LUGANSK STATE MEDICAL UNIVERSITY

DEPARTMENT OF INTERNAL MEDICINE

TOPIC: RIGHT VENTRICULAR MYOCARDIAL INFARCTION

BY: DR. IBEANU CHARLES

LUGANSK 2012

EPIDEMIOLOGY

In Ukraine, statistics shows that about 30% of all myocardial infarction is with right ventricular involvement and the combination of both left posterior and right myocardial infarction is about 50% of all cases. It is common in old age. In about 5% of right myocardial infarction there is presence of cardiogenic shock. After cardiogenic shock it progresses to right myocardial infarction in 75% case.

ETIOLOGYAtherosclerosis

Hypertension

Hypercholesterolemia

Progressive after left ventricular infarction

Risk factors

Non-Modification:

Age (>65 years)

Gender (50:50; male/female)

Genetic predisposition

Modification:

High risk coronary problem (Atherosclerosis)

Hypertensive history

Obesity

Diabetes mellitus

Hypodynamia

Alcohol consumption

Diet

PATHOPHYSIOLOGY OF RVMIThe right ventricle is a thin-walled chamber that functions at low oxygen demands and pressure. It is perfused throughout the cardiac cycle in both systole and diastole, and its ability to extract oxygen is increased during hemodynamic stress. All of these factors make the right ventricle less susceptible to infarction than the left ventricle.

The posterior descending branch of the right coronary artery usually supplies the inferior and posterior walls of the right ventricle. The marginal branches of the right coronary artery supply the lateral wall of the right ventricle. The anterior wall of the right ventricle has a dual blood supply: the conus branch of the right coronary artery and the moderator branch artery, which courses from the left anterior descending artery.

Interestingly, right ventricular infarction noted at necropsy usually involves the posterior septum and posterior wall rather than the right free wall. The relative sparing of the right ventricular anterior wall apparently arises from a high degree of collateralization. This collateral blood flow is thought to be derived from the thebesian veins and diffusion of oxygen directly from the ventricular cavity. A direct correlation exists between the anatomic site of right coronary artery occlusion and the extent of right ventricular infarction. Studies have demonstrated that more proximal right coronary artery occlusions result in larger right ventricular infarctions.On occasion, the right ventricle can be subjected to infarction from occlusion of the left circumflex coronary artery.

CASE STUDY CONDUCTED IN HOSPITAL 7

PASSPORT PART:

Name: Patient X

Age: 86years

Sex: Female

Occupation: Pensioner

Present complain:

General weakness

Dizziness

Severe chest pain (>30mins) radiates to the left arm, intrascapular region and neck

Difficulty in breathing

Anamnesis Morbi:

The patient arrived the hospital in an ambulance after which the patient was hospitalized in Intensive care unit (ICU) on the 24th september after 2hours of intensive clinical picture which occurred for the first time. The diagnosis after ECG in the ambulance was diaphragmatic myocardial infarction with subendocardial ischemia of the apex and lateral left ventricle and sinus bradycardia (46 bpm)

Anamnesis Vitae:

The patient has 17 years history of arterial hypertension with maximum blood pressure of 180/100 mmHg and 130/90 mmHg during normal life. The patient had diabetes mellitus type II for 10 years with absence of regular treatment, the patient occasionally took metformin 500mg/daily in the evening for 10 years. The patient was diagnosed with atherosclerosis in 2004. The patient has transitory ischemia of the brain for 8 years . There was presence of ischemic heart disease for 10years and was diagnosed to be sternocardia II stage and no specific treatment was given. The patient has non-obstructive chronic pulmonary disease with absence of treatment. There was absence of tuberculosis, Botkin’s disease, Malaria, Helminthosis, and any allergic disease.

ECG AT THE AMBULANCE

AV block in III lead, elevation of ST segment by 5mm in leads II, III, AVF & V1, depression of ST segment in I, AVL & reciprocal in V2 & V6. Rhythm of P wave and QRS complex are 75 & 45 per minute respectively.

