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Syndrome ofSyndrome of
Right VentricularRight Ventricular
InfarctionInfarction
Dr Asadullah Khan soomroDr Asadullah Khan soomro
Adult cardiologistAdult cardiologist
Prince sultan Cardiac centrePrince sultan Cardiac centre
Al-Hassa Kingdom of Saudi ArabiaAl-Hassa Kingdom of Saudi Arabia
2222ndnd
November 2011November 2011
INTRODUCTIOINTRODUCTIO
NNMMoore thanre than 11 million11 million Americans have CoronaryAmericans have Coronary
Artery disease , nearlyArtery disease , nearly 1.5 million1.5 million patients annually sufferpatients annually suffer
from Acute myocardial infarctionfrom Acute myocardial infarction ( one patient every 20( one patient every 20
seconds)seconds) .. 50%50% of deaths associated with AMI occurof deaths associated with AMI occur
with in one hour of event .with in one hour of event . 300,000-400,000300,000-400,000 die annuallydie annually
due to sudden cardiac death at USA,due to sudden cardiac death at USA, 80%80% SDC are due toSDC are due to
CAD and its consequences, it is the first clinicalCAD and its consequences, it is the first clinical
manifestation of CAD inmanifestation of CAD in 20-25 %20-25 % of patients, how everof patients, how ever
previous MI was identified in as many as 75 % patients whoprevious MI was identified in as many as 75 % patients who
die suddenly.die suddenly. LV dysfunction due to CAD is mostLV dysfunction due to CAD is most
powerful predictor of SCDpowerful predictor of SCD..
DDespite impressive strides in diagnosis and managementespite impressive strides in diagnosis and management
over the last three decades, acute MI continues to beover the last three decades, acute MI continues to be
most seriousmost serious public health problempublic health problem and top leadingand top leading
cause of death all over the world and in Kingdom ofcause of death all over the world and in Kingdom of
Saudi ArabiaSaudi Arabia indeed .indeed .
It was an epidemic in most industrialized countries andIt was an epidemic in most industrialized countries and
now threaten to accelerate in developing countries atnow threaten to accelerate in developing countries at
younger age .younger age .
It strikes an individual during mostIt strikes an individual during most productive yearsproductive years
withwith profound deleterious psychosocialprofound deleterious psychosocial
and economic remifications.and economic remifications.
INTRDUCTIO
N
INTRODUCTIO
NN
Right ventricular myocardial infarction was firstRight ventricular myocardial infarction was first
recognized inrecognized in 1958 by H-De-Mosquita1958 by H-De-Mosquita , Isolated, Isolated
acute RV infarction is rare event. Much moreacute RV infarction is rare event. Much more
commonly RV infarction is associated withcommonly RV infarction is associated with
infarction of the inferior wall of the LV,infarction of the inferior wall of the LV,
occurring in more thanoccurring in more than one thirdone third of suchof such
cases. Infarction typically involves the LVcases. Infarction typically involves the LV
infero-posterior wall ,septum, andinfero-posterior wall ,septum, and posteriorposterior
right ventricular free wallright ventricular free wall
Inferior myocardial infarction associated with RightInferior myocardial infarction associated with Right
ventricular infarction defines aventricular infarction defines a high risk subsethigh risk subset withwith
a mortality rate ofa mortality rate of 25-30%25-30% as opposed to an overallas opposed to an overall
mortality of aboutmortality of about 6%6% in inferior MI.in inferior MI.
Right ventricular infarction occurs whenRight ventricular infarction occurs when
there is an occlusion of thethere is an occlusion of the rightright
coronary artery proximal to thecoronary artery proximal to the
marginal branch,marginal branch, but it may alsobut it may also
occur with an occlusion of the leftoccur with an occlusion of the left
circumflex artery in patients who havecircumflex artery in patients who have
left-dominant coronary circulationleft-dominant coronary circulation
Right ventricular infarction complicatesRight ventricular infarction complicates
30-50%30-50% of inferior wall MI, andof inferior wall MI, and 10%10%
of anterior wall infarctsof anterior wall infarcts
When predominant infarction of the rightWhen predominant infarction of the right
ventricle is present, the patient may present withventricle is present, the patient may present with
unique combinationunique combination of clinical findings.of clinical findings.
This clinicalThis clinical acute ischemic RVacute ischemic RV
dysfunction syndromedysfunction syndrome also require uniquealso require unique
form of therapy clearly distinct from that ofform of therapy clearly distinct from that of
hypotension associated with predominant LVhypotension associated with predominant LV
infarction.infarction.
Nevertheless ,it is clear that this clinical syndromeNevertheless ,it is clear that this clinical syndrome
has better acute and long term prognosis thanhas better acute and long term prognosis than
that associated with predominant LV infarctionthat associated with predominant LV infarction
Susceptibility to RV IschemiaSusceptibility to RV Ischemia
Right ventricular function improves in the majority of patients withRight ventricular function improves in the majority of patients with
RV infarction, including those who areRV infarction, including those who are not reperfusednot reperfused. This. This
observation suggest that RV dysfunction is usually due toobservation suggest that RV dysfunction is usually due to
ischemic myocardium that remainsischemic myocardium that remains viableviable..
There are several factors that make RV less susceptible to ischemia;There are several factors that make RV less susceptible to ischemia;
1) Oxygen demand is significantly lower in RV because of its much1) Oxygen demand is significantly lower in RV because of its much
smaller muscle masssmaller muscle mass
2) Coronary perfusion in RV occurs in both systole and diastole2) Coronary perfusion in RV occurs in both systole and diastole
3) There is more extensive collateral flow from left to right.3) There is more extensive collateral flow from left to right.
RV may also be protected to a greater degree by ischemicRV may also be protected to a greater degree by ischemic
preconditioning. The preinfarction angina with in 72preconditioning. The preinfarction angina with in 72
hours of MI was associated with a reduction in incidencehours of MI was associated with a reduction in incidence
of RV infarction and combined hypotension and shock.of RV infarction and combined hypotension and shock.
