary Hypertension
Right ventricular hypertrophy
Significant tricuspid regurgitation - Using TR jet estimated RVSP is 4V2 + RAP
Right atrial enlargement
Right ventricular enlargement/dilatation - D-shaped LVon short axis
Right ventricular dysfunction
Pulmonary regurgitation - Using PR jet estimated PAEDP is 4V2 + RAP
Reduced RV outflow tract velocity, short acceleration time
Dilated IVC not collapsing with respiration (if patient not ventilated)
Patent foramen ovale (bubble contrast used)
Pericardial effusion
Dilated pulmonary arteries
25. Goals of therapy
• Reduce pulmonary artery pressure
• Reduce pulmonary vascular resistance
• Improve RV function
• Improve CI
• BEFORE RV failure becomes irreversible
• Maintain adequate preload
• Maintain SVR
• Avoid acidosis, hypercapnia,
hypothermia, hypoxia
26. Lifestyle modifications
• Na restrictions
• Abstinence from smoking
• Avoid high altitude
• Avoid exertion in settling of free or
frank syncope
29. Medical Therapy for PH
• Treat hypoxia and left heart failure
• Diuretics if right heart failure
• Calcium channel blockers
– Diltiazem if HR > 100 bpm
– Nifedipine if HR < 100 bpm
• Prostacyclin analogs (mortality benefit in
chronic)
– iv epoprostanol, inhaled iloprost, s/c Trepostinil
• Phosphodiesterase (PDE-5) inhibitors
– Sildenafil, Tadalafil
• Endothelin receptor antagonists e.g. Bosentan
• Nitric oxide (inhaled, continuous)
30. ANESTHETIC MANAGEMENT OF PH.
PH is a serious condition perioperative mortality
of 7-24%.
Peri-operative morbidity 14–42% includes:
Respiratory failure
Heart failure, dysrhythmias
Sepsis,
Renal insufficiency,
Myocardial infarction.
31. PRE OPERATIVE EVALUATION
Patient with established PH should be based on a risk
assessment :
Functional state
Severity of the disease
Type of surgery.
32.
33. Prognostication in Group
1 (PAH)
Determinant Low risk (good prognosis) High risk (bad prognosis)
Clinical RV failure NO YES
WHO functional class II/III IV
6 min walk distance > 400m < 300m
CPET results VO2 max > 10.4 ml/kg/min VO2 max < 10.4 ml/kg/min
Echo Minimal RV dysfunction Pericardial effusion
RV enlarged or dysfunction
RA enlarged
Haemodynamics RAP < 10 mmHg
CI > 2.5 L/min/m2
RAP > 20 mmHg
CI < 2.0 L/min/m2
BNP Minimal elevation Significant elevation
McLaughlin VV, McGoon MD. Pulmonary arterial hypertension. Circulation. 2006;114:1417–31.
35. PREOPERATIVE
MANEGMENT
Ideally before surgery, mean PAP should be reduced to a normal of
25 mm Hg.
If substantial RV dysfunction is present, the advisability of surgery
should be reexamined.
Any chronic pulmonary hypertensive therapies that patients
are currently taking should be continued perioperatively to
avoid rebound PH
Short acting anticoagulant like heparin should replace
indirect anticoagulant until the surgical procedure.
Avoid anxiety, pain, and sympathetic stimulation.
Avoid over sedation and hypoventilation.
Antibiotic prophylaxis must be given.
37. • Intraoperative “basic treatment” to
avoid an increase of pulmonary
• arterial pressure:
“Luxury”-oxygenation with inspiratory
FiO2 0.6 – 1.0
Moderate hyperventilation (goal: PaCO2
30-35 mmHg)
Avoidance of metabolic acidosis (pH >
7.4)
Recruitment-manoeuver to avoid
ventilation/perfusion-mismatch.
38. Low-tidal-volume ventilation to avoid
over-inflation of aveoli (goal: ml/kg
ideal body weight)
Temperature management to maintain
body temperature of 36-37°C
“Goal-directed” fluid- and volume-
therapy with hemodynamic
monitoring
39. INTRAOPERATIVE
MANAGEMENT
Optimize RV function and CO with adequate preload, SVR,
and avoid contractility, avoid myocardial depressants
Consider pulmonary vasodilators to decrease RV afterload
Maintain sinus rhythm.
