Pulmonary Hypertension and Pregnancy

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Pulmonary Hypertension and Pregnancy:

Pulmonary Hypertension and Pregnancy Aalap Shah Obstetric Anesthesiology September 20, 2012

Outline:

Outline Pulmonary Hypertension ( pHTN ) – Overview Introduction pHTN evaluation Treatment II. pHTN in the Parturient III. Goals of Anesthetic Care - Pre-Op - Monitoring - Intraop - Post-Op Care IV. Anesthetic Management in a pHTN Parturient

I. Introduction:

I. Introduction Definition: - Progressive increase in mean pulmonary arterial pressure (PAP) > 25 mmHg at rest; OR 30mmHg during exercise - PAP > 30/15 - Estimated PASP > 0.5 SBP PBF= ( mPAP-mPCWP )/PVR

I. Introduction:

I. Introduction Demographics: - Prevalence: 15 cases/1 million ( Humbert 2006) - Incidence: 2.4 cases/1 million/year ( Humbert 2006 ) - Average age: 53 +/- 14 years ( Badesch 2010) - Overall survival: Launay et al. - Comparison: Older, more obese, more comobordities

I. WHO Classification:

I. WHO Classification Simmoneau et al. 2009

I. NYHA Functional Assessment:

I. NYHA Functional Assessment ( Barst et al. 2004)

I. Introduction:

I. Introduction Normal anatomy: Pulmonary circulation Walls of PA & large branches are 30% as thick as aorta Small arterial vessels – small endothelial tubes with little muscle in wall

I. Introduction:

I. Introduction Normal Pressures: Courtesy of J. Rajesh MD

I. Introduction:

I. Introduction Pathology Muscularization of terminal portion of pulmonary arterial vasculature due to SMC hyperplasia Elevation of pulmonary pressure  medial hypertrophy & intimal fibrosis Morphological changes in vasculature are due to reactivity of vessels to high pressure

PowerPoint Presentation:

Plexiform Lesion of Pulmonary Hypertension Courtesy of Bulent Celasun , MD

PowerPoint Presentation:

Courtesy of Nationwide Children’s Hospital. Columbus, OH

I. Introduction :

I. Introduction Vicious cycle Increased mPAP  damage to pulmonary v asculature  Wall thickening/fibrosis/ plexiform lesions  impaired O2/CO2 transfer  hypoxemia  hypoxic vascoconstriction  increased mPAP

I. Introduction:

I. Introduction Acute physiological changes Increased RV afterload Decreased EDV Decreased RVEF and SV* (dynamic CO) Pulm HTN crisis: Rapid increase in PVR  > SBP  biventricular failure  death

I. Introduction:

I. Introduction Chronic physiological changes: Progressive RV overload  dilatation/hypertrophy  gradual RV dysfunction Paradoxical IVS movement Septal bowing  LV compression, impaired filling Low cardiac output state (fixed CO) Reduced arterial pressure Reduced coronary blood flow to RV

I. Introduction:

I. Introduction Common mechanism Positive intrathoracic pressure (PEEP)  alveolar overdistension + decreased venous return/RV preload  decreased PBF/increased PVR

I. pHTN Evaluation:

I. pHTN Evaluation H & P ECG – RVH, RAE CXR – cardiomegaly, prominent PA 2D TTE + Doppler flow studies Signs /symptoms - Exertional dyspnea/fatigue - Cool extremities - Poor peripheral pulse - Quiet precordium  systolic murmur over pulmonic valve - Prominent a waves in jugular vein - Loud P2 (increases w/ PAP) - L. parasternal heave - pulmonary valve regurgitation ( dilation of pulm valve annulus ) - S3 gallop (advanced RV failure ) Poor prognostic factors – RHF, syncope, chest pain

I. pHTN evaluation:

I. pHTN evaluation If non-cardiogenic pHTN confirmed  CBC, LFT, HIV, PT, aPTT , ABG , sleep study, LFTs Suspected pulmonary disease-mediated pHTN

I. Treatment:

I. Treatment Goals : = Short-term: Reduce PCWP and PVR, treat RVF = treat the cause = Oxygen = Treatment of RVF: Diuretics, ACEi , dobutamine

I. Treatment:

I. Treatment Medications CCBs: - only 15-25% of pts respond - may prevent pre-term labor ( Simhan 2007) Prostacyclins : Epoprostenol , Iloprost , Trepstinil , Beraprost (PGI2) - no discernible survival benefit *yet) - improved NYHA class and functional status

