Important yet a neglected topic

1. DR.VIJAYYADAV
DM RESIDENT 1STYEAR
MCVTC, IOM

2. Introduction
 Acute myocardial infarction (MI) involving only the right ventricle is an
uncommon event.
 In 1930, Sanders first described the syndrome of RVMI with the triad of
hypotension, increased JVP, and clear lung fields.
 RV involvement in myocardial infarction was first described in 1974.
 In 1979, Cohn published a classic report in which RVMI was described as
distinct entity.
 Occurs in 30-50% of Inferior wall STEMI.
 Isolated RVMI occurs in 3-5% of cases.
 RVMI is associated with higher in-hospital morbidity and mortality due to
profound hemodynamic and electrical complications which occur in
approximately 50 percent of affected individuals.
 Mortality from RV shock = Mortality from LV shock
 RV recovery >>>> LV recovery

3. RIGHTVENTRICLE
 Trabeculated endocardial
surface
 Thin walled (< 5mm)
 Three papillary muscles
 Moderator band
 Triangular shaped cavity
 Tricuspid atrioventricular
valve with relatively apical
insertion
 Crista supraventricularis
separates the tricuspid and
pulmonary valves
LEFTVENTRICLE
 Smooth endocardial surface
 Thick walled
 Two papillary muscles
 False tendon
 Elliptical shaped cavity
 Mitral atrioventricular valve
with relatively basal insertion
 The mitral and aortic valves
share fibrous continuity

4. RV PHYSIOLOGY AT A GLANCE
 The RV wall is thinner (< 5mm) and more complaint than the LV
wall.
 Composed of circumferential fibers in the subepicardium and
longtudional fibers in the subendocardium.
 There is inward, longitudinal, and circumferential traction in RV due
to LV contraction.
 Longitudinal shortening is the major contributor to the overall RV
performance.
 Normal RV contraction occurs as a peristaltic wave directed from
inflow to infundibulum.
 RV pumps the same stroke volume as the LV but uses only 25% of
the stroke work because of low resistance of pulmonary
vasculature.
 RV is closely connected to LV:
◦ Share a wall (IVS)
◦ RV free wall is attached to the anterior and inferior IVS
◦ Have mutually encircling epicardial fibers
◦ Share the same intrapericardial space
◦ Ventricular Interdependence

6. ARTERIAL
SEGMENT
ARTERIAL
BRANCH
PERFUSED
REGION
ECG EFFECTS
OF ISCHEMIA
Proximal segment Conus branch Outflow tract of
RV
SA nodal branch SA node Sinus bradycardia
Right atrial branch Atrial free wall Atrial fibrillation
Atrial infarct pattern
Middle segment Lateral RV branch Lateral RV free wall
STE and Q waves in
leads V3R – V6RAcute Marginal Inferior(Posterior)
RV free wall
Distal segment AV nodal branch AV node AV block
Posterior descending
segment
Posterior lateral LV
branch
Posterior descending
artery
Posterior LV
Inferior septum
Inferior LV free
wall
STE and Q waves in
II, III, aVF

7. Factors that make the right
ventricle less susceptible to
infarction:

8.  LC blood flow is impeded by
extravascular compressive forces
generated by systolic LV contraction.
 These forces are so high that LC blood
flow is briefly reversed.
 LC blood flow increases to a maximum
early in diastole and then falls
gradually following the decline in aortic
pressure during the remainder of
diastole.
 Because of a lower developed pressure
in the RV, there is no systolic inhibition
of RC blood flow.
 RC blood flow follows the shape of the
aortic pressure curve and remains
appreciable throughout the entire
cardiac cycle.

9. 2) Reduced myocardial oxygen demand because of smaller
muscle mass and low afteralod.
3) Reduced myocardial oxygen uptake and blood flow
4) Oxygen extraction reserve
5) More extensive collateral flow from left to right coronary
arteries
6) Greater degree of ischemic preconditioning
7) Ability to downregulate the metabolic demand during
coronary hypoperfusion.

10. Pathophysiology
 RVI results in reduced RV systolic contraction (RVSP and PP are
decreased)
 RVI results in RV diastolic dysfunction (elevated right sided filling
pressures like CVP, RA, and RVEDP).
 Reduction in RV output & blood supply to the lungs.
 Reduced pulmonary flow decreases pulmonary venous return to LA
and LV. (decreases LV preload and LV filling).
 Reduced LV output and systolic BP.
 RVI leads to RV dilatation which alters the motion of IVS; i.e. leftward
shift of septum during diastole which further impedes LV filling and
eventually reduces CO.
 LV dyssynchrony due to abnormal septal motion and loss of AV
synchrony when there is AV block also leads to decreased CO.
 Dilatation of RV enlarges tricuspid annulus which results in functional
TR that further reduces RV output.
 When RCA occlusion is proximal to right atrial branch, RA ischemia
occurs that diminishes its contraction and increases RA pressure and
further increases the probability of atrial arrhythmia.

