46 ARAS Forgotten Ventricle

1

Remembering the forgotten ventricle:Management of acute right ventricular failure in

Pulmonary Hypertension

Mandar Aras, MD, PhDAssistant Professor

Advanced heart failure and heart transplantUniversity of California, San Francisco

Objectives

• Review the descriptive and hemodynamic classification of pulmonary hypertension

• Discuss the significance of acute right heart failure (ARHF) in PH

• Discuss management principles for ARHF in setting of pre-capillary vs. post-capillary PH, including the role of:– Oxygenation– Pulmonary vasodilator therapies– Inopressors– MCS, transplantation

Pulmonary Hypertension(PH)

Sustained elevation of mean pulmonary artery pressure*:

mPAP > 25 mmHg

Simonneau et al, J Am Coll Cardiol. 2013;62:D34-41

* mPAP = Normal: 8 - 20 mmHgePASP Echo Doppler > 40 mmHg

PH ≠ PAH

2

5th WSPH Updated Classification of Pulmonary Hypertension, Nice 2013

GROUP 1 – Pulmonary Arterial Hypertension (PAH) 1.1 Idiopathic PAH1.2 Heritable PAH1.3 Drug- and Toxin-Induced1.4 Associated with:

1.4.1 Connective Tissue Disease1.4.2 Human Immunodeficiency Virus (HIV)

Infection1.4.3 Portal Hypertension1.4.4 Congenital Heart Disease1.4.5 Schistosomiasis

1’ PVOD and/or PCH

1” Persistent PH of the Newborn (PPHN)

GROUP 2 – PH Due to Left Heart Disease2.1 LV Systolic Dysfunction (HFrEF)2.2 LV Diastolic Dysfunction (HFpEF)2.3 Valvular Disease

2.4 Congenital/Acquired Left Heart Inflow/ Outflow Tract Obstruction and Congenital Cardiomyopathies

GROUP 3 –PH Due to Lung Disease and/or Hypoxia3.1 Chronic Obstructive Pulmonary Disease3.2 Interstitial Lung Disease3.3 Other Pulmonary Diseases With Mixed Restrictive

and Obstructive Pattern3.4 Sleep-disordered Breathing3.5 Alveolar Hypoventilation Disorders3.6 Chronic Exposure to High Altitude3.7 Developmental Lung Diseases

GROUP 4–Chronic Thromboembolic PH (CTEPH)

GROUP 5 – PH With Unclear Multifactorial Mechanisms5.1 Hematologic Disorders: Chronic Hemolytic Anemia,

Myeloproliferative Disorders, Splenectomy

5.2 Systemic Disorders: Sarcoidosis, Pulmonary Histiocytosis, Lymphangioleiomyomatosis

5.3 Metabolic Disorders: Glycogen Storage Disease, Gaucher Disease, Thyroid Disorders

5.4 Others: Tumoral Obstruction, Fibrosing Mediastinitis, Chronic Renal Failure, Segmental PH

Simmoneau G, et al. JACC. 2013; 62:D34-41.

Strange G et al. Heart 2012;98:1806-1811.

• Single center study from Australia • 6,994 screened 936 pts (9.1%) with PH on

ECHO Doppler (defined as ePASP >40 mmHg)

Etiology of PH on Echocardiogram

VC RA RV PA PVPC

LA LV Ao

PH Hemodynamic Profiles:

Vachiery JL et al, J Am Coll Cardiol 2013;62: D100-8Fang J et al, J Heart Lung Transplant 2012;31:913–33Galie N et al, Eur Respir J 2009;34(6):1219-63

VC RA RV PA PVPC

LA LV Ao

PH Hemodynamic Profiles:

Pre-capillaryPH

Vachiery JL et al, J Am Coll Cardiol 2013;62: D100-8Fang J et al, J Heart Lung Transplant 2012;31:913–33Galie N et al, Eur Respir J 2009;34(6):1219-63

Post-capillaryPH

Combined post-& pre-capillary

PH(Mixed PH)

3

VC RA PA PVPC

LA LV Ao

Group 1 – PAHGroup 3,4,5

Pre-capillary PHPA mean ≥ 25mmHg

PAWP < 15 mmHg

TPG > 12PVR > 3 Wu

RV

Modified from: Galie N et al. Eur Respir J. 2009. 34(6):1219-63

Fang J et al. J Heart Lung Transplant 2012;31:913–33Vachiery JL et al, J Am Coll Cardiol 2013;62: D100-8

