Source :Uptodate 2019

1.  The Majority of RV
infarcts results from
occlusion of the Proximal
Right coronary artery
 RVMI commonly
accompanies acute
infarction of inferior wall of
left ventricle ( in more than
13 of the cases )
Poor outcome  1-
Hemodynamic , electrical
complications
But long term prognosis
GOOD for those who
survive these events Up to date 2019

2. m
Right Coronary Artery (RCA (
1- Right atrium
2- Right ventricle
Area involved
in Inferior and
RV infarcts
1- SA node
2-AV node
Branch posterior
Descending (PD)
posterior left-infero
31posterior,ventricle
of the septum
Left coronary artery (LCA)
anterior
surface of the
left ventricle
Area involved
in Anterior
infarcts
anterior 23
of the
septum
Circumflex :
1- left atrium
2-lateral wall of
the left ventricle
Area involved
in lateral
infarcts
Up to date 2019

3. Electrical ConsequencesHemodynamic consequencesCulprit lesion site
Ischaemia ± activation of
cardioinhibitory reflexes 
SA ,AV nodal dysfunction
 Bradycardia
depends on 1 or both :
Extent of RV dysfunction ,
Extent of LV dysfunction
** Monitor hemodynamic 
patho physiology  ttt
Right ventricle is
supplied by RCA
through marginal
branches
Patients with acute RVMI
 high grade AV block OR
 Bradycardia
hypotension without AV
block
proximal occlusion  dec.
RV Free wall perfusion 
Dyskinesis  fall in blood
delivery to LV ( even with
intact LV systolic function )
Majority of RVMI 
occlusion of the RCA
proximal to the Right
marginal branches
Notes:
* Hypotension bradycardia
due to vagal afferent on LV
, RV or infero-posterior
* Tachycardia may be
present due to
sympathetic discharge to
raise CO )
Other factors :
1-Right Atrial ischaemia (
occlusion to proximal right
atrial branches )
2- depression of LV function
( prior MI)
3- Ticuspid valve
regargitation
4- mechanical complications
of MI
In 15 % of population
, or pts with left
predominant system
50 % of RV supplied
with left circulation (
chronic occlusion ,
significant collateral
flow from the left
anterior descending
or circumflex arteryUp to date 2019

4. ECHOcardiogramECGClinical presentation
ECHO Shows RV cavity dilatation ,
impaired RV free wall motion
** Urgent Echo  should be in pts
with an inferior MI + Evidence of
Hemodynamic compromise
RVMI Signs
1- Hypotension
2- JVP increased
3-Clear lung Fields
4- ECG : ST elevation of an
acute inferior MI
Major limitation : suboptimal
visualization of the cardiac structures
in some pts
Inferior wall infarction by 
ST Elevation in leads II ,III ,aVF
Right Sided pericordial leads
V4R ,V5 , V6 particularly V4R
Small RVMI : may not lead to
hypotension ,No JV distension
Most ECHO signs : 1-RV cavity
dilatation ( RA dilataion incase of
iscahemia )
2-impaired RV free wall motion
3-Diastolic reversed septal curvature
3- Dec. TAPSE & or reduced EF
4-plethora of inferior Vena Cava
** Note : PE & Pulmonary HTN 
ECHO abnormalities
≥ 1 mm doming ST elevation of Right
sided pericordial leads V4R, v5R
Note :
* pericarditis with pericardial temponade
may present with similar pic - Echo
shows RV dilatation in RVMI
Note :
LVMI : contrast of RVMI
* pulmonary congestion , S3, S4
heart sounds , mitral valve
murmur

