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Right ventricle infarction
Dr. Virbhan BalaiDepartment of cardiology
National heart institute, Delhi
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• General• Pathophysiology• RCA supply and occlusion• Clinical presentation• Examinations• Treatment• Conclusions• Examples
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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%
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• <10% hemodynamic unstable• Higher morbidity and mortality than inferior
MI• Mortality 25-30% - Inferior mi + RVI = 31%
- Inferior mi – RVI = 6%
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• Therapeutic implications. • Spectrum of disease: Asymptomatic mild RV
dysfunction to cardiogenic shock• Higher rates of hypotension, bradycardia and
in-hospital mortality.
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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.
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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)
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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
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• 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.
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• 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.
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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.
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Physical Examination
• Classic clinical triad of 1. Distended neck veins (↑ JVP)2. Clear lung fields3. Hypotension.
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• RV- S3, S4 +– Lower left sternal border – ↑with inspiration.
• Hemodynamic monitoring. – ↑right-sided filling pressures
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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.
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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
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Approach Considerations
• Non invasive techniques• Hemodynamic monitoring. • Cardiac MRI -most sensitive to assess RV
function.
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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.
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Leads Sensitivity (%) Specificity (%)
V1 28 92
V3 R 69 97
V4 R 93 95
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• 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).
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Echocardiography
• RV dilatation • RWMA- RV• Depressed RV function • Paradoxical motion of IVS• TR
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• 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
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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 %
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• 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%
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• 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.
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• 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.
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• 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.
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Angiography and Scintigraphy
• Radionuclide angiography • When technetium 99m pyrophosphate is
employed – The RV free wall is "hot," indicating significant
infarction.
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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
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• 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.
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Management
• Maintain RV preload • Lower RV afterload • Restore AV synchrony • Inotropic support
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• Nitrates and diuretics should be avoided. • Hemodynamic can be improved by a
combination of expansion of plasma volume to augment RV preload and CO.
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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.
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• 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.
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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%)
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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.
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• 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.
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• 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.
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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.
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Medication Summary
• Agents- – Dobutamine– tPA -alteplase.– Levosimendan (Simdax)- a calcium sensitizer, for
hospitalized pts with ACDF.
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• Dobutamine • Milrinone• Levosimendan (approved only in Europe)• Norepinephrine• Low-dose vasopressin. • Avoid dopamine and phenylephrine. • Consider combination therapy with inhaled
nitric oxide.
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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.
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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.
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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.
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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.
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• Mechanical circulatory support can be also used, including-
1. LVAD 2. RVAD3. Biventricular ventricular assist device.
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