Normal

PAH

FDA-Approved Specific Therapies for PAHEndothelin Receptor Antagonists (oral)

• Bosentan• Ambrisentan• Macitentan

Phosphodiesterase Type-5 Inhibitors (oral)

• Sildenafil• Tadalafil

Prostacyclin Derivatives

• Epoprostenol: IV

• Iloprost: inhalational

• Treprostinil: inhalational, oral, SQ or IV

Soluble Guanylate Cyclase Stimulators (oral)

• Riociguat (also approved for CTEPH)

Prostacyclin Receptor Agonist (oral)• Selexipag

Simonneau G et al, J Am Coll Cardiol 2013;62:D34-41Vachiery JL et al, J Am Coll Cardiol 2013;62: D100-8Fang J et al, J Heart Lung Transplant 2012;31:913–33Galie N et al, Eur Respir J 2009;34(6):1219-63

Group 2: PH due to left heart diseaseLV Systolic dysfunctionLV Diastolic dysfunctionValvular disease LH obstruction & Congenital CMP

VC RA RV

Isolated Post-Capillary PHPAWP>15 mmHg

TPG < 12PVR nl range

• Myocardial DiseaseCMP-ischemic/non-isc.

Hypertrophic CMPRestrictive/infiltrative CMP

• Pericardial disease

PA PVPVPPC

LALAP

LV Ao

Systemic HTNAoV Disease

LVEDP

MR

HFrEF, HFpEF

Combined post- & pre-capillary PH(CpcPH)

Mixed hemodynamic profile PAWP > 15 mmHg

TPG>12 PVR > 3 Wu

VC RA PAPC

LALAP

LV Ao

LVEDP

PVPVP

RV

Left sided filling pressure Neurohormones, cytokines, other mediators

Fang J et al, J Heart Lung Transplant 2012;31:913–33Galie N et al, Eur Respir J 2009;34(6):1219-63

Moraes et al, Circ 2000; 1718

Simonneau et al, J Am Coll Cardiol 2013;62:D34-41Vachiery JL et al, J Am Coll Cardiol 2013;62: D100-8

4

Combined post- & pre-capillary PH(CpcPH)

Mixed hemodynamic profile PAWP > 15 mmHg

TPG>12 PVR > 3 Wu

VC RA PAPC

LALAP

LV Ao

LVEDP

PVPVP

RV

Left sided filling pressure Neurohormones, cytokines, other mediators

Fang J et al, J Heart Lung Transplant 2012;31:913–33Galie N et al, Eur Respir J 2009;34(6):1219-63

Moraes et al, Circ 2000; 1718

Simonneau et al, J Am Coll Cardiol 2013;62:D34-41Vachiery JL et al, J Am Coll Cardiol 2013;62: D100-8

FDA-Approved Specific Therapies for PAHEndothelin Receptor Antagonists (oral)

• Bosentan• Ambrisentan• Macitentan

Phosphodiesterase Type-5 Inhibitors (oral)

• Sildenafil• Tadalafil

Prostacyclin Derivatives• Epoprostenol: IV

• Iloprost: inhalational

• Treprostinil: inhalational, oral, SQ or IV

Soluble Guanylate Cyclase Stimulators (oral)

• Riociguat (also approved for CTEPH)

Prostacyclin Receptor Agonist

• Selexipag

Pulmonary hypertension (PH) from any etiology is associated with:

• Worse prognosis due to right heart failure

• Increased morbidity and mortality • Reduced exercise capacity

A clinical syndrome due to an alteration ofstructure and/or function of the right heart systemthat leads to a sub-optimal delivery of blood flowto the pulmonary circulation and/or elevatedvenous pressures - at rest or with exercise.

Working Definition of Right Heart Failure

Right Heart Failure Summit: Towards a Common LanguageBoston, MA 2012, 2013

5

PAH: It’s all about the RV!!

Van de Veerdonk MC, et al. J Am Coll Cardiol. 2011;58:2511-2519.

100

80

60

40

20

0

Sur

viva

l, %

0 0 50 75 100 125

Time, months

1. RVEF > 35%, PVR < 650 (n=36)2. RVEF > 35%, PVR > 650 (n=20)3. RVEF < 35%, PVR < 650 (n=13)4. RVEF < 35%, PVR > 650 (n=41)

p < 0.01

PH in LHD: It’s all about the RV!

Voelkel NF, et al. Circulation. 2006;114:1883-1891.