At Hospitalization in ICUAnamnesis:

Presence of syncope, acrocyanosis of the lip, fingers and nose, cold feet and hands

After Auscultation of lung: absence of crepitation in lungs, tachypnea (16 beat/minutes)

After Auscultation of heart: sinus bradycardia, BP; 80/60

Laboratory findings:

Blood: WBC- 11.7 x 109 /L

Blood glucose: 9.0 mmol/L

Creatinine: 166 mg/dL

There was stabilization of haemodynamics after administration of:

Intravenous atropine 0.1%-1ml

Fluid upload (reosorbilact 400ml and Nacl 400ml)

Prednisolone 60mg and Nacl 100ml

Dopamine infusion 10mcg/kg/min

Oxygen therapy

Total infusion at admission in initial phase was about 1000ml while total fluid upload possible is1500ml

Medications contraindicated in treatment of RVMI:

Diuretics

Nitrates

Narcotic agent: Morphine

INTENSIVE CARE UNIT

AV block in III lead, elevated ST segment in V3,V4, Q(+) ST elevation in III lead. In Right position ECG; ST elevation, ventricular extrasystole (bigeminy) & QRST elevation.

STATUS PRESENT:

Respiratory: dyspnea, breathing rate-16 breaths per minutes . On auscultation; absence of crepitation

Cardiovascular: Angina status, increased jugular venous pressure, decreased blood pressure – 70/40, On percussion; shift of left relative heart border by 1.5cm, edema

Digestive system: Liver enlargement(hepatomegaly- +2.5cm in right) on palpation, the stomach and other organs were said to be normal

LABORATORY DIAGNOSISBlood

1st day

Hemoglobin: 128

Leukocyte: 10.3 x 109 /L

ESR: 8mm/hr

Lymphocyte: 23%

5th day

Hemoglobin: 121

Leukocyte: 3.8 x 109 /L

ESR: 28mm/hr

Biochemical analysis

Troponin I: 43ng/mL

Lipid: 6mmol/l

Alfa cholesterol: 0.37mmol/L

Total cholesterol: 6.85mmol/L

Beta cholesterol: 4.6mmol/L

Pre-Beta cholesterol: 1.03mmol/L

Triglyceride: 1.6

AI: 4.8

Creatinine: 166 mg/dL

In Urine: Protein: 0.6

AFTER 2 HOURS

AV block, no extrasystole, ST depression in line, T inverted and decrease reciprocal problem in anterior and AVL

AFTER 50 MINUTES

AV block stage II and ST elevation

AFTER TREATMENT IN ICU

Sinus rhythm , normal position heart. Rhythm 71/min. In III and AVF present Q(+) MI and T inverted in V4, V5, V6 right position ECG not present in the slide.

ECHOCARDIOGRAM

DIAGNOSIS

Ischemic heart disease

Acute Q(+) myocardial infarction (Left Posterior diaphragmatic and right ventricle MI) on 24th september 2012

Diffuse cardiosclerosis

Essential hypertension III stage (myocardial infarction, left ventricular hypertrophy, coronary disease stage III and transitory ischemic attack in 2004)

Heart decompensation stage IIa, Acute left ventricular dysfunction killip IV ( cardiogenic shock), systolic dysfunction left ventricle. Systolic fraction-38%

AV block stage III, normalization of sinus rhythm on the 30th of september.

Diabetes mellitus type II (compensatory stage) and decirculatory encephalopathy

Asthenic vegetative syndrome

TREATMENT IN HOSPITAL/HOME

Cardiomagnil 75mg, 1 tablet in the evening

Atovastatin 20mg, 1 tablet in the evening

Ramipril 5mg, 1 tablet in the morning

Eplerenone (inspra) 25mg, after breakfast everyday for chronic treatment and to control potassium level in blood

Clopidogrel 75mg, everyday in the evening

Metabolic treatment; Trimetazidine 35mg, 2 times a day for 6months

Nitrate therapy after stabilization

Diabetone 30mg, 30 minutes before breakfast

SUMMARY

1. Patient after posterior inferior MI acute stage, problem in proper diagnosis by ECG at the ambulance but standard right position ECG shows specific diagnostic criteria in V3R and V4R

2. Patient has acute posterior myocardial infarction and acute right ventricular myocardial infarction. At admission specific clinical picture; decrease BP, no crepitation, increase JVP.

3. The anatomical substrate for right ventricular MI-is characterized by proximal occulsion dominant in right coronary artery and high risk cardiogenic shock and lethal condition in prognosis.

4. Treatment of the patient in the ambulance was to increase volume infusion and absence of diuretic, nitrate and morphine therapy