Inferior wall MI and its complications

CLINICIAN IN CHARGE:

PROF. HILAL AH RATHER

Prof. Dept. of Cardiology

MODERATOR :

PROF. A R LONE

Dept of Medical oncology

45 yrs old male

Chronic smoker

Diabetic

HTN

presents with:

Retrosternal chest pain X 4 hrs

It was sudden onset,

Localised to left side of chest,

Stabbing in nature,

Feeling of heaviness on chest,

Radiation to left arm,( since 12 midnight)

On further enquiry, he gives History of:

Multiple episodes of vomiting,

Diaphoresis

Transient loss of consciousness(1-2 min)

Cough

Breathlessness

Sputum production

fever

Palpitations

Pain radiating to back

Headache

Weakness of any part of body.

Negative history

GPE:- Conscious, cooperative, oriented

VITALS:-

PULSE : 34 bts/min, regular,

BLOOD PRESSURE: 80/60mmHg

RR: 28 cycles/min

Spao2: 88%

Temp: Afebrile

JVP: Raised

Chest: NVBS, b/l symmetrical

CVS:- Normal precordium.

No murmur /s1s2+

P/A:- soft/ Non distended.

CNS:- GCS 15/15

Neck free, No meningeal Signs,

Cranial Nerves Normal

No neurological Deficit

HB TLC DLC PLT MCV ESR

14.2 21.54 87/6.

4

122 85/29 14

12.3 13.5 79/16 76 87/29 10

12.8 11.2 82/15 86 84/28

11.6 6.7 72/18 74

UREA CREATININE

58 1.12

65 .92

64 .86

69 .85

58 .90

Na K Ph PCo2 HCO3

136 2.5 7.46 33 23.5

149 4.1 7.35 41 16.7

135 3.1 7.44 44 22.6

138 3.8 7.43 42 22.5

141 4.4 7.26 12

ROUTINE URINE EXAM:

PC 3-4

RBC’S – NIL

SUGAR, ALB - NIL

CXR : wnl.

IWMI with Complete heart block with shock

with suspected RVMI.

IWMI with Complete heart block with shock

with RVMI with ? Proximal RCA Involvement.

O2 inhalation

IV Fluids

Inj stk 1.5 million units i/v in 100 ml of ns over 1hr.

Tab ecosprin 300mg stat f/b 150 od

Tab clopidogrel 300 mg stat f/b 150 mg od

Tab atorvastatin 80mg stat f/b 40 od

INJ Clexane 0.6ml S/C BD

Inj dopamine 5 ug/kg/min(4 days)

Inj dobutamine 5-10 ug/kg/min(6days)

Inj NA 7.5 to 10 ug/kg/min(5days)

Normal lV function

EF-68%

RWMA in inferior and inferoseptal segments

Mild PAH/TR.

In view of deteriorating hemodynamic status,

patient planned for pharmaco invasive PCI.

Mean pulmonary artery pressure: 18mmHg

LM: normal

LAD: mid lad-D1 long bifurcation lesion 80-90%

S2 septal lesion (ostial 80% lesion).

LCA: distal lcx 60-70% dis, proximal lCAplaquing.

RCA: Dominant, proximal plaquing, tight lesion in mid RCA (90% stenosis). Distal plaquing.

PCI to RCA(culprit vessel) done in the same setting with Nobori 3×18 stent

During pharmacoinvasive PCI he developed

multiple episodes of atrial tachycardia

managed with 200J synchronized DC shock.

Multiple episodes of hypotension responded

to inotropic support

TP lead placed in IVC prophylactically in

v/o of unstable rhythm and recurrent

bradycardia.

Post procedure when patient received inward he developed multiple episodes of venttachycardia.

Pt received multiple DC shock f/bAmiodarone infusion.(150mg I/V f/b 1mg/kgx6hr f/b .5mg/kgx 18hrs.)

In the same setting later patient developedmultiple episodes of SVT,AF,VT,AIVR(3-5episodes) and managed with multiple DCshocks..

Ph 7.26

Hco312.2

Pco2 26

Na 141

K 4.4

Urine for

ketones

++

Bsugar

468mg/dl

Again complicated by DKA with sev

acidosis in the evening..

Patient managed with insulin

infusion and i/v fluids DNS with

10meq k+ /500ml DNS @ 75ml/hr..

Patient developed severe junctional bradycardiaand hypotension.

Amiodarone infusion stopped.

I/v atropine given, but pt persisted with severebradycardia and hypotension.

TP lead advanced into RA and TPM switched on,Position confirmed on monitor.HR set on100/min.

Patient hemodynamically improved.

Patient developed again one episode of SVT

in the evening and managed with Inj

diltiazem 10mg I/v stat.

Patient again developed 3 episodes of

sustained VT in the evening at 10 pm..

Managed with DC shock and overdrive pacing

again started on amiodarone infusion..

Dopamine tapered off and stopped and

started on Dobutamine 2.5ug/kg/min and NA

continued and up titrated to from 10 to 15

ug/min

Patient remains hemodynamically stable on

dual inotropic support.

No fresh episode of any arrhythmia

documented..

Symptomatically better

Patient remained haemodynamically stable

on dual inotropic support being gradually

tapered off..