Site of Culprit lesionSite of Culprit lesion
Distal
Right
Coronary
Artery
Left
Circumflex
Artery LAD
Proximal
Occlusion of
Right
Coronary
artery
Site of Culprit lesionSite of Culprit lesion
Among patients with right CAD, the size of infarctAmong patients with right CAD, the size of infarct
is related in part to theis related in part to the site of culprit lesionsite of culprit lesion..
In a report ofIn a report of 522522 patients with inferior MI frompatients with inferior MI from
HIT-4 trialHIT-4 trial ,,52%52% of patients with large infarctof patients with large infarct
and RV involvement hadand RV involvement had proximal RCAproximal RCA lesionlesion
compared tocompared to 23%23% in those with large infarctsin those with large infarcts
but no RV involvement. In contrast thebut no RV involvement. In contrast the 28%28% ofof
patients withpatients with small infarctssmall infarcts primarily had lesionsprimarily had lesions
in thein the distal RCAdistal RCA. Similar findings were noted in. Similar findings were noted in
an autopsy study in whichan autopsy study in which proximal RCAproximal RCA
occlusion caused larger infarcts than distalocclusion caused larger infarcts than distal
occlusion.occlusion.
Right coronary artery with corresponding regionsRight coronary artery with corresponding regions
of perfusion& EKG findings for underperfusionof perfusion& EKG findings for underperfusion
Proximal
Segment
Middle
Segment
Distal
Segment
Posterior
Decending
segment
SA Nodal
Branch
Right atrial
branch
SA node
Atrial free wall
Sinus bradycardia
Atrial infarction
Pattern& atrial
Fibrillation
EKG effect
of ischemia
Perfused
region
Arterial
branch
Arterial
segment
Lateral&
Marginal RV
Branch
AV nodal
branch
Posterior
lateral LV
branch &
Lateral /
inferior RV
free wall
AV node
Posterior LV,
inferior septum&
LV free wall
ST segment elevation, later
Q waves( V3 to V6(
AV block
ST segment elevation,
later Q waves in leads
11,111,avf
Diagnosis ofDiagnosis of
Right Ventricular InfactionRight Ventricular Infaction
Because of the pathophysiology of RV infarction,Because of the pathophysiology of RV infarction,
its management differs substantially from theits management differs substantially from the
routine management of LV infarction.routine management of LV infarction.
Early accurate diagnosis isEarly accurate diagnosis is
imperativeimperative. Since hemodynamically. Since hemodynamically
important RV infarction occurs in patients withimportant RV infarction occurs in patients with
anan acute inferior wall myocardialacute inferior wall myocardial
infarction,infarction, there fore suspicion isthere fore suspicion is
warranted in any patient presenting withwarranted in any patient presenting with
such an infarction.such an infarction.
Right ventricle has remarkableRight ventricle has remarkable
tendency to recover functiontendency to recover function
rapidly, diagnostic tests are mostrapidly, diagnostic tests are most
reliable when performed soonreliable when performed soon
after presentation. Clinicalafter presentation. Clinical
suspicion and careful physicalsuspicion and careful physical
examination demonstrating theexamination demonstrating the
signs are first step.signs are first step.
Caution must be exercised in
relying on such findings, since
they are readily masked by
volume depletion and
because the physical and
hemodynamic signs of right
ventricular infarction often
emerge only after volume
loading.
By radionuclide ventriculography,By radionuclide ventriculography,
Echocardiography or right sidedEchocardiography or right sided
ECG RV involvement isECG RV involvement is
demonstrated in up todemonstrated in up to 40%40% of patientof patient
with acute inferior infarction,with acute inferior infarction,
however clinical or hemodynamichowever clinical or hemodynamic
evidence of RV infarction is presentevidence of RV infarction is present
in less thenin less then 10%10% of patients withof patients with
inferior infarction.inferior infarction.
On examinationThe clinical triad of hypotension,
elevated JVP and clear lung
fields, in a patient with an inferior
infarction is virtually pathognomonic for
RV infarction, however this triad has
sensitivity of less than 25%.
Caution must be exercised in relying on
such findings ,since they are readily
masked by volume depletion and
because the physical and hemodynamic
signs of RV infarction often emerge only
after volume loading.
Prominent jugular venous distension
Kussmauls sign and pulses paradoxus may be
present
In fact Kussmauls sign in the setting of
inferior MI is highly sensitive& specific for
RV infarction.
Other physical signs may include RV gallop,
murmur of tricuspid regurgitation, and
septal rupture, pericardial rub and AV
dissociation.
(CVP >PCWP)
ELECTROCARDIOGRAM
There is general consensus with respect to
the diagnosis of ST elevation MI,EKG is
obligatory tool in identifying patients with
STEMI.
12 lead EKG along with right sided leads V3R
through V6R should be recorded in all the
patients with acute inferior wall MI .
EKG must be interpreted as quickly as
possible after first medical contact and
ideally with in 10 minutes
Electrocardiography
A right precordial lead (V4R) is the
investigation of choice. ST-
segment elevation in lead V4R
remains the most predictive
electrocardiographic finding for
right ventricular infarction. A 1-mm
ST-segment elevation in this lead
was 70% sensitive and 100%
specific for right ventricular
infarction.
5454%% of inferior MI have ST elevation inof inferior MI have ST elevation in V4RV4R,,
1818%% of Pts with acute inferior MI had STof Pts with acute inferior MI had ST
elevation in leadelevation in lead V1V1,which is highly specific sign,which is highly specific sign
of RV infarctionof RV infarction..
Greater ST elevation in lead 111 than lead 11 is alsoGreater ST elevation in lead 111 than lead 11 is also
suggestive of RV infarctionsuggestive of RV infarction. In one study this. In one study this
finding had a sensitivity, specificity,and positivefinding had a sensitivity, specificity,and positive
and negative predictive value of 97,56,69 andand negative predictive value of 97,56,69 and
95%respectively.95%respectively.
It is usually associated with large infarct size and higherIt is usually associated with large infarct size and higher
incidence of major in hospitalincidence of major in hospital atrial & ventricularatrial & ventricular
arrhythmias and high grade AV blockarrhythmias and high grade AV block
ElectrocardiographyElectrocardiography
Electrocardiography
48% of the patients had resolution of
EKG changes within 10 hours of
the onset of symptoms.
