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Inferior myocardial infarction with Right
ventricular infarction & Posterior extension
Dr. Gias Uddin Md Salim
MD –Final Part Student
Department of Cardiology
Dhaka Medical College
A 60 year old women, diabetic and hypertensive patient
presented with H/O operation of carcinoma of breast on
4th POD
 Severe central chest tightness with epigastric discomfort
 Persistent for 2 hours,
 Associated with nausea, vomiting and severe shortness of
breath
 Calm and cold periphery, feeling of fainting with agitation.
Examination:
pulse: 108 b/min and feeble
BP: 80/50mmHg
JVP: elevated
Cyanosis present
Precordium: S1+S2,no murmur
Lungs: no basal crackles.
Temperature -101* F
????
Possibilities:
 ACS
 Acute pulmonary embolism
 Pericardial effusion/temponade
 Pneumothorax/collapse lungs
 Metabolic causes
Artery involved in Inferior MI
 RCA(Right dominant)
 LCX(left dominant)
 Type 4 LAD
CLINICAL FEATURES
 Symptoms:
 Chest pain > 30 min.
 Character of the pain –retrosternal,
constrciting,crushing,compressing sensation of heavy
weight.
 Predilection for left side.
 Radiates to the ulnar aspect of the left arm
 Tingling sensation of the wrist and fingers.
 In some patients, the symptom is epigastric, with a
feeling of indigestion or of fullness and gas.
 Nausea,Vomitings , why more common?
 Profound weakness
 Dizziness
 Palpitations,
 Cold perspiration
 Sense of impending doom.
 Urine output
Isolated Inferior MI
 Clinical features?
 Hemodynamically stable or not?
If not ,think followings:
 RV infarction
 Post extension
 RV+Post extension
 Associated anterior MI
 Old MI
 Arrythmias
 Atrial infarction
 Drugs: beta blocker
 Pericardial Effuusion
 VSR
 Acute pulmonary embolism
 Acute severe mitral regurgitation
 Bezold–Jerisch reflex
Why detection of RV /post infarction is
important?
Why detection of RV /post infarction is important?
 Clinical presentation is different
 ECG over looked
 Conventional ECG leads not representative of those
surface
 Special leads require to perform ECG
 Management different than anterior,inferior ,posterior
 Some drugs should be avoided
 Fluids may be needed for management
 In Exam important (OSPE ECG. medicine &
cardiology)
 Isolated RV infarction is extremely rare.
 RVI usually is noted in association with
inferior wall MI.
 • The incidence of RVI in such cases ranges
from 10-50%
 AV block is more common than infranodal block and
occurs in approximately 20% of IWMI.
 Sinus bradycardia is more common in IWMI
(tahcycardia in AWMI)
 Posterior wall MI is associated with 5% of IWMI or
lateral MI but rarely occurs alone.
 <10% hemodynamic unstable
 Higher morbidity and mortality than inferior
MI
 Mortality 25-30% - Inferior mi + RVI = 31%
- Inferior mi – RVI = 6%
 RV infarcttion +LV failure -80%
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
hemodynamic features of RVI:
 Prominent V wave, sharp Y descent
 ↑in RA pressure (JVP) with inspiration (ie,Kussmaul
sign)
 • Fall in systolic pressure >10 mm Hg with
inspiration (ie,pulsus paradoxus)
Mimic/DD of RV infarction
 Hypotension(without JVP raised)
 Pericardial temponade
 Acute pulmonary embolism
 ECG
 Cardiac biomarkers
Troponin -I (disproportionately increased)
CKMB,
 CBP
 RBS
 CXR-signs of LV failure, help to fluid
therapy,PE,Effsion
 Serum electrolytes
 Serum creatinine
Investigations:
 Lipid profile
 Technetium 99m pyrophosphate scintigraphy
 Scintigraphy with thallium 201
 Hemodynamic assesement with PA catheter---
cardiogenic shock
 Inferior wall MI –
ST segment elevation of > 1 mm in inferior leads
then look the following leads (Which coronary artery?)