I. Treatment:

I. Treatment Medications …continued Sildenafil: PDE5 inhibitor, FDA-approved 2005 ( Galie 2005) - reduced RV mass and remodeling - minimal effects on systemic vasculature - not recommended in parturients Endothelin antagonists : bosentan , sitaxsentan , ambrisentan (chronic tx ) - one parturient case report ( Molelewka 2005)

I. Treatment:

I. Treatment Medications … continued Inhaled NO - drop in PVR ( Budts 2001 Leucht 2004) Nitric oxide donors (L-arginine) Surgical therapy Exercise training - Improved 6MWD, functional class, VO2, HR , SpO2 at 3 and 15 weeks. ( Grunig 2012)

II. pHTN in the Parturient:

II. pHTN in the Parturient Question: Can my pHTN patient safely become pregnant and undergo delivery? Women are counseled to avoid pregnancy, then and now

II. pHTN in the Parturient:

II. pHTN in the Parturient Weiss et al. 1998 (1978-1996) - N = 125 (73 Eisenmenger’s , 27 primary PH, 25 secondary pH) - Median age: mid 20s - Exclusion criteria: pregnancy < 22 weeks or intention for TOP

II. pHTN in the Parturient:

II. pHTN in the Parturient Weiss et al. continued - Eisenmenger’s : - 26 peripartum deaths (36%) (3/26 died during pregnancy) - Fetal/neonatal mortality rate; 13% (95% CI: 6-23%) - 33 (47%) delivered at term - Primary PH: - 8 peripartum deaths (30%), all after delivery - Fetal/neonatal mortality rate: 11% (95% CI: 2-29%); all pre-mature - 11 (41%) delivered at term   - Secondary PH: - 14 peripartum deaths (56%), all after delivery - Fetal/neonatal mortality rate: 12% (95% CI: 3-31%)

II. pHTN in the Parturient:

Weiss et al. continued II. pHTN in the Parturient Weiss et al. 1998

II. pHTN and the Parturient:

II. pHTN and the Parturient Weiss et al. 1998

II. pHTN in the Parturient:

II. pHTN in the Parturient Weiss et al. continued Weiss et al. 1998

II. pHTN in the Parturient:

Weiss et al. continued Points of Discussion: secondary PH mortaliy - risk factors: age, gravida ( univariate ), late diagnosis, hospital admission first month after delivery = highest mortality rate decreased myocardial contractility and EBV increased PRV reactivity and thromboembolic risk - dependent on maternal tolerance of late pregnancy II. pHTN in the Parturient

II. pHTN in the Parturient:

II. pHTN in the Parturient Bedard et al. 2009 (1997-2007) N = 76  47 reports (73 patients) median age: 29

PowerPoint Presentation:

Bedard et al. 2009

II. pHTN in the Parturient:

II. pHTN in the Parturient Bedard et al continued iPAH : - 5 peripartum deaths (17%) (2 during pregnancy) - Fetal/neonatal mortality rate: 10% - 6 (15%) delivered at term - IUGR: 3% CHD-PAH : - 8 peripartum deaths (28%), all after delivery - Fetal/neonatal mortality rate: 7% - 4 (14%) delivered at term - IUGR: 24% oPH : - 5 peripartum deaths (33%) (1 during pregnancy) - Fetal/neonatal mortality rate: 13% 0 (0%) delievered at term - IUGR: 33%

II. pHTN and the Parturient:

II. pHTN and the Parturient Bedard et al. 2009

II. pHTN in the Parturient:

II. pHTN in the Parturient Jais et al. 2012 : (2007-2010) N =26 patients (6 with inducted abortions) Median age: 31 yrs 15 /16 planned C-section (31-36wk) - 12 (80%) under spinal anesthesia - 3 (20%) under general anesthesia   Overall mortality: 12% (+1 on ECMO) Primary PH (PAH) predictors of peripartum death: increased mPAP , PVR, non-responders to CCBs

II. pHTN in the Parturient:

II. pHTN in the Parturient Duarte et al. 2013: - N =18 patients (6 with induced abortions) - All received C/S @ 34w - Overall mortality: 16.7 % Ma 2010 (1998-2008) - N = 30 - Mortality rate: 5/30 (17%) (4 of 5 within 1 month of delivery) - Fetal /Neonatal mortality rate: 4/30 (13.5%) - Term deliveries: 14/30 (47%) No multivariate predictors of mortality

II. pHTN in the Parturient:

II. pHTN in the Parturient Bonin 2005 (1992-2002) - N =15 - Mortality rate : 36% (2 die during pregnancy ); all within 1 month

