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Right Ventricular Function<br />

Under Pressure<br />

<strong>Michael</strong> R. <strong>Pinsky</strong>, MD, Dr hc<br />

Department of Critical Care Medicine<br />

University of Pittsburgh


Background: Right Ventricle Failure<br />

• Occurs in many disease states<br />

– LV systolic dys<strong>function</strong> and CHF<br />

• Pulmonary disease (cor pulmonale)<br />

– Coronary artery disease (<strong>RV</strong> infarct) • Pulmonary hypertension<br />

– Valvular heart disease (MS, TR, PS)<br />

• Liver disease<br />

– Congenital heart disease<br />

• Worse Prognosis<br />

It is very common<br />

– HF due to systolic dys<strong>function</strong> (de Groote P, et. al. JACC 1998;32:948-54., Ghio S, et. al..<br />

JACC 2001;37:183-8.) 8.)<br />

– Ventricular Assist Device implantation ti (Rose EA, et. Al. NEJM 2001;345:1435-1443.)<br />

1435 1443.)<br />

– Acute myocardial infarction (Sakata, et. al.. Am J Cardiol 2000;85:939-44., Mehta, et. al. JACC<br />

2001;37:37-43.)<br />

– CABG (Eagle It<br />

KA, has et al.. JACC bad 1999;34(4):1262-347.)<br />

outcomes<br />

347.)<br />

– valve surgery (Bonow RO, et. al. JACC 1998;32:1486-588.)<br />

– primary PH (D'Alonzo GE, et. al. Ann Intern Med 1991;115:343–349.) 349.)<br />

– pulmonary arterial embolectomy (Gilbert TB, et. al.. World Journal of Surgery 1998;22:1029-<br />

1033.)<br />

– relative contraindication for liver transplant (Kuo et al. Transplantation 1999;67:1087-1093.) 1093.)


ECG-Gated Gated Multislice Computed<br />

Tomographic Angiography (MSCTA)<br />

to Assess Right Ventricular Function<br />

Simon et al. University of Pittsburgh


Rapid CT 3-D reconstruction of <strong>RV</strong> Cavity by MSCTA<br />

Main pulmonary artery<br />

Pulmonary valve<br />

Superior vena cava<br />

<strong>RV</strong> outflow tract<br />

Tricuspid valve<br />

Right atrium & appendage<br />

Inferior vena cava<br />

Simon et al. University of Pittsburgh


<strong>RV</strong> Systolic Function and Aortic Pressure<br />

<strong>RV</strong> <strong>pressure</strong> 20<br />

Brooks et al. J Clin Invest 50:2176-83, 1971


<strong>RV</strong> Systolic Function and Aortic Pressure<br />

<strong>RV</strong> <strong>pressure</strong> 40<br />

Brooks et al. J Clin Invest 50:2176-83, 1971


<strong>RV</strong> Systolic Function and Aortic Pressure<br />

Brooks et al. J Clin Invest 50:2176-83, 1971


Effects of Right Coronary Blood Flow on Cardiac<br />

Output during Supra-critical PA Pressures<br />

Start of coronary perfusion pump<br />

Brooks et al. J Clin Invest 50:2176-83, 1971


Effects of Pulmonary Hypertension on<br />

Right Coronary Blood Flow<br />

Brooks et al. J Clin Invest 50:2176-83, 1971


LV Pressure-Volume Loop<br />

LV<br />

Pressure<br />

(mm Hg)<br />

End-systole<br />

Ejection (stroke volume)<br />

Isometric<br />

Relaxation<br />

Aortic Valve<br />

Opening<br />

Isometric<br />

Contraction<br />

Mitral<br />

Valve<br />

Opening<br />

Diastolic filling<br />

LV Volume<br />

(mL)<br />

End-diastole<br />

diastole


On the Nature of LV Contraction<br />

Sequential P/V Loops during IVC Occlusion<br />

LV<br />

Pressure<br />

IVC<br />

Occlusion<br />

LV Volume


Right Ventricular Pressure-<br />

Volume Loops<br />

• Conductance Catheter measuring <strong>RV</strong> blood<br />

pool impedance (Leycom,NL)<br />

• High fidelity <strong>pressure</strong> tipped catheter in <strong>RV</strong><br />

(Millar)<br />

• Rapid changes in <strong>RV</strong> volumes or <strong>pressure</strong>s<br />