1.0

0.8

0.6

0.4

0.2

0.0

-0.2

Cum

ula

tive

Pro

po

rtio

n S

urv

ivin

g

0 10 20 30 40 50 60 70

months

P<0.001

Group 1: Normal PAP, preserved RVEF Group 2: Normal PAP, low RVEF Group 3: High PAP, preserved RVEF Group 4: High PAP, low RVEF

Category High Risk Variables Predicting RVF

Demographic • Age• Female gender

Clinical setting • Need for mechanical ventilation• Need for dialysis/CRRT

Biomarkers • High INR• High NT-proBNP (heterogenous)

Hemodynamic (RHC) • Low RVSWI• High CVP

Echocardiography • Moderate to severe RVD• Elevated RV/LV ratio• Low RV free wall longitudinal systolic

strain

Bellavia D et al.Eur J Heart Fail 2017; 9, 926–946

LVAD outcomes:It’s all about the RV (RV/PA

coupling)

Meta-analysis of:-36 studies-4428 pts-35% (995) pts developed RHF

Pulmonary hypertension

RV Pressure overload

Adaptive RV hypertrophy

Decreased wall stress

Maladaptive RV hypertrophy & fibrosisDiastolic dysfunction

De Marco T. Advances PH 2005;4:16Nootens et al. J Am Coll Cardiol 1995;26:1581 Voelkel et al. Circ 2006;114:1883

6

Pulmonary hypertension

RV Pressure overload

Adaptive RV hypertrophy

Decreased wall stress

Maladaptive RV hypertrophy & fibrosisDiastolic dysfunction

Compensated Phase

• Normal CO • Normal RAP

Decompensating Phase

• Higher RAP to maintain

adequate CO• CO with exercise

De Marco T. Advances PH 2005;4:16Nootens et al. J Am Coll Cardiol 1995;26:1581

Neurohormonal

Cytokine,

& other

mediator activation

Altered gene

expression

RV remodeling

Voelkel et al. Circ 2006;114:1883

De Marco T. Advances PH 2005;4:16 Haddad et al. Circ 2008;117;1717Belenkie et al. Ann Med 2001;33:236

Decompensated Phase

RAP CO

• Congestive hepatopathy/ascites/

peripheral edema

• Renal congestion

•Hypoperfusion

• Hypoxemia (PFO)

• Acidosis

• Life-threatening

dysrrhythmias

Morris-Thurgood et al, Heart Fail Rev 2000;5:307Watanabe et al, Circ Res 1990;67:923

Cont.

LV

RV

Normal PAH

LVRV

RA LA

Api

cal F

ou

r C

ha

mb

er

Par

aste

rnal

Sho

rt A

xis

PAHNormal

Echocardiogram in PAH Measuring RV systolic function

• TAPSE (Tricuspid annular plane systolic excursion)– TAPSE < 1.6 indicates RV systolic dysfunction

• Fractional area change (FAC)– Two-dimensional FAC (as a percentage) provides an estimate of RV

systolic function.

– Two-dimensional FAC < 35% indicates RV systolic dysfunction.

• Tissue doppler S’ – Easy to measure, reliable and reproducible.

– S’ velocity < 10 cm/s indicates RV systolic dysfunction.

J Am Soc Echocardiogr 2010;23:685-713.

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Management of Acute Right Heart Failure (ARHF) in PH

ARHF: Goals of Management

• Immediate– Restore oxygenation – Treat congested/ volume overload state– Restore vital organ perfusion (kidneys, brain, heart, liver)

• Short Term– Identify and treat precipitating factors– Initiate/readjust maintenance regimen– Minimize ICU time and length of stay

• Intermediate and Long Term– Prevent early readmission– Optimize medical regimen to

• Alleviate symptoms• Slow disease progression• Reduce morbidity & mortality• Successfully bridge patients to more definitive therapy

– PAH lung tx– PH in LHD with VAD Heart Transplant

De Marco T. Advances PH 2005;4:16 ; Haddad et al, Circ 2008;117;1717

Medical Management Principles in ARHF

Hoeper MH, et al. Am J Respir Crit Care Med.2011;184:1114-1124. (modified)

Identify and Treat Triggering Factor(s)

Reduce RV Afterload: - External (PVR, PAC) - Internal (Wall Stress)

Optimize Cardiac OutputCVO2 >65%, CI >2.0 l/min/m2

Optimize Perfusion Pressure

Optimize Preload




• Dietary indiscretion, infections, anemia, arrhythmias, co-morbidities

• Rule out PE, MI, other conditions• Discontinue use of NSAIAs, COX-2 inhibitors• Hypoxemia (Maintain SaO2 >90%); Avoid intubation in severe PAHReduce RV Afterload:

- External (PVR, PAC) - Internal (Wall Stress)



Optimize Preload

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Reduce RV Afterload: - External (PVR, PAC) - Internal (Wall Stress)

• iNO, IV and/or inhaled Prostanoids (PAH) • PDE5 inhibitors (IV, oral); others• Optimal fluid management



Optimize Preload

• Use of pulmonary vasodilators in chronic PAH differs from acute PH/ RH failure

• Potential adverse hemodynamic effects of non-selective pulmonary vasodilators VQ mismatch– Inhaled treatments most selective– iNO most selective; no effect on SVR,but may lead to pulmonary

edema in PH due to LHD • Systemic administration of pulmonary vasodilators can induce

hypotension worsen RV ischemia • In presence of fixed pulmonary venous hypertension (PVOD), in

transpulmonary flow may precipitate pulmonary edema• Monitor renal function closely!!

Kieler-Jensen N et al. J Heart Lung Transplant. 1995; 14:436. McNeil K et al. Thorax 2003;58:157.Galie N, Eur Respir J 2009;34:1219. Price LC et al. Critical Care 2010;14:169

Reducing RV External Afterload (PVR)Pulmonary Vasodilators - General Considerations:

• Oxygen

– Aim for SpO2 >90%

– Avoid intubation in severe PAH cardio-circulatory collapse

• Inhaled NO in pre-capillary PH (PAH)

– selective pulmonary vasodilator

– PVR, no Δ on SVR, MAP

– no V/Q mismatch

• Other inh. Prostanoids (iloprost, epoprostenol) beneficial in pre-capillary PH (PAH)

– enhanced effect with PDE 5-Inhibitors

• IV, oral PDE-5 Inhibitors Frostell CG et al. Anesthesiology 1993;78(3):427-35Hoeper MM et al. J Am Coll Cardiol 2000;35:176

McLaughlin VV et al. J Am Coll Cardiol 2009;53:1573. Sitbon O et al. J Am Coll Cardiol 2002,40:780. Preston IR et al. Pulm Circ 2013,;3:1

Reducing RV External Afterload (PVR): Pulmonary Vasodilators

Loe E et al. Circulation. 1994;90:2780-2785

19 patients with class III (n=5) to IV (n=14) HF; mean PVR 2.8 WUProtocol: 80 ppm inhaled nitric oxide (iNO) over 10 minutes

PH in LHD: iNO

PCWP

9

PA Vasodilation PA flow

No venous dilation(inactivated by Hgb)

Hydrostatic pressure in capillary bed Pulmonary edema

Effect of INO On Pulmonary CirculatoryIn Setting of PVH

Left sided filling pressure

Fixed PVH (PVOD)• IV prostacyclin derivatives initial treatment of choice in PAH

(epoprostenol, treprostinil, iloprost)

– All reduce PVR and improve RV performance

– Epoprostenol preferred agent in ARHF• Short acting

• Shown to improve survival

• Caveat: systemic hypotension which can limit use

– May need concomitant pressors

– Avoid tachyarrhythmia

Frostell CG et al. Anesthesiology 1993;78(3):427-35McLaughlin VV et al. J Am Coll Cardiol 2009;53:1573. Sitbon O et al. J Am Coll Cardiol 2002,40:780.

De Marco T. Advances PH 2005; 4:16;

Reducing RV External Afterload (PVR, PAC): Pulmonary Vasodilators

• Sildenafil highly selective (>4000 fold) for PDE-5 over PDE-3

– Shown to exert milrinone-like effect via PDE-3 inhibition, augmenting RV function

• No significant effect on SBP or heart rate

• Other effects:

– Increase in coronary perfusion– Enhances endothelial mediated vasodilation

– Attenuates adrenergic stimulated contractility– In severe HF: PCWP and CO

• Oral or IV sildenafil may provide a transition method from iNO or inhaled epoprostenol

Degerman E et al. J Biol Chem 1997;272:6823 Aladdini J et al. Am J Cardiol 2004;94:1475Katz SD et al. J Am Coll Cardiol 2000;36:845 Borlaug BA et al. Circulation 2005;112:2642Hermann HC et al. N Engl J Med 2000;342:1622 Vachiery JL et al. BJCP 2011; 71:289