Thus, it is imperative to record the EKG
through the accessory right precordial
leads as early as possible .
It is important to recognize the
transient nature of ST segment
elevation.
EchocardiographyEchocardiography::
Abnormal findings includeAbnormal findings include right ventricularright ventricular
dilatation, right ventricular walldilatation, right ventricular wall
asynergy,asynergy, and abnormal interventricularand abnormal interventricular
septal motion caused by a reversal of theseptal motion caused by a reversal of the
trans septal pressure gradient due to thetrans septal pressure gradient due to the
increased right ventricular end-diastolicincreased right ventricular end-diastolic
pressure.pressure.
The short-axis view has been shown toThe short-axis view has been shown to
have the highest sensitivity (82have the highest sensitivity (82
percent), with a specificity ranging frompercent), with a specificity ranging from
62 to 9362 to 93 percent for hemodynamicallypercent for hemodynamically
important right ventricular infarction .important right ventricular infarction .
EchocardiographyEchocardiography::
Interatrial septal bowingInteratrial septal bowing
towards the lefttowards the left
atrium,indicative of an increasedatrium,indicative of an increased
RA to LA pressure gradient is anRA to LA pressure gradient is an
important prognostic marker inimportant prognostic marker in
RV infarctionRV infarction..
Patients with this finding have morePatients with this finding have more
hypotension, more heart block, andhypotension, more heart block, and
higher mortality than patientshigher mortality than patients
without itwithout it..
EchocardiographyEchocardiography::
Doppler Echocardiography isDoppler Echocardiography is
particularly helpful in detectingparticularly helpful in detecting
complications of RV infarction suchcomplications of RV infarction such
asas tricuspid regurgitation, ventriculartricuspid regurgitation, ventricular
septal rupture, ASDseptal rupture, ASD or PFO andor PFO and
premature opening of pulmonarypremature opening of pulmonary
valve ( indicative of non compliantvalve ( indicative of non compliant
RVRV(.(.
Pericardial effusion andPericardial effusion and
cardiac tamponade, thrombuscardiac tamponade, thrombus
formation and plethora offormation and plethora of
inferior vena cavainferior vena cava
HemodynamicsHemodynamics
Hemodynamically significantHemodynamically significant
infarcts are associated withinfarcts are associated with
elevation in right atrialelevation in right atrial
pressure topressure to >10mmHg,>10mmHg, andand
in ratio of RA to PCWP toin ratio of RA to PCWP to
>0.8( normal mean value <>0.8( normal mean value <
0.6).0.6).
Other Imaging StudiesOther Imaging Studies
Radionuclide ventriculography and technetiumRadionuclide ventriculography and technetium
pyrophosphate scanning have acceptable sensitivitiespyrophosphate scanning have acceptable sensitivities
and specificities for making a diagnosis of RV infarction.and specificities for making a diagnosis of RV infarction.
They can detect wall motion abnormalties andThey can detect wall motion abnormalties and
hypoperfusion in affected Rv, it can also be used tohypoperfusion in affected Rv, it can also be used to
quantitate both LV & RV ejection fraction. Technitiumquantitate both LV & RV ejection fraction. Technitium
scan ,On the other hand ,is particularly useful for latescan ,On the other hand ,is particularly useful for late
diagnosis, since it shows areas of necrosis or dyingdiagnosis, since it shows areas of necrosis or dying
myocardium.myocardium.
However both methods areHowever both methods are cumbersome ,time consumingcumbersome ,time consuming
and frequently difficult to perform at bed sideand frequently difficult to perform at bed side, therefore, therefore
performed later rather than as primary diagnosticperformed later rather than as primary diagnostic
modalties.modalties.
RV Infarction & Cardiogenic Shock
It is a highly lethal disease patient
deteriorate dramatically and
catastrophically (80-90% mortality(.
Patients have large zones of “
STUNNED” but reversible ischemic
myocardium if reperfusion is
established with in 5 hours of
occlusion, potentially infarcted
myocardium may be salvaged.
RV infarction & cardiogenic shock posesRV infarction & cardiogenic shock poses
special problems,special problems, intra aorticintra aortic
baloonbaloon does not afford any measuresdoes not afford any measures
of relief to the infarcted RV and isof relief to the infarcted RV and is
rarely of use in the treatment of shockrarely of use in the treatment of shock
caused by RV infarction unless there iscaused by RV infarction unless there is
some concomitant LV dysfunction.some concomitant LV dysfunction.
It is best treated by IV fluids ,It is best treated by IV fluids ,
ionotropic drugs and earlyionotropic drugs and early
myocardial reperfusionmyocardial reperfusion
MANAGEMENT Of RV
INFARCTION
RECOGNITION
REPERFUSION
VOLUME
LOADING
INOTROPIC
SUPPORT
RATE &
RHYTHM
CONTROL
COMPLICATIONS
TreatmentTreatmentThe major objective in treating RV
infarction, at ER level is
recognition, by 12-15 lead EKG,&
Clinical triad.
Initiate volume loading ,thrombolysis,
ionotropic support, atropine for
symptomatic bradycardia and shift the
patient in CCU for primary PCI, pacing,
IABP, haemodynamic monitoring and
treatment of complications,
( Emergency surgical intervention)
TreatmentTreatmentMaintain Right Ventricular PreloadMaintain Right Ventricular Preload
Volume load – The initial step in managingVolume load – The initial step in managing
hypotension should consist of volume loadinghypotension should consist of volume loading
with 40ml per minutes up towith 40ml per minutes up to2 L2 L of isotonicof isotonic
sodium chloride solution over asodium chloride solution over a 1- to 2-1- to 2-
hour,keeping RA pressure at less thanhour,keeping RA pressure at less than
18mmHg18mmHg
Avoid nitrates, diuretics, morphineAvoid nitrates, diuretics, morphine
Maintain atrioventricular synchrony:Maintain atrioventricular synchrony:
AV sequential pacing for complete heart blockAV sequential pacing for complete heart block
Atropine ( 0.5 to 1mg every 5 min up to total 2.5mg)Atropine ( 0.5 to 1mg every 5 min up to total 2.5mg)
Prompt Cardioversion for atrial fibrillationPrompt Cardioversion for atrial fibrillation
TreatmentTreatment
Ionotropic supportIonotropic support
If volume loading does not correctIf volume loading does not correct
hypotension and restore cardiac output, thenhypotension and restore cardiac output, then
ionotropic support with dobutamine may beionotropic support with dobutamine may be
attemptedattempted ( 2-5micg per kg per min to 15-( 2-5micg per kg per min to 15-
20micg)20micg)
Dobutamine is the agent of choice, thenDobutamine is the agent of choice, then
adrenaline or noradrenaline, dopamine.adrenaline or noradrenaline, dopamine.