• Animal model in which measurement<br />

artifacts are minimized (rabbit, piglet)<br />

• Solda et al. J Appl Physiol 73:1770-5, 1992<br />

• <strong>Pinsky</strong> et al. J Crit Care 11: 65-76, 1996


Bi-Ventricular End-Systolic<br />

Pressure Volume Relationships<br />

(generated by IVC occlusion)<br />

Left Ventricle<br />

Right Ventricle<br />

E es<br />

Occlusion<br />

Ees<br />

Occlusion<br />

Diastolic compliance<br />

Diastolic compliance


Assessment of Right Ventricular<br />

Function<br />

<strong>RV</strong> Pressure Assumption:<br />

<strong>RV</strong> end-systolic <strong>pressure</strong>-<br />

volume relation (ESPVR)<br />

correlates with <strong>RV</strong><br />

contractility


Left Ventricular Function<br />

(generated by IVC occlusion)<br />

E es<br />

O l i<br />

m Hg)<br />

ure (mm<br />

V pressu<br />

LV<br />

Ejection<br />

Occlusion<br />

Diastolic compliance<br />

LV volume (ml)


Right Ventricular Function<br />

IVC Occlusion<br />

Hg)<br />

<strong>RV</strong><br />

pressur<br />

re (mm<br />

E es<br />

Diastolic filling<br />

Diastolic compliance<br />

<strong>RV</strong> volume (ml)


