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Definition Progressive increase in mean pulm arterial pressure (PAP) >25mmHg at rest or 30mmHg during exercise .

Severity of Pulmonary Hypertension:

Severity of Pulmonary Hypertension Degree of disease Mild Moderate Severe Mean PAP (mmHg) 25 - 40 41 - 55 >55


Classification Pulmonary arterial hypertension". 1. Idiopathic (IPAH) 2. Familial (FPAH) 3. Associated with (APAH): Collagen vascular disease Congenital systemic-to-pulmonary shunts Portal hypertension HIV infection Drugs and toxins

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Other (thyroid disorders, glycogen storage disease, Gaucher disease) 4. Associated with significant venous or capillary involvement Pulmonary veno -occlusive disease (PVOD) Pulmonary capillary hemangiomatosis (PCH) 5. Persistent pulmonary hypertension of the newborn

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Pulmonary venous hypertension 1. Left-sided atrial or ventricular heart disease 2. Left-sided valvular heart diseases.

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Pulmonary hypertension associated with disorders of the respiratory system or hypoxemia". 1. Chronic obstructive pulmonary disease 2. Interstitial lung disease 3. Sleep-disordered breathing 4. Alveolar hypoventilation disorders 5. Chronic exposure to high altitude 6. Development abnormalities

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Pulmonary hypertension caused by chronic thrombotic or embolic disease 1. Thromboembolic obstruction of proximal pulmonary arteries 2. Thromboembolic obstruction of distal pulmonary arteries 3. Non-thrombotic pulmonary embolism (tumor, parasites, foreign material)

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VC RA RV PA PV PC LA LV Ao Post-Capillary PH (PCWP>15 mmHg ; PVR nl) Systemic HTN AoV Disease Myocardial Disease Dilated CMP-ischemic/non-isc. Hypertrophic CMP Restrictive/infiltrative CMP Obesity and others Atrial Myxoma Cor Triatriatum PV compression PVOD PAH Respiratory Diseases PE Pulmonary Hypertension: Lesion MV Disease  LVEDP Mixed PH Pre-capillary PH PCWP < 15 mmHg PVR > 3 Wu

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NORMAL REVERSIBLE DISEASE IRREVERSIBLE DISEASE Pathogenesis of Pulmonary Arterial Hypertension

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PAH: Pathophysiology

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Dilated RV- Intact pericardium  RAP   Intrapericardial pressure (IPP)   LV transmural filling pressure= LVEDP-IPP + Shift of IV septum toward LV   LV preload and  LV distensibility   Systemic Cardiac Outpu t

Clinical Evaluation of PAH:

Clinical Evaluation of PAH Symptoms: Insidious onset of shortness of breath Chest pain Syncope Peripheral edema or ascites Hemoptysis (rare)

Physical Findings in Pulmonary HTN:

Physical Findings in Pulmonary HTN C lear lungs Central and peripheral cyanosis H oarseness of voice No clubbing (if present implicates CHD)

Physical Findings in Pulmonary HTN:

Physical Findings in Pulmonary HTN Accentuated P2 Right ventricular S4 RV heave along left sternal border Large A waves from stiff RV Large V waves from TR Elevated JVP Graham-Steel murmur of PR Right ventricular S3

Assessment of Disease Severity:

Assessment of Disease Severity History Etiology Effort tolerance 6 minute walk test Hemodynamics (Pressure and Flow) CO, and RA (right heart failure) Response to acute vasodilator challenge Inhaled NO IV prostacyclin IV adenosine

Predictors of Prognosis:

Predictors of Prognosis  NYHA Class Median Survival I and II 5 years III 2.5 years IV 6 months 5-year survival: 27% NYHA Class III/IV

Predictors of Poor Prognosis:

Predictors of Poor Prognosis Poor exercise capacity (6 MWT) Cardiopulmonary hemodynamics High right atrial pressure Low cardiac index High mean pulmonary artery pressure Enlarged right atrium on echo Pericardial effusion on echo Absence of anticoagulant use Absence of initial acute vasodilator response

Goals of Therapy:

Goals of Therapy Alleviate symptoms, improve exercise capacity and quality of life Improve cardiopulmonary hemodynamics and prevent right heart failure Delay time to clinical worsening Reduce morbidity and mortality

PAH Therapy: Life style considerations:

PAH Therapy: Life style considerations Sodium restriction Abstinence from smoking Avoid high altitude <4,000 feet above sea level Avoid physical exertion in setting of pre- or frank syncope sx Avoid pregnancy

PAH: Therapy:

PAH: Therapy Pharmacologic Vasodilators/Vasoremodeling therapy (CCB, oral bosentan, inhaled iloprost; SQ/IV treprostinil; IV epoprostenol, oral sildenafil) Supplemental O 2 Anticoagulation (INR≈ 2-3) Diuretics ( excessive preload) Digoxin IV inotropes (low dose dobutamine, dopamine 1-2 mcg/kg/min ) Rx for RV failure }



Recommended Tests before Anesthesia:

Recommended Tests before Anesthesia ECG: RV/RA enlargement CXR: enlarged central and R/L pulmonary arteries,  cardiac silhouette ABG ECHO: TR, estimation of pulmonary pressure, RV hypertrophy, dilatation of RV with impairment of LV filling, paradoxical mvmt of IV septum Cardiac Catheterization: pulm pressures, CO, response to vasodilators, status of coronary circulation

Anesthetic Considerations: Pre-op:

Anesthetic Considerations: Pre-op Maintain all pulm vasodilators ex. prostacyclin , Ca2+ antagonists, phosphodiesterase-5-inhibitors ( sildenafil , dypiridamole ), endothelin receptor antagonists ( Bosentan ) and O2 If pulm HTN diagnosed immediately pre-op and OR can’t be delayed, start sildenafil (0.1mg/kg daily up to 0.5mg/kg q6hrs, adults 50-100mg daily, IV 0.2mg/kg/hr) and l- arginine (15gm daily) if clinical signs of pulm HTN or poor ex tolerance Heparin should replace indirect anticoagulant ( ie . Coumadin) until OR


Premedication Premedication: slight midazolam can be given but respiratory acidosis and hypotension should be taken care of.