 ST segment elevation lead III>ST segment lead II-RCA
 Reciprocal change in lead I & aVL-RCA
 If no reciprocal change in lead I & aVL- LcX
 Signs of lateral infarction I,aVL,V5,V6-LcX
 Look anterior lead –LAD
ECG -----
 Then look for V1,V2,,V3,V4(Don’t Missed)
 In VI isoelectric/elevated
 V2,V3, V4 ST segment depression
 ST elevation in right sided chest lead(V3R/V4R)
----RV infarction
ECG -----
Leads Sensitivity (%) Specificity (%)
V3 R 69 97
V4 R 93 95
V1 28 92
 R/S ratio >1 in V1 & V2
 ST depression
 T upright
 ST segment elevation in pV7,pV8 and pV9
----post extension
ECG ----
Position of post leads
 Is it inferior MI?
Echo
 Exclude d/d
 PE
 Acute pulmonary embolism
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
 MRI with gadolinium contrast enhancement –most
sensitive –2 gm of MI can be detected.
 Techntium scan – hot spot with calcium – insensitive
to small infarctions.
 Thallium scan –cold spots in regions of diminished
perfusion –does not differentiate old from new.
Other imaging
Principle of Management:
 Management of ACS
 Maintain RV preload
 Lower RV afterload
 Restore AV synchrony
 Arrythmias
 Inotropic support
 Risk factors
 Mobilization & rehabilitation
Initial management
 Complete bed rest
 High flow O2
 Loading dose of aspirin, clopidogrel, statin
 IV channel
 Analgesic
 Antiemetic
 Continuous ECG monitoring
 CV and arterial line insertion and monitoring of CVP
 Alternate to CVP—JVP,Lungs crakles
management
Primary PCI
Pharmaco- invasive
Reperfusion with Thrombolysis
Fluid challange
Inj.Atropine
pulse,BP, JVP, Lungs,Urine output-hourly
Antidiabetic with short acting insulin
Risk stratification (TIMI /GRACE risk score)
Caution…
 Nitrates
 Beta blocker, rate limiting CCB
 Vasodilators
 Diuretic
 Opiods(morphine)
Cardiogenic shock with RVI
Target: CVP:8-10mmHg or PCWP:18mmHg
Early reperfusion should achieved if possible
RV preload should be optimized by:
Fluid challenge:(Fluid in fluid)
Inotropes: dobutamine.
RV after load should be optimized when associated with
LV dysfunction.
Management of RV Infarction
 Fluids challenges
Management of RV Infarction
Fluids challenges
 Normal saline
 Careful administration of fluid boluses
 Bolus 200-300 ml running(aliquts),several liters in one
hour,
 Frequently auscultate lungs bases
 Upto-1500mL; then measure
 PCWP-<15 mm of hg
 Continue fluid
 Not responded to fluid?/
 • RV failure may limit filling via ↓in CO,
 • 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
Right Ventricular Dysfunction and
Shock, use of excessive fluids??
 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.
 Inotropic support(principle?)
 Dobutamine, 2 to 5 μg per kg per minute given IV, with
dose increased every 5 to 10 minutes up to 15 to 20 μg per
kg per minute (why?)
 Milrinone
 Levosimendan (approved only in Europe)
 Norepinephrine
 Low-dose vasopressin.
 Nitropruside and hydralazine
 Avoid dopamine(?) and phenylephrine(?).
 Consider combination therapy with inhaled
nitric oxide.
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 treatmen of
acute RV failure.
Rate and rhythm control
 Symptomatic bradycardia: atropine, 0.5 to 1 mg given IV
every 5 minutes up to total of 2.5 mg
 Salbutamol
 Theophyline
 propantheline
 Isoprenaline
 A-V sequential pacing is the modality of choice
when a pacemaker is required
Other options:
 Nitroprusside,hydralazine infusion for afterload
reduction.
