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Pulmonary hypertension
By:-
Dr. Prateek Gupta
PG Anesthesia (2nd Year)
• 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
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,.
• 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).
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
PAH
• Idiopathic
• Hereditary- BMPR2, ALK-1, endoglin
• Drug and toxin induced
• Associated PAH.
- connective tissue disorders
-HIV
-portal HTN
-schistosomiasis
-CH. Hemolytic anemia
-persistent newborn PH
• Pulmonary veno-occlusive disease and/or
pulmonary capillary hemangiomatosis (PCH)
Pulmonary hypertension owing
to left heart disease
• Systolic dysfunction
• Diastolic dysfunction
• Valve disease
• Congenital/acquired left heart
inflow/outflow tract obstruction
Pulmonary Hypertension owing to
lung disease
• Chronic obstructive pulmonary disease
• Interstitial pulmonary diseas
• Sleep-disordered breathing
• Alveolar hypoventilation disorders
• Chronic high-altitude exposure
• Developmental abnormalities
• Other pulmonary diseases with mixed
restrictive and obstructive patterns
MISCELLENOUS
• Hematological disorders: myeloproliferative
and splenectomy, chronic anemia
• Systemic disorders: sarcoidosis, pulmonary
Langerhans cell histiocytosis,
lymphangioleiomyomatosis,
neurofibromatosis, and vasculitis
• Metabolic disorders: glycogen storage
disease, Gaucher's disease, and thyroid
disorders
• Others: tumoral obstruction, fibrous
mediastinitis, and chronic renal failure with
dialysis
CLASIFICATION
Mean PAP (mmHg)
25 - 40
41 - 55
>55
Degree of disease
 Mild
 Moderate
 Severe
VC RA RV PA PV
PC
LA LV Ao
Post-Capillary PH
(PCWP>15 mmHg; PVR nl)
Systemic HTN
AoV Disease
Myocardial Disease
DCM,HCM,ischemic CM
RCM,Obesity , others
PV
compression
PVOD
PAH
Respiratory
Diseases
PE
PULMONARY
HYPERTENSION:LESIONS
Atrial Myxoma
Cor Triatriatum MV Disease
LVEDP
Pre-capillary PH
PCWP<15 mmHg
PVR > 3 Wu
DIAGNOSIS OF PH
Symptoms of PH
 Dyspnea
 Fatigue
 Near
syncope/syncope
 Chest pain
 Palpitations
 Leg edema
60%
19%
13%
7%
5%
3%
PHYSICAL EXAMINATION
 Loud pulmonary component of the 2nd heart sound
P2 (increases PAP)
 Left parasternal lift (RV heave=R sided overload)
 Right ventricular S4
 Systolic ejection murmur of TR
 S3 gallop (advanced RV failure)
 GRAHAM STEEL MURMUR OF PR
 Signs of RV failure:
 -Jugular venous distention
 -Hepatomegaly
 -Perepheral edema
CLEAR LUNGS
Investigations
• Right heart catheterization
• TTE
• CXR
• ECG
• PFT
• SPIROERGOMETRY
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
ECG
• Tachycardia
• RBBB/RVH strain
• Right axis deviation
• Right atrial enlargement
Right heart catheterization
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
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
Lifestyle modifications
• Na restrictions
• Abstinence from smoking
• Avoid high altitude
• Avoid exertion in settling of free or
frank syncope
Therapeutic treatment
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)
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.
PRE OPERATIVE EVALUATION
Patient with established PH should be based on a risk
assessment :
 Functional state
 Severity of the disease
 Type of surgery.
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.
PREOPERATIVE
MANEGMENT
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.
INTRAOPERATIVE
MANAGEMENT
Anesthetic and Hemodynamic goals for PH :
• 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.
 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
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
ANESTHETIC TECHNIQUES
All standard anesthetic techniques
can, in principle applied to patients with
PH
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
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.
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.
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.
• 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.
• -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.
• 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.
• . 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.
• 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
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
 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
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.
PERI-OPERATIVE MANAGEMENT OF PH
CRISIS
Pulmonary hypertension and its anesthetic management

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Pulmonary hypertension and its anesthetic management

  • 1. Pulmonary hypertension By:- Dr. Prateek Gupta PG Anesthesia (2nd Year)
  • 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
  • 6. PAH • Idiopathic • Hereditary- BMPR2, ALK-1, endoglin • Drug and toxin induced • Associated PAH. - connective tissue disorders -HIV -portal HTN -schistosomiasis -CH. Hemolytic anemia -persistent newborn PH • Pulmonary veno-occlusive disease and/or pulmonary capillary hemangiomatosis (PCH)
  • 7. Pulmonary hypertension owing to left heart disease • Systolic dysfunction • Diastolic dysfunction • Valve disease • Congenital/acquired left heart inflow/outflow tract obstruction
  • 8. Pulmonary Hypertension owing to lung disease • Chronic obstructive pulmonary disease • Interstitial pulmonary diseas • Sleep-disordered breathing • Alveolar hypoventilation disorders • Chronic high-altitude exposure • Developmental abnormalities • Other pulmonary diseases with mixed restrictive and obstructive patterns
  • 9. MISCELLENOUS • Hematological disorders: myeloproliferative and splenectomy, chronic anemia • Systemic disorders: sarcoidosis, pulmonary Langerhans cell histiocytosis, lymphangioleiomyomatosis, neurofibromatosis, and vasculitis • Metabolic disorders: glycogen storage disease, Gaucher's disease, and thyroid disorders • Others: tumoral obstruction, fibrous mediastinitis, and chronic renal failure with dialysis
  • 10. CLASIFICATION Mean PAP (mmHg) 25 - 40 41 - 55 >55 Degree of disease  Mild  Moderate  Severe
  • 11. VC RA RV PA PV PC LA LV Ao Post-Capillary PH (PCWP>15 mmHg; PVR nl) Systemic HTN AoV Disease Myocardial Disease DCM,HCM,ischemic CM RCM,Obesity , others PV compression PVOD PAH Respiratory Diseases PE PULMONARY HYPERTENSION:LESIONS Atrial Myxoma Cor Triatriatum MV Disease LVEDP Pre-capillary PH PCWP<15 mmHg PVR > 3 Wu
  • 12.
  • 13.
  • 14.
  • 15. DIAGNOSIS OF PH Symptoms of PH  Dyspnea  Fatigue  Near syncope/syncope  Chest pain  Palpitations  Leg edema 60% 19% 13% 7% 5% 3%
  • 16. PHYSICAL EXAMINATION  Loud pulmonary component of the 2nd heart sound P2 (increases PAP)  Left parasternal lift (RV heave=R sided overload)  Right ventricular S4  Systolic ejection murmur of TR  S3 gallop (advanced RV failure)  GRAHAM STEEL MURMUR OF PR  Signs of RV failure:  -Jugular venous distention  -Hepatomegaly  -Perepheral edema CLEAR LUNGS
  • 17.
  • 18. Investigations • Right heart catheterization • TTE • CXR • ECG • PFT • SPIROERGOMETRY
  • 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
  • 20.
  • 21. ECG • Tachycardia • RBBB/RVH strain • Right axis deviation • Right atrial enlargement
  • 22.
  • 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
  • 27.
  • 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
  • 40.
  • 41. ANESTHETIC TECHNIQUES All standard anesthetic techniques can, in principle applied to patients with PH
  • 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.