Reducing RV External Afterload (PVR): Pulmonary Vasodilators: Sildenafil

Sildenafil in PH due to Advanced HF

• 14 pts with AHF (EF<24+14%) and Cpc PH refractory to milrinone, dobutamine, nitroprusside, nesiritide

• Sildenafil 25-50 mg administered orally q 8hr <3 doses• 93% of pts:mPAP >20%; 20% pts PVR/SVR (relative PA

selectivity); 50 mg more effective; sildenafil safe & effective to improve candidacy for OHT

Aleaddini et al. Am J Cardiol 2004; 94; 1475

Baseline Post-sild. P value

mPAP (mmHg) 44+11 31+14 <0.001

PAWP (mmHg) 25+6 18+6 <0.001

CI (L/min/m2) 2.4+0.9 2.8+1.0 <0.01

PVR

(dyne.s/cm5)311+115

(3.9 Wu)

191+74

(2.4 Wu)

<0.01

SAP (mmHg) 108+19 104+21 NS

DAP (mmHg) 62+10 59+11 NS

10

VADs in PH due to Advanced HF

Masri CS et al. ASAIO J. 2017 Mar/Apr;63(2):139-143.

Hemodynamics were collected and analyzed both pre and post (w/in 48-72 hrs) LVAD implantation on a cohort of 64 HFrEF pts.

RV afterload almost always declines with LVAD insertion and does so rapidly

LVADs Decrease “Fixed” PH in Cardiac Transplant Candidates(Reduction in Left Sided Filling Pressures)

Zimpfer et al. J Thorac Cardiovsc Surg 2007;133:689

• Prospective, 6 week study• N= 35 pts• Severe HF and indication for LVAD• “Fixed” Cpc PH: PVR >3.5 Wu despite vasodilators/inodilators• RH cath before LVAD, then 3 days and 6 weeks post- LVAD• Device: MicroMed DeBakey (24), DuraHeart (3), Novacor (8)

Baseline 3 Days 6 Weeks

MPAP (mmHg) 44.0+6.2 28.6+7.3* 18.4+4.3*

PAWP (mmHg) 28.1+6.0 12.0+5.7* 10.0+3.6*

CO (L/min) 3.1+0.8 5.7+0.7* 4.0+0.9**

PVR (Wood units) 5.1+2.6 2.9+1.3* 2.0+0.8*

* P< .0001; **P= .002 [ TPG from >16 to <8 mmHg]

PDE-5 Inhibitor Treatment for Persistent PH after MCS

Study N Design Results

Tedford

2008

138

LVAD

PVR> 3 W u

N=58 : no in PVR 1-2 wks post VAD despite in PAWP

•26 consecutive pts received sildenafil (mean dose 52 mg TID)

•32 controls

Sildenafil Group (12-15 wks post-LVAD):

PVR 5.87 + 1.9 to 2.96+ 0.92*

MPAP 36.5 + 24.3 to 24.3 + 3.6*

• PVR sign. lower in sildenafil rx pts vs control

• Sildenafil resulted in improved RV function (dp/dt; TAPSE) vs control

Tedford et al. Circ Heart Fail 2008; 1:213

*P< .001

In patients with persistent mixed PH after LVAD, sildenafil is a useful adjunctive therapy to PVR and

potentially facilitate heart transplantation




Reduce RV Afterload: - External (PVR, PAC)

- Internal (Wall Stress)



Optimize Preload

• Hypervolemia IV diuresis/hemofiltration • Hypovolemia with hypoperfusion (no evidence

for congestion, rare) Administer fluid

11

Reduce RV internal afterload (Wall Stress ≈ P x R/ h)Decompress RV to preload/wall stress MVO2 , CPP, RV ischemia; improve LV filling and systemic CO ; relieve organ congestion

•Avoid volume loading in setting of hypotension or pre-renal azotemia

– No benefit from RV Frank-Starling mechanism

– Dilates RV LV filling CO

•Diuretics

– intermittent or continuous infusion loop diuretics, +/-thiazide, +/-aldosterone antagonists

•Mechanical fluid removal: CVVH/Aquapheresis

De Marco T. Advances PH 2005; 4:16Brown N. Curr Opinion Nephrol Hyperten 2005;14:235

Mebazaa et al. Int Care Med 2004;30:185Haddad et al. Circ 2008;117:1717







• Dobutamine/dopamine (monitor fortachyarrhythmia)

• Milrinone (caveat: systemic hypotension in PAH) favored in PH due to LHD)


