Right ventricle infarction

Dr. Virbhan Balai

Department 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 fields
3. 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 Pericarditis
2. Constrictive Pericarditis
3. Cor Pulmonale
4. Endomyocardial Fibrosis
5. Hypertrophic Cardiomyopathy
6. Pneumothorax Imaging
7. Primary Pulmonary Hypertension
8. Pulmonary Embolism
9. Restrictive Cardiomyopathy
10. Secondary Pulmonary Hypertension
11. 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. RVAD
3. Biventricular ventricular assist device.
THANKYOU