Inferior myocardial infarction

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Inferior Wall MyocardialInfarctionDr.K.Prashanthi

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Sir William Oslersaid, “Variability is the law of life, and as no two faces are the same, so no two bodies are alike, and no two individuals react alike and behave alike under the abnormal conditions which we know as disease

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INTRODUCTION

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DEFINITION

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EPIDEMIOLOGY

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ETIOLOGY

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CLINICAL FEATURES

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DIAGNOSIS

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TREATMENT

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COMPLICATIONS

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CONCLUSION

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TAKE HOME MESSAGETHEPIONEERSHAROLD ENSIGN BENNET PARDEEEINTHOVENPAUL DUDLEY WHITE

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2D ECHO

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CHARLES THEODORE DOTTERPERCUTANEOUSTRANSLUMINAL ANGIOPLASTY

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DR.andreasgruentzigBalloon angioplasty

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Dr.bernardlownEXTERNAL DEFIBRILLATOR

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THE LIFE SAVINGDRUGS

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STREPTOKINASE

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The saviour –ATROPINE

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Coronary circulation

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DEFINITIONCriteria for Acute,Evolving ,Recent MI :Either of the following criteria satisifies the diagnosis:1.Typical rise and /or fall of biochemical markers of myocardial necrosis with atleast one of the following :A.Ischemic symptomsB.Development of the pathological q waves in the ECG.C.Ecg changes indicative of ischemia.(ST segment elevation or depression).D.Imaging evidence of new loss of viable myocardium or new RWMA.2.Pathological findings of an acute myocardial infarction.

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EPIDEMIOLOGYMyocardial infarction isa common presentation of Ischemic heart disease.

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Worldwide more than3 million people have STEMIs and 4 million have NSTEMIs a year.

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Coronary heart diseaseis responsible for 1 in 5 deaths in the United States.EPIDEMIOLOGY-IndiaIn India, cardiovascular disease (CVD) is the leading cause of death. 32% of all deaths in 2007 .Relatively new epidemic in India.Mortality estimates due to CVD vary widely by state, ranging from 10% in Meghalaya to 49% in Punjab (percentage of all deaths). Punjab (49%), Goa (42%), Tamil Nadu (36%) and Andhra Pradesh (31%) have the highest CVD related mortality estimates.State-wise differences are correlated with prevalence of specific dietary risk factors in the states. Moderate physical exercise is associated with reduced incidence of CVD in India (those who exercise have less than half the risk of those who don't).

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EPIDEMIOLOGYUsually anterior wallMI is more than other segment MI because of conjunction of HTN and diabetes along with the presence of hypercholeosterolemias in C.A.D -----Br heart journal 2000..ncbi.nch.gov/pmc

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RVMI is presentin one third of patients with IWMI ,but clinically significant in less than 50 % of the one third…. CMDT 2009.

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AV block ismore common than infranodal block and occurs in approximately 20% of IWMI. (infranodal – AWMI) ………CMDT 2009 .

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Sinus bradycardia ismore common in IWMI (tahcycardia in AWMI)

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Posterior wall MIis assosciated with 5% of IWMI or lateral MI but rarely occurs alone.ETIOLOGYAtherosclerosis. 90% of MIs result from an acute thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture and erosion - the major triggers for coronary thrombosis.CAD without atherosclerosisSecondary to vasculitis

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Ventricular hypertrophy

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Coronary artery emboli

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Congenital coronary anomalies

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Coronary trauma

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Primary coronary vasospasm(variant angina)

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Drug use (eg,cocaine, amphetamines, ephedrine)

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Arteritis

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Heavy exertion, fever,or hyperthyroidism

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Hypoxemia of severeanemia

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Aortic dissection with retrograde involvement of the coronary arteries

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Infected cardiac valvethrough a patent foramen ovale (PFO)

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Significant GI bleed

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CO PoisoningClinical featuresProdromal symptoms:

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Fatigue,

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Chest discomfort,

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Malaise in thedays preceding the event;

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May occur suddenlywithout warning

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Nausea and/or abdominalpain often are present in infarcts involving the inferior or posterior wall. CLINICAL FEATURESSymptoms:

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Chest pain >30 min.