Optimize Preload

Augment RV contractility• Inotropes

– Dobutamine/dopamine – Other adrenergic agents (NE, epinephrine)– Milrinone in PH due to LHD (Ipc-PH; Cpc-PH)– Addition of IV epoprostenol (PAH)– Combination– Caveat: tachyarrhythmias, hypotension

(HTN concerning esp with milrinone in PAH)

De Marco T. Advances PH 2005: 4:16Montalescot et al. Am J Cardiol 1998;82:749


Medical Management Principles in ADRHF







Optimize Preload

•Norepinephrine•Vasopressin

12

Optimize Perfusion Pressure– Systemic vasodilatory state:

Vasopressors norepinephrine vasopressin (PVR/SVR ratio)

– Systemic vasodilatory state + tachycardia Vasopressors vasopressin

phenylephrine (caution PVR)Dysrrhythmias:– usual therapy – avoid β-blockers, CCB in acute RHF

De Marco T. Advances PH 2005: 4:16Montalescot et al. Am J Cardiol 1998;82:749


Non- Pharmacologic Treatment ofARHF in PAH

Percutaneous graded blade-balloon atrial septostomywith stent• R L shunt: decompresses failing RV & improves LV filling systemic CO

• Recurrent ARHF, syncope, BTT, no other options

Mechanical support (BTR/BTT)

• ECLS: Traditional ECMO, Artificial lung [PA-LA]

Bilateral lung transplantation

• Viable option: 1 yr survival: 70-90%; 5 yr survival: 50-60%

• Mortality on waiting list remains high (20% yr despite LAS)

• Aggressive pre-transplant management can mortality

Keogh AM, et al. J Am Coll Cardiol 2009;54:S67Chen H, et al. Am J Resp Crit Care Med 2009;180:468

Proposed Algorithm:Treatment of ADRHF in PAH

Identify and treat underlying precipitating factors(Dietary indiscretion, infection, anemia/erythrocytosis, thyroid disorders,

dysrrhythmia, ischemia, PE, NSAID’s, COX-2 I)

Restore oxygenation•Supplemental/ high flow O2

•Avoid mechanical ventilation•Avoid excess PEEP, • Avoid acidosis

Restore vital organ perfusion•Pulmonary vasodilators ( afterload)

•O2/iNO/ prostanoids (IV, Inh.)•Combination therapy

•Inotropes / vasopressors•Adrenergic agents,?PDE-3 Inh.•Add/change to IV epoprostenol

Relieve congestion•IV loop diuretics•IV, oral thiazide diuretic•Oral aldosterone antagonist•Mechanical fluid removal(CVVH or Aquapheresis)

Stabilization achievedTransition to chronic therapy

•Wean NO with epoprostenol•Wean IV inotropes•Optimize chronic therapies•Evaluate for transplantation

Unresponsive/refractoryTransplant Candidates: Bridge to Transplant• Continuous IV inotropes• Atrial Septostomy• ECLS (ECMO, Artificial lung)Not Transplant Candidate• Palliation of symptoms• Hospice Care

De Marco T. Advances PH 2005;4:16Haddad et al. Circ 2008;117:1717

Proposed Algorithm for Management of Cpc-PH due to LHD On optimal, guideline directed therapy for HFrEF

Transplant eligible Not transplant eligible

Vasoreactive Not vasoreactive

Heart transplant

PH resolves or becomes vasoreactive

Persistent PH• Continue HF

Therapy

• DT VAD

•Investigational Trials

•Aggressive chronicpharmacologic rx

(IV inodilators, po PDE5-I)•MCS•Combination rx;trials

Considerheart-lungtransplantation

Acutevasoreactivitytesting

(q 3-6mosRHC)

Adapted from Murali S, Adv in PH 2006;5:33 Mehra et al. J Heart Lung Transplant 2006; 25:1024

(FrequentRHC q 3-6 mos)

13

• ARHF in PH is associated with morbidity and mortality• ARHF is a syndrome with complex pathophysiology

– Characterized by dyspnea, fatigue, edema, syncope, CVP, vital organ congestion +/- hypoperfusion

• Pharmacologic strategies should be aimed at:– Restoring oxygenation– Relieving congestion and hypoperfusion maintaining vital organ perfusion is critical

• Management includes judicious- individualized use of: – Pulmonary vasodilators – Diuretics/ hemofiltration– Inotropes– Vasopressors– Atrial septostomy, mechanical circulatory support (BTT), and

transplantation

Conclusions

Thank you!!

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46 ARAS Forgotten Ventricle