 IABP- Concomitant LV dysfunction
 Mechanical circulatory support can be also
used, including-
1. LVAD
2. RVAD
3. Biventricular ventricular assist device.
 pericardiotomy
 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
Is it reversible ?less
extensive
Risk factors Mx
Control DM and HTN
Cessation of smoking
Low fat diet
Eat more vegetables, fruits and fiber containing foods
Control body weight
Regular walking and exercise
Mobilization and Rehabilitation
In uncomplicated cases:
 Sit on the chair in Day2
 Walk to toilet Day3
 Return to home on Day 5-7
 To normal work 4-6 wks
 Counseling and reassurance
Complicated cases:
 Process of mobilization and rehabilitation varies and
depends upon the patient functional capacity.
যাহা কিছু মনে রাকিনে হইনে
Inferior MI(ST elevation in II,III,aVF)
1. Look for RV & Post extension(V1-V4)
2. Do rt site & post ECG
3. Look for arrythmias
4. Fluid challange
5. Avoid drugs (nitrates,diuretics,b –
blocker,vasodilator)
6. Ionotrops(dobutamine)
OSPE??
 Write down the complete ECG diagnosis
 Write the three points in favour of your diagnosis
 What do you expect in auscultation of lung base
 Mention 2 other positive clinical findings support
your diagnosis
 What is the site of lesion
 Mention one treatment option usually not given in
lesion of he other site
Thank you
??
Inferior Myocardial Infarction with Right Ventricular Infarction & Posterior Extension
Inferior Myocardial Infarction with Right Ventricular Infarction & Posterior Extension
Inferior Myocardial Infarction with Right Ventricular Infarction & Posterior Extension
Inferior Myocardial Infarction with Right Ventricular Infarction & Posterior Extension
Inferior Myocardial Infarction with Right Ventricular Infarction & Posterior Extension
Inferior Myocardial Infarction with Right Ventricular Infarction & Posterior Extension

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Inferior Myocardial Infarction with Right Ventricular Infarction & Posterior Extension

  • 1. Inferior myocardial infarction with Right ventricular infarction & Posterior extension Dr. Gias Uddin Md Salim MD –Final Part Student Department of Cardiology Dhaka Medical College
  • 2. A 60 year old women, diabetic and hypertensive patient presented with H/O operation of carcinoma of breast on 4th POD  Severe central chest tightness with epigastric discomfort  Persistent for 2 hours,  Associated with nausea, vomiting and severe shortness of breath  Calm and cold periphery, feeling of fainting with agitation.
  • 3. Examination: pulse: 108 b/min and feeble BP: 80/50mmHg JVP: elevated Cyanosis present Precordium: S1+S2,no murmur Lungs: no basal crackles. Temperature -101* F
  • 5. Possibilities:  ACS  Acute pulmonary embolism  Pericardial effusion/temponade  Pneumothorax/collapse lungs  Metabolic causes
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  • 11. Artery involved in Inferior MI  RCA(Right dominant)  LCX(left dominant)  Type 4 LAD
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  • 14. CLINICAL FEATURES  Symptoms:  Chest pain > 30 min.  Character of the pain –retrosternal, constrciting,crushing,compressing sensation of heavy weight.  Predilection for left side.  Radiates to the ulnar aspect of the left arm  Tingling sensation of the wrist and fingers.
  • 15.  In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas.  Nausea,Vomitings , why more common?  Profound weakness  Dizziness  Palpitations,  Cold perspiration  Sense of impending doom.  Urine output
  • 16. Isolated Inferior MI  Clinical features?  Hemodynamically stable or not?
  • 17. If not ,think followings:  RV infarction  Post extension  RV+Post extension  Associated anterior MI  Old MI  Arrythmias  Atrial infarction  Drugs: beta blocker
  • 18.  Pericardial Effuusion  VSR  Acute pulmonary embolism  Acute severe mitral regurgitation  Bezold–Jerisch reflex
  • 19. Why detection of RV /post infarction is important?
