Right ventricle infarction

Dr. Virbhan BalaiDepartment of cardiology

National heart institute, Delhi

• General• Pathophysiology• RCA supply and occlusion• Clinical presentation• Examinations• Treatment• Conclusions• Examples

Epidemiology

• Isolated infarction of the RV is extremely rare.• RVI usually is noted in association with

inferior wall MI.• The incidence of RVI in such cases ranges

from 10-50%

• <10% hemodynamic unstable• Higher morbidity and mortality than inferior

MI• Mortality 25-30% - Inferior mi + RVI = 31%

- Inferior mi – RVI = 6%

• Therapeutic implications. • Spectrum of disease: Asymptomatic mild RV

dysfunction to cardiogenic shock• Higher rates of hypotension, bradycardia and

in-hospital mortality.

Pathophysiology

• RV is a thin-walled chamber that functions at low O2 demands and pressure.

• It is perfused throughout the cardiac cycle in both systole and diastole.

• Its ability to extract O2 is increased during hemodynamic stress.

• Collateral blood supply ( Esp. anterior wall of RV)• All of these factors make the RV less susceptible

to infarction than the LV.

Right coronary artery• Posterior descending branch

- Inferior and posterior wall of RV• Marginal branches

- Lateral wall of RV• Conus branch

- Anterior wall ( also supplied by LAD- moderator branch)

Right coronary artery occlusion

• Mostly ateriosclerotic occlusion of proximal RCA

• Direct correlation between anatomic site of RCA occlusion and extent of RVI.

• More proximal occlusion causes a larger RVI

• Proximal to RV occlusion of RCA causes:RV free wall injury compromises blood supply to SA node, atrium and AV node sinus brady, atrial infarction, AF, AV block.

• Extent of infarction depends somewhat on flow through the thebesian veins.

• The potential hemodynamic derangements associated with RVI render the pt. – Sensitive to diminished preload (i.e volume) – Loss of A-V synchrony.

• These 2 circumstances can result in a severe decrease in RV and LV output.

History

• Should be considered in all pt’s with an acute inf wall MI (esp. low CO).

• Marked sensitivity to preload-reducing agents such as nitrates, morphine, or diuretics.

• High-grade A-V block, TR, cardiogenic shock, RV free wall rupture, and cardiac tamponade.

Physical Examination

• Classic clinical triad of 1. Distended neck veins (↑ JVP)2. Clear lung fields3. Hypotension.

• RV- S3, S4 +– Lower left sternal border – ↑with inspiration.

• Hemodynamic monitoring. – ↑right-sided filling pressures

Diagnostic Considerations

• If a pt. with RVI experience unexplained hypoxia (Despite administration of 100% O2). 1. Rt.-Lt shunting at atrial level in the presence of

RV failure 2. ↑RA pressure should be considered.

Differential Diagnosis

1. Acute Pericarditis2. Constrictive Pericarditis3. Cor Pulmonale4. Endomyocardial Fibrosis5. Hypertrophic Cardiomyopathy6. Pneumothorax Imaging7. Primary Pulmonary Hypertension8. Pulmonary Embolism9. Restrictive Cardiomyopathy10. Secondary Pulmonary Hypertension11. Tricuspid Regurgitation

Approach Considerations

• Non invasive techniques• Hemodynamic monitoring. • Cardiac MRI -most sensitive to assess RV

function.

Electrocardiography

• All pt's with inf. wall MI should have a Rt.-sided ECG.

• ST↑ - V4 R most sp.• The ST-segment ↑ is transient, disappearing in

<10 hrs.

Leads Sensitivity (%) Specificity (%)

V1 28 92

V3 R 69 97

V4 R 93 95

• Isolated RVI is extremely rare • May be interpreted erroneously as LV antero

septal MI on ECG (ST ↑V1 -V4).• ST segments are oriented to the Rt. with

RVI(e.g., +120 degrees). • They are oriented to the Lt with antero septal

MI (e.g., −30 degrees).

Echocardiography

• RV dilatation • RWMA- RV• Depressed RV function • Paradoxical motion of IVS• TR

• In vast majority of pts RWMA recovers within 3 months.

• TAPSE• MPI - derived from the sum of the IVRT and

contraction time divided by the ET. • MPI ≥0.30 = RVI• Can detect shunting through a PFO

 Right Systolic Function

• RVOT-SF• Parasternal short-axis view at the base of the

heart • ED-RVOT-D and (ES-RVOT-D) measured. • RVOT-SF (%) = (EDRVOTD -

ESRVOTD)/EDRVOTD • Normal values: 61±13 %

• RVFAC• RVFAC -percentage change in RV area b/w

end-diastole and end-systole.• Four-chamber view • RV - EDA and RV - ESA are measured.• RV FAC (%) = (RV EDA – RV ESA)/RV EDA

x 100• Normal value for RV FAC: above 35%

• TAPSE• TAPSE -distance of systolic excursion of the

RV annular plane towards the apex.• M-mode - tricuspid lateral annulus in a four-

chamber view.• Measuring the amount of longitudinal

displacement of the annulus at peak-systole.• Normal value for TAPSE: above 16 mm.

• Right ventricular dp/dt• Rate of pressure rise in the ventricle and it is

used as a parameter of systolic function.• rarely used in daily practice.

• MPI or Tei index• Ratio of total isovolumic time divided by ejection time.• MPI = IVRT + IVCT/ET• The pulsed Doppler method: ET is determined from the parasternal

short-axis view at the pulmonary valve, based on the pulsed – wave Doppler signal at the right ventricular outflow tract while

• Isovolumic intervals –pulsed wave Doppler envelope of the tricuspid flow.