III. Goals of Anesthetic Care:

III. Goals of Anesthetic Care Hemodynamic changes in pregnancy - 1 st 6 weeks: hormonal activation / prostaglandins decrease SVR, increase EBV and CO (up to 50%) - Labor contractions increase CO 10-40% - Aortocaval compression  decreased preload

III. Goals of Anesthetic Care:

III. Goals of Anesthetic Care Pre-Operative - Pre-operative assessment of severity - Maintain all pulmonary vasodilators infusions ( Humbert 2004) !! - sildenafil (PO: 0.1-0.5mg/kg q6h; IV 0.2mg/kg/ hr ) - L.arginine (15gm daily) if overt signs of pHTN and/or <4METs - acute discontinuation  vasoconstriction, hypoxia, and death - Heparin - Pre-medication – nociception increases PVR - Avoid hypotension and acidosis - CCB reactivity*** ( Sitbon 2005, Jais 2012)

III. Goals of Anesthetic Care:

III. Goals of Anesthetic Care Intraoperative - Maintain NSR, avoid tachycardia - Avoid hypotension/ hypertension - Avoid increased cardiac output associated with contraction and pain - Avoid increases in PVR or decreased contractility - hypoxia - hypercarbia - acidosis - pain/noxious stimuli - low lung volumes/ overdistension

III. Goals of Anesthetic Care:

III. Goals of Anesthetic Care Monitoring - ASA standards - Arterial line - CVP (+/-PAC) ( Warnes 2004, Connoly 2003) - TEE

III. Goals of Anesthetic Care:

III. Goals of Anesthetic Care PCWP monitoring: When is it indicated? - Assessment of respiratory distress - Assessment of shock - Severe preeclampsia management - Management of complicated MI = No consensus given risks (risk of PA rupture, arrhythmias ) ( Barash 1981 ) = No impact on outcomes ( Bedard 2009)

III. Goals of Anesthetic Care:

III. Goals of Anesthetic Care

III. Goals of Anesthetic Care:

III. Goals of Anesthetic Care

III. Goals of Anesthetic Care:

III. Goals of Anesthetic Care Post-Op Care - Continue epidural - Avoid hypoxemia, hypotension, hypovolemia - Increased risk of pulmonary vasospasm, PE, - Increased incidence of arrhythmia - Increased sympathetic/ pulm vascular tone

IV. Parturient Anesthetic Management:

IV. Parturient Anesthetic Management Mode of delivery: Vaginal delivery - smaller fluid shifts, lower clotting/bleeding complications , lower infection risk - C - section - indicated for fetal distress - uterine contraction  harmful large bolus of blood (Weiss 2000) - increased rate in recent decade  increased premature delivery rate (Bonin 2005)

IV. Parturient Anesthetic Management:

IV. Parturient Anesthetic Management Maxwell et al. 2013

IV. Parturient Anesthetic Management:

IV. Parturient Anesthetic Management Maxwell et al. 2013

IV. Parturient Anesthetic Management:

Regional Anesthesia - Combination>= Epidural > General - Epidural - Reduce local anesthetic dosage w/ opioids to decrease hemodynamic fluctuations - Medical indication for pain control - Ma 2006: Spinal (NYHA I-II), GA (NYHA III-IV ) Adjuncts: IV midazolam, fentanyl - Chohan 2006: low-dose epidural, CSA IV. Parturient Anesthetic Management

IV. Parturient Anesthetic Management:

IV. Parturient Anesthetic Management Maxwell et al. 2013

IV. Parturient Anesthetic Management:

IV. Parturient Anesthetic Management General Anesthesia - increased mortality risk ( Bedard et al. ) Induction : - Opioids – blunt intubation response, NO effect on pulmonary vessels - Lidocaine (1mg/kg) can suppress response to intubation - Induction agents: Propofol (dropped SVR), etomidate (PV reactivity) - Ketamine – increase in PVR/PAP ( Morray 1984, Berman 1990, Wolfe 1991) - Controversial (Hickey 1985, Maass 2006) - selectively attenuates endothelial dependent pulmonary vasorelaxation by inhibiting NO - Depolarizing or nondepolarizing muscle relaxants (avoid histamine - relasting Rx)

IV. Parturient Anesthetic Management:

IV. Parturient Anesthetic Management General Anesthesia continued Maintenance - Isoflurane : - attenuates hypoxic pulmonary vasoconstriction - Potential vasodilator response to B1 adrenoreceptor vasoconstriction - No effect on alpha 1 vasoconstriction - Desflurane : potentiates hypoxic pulmonary vasoconstriction to adrenoreceptor activation - N2O: transient increase in intrathoracic pressure, depressed myocardial contractility