5. Differential DiagnosisHemodynamic monitoring
Percarditis TemponadesPERVMIIn minority of pts,  placement of
Pulmonary artery catheter ( **
ischaemic RV is prone to catheter induced
Ventricular arrithmyia )
ST elevation in
inferior leads : lead III ,II
, aVR
ECG : ST Elevation in
Right percordial
leads V1 , V2
No Inferior
ECG : ST elevation in
right Percordial leads
V4R ,V5R ,V3R
inferior leads : lead III
,II , aVRHemodynamically significant RV
infarcts  inc . in RA pressure to
pulmonary wedge pressure > 0.8 (
normal<0.6)
Diastolic filling pressures of RA ,RV ,
PCW ,LV may be elevated or equalized
Kussamaul’s sign  in JVP
if LV dysfunction may prevent
manifestation
Plerutic chest pain ,
clear lung fields ,
hypotension ( shock
Troponin +ve
Ischemic Chest pain ,
clear lung fields ,
hypotension ( shock )
troponin +ve
ECHO No DilatationECHO , right
ventricular systolic
dysfunction
McConenell’s sign n
large PE
- Additional
testing :
VQ perfusion
helical CT scanning
ECHO , right
ventricular systolic
dysfunction
RV Cavity dilatation ,
RV free wall motion
Other Studies : Cardiac MRI is more
sensitive in inferior MI but not
recommended to be used

6. Outline of Treatment of RVMI
General treatment :
 Dual Antiplatet
therapy ( Aspirin +
P2Y12 inhibitor )
 Anticoagulant
 Statin Therapy
Use with Caution
ø Drugs that
Decrease Preload (
nitrates , diuretics )
ø decrease
contactility ( CCB )
ø slow HR (ββ)
Incase of Low cardiac output , clear lung field , low or normal JVP 
optimization of preload
Small boluses of
normal Saline to
increase preload
Presistant Hypotension even after salin
Dopamine ( grade 2C)usual starting dose 5 mcg kg
min
RVMI don’t benefit from
afterload reducing therapy
“Some “ pts may benefit from
afterload reducing therapy (
either : Vasodilating agents
,intraaortic ballon )
Bradycardia , AV
abnormalities 
Atropine
(parasympatholytic) &
Transvenous pacing
AVOID drugs
that decrease
preload :
Nitrates,
opioids ,
Diuretics

7. Optimization of HR &AV
synchronny
Optimization of RV after loadOptimization of RV preloadGeneral Management
In pts with RVMI  Atropine (
parasympatholytic)
 Temporary Pacemaker
** Ischemic right ventricle has
fixed StrokeVolume  then RV
Output depends on the HR &
AV transport
RV output may be comprimised
Incases of LV dysfunction with
elevation of pulmonary venous
pressure , Hypoxemia with
pulmonary artery VC ,α
agonists pulmonary VC,
mechanical Ventillation
Incase of evidence of low CO : (
Hypotension , hypoperfusion ,
normal low JVP ) who don’t have
Rv failure or pulmonary
congestion  intravenous
fluids :Saline
Coronary Reperfusion 
fibrinolytics PCI  Show better
prognosis RV Recovery
Like the management of STEMI
 Dual Antiplatelet therapy (
Aspirin + P2Y12 inhibitor )
 Anticoagulant
 Statin Therapy
Use with Caution
ø Drugs that Decrease Preload (
nitrates , diuretics
ø Antiischaemic
used with caution insatble pts (
decrease contactility ( CCB )
ø slow HR (ββ
Some give atropine before PCI
in the case of vagotonia HR <
55 beatsmin even if BP normal
RV Afterload reducing agent is
not indicated
But RV MI with LV dysfunction 
use intraaortic balloon pump
 Occasionally afterload
reducing agents
• 200 -300 ml of saline +
assessing JVP & BP
•Once increases in JVP > 15
mmHg without increases in
aortic pressure further
expansion won’t improve
hemodynamics
- Severe Hypotension
stabilized by inotropic agents ,
vasopressors
Inotropic agents  hypotension
not responding to fluid
resusitation
Dopamine 5 mcgkgmin up to
15 mcg kgmin depending on
response ( monitor for
ventricular ectopy &tachycardia
Dubtamine 5 mcgkgmin->
upto 20 mcgkgmin ( same as
Dopamine)
- Dec. PR higher doses
dec BP
Mechanical Assist devices 
intraaortic balloon pump in
cardiogenic shock due to LV
dysfunction
Impella PR  improves
hemodynamics in RV failure
øAvoid use of Nitrates ,diuretics
as they reduced RV Preload
Øinsertion of a bladder catheter
can cause inc. vagal tone dec
preload , cardiogenic shock
Reperfusion with primary PCI or
fibrinolytics
( check pharmacotherapy
practice guide)

8. Pharmacotherapy principles & practice :ACS