• Normal values: The upper reference limit for the right-sided MPI is 0.40 using the pulsed Doppler method and 0.55 using the pulsed tissue Doppler method. 

Angiography and Scintigraphy

• Radionuclide angiography • When technetium 99m pyrophosphate is

employed – The RV free wall is "hot," indicating significant

infarction.

Hemodynamic Monitoring

• ↑↑Rt.-sided filling pressures as compared with Lt-sided ---hallmark of RVI

• Hemodynamic criteria for RVI include – RA pressure >10 mm Hg  (CVP)– Rt atrial–to–PCWP ratio >0.8 – RA pressure within 5 mm Hg of the PCWP

• Other interesting hemodynamic features of RVI: • Prominent y descent of the RA pressure• ↑in RA pressure (JVP) with inspiration (ie,

Kussmaul sign)• Fall in systolic pressure >10 mm Hg with

inspiration (ie,pulsus paradoxus)• Elevation of RV filling pressure with early diastolic

dip and plateau (“square root sign”).• Resemble restrictive or constrictive physiology.

Management

• Maintain RV preload • Lower RV afterload • Restore AV synchrony • Inotropic support

• Nitrates and diuretics should be avoided. • Hemodynamic can be improved by a

combination of expansion of plasma volume to augment RV preload and CO.

Approach Considerations

• Should always be considered in any pt with IWMI + Hypotension, esp in the absence of rales.

• Ensuring adequate Rt-sided filling pressures-in pt’s with RV dysfunction and shock.

• If cardiogenic shock persists after optimization of RV-EDP, inotropic therapy should be instituted.

• IABP- Concomitant LV dysfunction • Nitroprusside infusion for afterload reduction.• Because of the critical role of A-V synchrony

and atrial transport in maintaining CO, • A-V sequential pacing is the modality of choice

when a pacemaker is required.

PPCT Vs Thrombolysis• A study by Lupi-Herrera et al indicated that primary PCI

leads to lower mortality rates than thrombolytic therapy. • Patients were divided into three groups:• In-hospital mortality rates at 30 days were as follows:1. Pts without RV failure: Thrombolytic therapy (4.4%);

PPCI (3.2%)2. Pts with RV failure: Thrombolytic therapy (13%); PPCI

(8.3%)3. Pts with cardiogenic shock: Thrombolytic therapy

(100%); PPCI (44%)

Right Ventricular Dysfunction and Shock

• RV failure may limit filling via a ↓in CO, ventricular interdependence, or both.

• Traditionally -focused on ensuring adequate Rt-sided filling pressures to maintain CO and adequate LV preload.

• Pts with cardiogenic shock due to RV dysfunction have very high RV-EDP, often >20 mm Hg.

• This elevation of RV-EDP may result in shifting of the IVS toward the LV cavity

• Which raises LA pressure but impairs LV filling due to the mechanical effect of the septum bowing into the LV.

• This alteration in geometry also impairs LV systolic function.

• The common practice of aggressive fluid resuscitation for RV dysfunction in shock may be misguided.

• Careful administration of fluid boluses• In conjunction with non invasive or invasive

assessment of CO,• 500-1000 mL; no further volume challenge is

needed if no effect.

Inotropic Therapy in Cardiogenic Shock

• Inotropic therapy is indicated for RV failure when cardiogenic shock persists after RV-EDP has been optimized.

• Inotropes should be used until more data are available.

• RV-EDP of 10-15 mm Hg has been associated with higher output than lower or higher pressures.

Medication Summary

• Agents- – Dobutamine– tPA -alteplase.– Levosimendan (Simdax)- a calcium sensitizer, for

hospitalized pts with ACDF.

• Dobutamine • Milrinone• Levosimendan (approved only in Europe)• Norepinephrine• Low-dose vasopressin. • Avoid dopamine and phenylephrine. • Consider combination therapy with inhaled

nitric oxide.

Management of Persistent Hypotension

• If hypotension persists, consider hemodynamic monitoring with a pulmonary artery catheter.

• Pts with extensive RV necrosis are at risk for RV catheter–related perforation.

Early Treatment Survival Benefit

• Current available evidence indicates that pts presenting within 6 hrs of onset of IWMI with RVI diagnosed by ECG or other non invasive criteria have a definite early survival benefit from thrombolytic therapy or coronary angioplasty.

• Scant data exist regarding improvement in pts who present >12 hours after onset.

• These pts most likely would do well with a conservative management strategy, considering the often spontaneous resolution of RV dysfunction.

Inhaled Nitric Oxide

• Inhaled NO – in pts with RVI complicated by cardiogenic shock.

• Principle- ↓PVR without compromising SVR, the filling of the LV can be improved with a resultant improvement of systemic CO.

• Inhaled NO in this setting has been associated with rapid improvement of hemodynamics.

• The combination of inhaled NO with dobutamine is best supported by current evidence in the Tt of acute RV failure.

• Beta-blocking agents and ACE inhibitors improve RV hemodynamics in pts with biventricular failure.

Valve Replacement and Repair

• Severe TR - valve replacement or repair with angioplasty rings.

• If a pt develop arterial hypoxemia secondary to rt-lt shunting at the atrial level, then an ASD –occluding device should be considered immediately.

• If delay- inhaled NO can ↓ the right-to-left shunting and ↑systemic oxygenation.

• Mechanical circulatory support can be also used, including-

1. LVAD 2. RVAD3. Biventricular ventricular assist device.

THANKYOU