Dobutamine increases cardiac output,Dobutamine increases cardiac output,
stroke volume index and RVEP,stroke volume index and RVEP,
consequently unloading the rightconsequently unloading the right
ventricle.ventricle.
TreatmentTreatment
ReperfusionReperfusion
Thrombolysis, primary PCI, and CABGThrombolysis, primary PCI, and CABG
ComplicationsComplications
LV ischemic dysfunction; judicious after loadLV ischemic dysfunction; judicious after load
reduction (ACE & Volume restriction)reduction (ACE & Volume restriction)
Cardiogenic shock, Intra aortic balloon pump,Cardiogenic shock, Intra aortic balloon pump,
Interventricular septal rupture, RV papillaryInterventricular septal rupture, RV papillary
muscle rupture and tricuspid regurgitaion,muscle rupture and tricuspid regurgitaion,
need emergency surgical repairneed emergency surgical repair
Coronary ReperfusionCoronary Reperfusion
Early reperfusion using either primary PCI orEarly reperfusion using either primary PCI or
thrombolysis can preserve both right and leftthrombolysis can preserve both right and left
ventricular function and reduce mortality andventricular function and reduce mortality and
morbadity. As in LV infarction the likelyhood ofmorbadity. As in LV infarction the likelyhood of
successful reperfusion appears to be greater withsuccessful reperfusion appears to be greater with
primary PCI compared to thrombolysisprimary PCI compared to thrombolysis..
Patients in whom reperfusion is achieved typicallyPatients in whom reperfusion is achieved typically
show a dramatic improvement in hemodynamicshow a dramatic improvement in hemodynamic
profile with inprofile with in 24 hours24 hours .In series of.In series of 5353 patientspatients
with symtomatic acute RV infarction who werewith symtomatic acute RV infarction who were
treated withtreated with primary PCIprimary PCI was attained inwas attained in
41(77%).41(77%).Successful reperfusion was associatedSuccessful reperfusion was associated
with prompt and striking recovery in rightwith prompt and striking recovery in right
ventricular function that begin with inventricular function that begin with in one hourone hour
and normalized in 95% patients at 3-5 daysand normalized in 95% patients at 3-5 days..
Key PointsKey Points
1)1) The Right Ventricle is anatomicallyThe Right Ventricle is anatomically
and physiologically designed to serveand physiologically designed to serve
the low pressure pulmonary circulationthe low pressure pulmonary circulation
2)2) Right ventricular infarction occursRight ventricular infarction occurs
when there is an occlusion of the rightwhen there is an occlusion of the right
coronary artery proximal to the acutecoronary artery proximal to the acute
marginal branches.marginal branches.
3)3) Right ventricular infarction complicatesRight ventricular infarction complicates
30-50%30-50% of inferior wall MIs, andof inferior wall MIs, and 10%10%
of anterior wall infarcts.of anterior wall infarcts.
Key PointsKey Points
44))The clinical triad ofThe clinical triad of hypotension,hypotension,
elevated JVP, and clear lung fieldselevated JVP, and clear lung fields
in patients with an inferior wallin patients with an inferior wall
infarction is virtually pathognomonic forinfarction is virtually pathognomonic for
right ventricular infarctionright ventricular infarction..
55))The most reliable ECG finding is STThe most reliable ECG finding is ST
segment elevation in the right precordialsegment elevation in the right precordial
leads, particularlyleads, particularly V4R,V4R,with associatedwith associated
ST segment elevation in 11,111,avfST segment elevation in 11,111,avf..
Key PointsKey Points
4)Haemodynamic insufficiency in the4)Haemodynamic insufficiency in the
presence of inferior wall myocardialpresence of inferior wall myocardial
infarction suggests additional rightinfarction suggests additional right
ventricular infarctionventricular infarction
Meta analysis have shown that RVMeta analysis have shown that RV
infarction with persistent hypotension isinfarction with persistent hypotension is
associated with worse in hospitalassociated with worse in hospital
outcome.outcome.
Long-term outcome depends on theLong-term outcome depends on the
degree of concomitant left ventriculardegree of concomitant left ventricular
dysfunction.dysfunction.
Why is Right Ventricle ImportantWhy is Right Ventricle Important
1)1) RV is anatomically and physiologically designed to serve the lowRV is anatomically and physiologically designed to serve the low
pressure pulmonary circulation.pressure pulmonary circulation.
2)2) Muscle mass of RV is 15% of LV.Muscle mass of RV is 15% of LV.
3)3) RV stroke work is 25% of LV.RV stroke work is 25% of LV.
4)4) Pulmonary is 10% of systemic vascular resistance.Pulmonary is 10% of systemic vascular resistance.
5)5) Coronary blood flow occurs in both systole and diastole in RVCoronary blood flow occurs in both systole and diastole in RV
absence of RV hypertrophy.absence of RV hypertrophy.
6)6) The main blood vessel is the right coronary artery( serves theThe main blood vessel is the right coronary artery( serves the
lateral wall ,posterior wall and posterior interventricularlateral wall ,posterior wall and posterior interventricular
septum by PDA)septum by PDA)
7)7) The anterior wall is supplied by conus artery and the LAD.The anterior wall is supplied by conus artery and the LAD.
8)8) The increased incidence of RV infarction in patients without aThe increased incidence of RV infarction in patients without a
history of preinfarction angina may result from a lack ofhistory of preinfarction angina may result from a lack of
adequately formed collateral vessels.adequately formed collateral vessels.