11. Elevated right sided filling pressure in the
presence of normal pulmonary artery and left
sided filling pressure is the hallmark of RVI
RA pressure: 10 mm Hg
PCWP: 1-5 mm Hg
 Sensitivity: 73%
 Specificity: 100%

12. DIAGNOSIS

13. Symptoms Signs
Clinical Features
 Chest pain
 Diaphoresis
 Nausea and Vomiting
 Syncope (if AV block)
 Palpitation
 Dizziness
 Anxiety
 Triad of hypotension, raised
JVP, and clear chest
 Jugular venous pressure:
 Prominent a wave & x descent if
RA ischemia is absent
 Diminished a wave, x & y
descents if RA ischemia is
present
 If TR present: Prominent a wave,
c-v wave (Lancisi’s sign), & y
descent and absent x descent
 Kussmaul’s sign: Highly
predictive of RVMI in the setting
of IWMI
 Pulsus paradoxus
 Right sided S3

14. INFERIOR WALL MI
RIGHT CORONARY
ARTERY
LEFT CIRCUMFLEX
ARTERY
 STE III > II
 ST depression aVL > I
 S/R ratio in aVL > 3
 V3/III sign (ST↓ V3/
STE III ratio)
 <0.5: Prox RCA
 0.5-1.2: Distal
RCA
 >1.2: LCx
 RAD of ST vector
(lead III)
 STE II > III
 No ST ↓ in aVL
 S/R ratio in aVL < 3
 V3/III sign > 1.2
 LAD of ST vector
(lead II)

15. RVMI FROM 12 LEAD ECG
 ST elevation in III > II (Pathognomonic of RVMI)
 ST elevation in V1 > V2
 ST elevation in V1 + ST depression in V2 (Highly specific for RVMI)
 ST elevation in aVF > ST depression in V2
 Isoelectric ST segment in V1 with marked ST depression in V2
 ST depression in I + aVL > 2 mm
 ST depression in V2 ≤ 50% of STE in aVF
 ST depression in V3 < ½ STE in III
 Isolated RVMI from non-dominant RCA: ST elevation in V1-V4 (mimics AWMI; ST
segment maximal in V1 in RVMI whereas it is minimal in AWMI)
ST elevation in the right sided leads is a transient phenomenon, lasting
less than 10 hours in 50% of patients with RV infarction

16. RVMI FROM A RIGHT SIDED
ECG
 The precordial leads are placed
over the right side of the chest in
a mirror image pattern to normal.
 Right sided leads V4R, V5R, &
V6R should be obtained in any
patient with inferior wall
infarction.
 ST elevation in V4R > 1mm:
 Sensitivity: 100%
 Specificity: 87%
 Positive predictive value: 92%
 Correlates with occlusion of proximal
RCA.

17. Diagnosing RVMI
is a rule in IWMI
STE in V1 and III>II in
IWMI

18. *
*Sensitivity: 82% & Specificity: 93% for detection of RVI.
*The specificity may be decreased by pre-existent pulmonary
diseases (COPD, PE)
*Most specific: RV free wall hypokinesia
*RV dilatation with paradoxical septal motion
*RA dilatation and increased RAP
*RV systolic dysfunction
*Functional tricuspid regurgitation : Hallmark
*Persistent bowing of IAS from right to left (RAP > LAP)
*Patent PFO on saline contrast echo leading to profound
hypoxemia
*Dilated IVC with poor respirophasic variation

19. Qualitative
Quantitative
RV dilatation
 In A4CH view
 Mildly enlarged:
 RV is enlarged but < LV
 Moderately enlarged:
 RV = LV
 Severely enlarged:
 RV > LV
 Apex of heart comprised of
RV
 In RV focused A4CH at end-
diastole
 RV basal diameter > 4.2 cm
 RV midcavity diameter > 3.5 cm
 RV longitudional diameter > 8.6
cm
 RVOT PLAX proximal diameter
> 3.5 cm
 RVOT PSAX distal diameter >
2.7 cm

20.  Measured at end-diastole
 Major dimension: >
53mm
 Distance from the
superior wall to the TA
 Minor dimension: >
44mm
 Distance from interatrial
septum to the
anterolateral wall
 RA area: > 18 cm2
IVC
diameter
(cm)
Respons
e to sniff
RA
pressure
(mm Hg)
≤ 2.1 > 50%
collapsibl
e
3
≤ 2.1 < 50%
collapsibl
e
8
> 2.1 < 50%
collapsibl
e
15
RA dilatation Estimation of RAP

21.  Tricuspid Annular Plane Systolic Excursion (TAPSE): < 16 mm
 Pulsed doppler peak velocity at the annulus: < 10 cm/sec
 RV Fractional Area Change (FAC): < 35%
 Normal: 32-60%
 Mildly reduced: 25-31%
 Moderately reduced: 18-24%
 Severely reduced: < 17%
 Reduced RV stroke volume: RVOTVTI < 12 cm = RV CO < 2.2 l
 Pulsed Doppler MPI > 0.40
 Tissue Doppler MPI > 0.55