No further episode of any arrhythmia

documented

TP lead removed on day 6th..

Patient gradually tapered off support…

Since day 9th patient was ambulatory.

Young male, chronic smoker ,diabetic,hypertension. Admitted as a case of IWMIwith RVMI.

Managed pharmacoinvasively, stented inRCA..complicated post operatively bymultiple episodes of Tachyarrythmias, Af, VT,AIVR managed with multiple DC shocks ,RVand Atrial pacing.

Discharged in a stable condition and plannedfor PCI to LAD-DI later On..

DISCHARGE

Right ventricle myocardial infarctions (RVMIs)accompany inferior wall ischemia(usuallyinvolves inferior wall of left ventricle) in up toone-half of cases.

The clinical sequelae of RVMIs vary from nohemodynamic compromise to severe hypotensionand cardiogenic shock.

Diagnosis is based on physical examination,ECG,ECHO and CAG.right-sided precordial leadsparticularly lead V4R must always be included.(ACC guidelines)

RVMI leads to reduced LV filling which translates intopoor LV pre load in addition ischemia to theconduction pathways disrupts normal rate andrhythm.

Adequate fluid administration in combination withpositive inotropic agents and early coronaryreperfusion are crucial components of treatment.

Diuretics and nitrates should be avoided.

Intra-aortic balloon counter pulsation and rightventricle assist devices may be used with success inRVMIs associated with medically refractory heartfailure.

The occurrence of RV impairment depends primarilyon the location of the MI, which ranges from rarecases in the anterior heart wall to more commonlocations such as in the inferior wall in 24% to 50% ofcases.

The relatively small percentage of RVMIs may beexplained by several factors:

1. Lower oxygen requirements of the RV due to itssmaller muscle mass and workload.

2. Increased blood flow during diastole and systole;

3. More extensive collateralization of the RV, primarilyfrom the left coronary system; and

4. Diffusion of oxygen from intrachamber bloodthrough the thin wall of the RV and into theThebesian veins .

Physical examination

1. The typical triad observed on physical

examination is hypotension occurring with

jugular vein distention and clear lungs.

2. A tricuspid regurgitation murmur,

Kussmaul’s sign and pulsus paradoxus are

signs of significant hemodynamic effects

due to RV ischemia.

ST segment elevations in leads II, III and aVF.

Disproportionate ST segment elevation with

greater ST elevation in lead III than in lead II

is pathognomonic for an RVMI.

ST segment elevation across the entire right

precordium from V1R through V6R; a sole ST

segment elevation in lead V4R >1.0 mm is a

reliable marker of an RV infarction, with

100% sensitivity, 87% specificity.

RV dilation with depressed systolic function

RV free wall dyskinesia with paradoxical

septal motion.

Asses the LV function secondary to RWMI—in

case of refractory to IV fluids—to rule out

cardiogenic shock.

Angiography often reveals occlusion of the

right coronary artery (RCA) proximal to the

acute marginal branch, while more proximal

occlusions usually suggest more extensive

necrosis of the posterior and, potentially, the

anterior RV myocardial wall.

In patients with left coronary artery

dominance, a left circumflex coronary artery

(LCX) occlusion may also be found

1. Post infarction ischaemia.

2. RVMI

3. VPCs/VT/VF

4. AF

5. AFL

6. AIVR

7. Sinus bradycardia

8. Pericarditis

9. Septum rupture

10. Cardiogenic shock

RVMIs are more often complicated by all

types of arrhythmias compared with ‘simple’

inferior or anterior wall LVMIs.

Barrillon et al were the first to recognize the

significantly higher risk of severe conduction

disorders in patients with RV involvement.

Complete atrioventricular (AV) or sinoatrial

blocks occurred in onehalf of cases in which

ST segment elevation or a QS pattern in V3R

and/or V4R were present.

Initial therapy, requires the administration of sufficient

volume to increase RV filling; it is critically important to

avoid drugs that cause venodilation and a decrease in RV

filling (eg, nitrates, diuretics). Treatment is generally

recommended to begin with a volume challenge of 300 mL to

600 mL normal saline over 10 min to 15 min.

Invasive hemodynamic monitoring is recommended, because

further infusion may be harmful in some patients, who don’t

respond to fluid challenge if additional increases in RV

volume prevent sufficient LV filling via interventricular

interactions and intrapericardial pressure equalization.

Based on hemodynamic monitoring studies, exceeding a RAP

or PCWP of 20 mmHg is generally not recommended .

If initial volume loading fails to improve arterial

pressure and cardiac output despite significant

increases in RAP and PCWP, then positive

inotropic agent therapy, can be effective in

stabilizing patients.

Restoration of sufficient coronary blood flow

represents the only treatment that addresses the

underlying problem, and early reperfusion

improves RV performance as well as the clinical

course and survival.

1. IWMI in 30-50% cases associated with RVMI.

2. Triad of raised jvp ,hypotension ,and clear

lungs think of RVMI.

3. Take Rt sided V4R in all patients with IWMI.

4. Presence of RVMI increases mortality of

patients.

5. IV fluids and ionotropes ,A-V sequential

pacing play a equally contributing role in

the managements of patients on

presentation.

Thank You

Dr. piyush khajuriaPG Student