IV. Parturient Anesthetic Management:

IV. Parturient Anesthetic Management Other medications Thromboprophylaxis - Low dose subcutaneous prophylactic heparin for PAH patients (Ginsberg 2003) - Higher doses may be indicated in underlying disorders or h/o thromboembolic events PPH /Uterine atony management - Careful use of oxytocin (dropped SVR and increased PVR, carboprost - methergine contraindicated

Conclusions:

Conclusions Improved mortality, unchanged fetal/neonatal mortality, increased pre-term delivery Mortality: Cesearean > Vaginal Increased number of treatments; studies in progress Should be continued ! CCB vasoreactivity is a strong positive prognostic factor for survival intrapartum and 1-month post-partum

Conclusions:

Conclusions Analgesia is medically indicated (due to nociceptive effects on PVR) Low-dose and sequential CSEs can maintain hemodynamic stability No prospective randomized studies on anesthetic technique and M& M Appropriate monitoring, scrupulous fluid management, awareness of PVR effectors

References:

References Badesch DB, Raskob GE, Elliott CG, et al. Pulmonary arterial hypertension: baseline characteristics from the REVEAL Registry. Chest 2010; 137:376 –387. Jais X, Olsson KM, Barbera JA, et al. Pregnancy outcomes in pulmonary arterial hypertension in the modern management era. Eur Respir J 2012; 40:881–885 . Duarte AG, Thomas S, Safdar Z, et al. Management of pulmonary arterial hypertension during pregnancy: a retrospective, multicenter experience. Chest 2013; 143:1330–1336 . Bédard E, Dimopoulos K, Gatzoulis MA. Has there been any progress made on pregnancy outcomes among women with pulmonary arterial hypertension ? Eur Heart J. 2009 Feb;30(3):256- 65 Weiss BM, Zemp L, Seifert B, Hess OM. Outcome of pulmonary vascular disease in pregnancy: a systematic overview from 1978 through 1996. J Am Coll Cardiol 1998;31 :1650–1657 . Sitbon O, Humbert M, Jais X, Ioos V, Hamid AM, Provencher S, Garcia G , Parent F, Herve P, Simonneau G. Long-term response to calcium channel blockers in idiopathic pulmonary arterial hypertension. Circulation 2005;111:3105–3111 . Hickey PR, Hansen DD, Cramolini GM, Vincent RN, Lang P. Pumonary and systemic hemodynamic responses to ketamine in infants with normal and elevated pulmonary vascular resistance. Anesthesiology. 1985 Mar;62(3):287-93

References:

References Morray JP, Lynn AM, Stamm SJ. Hemodynamic effects of ketamine in children with congenital heart disease.. Maxwell BG, El- Sayed YY, Riley ET, Carvalho B. Peripartum outcomes and anaesthetic management of parturients wth moderate to complex congenital heart disease or pulmonary hypertension. Anaesthesia . 2013 Jan;68(1):52-9 Bonnin M, Mercier FJ, Sitbon O, et al. Severe pulmonary hypertension during pregnancy: mode of delivery and anesthetic management of 15 consecutive cases. Anesthesiology 2005; 102: 1133–1137 Simhan HN, Caritis SN. Prevention of preterm delivery. New Engl J Med 2007;357:;477–487. Molelekwa V, Akhter P, McKenna P,Eisenmenger's syndrome in a 27 week pregnancy--management with bosentan and sildenafil. Ir Med J. 2005 Mar;98(3):87-8 Warnes CA. Pregnancy and pulmonary hypertension. Int J Cardiol . 2004 Dec;97 Suppl 1:11-3 Barash PG, Nardi D, Hammond G. Catheter-induced pulmonary artery perforation. Mechanisms , management, and modifications. J Thorac Cardiovasc Surg. 1981 Jul;82(1):5-12

References:

References Simonneau G, Robbins IM, Beghetti M, et al. Updated clinical classification of pulmonary hypertension. J Am Coll Cardiol . 2009;54( suppl 1):S43-S54. - Barst RJ, McGoon M, Torbicki A, Sitbon O, Krowka MJ, Olschewski H, et al . Diagnosis and differential assessment of pulmonary arterial hypertension. J Am Coll Cardiol 2004;43:40S-7S Rajesh JP. Pulmonary Hypertension – Anesthesiologist’s View. AuthorSTREMA Online Presentation. 2010 December 10 Ma LL. Management of parturients with pulmonary hypertension: experience with 30 cases. Front Med. 2012 Sep;6(3):307-10 Ginsberg JS, Bates SM. Management of venous thromboembolism during pregnancy. J Thromb Haemost . 2003 Jul;1(7):1435-42

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