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Character of thepain –retrosternal,constrciting,crushing,compressing sensation of heavy weight.

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Predilection for leftside.

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Radiates to theulnar aspect of the left arm

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Tingling sensation ofthe wrist and fingers.

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In some patients,the symptom is epigastric, with a feeling of indigestion or of fullness and gas.

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Nausea,Vomitings

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Profound weakness

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Dizziness

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Palpitations,

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Cold perspiration

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Sense of impendingdoom.occurs most often in the early morning hours, -- increase in catecholamine-induced platelet aggregation and ↑ serum concentrations of plasminogen activator inhibitor-1 (PAI-1) that occur after awakening.

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In general, theonset is not directly associated with severe exertion. Instead, it is concomitant with exertion.

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The immediate riskof myocardial infarction increases 6-fold on average post MI,CAD and by as much as 30-fold in sedentary people. ncbi.nbl.com

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Anginal equivalent --abdominal pain,jaw pain,sharp pain in women,elderly.High index of suspicionwomen,

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diabetics,

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older patients,

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dementia,

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history of heartfailure,

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cocaine users,

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hypercholesterolemia,

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positive family historyfor early coronary disease ---- any first-degree Male aged≤ 45 years, female relative aged ≤ 55 years who MI Silent MIHalf of myocardial infarctions are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient.

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In as manyas 25% of elderly patients, a population in whom 50% of myocardial infarctions occur; in such patients, the diagnosis is often established only retrospectively, by applying electrocardiographic criteria or by scanning the patients using 2-dimensional (2D) echocardiography or magnetic resonance imaging (MRI).

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On clinical evaluation,ventricular aneurysms may be recognized late, with symptoms and signs of heart failure, recurrent ventricular arrhythmia, or recurrent embolization. Physical examinationPhysical examination findings can vary; comfortable in bed, with normal examination results, may be in severe pain, with significant respiratory distress and a need for ventilatory support.

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Ongoing pain ---pale and diaphoretic.

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Hypotension may indicateventricular dysfunction due to ischemia.

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Hypotension in thesetting of myocardial infarction usually indicates a large infarct secondary to either decreased global cardiac contractility or a right ventricular infarct.SignsBradycardia

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Hypotension----due to parasympathetichyperactivity.

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Increased respiration –cheynes stokes –anxiety and pain.

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Raised JVP.--- RVMI.—kussmaul’ssign

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Clear lung fields.

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On cardiac auscultation--S4is almost universally present in patients in SR with STEMI.but non specific.

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S3 ,S4 heardalong the left sternal border and increases on inspiration.—RVMI –RVFIWMI with RVMI The evidence of right ventricular ischemia should be sought in all patients with acute inferior MI at the time of admission. RT precordial leads, in particular lead V4R must be recorded in all patients with inferior MI. –ACC guidelines

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1-mm ST segmentelevation in the right precordial lead V4R is the single most predictive ECG finding in patients with right ventricular ischemia This finding, however, may be transient; half of the patients show resolution of ST elevation within 10 hours of the onset of symptoms .IWMI with RVMIDistention of neck veins is commonly described as a sign of failure of the RV.

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Impaired right ventriculardiastolic function also leads to systemic venous hypotension, edema, and hepatomegaly with abdominojugular reflux, which may result in saline-response underfilling of the LV and a concomitant reduction in cardiac output.

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Peripheral cyanosis, edema,pallor, diminished pulse volume, delayed rise, and delayed capillary refill may indicate vasoconstriction, diminished cardiac output, and right ventricular dysfunction or failure.DiagnosisECG

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Cardiac imaging

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Cardiac biomarkers

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Troponin T levels

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CKMB,CK

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Myoglobin levels

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CBP

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ESR

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LDH

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Lipid profile

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CRP

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MRI ,technetium 99mpyrophosphate scintigraphy

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Scintigraphy with thallium201

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Hemodynamic assessement withPA catheter---cardiogenic shockECGMost important tool in the initial evaluation

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Triage of patientsin whom an ACS is suspected.

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Confirmatory of thediagnosis - 80% of cases.

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In Inferior myocardialinfarction, record a right-sided ECG to rule out right ventricular infarct.