9)9) RV is like a pocket wraped around the LV sharing theRV is like a pocket wraped around the LV sharing the
interventricular septum and pericardium.interventricular septum and pericardium.
10)10) The right ventricle has same cardiac out put as left.The right ventricle has same cardiac out put as left.

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Right Ventricular Infarction Diagnosis, Signs, and Management

  • 1. Syndrome ofSyndrome of Right VentricularRight Ventricular InfarctionInfarction Dr Asadullah Khan soomroDr Asadullah Khan soomro Adult cardiologistAdult cardiologist Prince sultan Cardiac centrePrince sultan Cardiac centre Al-Hassa Kingdom of Saudi ArabiaAl-Hassa Kingdom of Saudi Arabia 2222ndnd November 2011November 2011
  • 2. INTRODUCTIOINTRODUCTIO NNMMoore thanre than 11 million11 million Americans have CoronaryAmericans have Coronary Artery disease , nearlyArtery disease , nearly 1.5 million1.5 million patients annually sufferpatients annually suffer from Acute myocardial infarctionfrom Acute myocardial infarction ( one patient every 20( one patient every 20 seconds)seconds) .. 50%50% of deaths associated with AMI occurof deaths associated with AMI occur with in one hour of event .with in one hour of event . 300,000-400,000300,000-400,000 die annuallydie annually due to sudden cardiac death at USA,due to sudden cardiac death at USA, 80%80% SDC are due toSDC are due to CAD and its consequences, it is the first clinicalCAD and its consequences, it is the first clinical manifestation of CAD inmanifestation of CAD in 20-25 %20-25 % of patients, how everof patients, how ever previous MI was identified in as many as 75 % patients whoprevious MI was identified in as many as 75 % patients who die suddenly.die suddenly. LV dysfunction due to CAD is mostLV dysfunction due to CAD is most powerful predictor of SCDpowerful predictor of SCD..
  • 3. DDespite impressive strides in diagnosis and managementespite impressive strides in diagnosis and management over the last three decades, acute MI continues to beover the last three decades, acute MI continues to be most seriousmost serious public health problempublic health problem and top leadingand top leading cause of death all over the world and in Kingdom ofcause of death all over the world and in Kingdom of Saudi ArabiaSaudi Arabia indeed .indeed . It was an epidemic in most industrialized countries andIt was an epidemic in most industrialized countries and now threaten to accelerate in developing countries atnow threaten to accelerate in developing countries at younger age .younger age . It strikes an individual during mostIt strikes an individual during most productive yearsproductive years withwith profound deleterious psychosocialprofound deleterious psychosocial and economic remifications.and economic remifications. INTRDUCTIO N
  • 4. INTRODUCTIO NN Right ventricular myocardial infarction was firstRight ventricular myocardial infarction was first recognized inrecognized in 1958 by H-De-Mosquita1958 by H-De-Mosquita , Isolated, Isolated acute RV infarction is rare event. Much moreacute RV infarction is rare event. Much more commonly RV infarction is associated withcommonly RV infarction is associated with infarction of the inferior wall of the LV,infarction of the inferior wall of the LV, occurring in more thanoccurring in more than one thirdone third of suchof such cases. Infarction typically involves the LVcases. Infarction typically involves the LV infero-posterior wall ,septum, andinfero-posterior wall ,septum, and posteriorposterior right ventricular free wallright ventricular free wall Inferior myocardial infarction associated with RightInferior myocardial infarction associated with Right ventricular infarction defines aventricular infarction defines a high risk subsethigh risk subset withwith a mortality rate ofa mortality rate of 25-30%25-30% as opposed to an overallas opposed to an overall mortality of aboutmortality of about 6%6% in inferior MI.in inferior MI.
  • 5. Right ventricular infarction occurs whenRight ventricular infarction occurs when there is an occlusion of thethere is an occlusion of the rightright coronary artery proximal to thecoronary artery proximal to the marginal branch,marginal branch, but it may alsobut it may also occur with an occlusion of the leftoccur with an occlusion of the left circumflex artery in patients who havecircumflex artery in patients who have left-dominant coronary circulationleft-dominant coronary circulation Right ventricular infarction complicatesRight ventricular infarction complicates 30-50%30-50% of inferior wall MI, andof inferior wall MI, and 10%10% of anterior wall infarctsof anterior wall infarcts
  • 6. When predominant infarction of the rightWhen predominant infarction of the right ventricle is present, the patient may present withventricle is present, the patient may present with unique combinationunique combination of clinical findings.of clinical findings. This clinicalThis clinical acute ischemic RVacute ischemic RV dysfunction syndromedysfunction syndrome also require uniquealso require unique form of therapy clearly distinct from that ofform of therapy clearly distinct from that of hypotension associated with predominant LVhypotension associated with predominant LV infarction.infarction. Nevertheless ,it is clear that this clinical syndromeNevertheless ,it is clear that this clinical syndrome has better acute and long term prognosis thanhas better acute and long term prognosis than that associated with predominant LV infarctionthat associated with predominant LV infarction
  • 7. Susceptibility to RV IschemiaSusceptibility to RV Ischemia Right ventricular function improves in the majority of patients withRight ventricular function improves in the majority of patients with RV infarction, including those who areRV infarction, including those who are not reperfusednot reperfused. This. This observation suggest that RV dysfunction is usually due toobservation suggest that RV dysfunction is usually due to ischemic myocardium that remainsischemic myocardium that remains viableviable.. There are several factors that make RV less susceptible to ischemia;There are several factors that make RV less susceptible to ischemia; 1) Oxygen demand is significantly lower in RV because of its much1) Oxygen demand is significantly lower in RV because of its much smaller muscle masssmaller muscle mass 2) Coronary perfusion in RV occurs in both systole and diastole2) Coronary perfusion in RV occurs in both systole and diastole 3) There is more extensive collateral flow from left to right.3) There is more extensive collateral flow from left to right. RV may also be protected to a greater degree by ischemicRV may also be protected to a greater degree by ischemic preconditioning. The preinfarction angina with in 72preconditioning. The preinfarction angina with in 72 hours of MI was associated with a reduction in incidencehours of MI was associated with a reduction in incidence of RV infarction and combined hypotension and shock.of RV infarction and combined hypotension and shock.