Right Ventricular Ejection<br />

Although <strong>RV</strong> Ees can be measured,<br />

does it reflect <strong>RV</strong> contractility tilit<br />

or<br />

the influence of LV ejection<br />

Systolic ventricular<br />

interdependence


Effect of isolated LV contraction on<br />

<strong>RV</strong> Developed Pressure<br />

63.5 LV vs. 36.5% <strong>RV</strong> contribution<br />

to <strong>RV</strong> developed <strong>pressure</strong><br />

Damiano et al. Am J Physiol 261:1514-24, 24, 1991


Effect of isolated LV contraction<br />

on <strong>RV</strong> Developed Pressure<br />

• LV contraction creates 70% of the<br />

developed <strong>RV</strong> systolic <strong>pressure</strong><br />

• Septal contraction not required for this<br />

effect<br />

•The right ventricle is squeezed by the<br />

left ventricular contraction through the<br />

free wall<br />

– Damiano et al. Am J Physiol 261:1514-24, 24, 1991


Effect of Partial Aortic Occlusion<br />

On LV and d<strong>RV</strong>P Pressure-Volume Vl Loops<br />

End-systolic shift<br />

Increased ejection force<br />

<strong>Pinsky</strong> et al. J Crit Care 11: 65-76, 1996


Partial lA Aortic Occlusion<br />

Left ventricle<br />

Closed Pericardium<br />

Right ventricle<br />

E es<br />

End-systolic shift<br />

Shi & <strong>Pinsky</strong> 1994


<strong>RV</strong> elastance in vivo<br />

Cannot Be Defined<br />

• The <strong>RV</strong> ESPVR is directly<br />

dt determined db by the force of fLV<br />

contraction<br />

• Changes in <strong>RV</strong> end-diastolic diastolic volume<br />

and ejection <strong>pressure</strong> may variably<br />

alter contractility


Ventricular Interdependence<br />

• Traditional Concept: Changes in<br />

Right Ventricular volume alters<br />

Left Ventricular <strong>function</strong><br />

• Diastolic interaction Right to Left<br />

–Increased <strong>RV</strong> end-diastolic diastolic volume<br />

decreases LV diastolic compliance<br />

– Decreased <strong>RV</strong> end-diastolic diastolic volume<br />

increases LV diastolic compliance


Increases in <strong>RV</strong> volume decrease<br />

mm Hg)<br />

ssure (m<br />

lar Pres<br />

ntricul<br />

Left Ve<br />

20<br />

LV diastolic compliance<br />

12<br />

<strong>RV</strong> volume:<br />

0 ml<br />

23 ml<br />

2<br />

35 ml<br />

0<br />

47 ml<br />

10<br />

0 10 20 30 40<br />

Left Ventricular Volume (ml)<br />

Taylor et al. Am J Physiol 213:706-10, 10, 1967


Effect of Partial Pulmonary Artery Occlusion<br />

On LV and d<strong>RV</strong>P Pressure-Volume Vl Loops<br />

70 mm Hg<br />

End-diastolic diastolic shift<br />

Decreased compliance<br />

70 mm Hg<br />

LVP<br />

<strong>RV</strong>P<br />

LVV<br />

3.30 ml<br />

<strong>RV</strong>V<br />

<strong>Pinsky</strong> et al. J Crit Care 11: 65-76, 1996


Volume Expansion in Cor Pulmonale<br />

Before Volume Expansion<br />

After Volume Expansion<br />

(500 mL plasma expander)<br />

ΔPP 21% ΔPP 29%<br />

RA<br />

LA<br />

RA<br />

LA<br />

<strong>RV</strong><br />

LV<br />

<strong>RV</strong><br />

LV<br />

CI: 1.3 L/min/m 2<br />

CI: 1.4 L/min/m 2<br />

from Jardin personal communication


Right Ventricular Afterload<br />

Question: Does pulmonary artery <strong>pressure</strong><br />

vary with ih right ventricular outflow<br />

Sometimes,<br />

but at the Extremes of blood flow<br />

(exercise) and in the setting of increased<br />

pulmonary vascular resistance<br />

(pulmonary vascular disease)


Question: Does <strong>RV</strong> Afterload<br />

Change Independent of Pressure<br />

• Afterload is wall stress and varies<br />

with wall tension<br />

– LaPlace’s Law:<br />

Tension = Pressure x radius of<br />

curvature<br />

• Decreasing <strong>RV</strong> radius of curvature<br />

should reduce <strong>RV</strong> afterload<br />

r<br />

P


Mild <strong>RV</strong> Loading Decreases <strong>RV</strong> Wall Stress<br />

<strong>RV</strong> free wall radius decreases!