Anesthetic Considerations: Goals:

Anesthetic Considerations: Goals Maintain NSR Avoid tachycardia Avoid hypotension/hypertension Avoid all factors that increase PVR: Hypoxia Hypercarbia Acidosis Pain/noxious stimuli Low lung volumes/overdistension

Anesthetic Considerations: Induction:

Anesthetic Considerations: Induction Opioids used at a dose to block the cardioresp response of intubation. Lidocaine (1mg/kg) can help suppress response to intubation Propofol, thiopentone or etomidate may be used Depolarizing or nondepolarizing muscle relaxants could be used (avoid MR releasing histamine)

Anesthetic Considerations: Maintenance:

Anesthetic Considerations: Maintenance Volatiles iso -most common Desflurane Potentiates pulm vasoconstriction to adrenoceptor activation Isoflurane Attenuates magnitude of hypoxic pulm vasoconstriction Potentiates vasodilator response to B1 adrenoceptor activation No effect on alpha 1 vasoconstriction Maintain opioids at a surgical analgesic level Maintain muscle relaxation


Monitoring Arterial line CVP or PAC TEE if available

Treatment of Pulm HTN During Surgery:

Treatment of Pulm HTN During Surgery Inhaled NO (20-40 ppm ) Milrinone (50ug/kg bolus then 0.5-0.75ug/kg/min) Dypiridamole (0.2-0.6 mg/kg IV over 15min q 12hrs) Inhaled prostacyclin ( nebulized or IV 2-20 mcg/kg/min) Mg: smooth muscle relaxant, attenuates the effect of hypoxia on PVR (serum conc 3-5mmol/L)

Nitric Oxide:

Nitric Oxide Selective pulmonary vasodilation, improves oxygenation ↑ cGMP Used in ARDS, PPHN, cardiogenic shock, post CPB Risks: methemoglobinemia and carboxyhemoglobinemia, rebound pulm HTN when stopped Requires closed inhalational circuit

Phosphodiesterase inhibitors:

Phosphodiesterase inhibitors Inhibition of nitric oxide degradation Sildenafil (PDE-5 inhibitor): ↓ PAP/PVR Min effects on systemic vasculature Synergistic with NO Reduction in RV mass: role in prevention or reversal of remodeling of RV Milrinone (PDE-3 inhibitor): ↓ PVR/PAP/SVR in setting of CV shock Nebulized minimizes systemic vasodilation


Prostacyclins Potent pulm and systemic vasodilators with antiplatelet properties Epoprostenol (IV): ↓ PVR, better CO/ex. Tolerance s/e: ↓BP, need for central line (risk of infection) Beraprost (PO): Longer duration Iloprost (nebulized)

Endothelin receptor antagonists:

Endothelin receptor antagonists Endothelin-1: neurohormone that causes pulm vasoconstriction, smooth muscle proliferation, fibrosis Stimulates endothelin receptors A & B A: vasconstriction B: vasodilation Nonselective: Bosentan A selective: sitaxsentan, ambrisentan Chronic pulm htn tx given long ½ life and no IV preparation s/e: hepatic toxicity

Ca channel blockers:

Ca channel blockers Chronic pulm HTN Rx s/e: hypotension causing reflex tachycardia Only 15-25% of pts respond Need to undergo vasoreactivity testing prior to starting


Post-op ICU Optimal analgesia with continuous epidural, regional block or parenteral opioids Avoid, hypoxemia, ↓BP, hypovolemia Risk of acute pulm vasospasm, PE, arrhythmia, fluid shifts, ↑ sympathetic tone, ↑ pulm vasc tone Wean any pulmonary vasodilators progressively

Periop Complications in Children with Pulm HTN undergoing Noncardiac Surgery or Cardiac Cath:

Periop Complications in Children with Pulm HTN undergoing Noncardiac Surgery or Cardiac Cath ↑ complication in pts with systemic (PAP 70-100% of systemic BP) or suprasystemic (PAP >100% systemic BP) Major complications more frequent during cardiac cath: 3/141 cardiac arrests, 2/141 deaths associated with pulm THN crises No association with age, etiology of PAH, type of anesthetic, or airway mngt technique

Pulm HTN Crises:

Pulm HTN Crises Rapid ↑ in PVR where PAP > syst BP R heart failure →↓PBF, ↓ CO, hypoxia and Biventricular failure Rx: 100% O2, hyperventilation, attenuation of noxious stimuli, pulm vasodilators

Obstetric Anesthesia:

Obstetric Anesthesia Epidurals used successfully Risk of ↓ venous return/BP from sympathetic blockade Keep BP within 15% of baseline and below basal level Systemic pressure should always be higher than pulm pressure Use a low concentration of LA/opioids to reduce drop in BP


C-section Uterine contraction: large bolus of blood to circulation may be poorly tolerated if severe pulm HTN or MS Vasodilators eg. NTG Diuretics



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