23. PULSED WAVE
DOPPLER MPI
1) Tricuspid valve inflow &
Pulmonary valve outflow
doppler tracings are
acquired in RV modified
A4CH and PSAX views.
2) Time duration from the
end of A wave to the
onset of E wave is
calculated. (TV closure
to opening time)
3) RVET from pulmonary
doppler tracing is
measured.
4) Isovolumic time =
(RVET – TV A to E
duration)
5) RVMPI = Isovolumic
time/RVET
6) In this case it is (386 –
271)/271 = 0.43

24. RV wall motion assessment
Lateral & Inferior wall hypokinesia: Proximal RCA
Anterior wall hypokinesia: LAD
Inferior wall hypokinesia: PDA

25. OTHER IMAGING STUDIES FOR RVMI
 Radionuclide
ventriculography &
99mTC-pyrophosphate
myocardial scintigraphy
are sometimes used.
 Standard imaging
technique for detailed
evaluation of RV
structure & function.
 RV free wall
myonecrosis is
indicated by late
gadolinium
enhancement.
Nuclear Imaging Cardiac MRI

26. Hemodynamic monitoring
O Done if a secure diagnosis of RVMI by echo is not
possible.
O Done by placement of a pulmonary artery catheter.
O Done cautiously as ischemic RV is prone to catheter-
induced ventricular arrhythmias.
Characteristics of a hemodynamically significant RV
infarct
RA pressure ≥10 mm Hg
Ratio of RAP to PCWP > 0.8 (Normal is < 0.6)
Decreased cardiac index
Equalization of diastolic filling pressures of RA, RV, PCWP
& LV
Square root sign

27.  Acute pulmonary embolism
 Cardiac tamponade
 Constrictive pericarditis
 Restrictive cardiomyopathy
 Severe pulmonary hypertension
 Acute anteroseptal wall MI (STE inV1 andV2
seen with an RV injury pattern)

28. MANAGEMENT
Optimization of RV preload:
• IV Fluid ( Isotonic saline) in patients with hypotension & low/N JVP
• 300-600ml preferably through central line over 10-15 minutes while
serially assessing JVP and BP
• Invasive hemodynamic monitoring with a Swan Gang Catheter
• Target PCWP: not to exceed 20 mm Hg
Avoidance of Nitrates, Diuretics, & Opoids:
• Cause venodilatation and further reduces RV preload
Ionotropic agents:
• Hemodynamic instability (raised RAP & PCWP) despite adequate IVF
• Dopamine is the initial agent of choice (5 – 15 mcg/kg/min)
• Dobutamine @ 5 – 20 mcg/kg/min
• Milrinone
• Levosimenden

29.  Coronary reperfusion:
◦ Either PPCI or thrombolysis can preserve both LV and RV
function thereby improving clinical, hemodynamic, and survival
parameters.
◦ Reduces chances of ventricular arrhythmias.
◦ RV function recovers completely within 24 hours.

30. Intra-Aortic Balloon Pump (IABP):
• Cardiogenic shock due to LV dysfunction
• Little benefits in shock due to RVMI
• Still can be used for temporary stabilization
• Increases RV perfusion pressure & improves septal
contraction
RV Mechanical assist devices:
• Medically refractory cases despite successful reperfusion
• Tandem-Heart Percutaneous Ventricular Assist Device

31. AV sequential pacing:
• The ischemic RV has a fixed stroke volume
• RV output depends upon heart rate & atrioventricular transport
• In patients requiring pacing, ventricular pacing alone may fail to
increase cardiac output
• Atropine and Temporary pacemaker
Inhaled Nitric Oxide:
• Decreases PVR without any effect on SVR
• Decreases RV afterload and increases BP
Valve replacement or repair with annuloplasty rings
PFO Occluder device for hypoxemia due to right to left
shunt across IAS.

32. STANDARD MI TREATMENT
 Aspirin
 P2Y12 receptor blocker
 Statin
 Anticoagulant
 Nitrate
 Opoids
 Beta blocker
 Diuretics
GIVE DO NOT GIVE

33. PROGNOSIS
 Higher incidence of
cardiogenic shock, ventricular
arrhythmia, advanced AV
block, and death if PCI not
done.
 In-hospital mortality: 23 and
53% with cardiogenic shock
in 2 different studies.
 PPCI results in prompt &
dramatic improvement in
hemodynamics with excellent
clinical outcomes.
 Determined by extent of LV
involvement.
 Near complete RV recovery
in 62-82% of patients within
first few months
Short term prognosis Long term prognosis

34. Anterior wall MI vs.
Inferior wall MI

36. THANK YOU