  • 20. Why detection of RV /post infarction is important?  Clinical presentation is different  ECG over looked  Conventional ECG leads not representative of those surface  Special leads require to perform ECG  Management different than anterior,inferior ,posterior  Some drugs should be avoided  Fluids may be needed for management  In Exam important (OSPE ECG. medicine & cardiology)
  • 21.  Isolated RV infarction is extremely rare.  RVI usually is noted in association with inferior wall MI.  • The incidence of RVI in such cases ranges from 10-50%
  • 22.  AV block is more common than infranodal block and occurs in approximately 20% of IWMI.  Sinus bradycardia is more common in IWMI (tahcycardia in AWMI)  Posterior wall MI is associated with 5% of IWMI or lateral MI but rarely occurs alone.
  • 23.  <10% hemodynamic unstable  Higher morbidity and mortality than inferior MI  Mortality 25-30% - Inferior mi + RVI = 31% - Inferior mi – RVI = 6%  RV infarcttion +LV failure -80%
  • 24. Classic clinical triad of  1. Distended neck veins (↑ JVP)  2. Clear lung fields  3. Hypotension.
  • 25.  RV- S3, S4 + – Lower left sternal border – ↑with inspiration.  • Hemodynamic monitoring. – ↑right-sided filling pressures
  • 26. hemodynamic features of RVI:  Prominent V wave, sharp Y descent  ↑in RA pressure (JVP) with inspiration (ie,Kussmaul sign)  • Fall in systolic pressure >10 mm Hg with inspiration (ie,pulsus paradoxus)
  • 27. Mimic/DD of RV infarction  Hypotension(without JVP raised)  Pericardial temponade  Acute pulmonary embolism
  • 28.  ECG  Cardiac biomarkers Troponin -I (disproportionately increased) CKMB,  CBP  RBS  CXR-signs of LV failure, help to fluid therapy,PE,Effsion  Serum electrolytes  Serum creatinine Investigations:
  • 29.  Lipid profile  Technetium 99m pyrophosphate scintigraphy  Scintigraphy with thallium 201  Hemodynamic assesement with PA catheter--- cardiogenic shock
  • 30.  Inferior wall MI – ST segment elevation of > 1 mm in inferior leads then look the following leads (Which coronary artery?)  ST segment elevation lead III>ST segment lead II-RCA  Reciprocal change in lead I & aVL-RCA  If no reciprocal change in lead I & aVL- LcX  Signs of lateral infarction I,aVL,V5,V6-LcX  Look anterior lead –LAD ECG -----
  • 31.  Then look for V1,V2,,V3,V4(Don’t Missed)  In VI isoelectric/elevated  V2,V3, V4 ST segment depression  ST elevation in right sided chest lead(V3R/V4R) ----RV infarction ECG -----
  • 32.
  • 33.
  • 34. Leads Sensitivity (%) Specificity (%) V3 R 69 97 V4 R 93 95 V1 28 92
  • 35.  R/S ratio >1 in V1 & V2  ST depression  T upright  ST segment elevation in pV7,pV8 and pV9 ----post extension ECG ----
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  • 53.  Is it inferior MI?
  • 54.
  • 55. Echo  Exclude d/d  PE  Acute pulmonary embolism
  • 56.
  • 57.
  • 58. 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
  • 59.  MRI with gadolinium contrast enhancement –most sensitive –2 gm of MI can be detected.  Techntium scan – hot spot with calcium – insensitive to small infarctions.  Thallium scan –cold spots in regions of diminished perfusion –does not differentiate old from new. Other imaging
  • 60. Principle of Management:  Management of ACS  Maintain RV preload  Lower RV afterload  Restore AV synchrony  Arrythmias  Inotropic support  Risk factors  Mobilization & rehabilitation
  • 61.