  • 8. Site of Culprit lesionSite of Culprit lesion Distal Right Coronary Artery Left Circumflex Artery LAD Proximal Occlusion of Right Coronary artery
  • 9. Site of Culprit lesionSite of Culprit lesion Among patients with right CAD, the size of infarctAmong patients with right CAD, the size of infarct is related in part to theis related in part to the site of culprit lesionsite of culprit lesion.. In a report ofIn a report of 522522 patients with inferior MI frompatients with inferior MI from HIT-4 trialHIT-4 trial ,,52%52% of patients with large infarctof patients with large infarct and RV involvement hadand RV involvement had proximal RCAproximal RCA lesionlesion compared tocompared to 23%23% in those with large infarctsin those with large infarcts but no RV involvement. In contrast thebut no RV involvement. In contrast the 28%28% ofof patients withpatients with small infarctssmall infarcts primarily had lesionsprimarily had lesions in thein the distal RCAdistal RCA. Similar findings were noted in. Similar findings were noted in an autopsy study in whichan autopsy study in which proximal RCAproximal RCA occlusion caused larger infarcts than distalocclusion caused larger infarcts than distal occlusion.occlusion.
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  • 11. Right coronary artery with corresponding regionsRight coronary artery with corresponding regions of perfusion& EKG findings for underperfusionof perfusion& EKG findings for underperfusion Proximal Segment Middle Segment Distal Segment Posterior Decending segment SA Nodal Branch Right atrial branch SA node Atrial free wall Sinus bradycardia Atrial infarction Pattern& atrial Fibrillation EKG effect of ischemia Perfused region Arterial branch Arterial segment Lateral& Marginal RV Branch AV nodal branch Posterior lateral LV branch & Lateral / inferior RV free wall AV node Posterior LV, inferior septum& LV free wall ST segment elevation, later Q waves( V3 to V6( AV block ST segment elevation, later Q waves in leads 11,111,avf
  • 12. Diagnosis ofDiagnosis of Right Ventricular InfactionRight Ventricular Infaction Because of the pathophysiology of RV infarction,Because of the pathophysiology of RV infarction, its management differs substantially from theits management differs substantially from the routine management of LV infarction.routine management of LV infarction. Early accurate diagnosis isEarly accurate diagnosis is imperativeimperative. Since hemodynamically. Since hemodynamically important RV infarction occurs in patients withimportant RV infarction occurs in patients with anan acute inferior wall myocardialacute inferior wall myocardial infarction,infarction, there fore suspicion isthere fore suspicion is warranted in any patient presenting withwarranted in any patient presenting with such an infarction.such an infarction.
  • 13. Right ventricle has remarkableRight ventricle has remarkable tendency to recover functiontendency to recover function rapidly, diagnostic tests are mostrapidly, diagnostic tests are most reliable when performed soonreliable when performed soon after presentation. Clinicalafter presentation. Clinical suspicion and careful physicalsuspicion and careful physical examination demonstrating theexamination demonstrating the signs are first step.signs are first step.
  • 14. Caution must be exercised in relying on such findings, since they are readily masked by volume depletion and because the physical and hemodynamic signs of right ventricular infarction often emerge only after volume loading.
  • 15. By radionuclide ventriculography,By radionuclide ventriculography, Echocardiography or right sidedEchocardiography or right sided ECG RV involvement isECG RV involvement is demonstrated in up todemonstrated in up to 40%40% of patientof patient with acute inferior infarction,with acute inferior infarction, however clinical or hemodynamichowever clinical or hemodynamic evidence of RV infarction is presentevidence of RV infarction is present in less thenin less then 10%10% of patients withof patients with inferior infarction.inferior infarction.
  • 16. On examinationThe clinical triad of hypotension, elevated JVP and clear lung fields, in a patient with an inferior infarction is virtually pathognomonic for RV infarction, however this triad has sensitivity of less than 25%. Caution must be exercised in relying on such findings ,since they are readily masked by volume depletion and because the physical and hemodynamic signs of RV infarction often emerge only after volume loading.
  • 17. Prominent jugular venous distension Kussmauls sign and pulses paradoxus may be present In fact Kussmauls sign in the setting of inferior MI is highly sensitive& specific for RV infarction. Other physical signs may include RV gallop, murmur of tricuspid regurgitation, and septal rupture, pericardial rub and AV dissociation. (CVP >PCWP)
  • 18. ELECTROCARDIOGRAM There is general consensus with respect to the diagnosis of ST elevation MI,EKG is obligatory tool in identifying patients with STEMI. 12 lead EKG along with right sided leads V3R through V6R should be recorded in all the patients with acute inferior wall MI . EKG must be interpreted as quickly as possible after first medical contact and ideally with in 10 minutes
  • 19. Electrocardiography A right precordial lead (V4R) is the investigation of choice. ST- segment elevation in lead V4R remains the most predictive electrocardiographic finding for right ventricular infarction. A 1-mm ST-segment elevation in this lead was 70% sensitive and 100% specific for right ventricular infarction.
  • 20. 5454%% of inferior MI have ST elevation inof inferior MI have ST elevation in V4RV4R,, 1818%% of Pts with acute inferior MI had STof Pts with acute inferior MI had ST elevation in leadelevation in lead V1V1,which is highly specific sign,which is highly specific sign of RV infarctionof RV infarction.. Greater ST elevation in lead 111 than lead 11 is alsoGreater ST elevation in lead 111 than lead 11 is also suggestive of RV infarctionsuggestive of RV infarction. In one study this. In one study this finding had a sensitivity, specificity,and positivefinding had a sensitivity, specificity,and positive and negative predictive value of 97,56,69 andand negative predictive value of 97,56,69 and 95%respectively.95%respectively. It is usually associated with large infarct size and higherIt is usually associated with large infarct size and higher incidence of major in hospitalincidence of major in hospital atrial & ventricularatrial & ventricular arrhythmias and high grade AV blockarrhythmias and high grade AV block ElectrocardiographyElectrocardiography
  • 21. Electrocardiography 48% of the patients had resolution of EKG changes within 10 hours of the onset of symptoms. Thus, it is imperative to record the EKG through the accessory right precordial leads as early as possible . It is important to recognize the transient nature of ST segment elevation.