It is good practice to remove air from intravenous syringes
and lines
42. Regional anesthetic techniques:
Not impairing spontaneous breathing
postoperative analgesic therapy
Nearly all patients with pulmonary hypertension receive
continuous anticoagulant therapy;
In severe PH or in diseases affecting the lung, patients
cannot be subjected to remaining in a flat position for
long period of time.
Regional anesthesia combined with careful GA to
ensure adequate oxygenation.
ANESTHETIC TECHNIQUES
43. GENERAL ANESTHESIA
the main advantages are
Safe oxygenation ,
uncomplicated airway management, and
intraoperative selective pulmonary vasodilation can
– if necessary – easily be administered through
the breathing circuit.
44. GENERAL
ANESTHESIA
All standard induction anesthetics can be used in
combination with opioids, as they have no influence on
pulmonary vascular resistance and oxygenation.
Ketamine may PVR due to catecholamine effect. However
patients with RV failure may be catecholamine depeleted.
Histamine-releasing muscle relaxants (atracurium ,
mivacurim) should be avoided for patients with PH,
PVR.
45. Volatile anesthetic agents of concentrations up to
1 MAC can be administered without any negative
effects on pulmonary pressure and resistance.
Nitrous oxide better avoided as it may raise PVR.
So use balanced technique, mixing higher doses of
opioids and low-dose volatile anesthetic agents
,careful with stress response during intubation.
46. • Inhaled nitric oxide (NO): Potent, rapidly
acting and selective pulmonary
vasodilator. it activates the enzyme
guanylate cyclase
• Milrinone/Amrinone (phosphodiesterase
III inhibitor): 50 mcg/kg bolus of
milrinone followed by a perfusion of 0.5-
0.75 mcg/kg/min.
• Dypiridamole: 0.2-0.6 mg/kg
intravenously over 15 min; to be
repeated every 12 hours.
47. • -Inhaled prostacyclin or iloprost: Two
modalities of application
• 1. Intermittent administration: 50
mcg is diluted in 50 ml saline and
nebulized in 15 min, which aerosolizes
a dose between 14 and 17 mcg. This
treatment must be repeated every
hour.
• 2 Continuous administration at a
concentration of 50 ng/kg/min.
48. • Prostaglandin E1 (alprostadyl) and
prostacyclin (PGI2):. They activate
adenylate cyclase to increase camp.
Prostacyclin, 1.5 mg, can be dissolved in
100 ml sterile glycine buffer (final
concentration, 15 mcg/ml);
• administered by means of an inline
nebulizer connected to the inspiratory
line.
• can be infused intravenously at a dose
between 2 and 10 ng/kg/min.
49. • . Epinephrine and norepinephrine31
have been used to treat persistent
systemic hypertension;
norepinephrine has the advantages
of being both a vasoconstrictor and a
positive inotropic agent. This
medication should be titrated
according to the clinical response.
50. • Nitroglycerine
• Dobutamine: is a beta agonist. It stimulates
cyclic adenosine monophosphate (cAMP). It
may induce arrhythmias and increase
oxygen demand.
• Isoproterenol: nonselective beta agonist that
causes pulmonary and peripheral
vasodilatation. It should be gradually
reduced because PVR may return quickly to
elevated baseline levels after discontinuation
51.
52. During Extubation:
Maintaining haemodynamic stability and adequate
ventilation can be difficult.
Deep extubation
May decrease SVR, contractility
Hypoxia and hypercarbia will increase PVR
Awake extubation
Can cause severe pulmonary vasoconstriction
Need tube tolerance without increased sympathetic
tone
Patient may need post-op ventilation with ICU
admission
53. postoperative monitoring until pulmonary pressures
and right-sided heart functions have stabilized at
the preoperative level.
sufficient analgesic therapy in the form of continuous
regional anesthesia
The specific therapy for PH should be resumed
at the preoperative dosage as soon as
possible.
In the postoperative course, it is also advisable to
treat pressure elevations.
Post operative management
54. laparoscopy
• An increase in end tidal carbon dioxide.
Acidosis, arrhythmias ,decrease preload PH
crisis.
• post operative benefits of laparoscopic surgery
must be balanced with intraoperative risk
involved.
• IAP to be maintained at 10-12 mm of Hg.
• CO2 insufflation slow rate to attenuate
abdominal stretch response
• Combined general with epidural anaesthesia
decreasing intraoperative anaesthetic
requirement.