  • 62. Initial management  Complete bed rest  High flow O2  Loading dose of aspirin, clopidogrel, statin  IV channel  Analgesic  Antiemetic  Continuous ECG monitoring  CV and arterial line insertion and monitoring of CVP  Alternate to CVP—JVP,Lungs crakles
  • 63. management Primary PCI Pharmaco- invasive Reperfusion with Thrombolysis Fluid challange Inj.Atropine pulse,BP, JVP, Lungs,Urine output-hourly Antidiabetic with short acting insulin Risk stratification (TIMI /GRACE risk score)
  • 64.
  • 65.
  • 66. Caution…  Nitrates  Beta blocker, rate limiting CCB  Vasodilators  Diuretic  Opiods(morphine)
  • 67. Cardiogenic shock with RVI Target: CVP:8-10mmHg or PCWP:18mmHg Early reperfusion should achieved if possible RV preload should be optimized by: Fluid challenge:(Fluid in fluid) Inotropes: dobutamine. RV after load should be optimized when associated with LV dysfunction.
  • 68.
  • 69. Management of RV Infarction  Fluids challenges
  • 70. Management of RV Infarction Fluids challenges  Normal saline  Careful administration of fluid boluses  Bolus 200-300 ml running(aliquts),several liters in one hour,  Frequently auscultate lungs bases  Upto-1500mL; then measure  PCWP-<15 mm of hg  Continue fluid  Not responded to fluid?/
  • 71.  • RV failure may limit filling via ↓in CO,  • 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 Right Ventricular Dysfunction and Shock, use of excessive fluids??
  • 72.  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.
  • 73.  Inotropic support(principle?)  Dobutamine, 2 to 5 μg per kg per minute given IV, with dose increased every 5 to 10 minutes up to 15 to 20 μg per kg per minute (why?)  Milrinone  Levosimendan (approved only in Europe)  Norepinephrine  Low-dose vasopressin.  Nitropruside and hydralazine  Avoid dopamine(?) and phenylephrine(?).  Consider combination therapy with inhaled nitric oxide.
  • 74. 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 treatmen of acute RV failure.
  • 75. Rate and rhythm control  Symptomatic bradycardia: atropine, 0.5 to 1 mg given IV every 5 minutes up to total of 2.5 mg  Salbutamol  Theophyline  propantheline  Isoprenaline  A-V sequential pacing is the modality of choice when a pacemaker is required
  • 76. Other options:  Nitroprusside,hydralazine infusion for afterload reduction.  IABP- Concomitant LV dysfunction  Mechanical circulatory support can be also used, including- 1. LVAD 2. RVAD 3. Biventricular ventricular assist device.  pericardiotomy
  • 77.  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 Is it reversible ?less extensive
  • 78. Risk factors Mx Control DM and HTN Cessation of smoking Low fat diet Eat more vegetables, fruits and fiber containing foods Control body weight Regular walking and exercise
  • 79. Mobilization and Rehabilitation In uncomplicated cases:  Sit on the chair in Day2  Walk to toilet Day3  Return to home on Day 5-7  To normal work 4-6 wks  Counseling and reassurance Complicated cases:  Process of mobilization and rehabilitation varies and depends upon the patient functional capacity.
  • 80. যাহা কিছু মনে রাকিনে হইনে Inferior MI(ST elevation in II,III,aVF) 1. Look for RV & Post extension(V1-V4) 2. Do rt site & post ECG 3. Look for arrythmias 4. Fluid challange 5. Avoid drugs (nitrates,diuretics,b – blocker,vasodilator) 6. Ionotrops(dobutamine)
  • 82.
  • 83.  Write down the complete ECG diagnosis  Write the three points in favour of your diagnosis  What do you expect in auscultation of lung base  Mention 2 other positive clinical findings support your diagnosis  What is the site of lesion  Mention one treatment option usually not given in lesion of he other site