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  • 29. EchocardiographyEchocardiography:: Abnormal findings includeAbnormal findings include right ventricularright ventricular dilatation, right ventricular walldilatation, right ventricular wall asynergy,asynergy, and abnormal interventricularand abnormal interventricular septal motion caused by a reversal of theseptal motion caused by a reversal of the trans septal pressure gradient due to thetrans septal pressure gradient due to the increased right ventricular end-diastolicincreased right ventricular end-diastolic pressure.pressure. The short-axis view has been shown toThe short-axis view has been shown to have the highest sensitivity (82have the highest sensitivity (82 percent), with a specificity ranging frompercent), with a specificity ranging from 62 to 9362 to 93 percent for hemodynamicallypercent for hemodynamically important right ventricular infarction .important right ventricular infarction .
  • 30. EchocardiographyEchocardiography:: Interatrial septal bowingInteratrial septal bowing towards the lefttowards the left atrium,indicative of an increasedatrium,indicative of an increased RA to LA pressure gradient is anRA to LA pressure gradient is an important prognostic marker inimportant prognostic marker in RV infarctionRV infarction.. Patients with this finding have morePatients with this finding have more hypotension, more heart block, andhypotension, more heart block, and higher mortality than patientshigher mortality than patients without itwithout it..
  • 31. EchocardiographyEchocardiography:: Doppler Echocardiography isDoppler Echocardiography is particularly helpful in detectingparticularly helpful in detecting complications of RV infarction suchcomplications of RV infarction such asas tricuspid regurgitation, ventriculartricuspid regurgitation, ventricular septal rupture, ASDseptal rupture, ASD or PFO andor PFO and premature opening of pulmonarypremature opening of pulmonary valve ( indicative of non compliantvalve ( indicative of non compliant RVRV(.(. Pericardial effusion andPericardial effusion and cardiac tamponade, thrombuscardiac tamponade, thrombus formation and plethora offormation and plethora of inferior vena cavainferior vena cava
  • 32. HemodynamicsHemodynamics Hemodynamically significantHemodynamically significant infarcts are associated withinfarcts are associated with elevation in right atrialelevation in right atrial pressure topressure to >10mmHg,>10mmHg, andand in ratio of RA to PCWP toin ratio of RA to PCWP to >0.8( normal mean value <>0.8( normal mean value < 0.6).0.6).
  • 33. Other Imaging StudiesOther Imaging Studies Radionuclide ventriculography and technetiumRadionuclide ventriculography and technetium pyrophosphate scanning have acceptable sensitivitiespyrophosphate scanning have acceptable sensitivities and specificities for making a diagnosis of RV infarction.and specificities for making a diagnosis of RV infarction. They can detect wall motion abnormalties andThey can detect wall motion abnormalties and hypoperfusion in affected Rv, it can also be used tohypoperfusion in affected Rv, it can also be used to quantitate both LV & RV ejection fraction. Technitiumquantitate both LV & RV ejection fraction. Technitium scan ,On the other hand ,is particularly useful for latescan ,On the other hand ,is particularly useful for late diagnosis, since it shows areas of necrosis or dyingdiagnosis, since it shows areas of necrosis or dying myocardium.myocardium. However both methods areHowever both methods are cumbersome ,time consumingcumbersome ,time consuming and frequently difficult to perform at bed sideand frequently difficult to perform at bed side, therefore, therefore performed later rather than as primary diagnosticperformed later rather than as primary diagnostic modalties.modalties.
  • 34. RV Infarction & Cardiogenic Shock It is a highly lethal disease patient deteriorate dramatically and catastrophically (80-90% mortality(. Patients have large zones of “ STUNNED” but reversible ischemic myocardium if reperfusion is established with in 5 hours of occlusion, potentially infarcted myocardium may be salvaged.
  • 35. RV infarction & cardiogenic shock posesRV infarction & cardiogenic shock poses special problems,special problems, intra aorticintra aortic baloonbaloon does not afford any measuresdoes not afford any measures of relief to the infarcted RV and isof relief to the infarcted RV and is rarely of use in the treatment of shockrarely of use in the treatment of shock caused by RV infarction unless there iscaused by RV infarction unless there is some concomitant LV dysfunction.some concomitant LV dysfunction. It is best treated by IV fluids ,It is best treated by IV fluids , ionotropic drugs and earlyionotropic drugs and early myocardial reperfusionmyocardial reperfusion
  • 37. TreatmentTreatmentThe major objective in treating RV infarction, at ER level is recognition, by 12-15 lead EKG,& Clinical triad. Initiate volume loading ,thrombolysis, ionotropic support, atropine for symptomatic bradycardia and shift the patient in CCU for primary PCI, pacing, IABP, haemodynamic monitoring and treatment of complications, ( Emergency surgical intervention)
  • 38. TreatmentTreatmentMaintain Right Ventricular PreloadMaintain Right Ventricular Preload Volume load – The initial step in managingVolume load – The initial step in managing hypotension should consist of volume loadinghypotension should consist of volume loading with 40ml per minutes up towith 40ml per minutes up to2 L2 L of isotonicof isotonic sodium chloride solution over asodium chloride solution over a 1- to 2-1- to 2- hour,keeping RA pressure at less thanhour,keeping RA pressure at less than 18mmHg18mmHg Avoid nitrates, diuretics, morphineAvoid nitrates, diuretics, morphine Maintain atrioventricular synchrony:Maintain atrioventricular synchrony: AV sequential pacing for complete heart blockAV sequential pacing for complete heart block Atropine ( 0.5 to 1mg every 5 min up to total 2.5mg)Atropine ( 0.5 to 1mg every 5 min up to total 2.5mg) Prompt Cardioversion for atrial fibrillationPrompt Cardioversion for atrial fibrillation
  • 39. TreatmentTreatment Ionotropic supportIonotropic support If volume loading does not correctIf volume loading does not correct hypotension and restore cardiac output, thenhypotension and restore cardiac output, then ionotropic support with dobutamine may beionotropic support with dobutamine may be attemptedattempted ( 2-5micg per kg per min to 15-( 2-5micg per kg per min to 15- 20micg)20micg) Dobutamine is the agent of choice, thenDobutamine is the agent of choice, then adrenaline or noradrenaline, dopamine.adrenaline or noradrenaline, dopamine. Dobutamine increases cardiac output,Dobutamine increases cardiac output, stroke volume index and RVEP,stroke volume index and RVEP, consequently unloading the rightconsequently unloading the right ventricle.ventricle.