Representative Images<br />

ECG-Gated Gated Multislice Computed Tomographic Angiography (MSCTA)<br />

to Assess Right Ventricular Function<br />

Normal:<br />

<strong>RV</strong>FAC 0.72<br />

RAP 4 mmHg, MPAP 17 mmHg,<br />

CI 4.9 L/min<br />

PH and <strong>RV</strong> Failure:<br />

Dx: IPF; <strong>RV</strong>FAC 0.18<br />

RAP 18 mmHg, MPAP 50 mmHg,<br />

CI 1.8 L/min<br />

Simon et al. Clin Tranlational Sci 2: 294-9, 9, 2009


Computed Tomography of <strong>RV</strong><br />

Normal<br />

<strong>RV</strong> FAC = 72 %<br />

RA <strong>pressure</strong> 4 mm Hg<br />

mean PA 17 mm Hg<br />

cardiac index 4.9 L/min<br />

End-Diastole<br />

End-Systole<br />

PH/<strong>RV</strong> Failure<br />

<strong>RV</strong> FAC = 18 %<br />

RA <strong>pressure</strong> 10 mm Hg<br />

mean PA 75 mm Hg<br />

cardiac index 1.8 L/min<br />

Simon et al. Clin Translat Sci 2:294-9, 9, 2009


Regional wall stress vs.<br />

Thickness<br />

Infund dibular En nd-Systol lic Wall Stress (kP Pa)<br />

40<br />

30<br />

20<br />

10<br />

0<br />

PH-C<br />

Normal<br />

PH-D<br />

Infundibular End-systolic Wall Thickness (mm)<br />

Normal<br />

PH-C<br />

PH-D<br />

0 2 4 6 8 10 12 14<br />

Simon et al. Clin Translat Sci 2:294-9, 9, 2009


<strong>RV</strong>OT ES Wall Stress vs. Wall Thickness<br />

40<br />

PAH without <strong>RV</strong><br />

Decompensation<br />

P


<strong>RV</strong> Adapts to Increased Pressure<br />

Loads in Response to Increased<br />

Wall Stress<br />

• Hypertrophy is initially heterogeneous<br />

– Outflow track hypertrophies first because<br />

it contracts last and thus sees the highest<br />

wall stress during systole<br />

•<strong>RV</strong> remodeling occurs with pulmonary<br />

hypertension before Pra


Modeling <strong>RV</strong> Wall Strain during<br />

Pulmonary Hypertension<br />

1. Tension in one<br />

principal curvature<br />

T = ⎛ P ⎞<br />

⎛<br />

⎜ ab ⎝ 2 ⎟ a 1+ b2<br />

⎠ a + ⎞<br />

⎜<br />

b2<br />

⎟<br />

⎝<br />

2 c 2<br />

⎠<br />

2A 2. Applied lidto each<br />

T ab<br />

,TT ac<br />

,TT ba<br />

,TT bc<br />

,TT ca<br />

,TT<br />

cb<br />

direction a, b and c<br />

3. Average Orthogonal ⎛<br />

T ab<br />

+ T ac<br />

⎞<br />

T a<br />

= ⎜<br />

⎟ ⎡ ⎛ T<br />

Tension<br />

⎝ 2 ⎠<br />

a<br />

⎞<br />

⎜ ⎟ x 2<br />

⎝ a ⎠ a + ⎛ T ⎞<br />

b<br />

⎜ ⎟ y 2 ⎛<br />

⎢<br />

⎜<br />

⎣<br />

2 ⎝ b ⎠ ⎝<br />

T<br />

4. Average Tension<br />

avg<br />

=<br />

x 2 tA<br />

+ y 2 + z2 at Any Point a 4 b 4 c 4<br />

5. Product of Principal<br />

( T gv ) 2 = T ab<br />

T ac<br />

+ T T 2 ba bc<br />

+ T T 2 ca cb<br />

Tensions a b c<br />

( ) x 2<br />

6. Maximal Tension<br />

at a Point T max<br />

= T avg<br />

+ ( T ac ) 2 − T gv<br />

7. Maximal Stress<br />

( ) y 2<br />

( ) z2<br />

b + T ⎞<br />

c<br />

2 c ⎠<br />

c 2<br />

⎟ z2<br />

c 2<br />

( ) 2 σ max<br />

= T max<br />

max<br />

h<br />

Regen. Ann Biomed Eng 24:400-17, 1996<br />

⎤<br />

⎥<br />


Modeling <strong>RV</strong> Wall Strain during<br />

Pulmonary Hypertension<br />

Modified 4 Chamber view<br />

Short Axis view


Modeling <strong>RV</strong> Wall Strain during<br />

Pulmonary Hypertension<br />

Str<br />

ress (kPa)<br />

Thickness (mm)


Does <strong>RV</strong> Ejection Efficiency<br />

Vary with Changes in <strong>RV</strong> end-<br />

diastolic volume<br />

Sometimes:<br />

with <strong>RV</strong> overdistention,<br />

ischemia and<br />

pulmonary hypertension


<strong>RV</strong> Adaptation to Pressure<br />

4CH Longitudinal Strain:<br />

Normal patient<br />

0%<br />

-39%


<strong>RV</strong> Adaptation to Mild PAH<br />

4CH Longitudinal Strain:<br />

Pra<br />

Ppa<br />

7 mm Hg<br />

40/16 mm Hg<br />

Mean Ppa 26 mm Hg<br />

Ppao<br />

7 mm Hg<br />

CI 3.73 l/min/m 2<br />

0%<br />

-24%


Severe PAH with Decompensated <strong>RV</strong><br />

4CH Longitudinal Strain<br />

Pra 13 mm Hg<br />

Ppa 111/51 mm Hg<br />

M Ppa 70 mm Hg<br />

Ppao 10 mm Hg<br />

CI<br />

1.3 l/min/m 2<br />

0%<br />

-14%


Echocardiographic Speckle Tracking<br />

Normal<br />

Pulm Hypertension, <strong>RV</strong> Failure<br />

Simon et al. Congestive Heart Failure 15:271-6, 2009


Clinical i l Implications<br />

• Right ventricular diastolic <strong>function</strong> is wedded<br />

to LV filling and cardiac fossal restraint<br />

– Remodelong occurs before Pra increases<br />

–End-diastolic diastolic volume and LV diastolic compliance<br />

– <strong>RV</strong> preload may not vary as <strong>RV</strong> EDV varies<br />

• Right ventricular systolic <strong>function</strong> is wedded<br />

to LV ejection<br />

– Etiology of Backward Circulatory Failure<br />

– Implications for LV Assist Device Use<br />

– Maintain arterial perfusion <strong>pressure</strong> > Ppa


Some Overly Simplistic Rules<br />

to Follow<br />

• Decreasing <strong>RV</strong>ef if not associated with an<br />

increase in stroke volume is bad<br />

• For cardiac output to increase <strong>RV</strong> ESV must<br />

also increase<br />

• The primary treatment for <strong>RV</strong> failure is to<br />

decrease pulmonary artery <strong>pressure</strong><br />

• The primary rescue of <strong>RV</strong> failure is by<br />

increasing arterial <strong>pressure</strong> > Ppa so as to<br />

sustain <strong>RV</strong> coronary perfusion

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