  • 40. TreatmentTreatment ReperfusionReperfusion Thrombolysis, primary PCI, and CABGThrombolysis, primary PCI, and CABG ComplicationsComplications LV ischemic dysfunction; judicious after loadLV ischemic dysfunction; judicious after load reduction (ACE & Volume restriction)reduction (ACE & Volume restriction) Cardiogenic shock, Intra aortic balloon pump,Cardiogenic shock, Intra aortic balloon pump, Interventricular septal rupture, RV papillaryInterventricular septal rupture, RV papillary muscle rupture and tricuspid regurgitaion,muscle rupture and tricuspid regurgitaion, need emergency surgical repairneed emergency surgical repair
  • 41. Coronary ReperfusionCoronary Reperfusion Early reperfusion using either primary PCI orEarly reperfusion using either primary PCI or thrombolysis can preserve both right and leftthrombolysis can preserve both right and left ventricular function and reduce mortality andventricular function and reduce mortality and morbadity. As in LV infarction the likelyhood ofmorbadity. As in LV infarction the likelyhood of successful reperfusion appears to be greater withsuccessful reperfusion appears to be greater with primary PCI compared to thrombolysisprimary PCI compared to thrombolysis.. Patients in whom reperfusion is achieved typicallyPatients in whom reperfusion is achieved typically show a dramatic improvement in hemodynamicshow a dramatic improvement in hemodynamic profile with inprofile with in 24 hours24 hours .In series of.In series of 5353 patientspatients with symtomatic acute RV infarction who werewith symtomatic acute RV infarction who were treated withtreated with primary PCIprimary PCI was attained inwas attained in 41(77%).41(77%).Successful reperfusion was associatedSuccessful reperfusion was associated with prompt and striking recovery in rightwith prompt and striking recovery in right ventricular function that begin with inventricular function that begin with in one hourone hour and normalized in 95% patients at 3-5 daysand normalized in 95% patients at 3-5 days..
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  • 43. Key PointsKey Points 1)1) The Right Ventricle is anatomicallyThe Right Ventricle is anatomically and physiologically designed to serveand physiologically designed to serve the low pressure pulmonary circulationthe low pressure pulmonary circulation 2)2) Right ventricular infarction occursRight ventricular infarction occurs when there is an occlusion of the rightwhen there is an occlusion of the right coronary artery proximal to the acutecoronary artery proximal to the acute marginal branches.marginal branches. 3)3) Right ventricular infarction complicatesRight ventricular infarction complicates 30-50%30-50% of inferior wall MIs, andof inferior wall MIs, and 10%10% of anterior wall infarcts.of anterior wall infarcts.
  • 44. Key PointsKey Points 44))The clinical triad ofThe clinical triad of hypotension,hypotension, elevated JVP, and clear lung fieldselevated JVP, and clear lung fields in patients with an inferior wallin patients with an inferior wall infarction is virtually pathognomonic forinfarction is virtually pathognomonic for right ventricular infarctionright ventricular infarction.. 55))The most reliable ECG finding is STThe most reliable ECG finding is ST segment elevation in the right precordialsegment elevation in the right precordial leads, particularlyleads, particularly V4R,V4R,with associatedwith associated ST segment elevation in 11,111,avfST segment elevation in 11,111,avf..
  • 45. Key PointsKey Points 4)Haemodynamic insufficiency in the4)Haemodynamic insufficiency in the presence of inferior wall myocardialpresence of inferior wall myocardial infarction suggests additional rightinfarction suggests additional right ventricular infarctionventricular infarction Meta analysis have shown that RVMeta analysis have shown that RV infarction with persistent hypotension isinfarction with persistent hypotension is associated with worse in hospitalassociated with worse in hospital outcome.outcome. Long-term outcome depends on theLong-term outcome depends on the degree of concomitant left ventriculardegree of concomitant left ventricular dysfunction.dysfunction.
  • 46. Why is Right Ventricle ImportantWhy is Right Ventricle Important 1)1) RV is anatomically and physiologically designed to serve the lowRV is anatomically and physiologically designed to serve the low pressure pulmonary circulation.pressure pulmonary circulation. 2)2) Muscle mass of RV is 15% of LV.Muscle mass of RV is 15% of LV. 3)3) RV stroke work is 25% of LV.RV stroke work is 25% of LV. 4)4) Pulmonary is 10% of systemic vascular resistance.Pulmonary is 10% of systemic vascular resistance. 5)5) Coronary blood flow occurs in both systole and diastole in RVCoronary blood flow occurs in both systole and diastole in RV absence of RV hypertrophy.absence of RV hypertrophy. 6)6) The main blood vessel is the right coronary artery( serves theThe main blood vessel is the right coronary artery( serves the lateral wall ,posterior wall and posterior interventricularlateral wall ,posterior wall and posterior interventricular septum by PDA)septum by PDA) 7)7) The anterior wall is supplied by conus artery and the LAD.The anterior wall is supplied by conus artery and the LAD. 8)8) The increased incidence of RV infarction in patients without aThe increased incidence of RV infarction in patients without a history of preinfarction angina may result from a lack ofhistory of preinfarction angina may result from a lack of adequately formed collateral vessels.adequately formed collateral vessels. 9)9) RV is like a pocket wraped around the LV sharing theRV is like a pocket wraped around the LV sharing the interventricular septum and pericardium.interventricular septum and pericardium. 10)10) The right ventricle has same cardiac out put as left.The right ventricle has same cardiac out put as left.