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Daily serial ECGsfor the first 2-3 days and additionally as needed. High probability of myocardial infarction is indicated either by ST-segment elevation greater than 1 mm in 2 anatomically contiguous leads ,2mm in chest leads or by the presence of new Q waves.

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intermediate probability ofmyocardial infarction are ST-segment depression, T-wave inversion, and other nonspecific ST-T wave abnormalities.

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low probability ofmyocardial infarction are normal findings on ECGs

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however, normal ornonspecific findings on ECGs do not exclude the possibility of myocardial infarction. Inferior wall MI –ST segment elevation of > 1mm in inferior leads with reciprocal ST segement depression in anterior leads.

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Right ventricular -RV4, RV5

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Posterior wall -R/S ratio greater than 1 in V1 and V2; T-wave changes (ie, upright) in V1,ST segment elevation in V8, and V9

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Right ventricular myocardialinfarction commonly is manifested by ST-segment elevation or Q waves detectable in right-sided precordial leads.2D ECHORWMA

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RV dysfunction.

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Assess the LVfunction secondary to RVMI --- in case of refractory to IV Fluids --- to rule out cardiogenic shock.

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MRI with gadolinium contrast enhacement –most sensitive –2 gm of MI can be detected.

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Techntium scan –hot spot with calcium – insensitive to small infarctions.

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Thallium scan –coldspots in regions of diminished perfusion –does not differentiate old from new.Cardiac markersTroponin T and troponin I

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Highly specific monoclonalantibodies - not normally detectable in the blood of the healthy individuals but may increase after STEMI to levels greater than 20 times.

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Normal troponin T 0-0.1 µg/l,I --- 0 – 0.08 µg/l

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Cut off forMI t>0.1µg/l, I . 0.4 µg/l

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CK, CKMB --- CK rises within 4-8 hrs and returns to normal by 48-72 hrs.

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A ratio (relativeindex) CKMB mass :CK actvity > 2.5 suggests but not diagnostic of acute MI rather than the skeletal source of CKMB elevation.Treatment golden period is 1 hr ….Door to needle time -30 min,door to balloon time is <90 min< 6 hrs PCI = thrombolysis <6 hrs with hypotension,cardiogenic shockPCI < 6 hrs with hypotension ,no PCI center Give IV fluids --

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Then thrombolysis withcardiac monitoring. In presenceofbradycardiaGive atropine In presence of CHBTemporary pacemaker Management1.Aspirin

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Block the formationof thromboxane A2 in the platelets by COX inhibition.

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Dose is 160-325mg.

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2.Clopidogrel

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Thienopyridine class antiplateletagent

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Inhibits P2Y12 subtypeof ADP receptor

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300 mg

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CLARITY trial –loadingdose of 300 mg,75 mg /day therafter along with thormbolysis---coronary patency –no increase in bleed.

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COMMIT/CCS2 trial inchina

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Clopidogrel to beadded to apsirin to all patients with STEMI regardless of whether or not perfusion is given and continued for atleast 14 days,and generally for 1 year.Reperfusion therapyLimitation of the infarct size

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PCI --

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Fibrinolysis

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Option depends uponthe duration and the availability of the PCI nearby.

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< 6 hrs---PCI – fibrinolysis

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>6 hrs --- PCI > fibrinolysis

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The patient atdischarge should be sent for angiography in case of absence of PCI not done < 6 hrs….but thrombolysis given, for the evaluation of the vessel blockage …and extent of vessel disease,. Thrombolysis/fibrinolysisTo maintain the patency of the coronary artery.Fibrinolytics agents used :Tissue plasminogen activatorTenectplaseReteplaseAlteplase ---GUSTO trialtpA---- 15 mg bolus followed by 50 mg intravenously IV over the first 30 min followed by 30 mg over the next 60 min.Tenectplase – IV bolus of 0.53 mg/kg over 10 secReteplase – 10 MU bolus given over 2 -3 min followed by 2nd 10 MU units 30 min later.Streptokinase--- 15 MU given over 1 hr –hypotension.

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Contraindications and complicationsAbsolute– cerebrovascular hemorrhage ,ischemia,marked hypertensionSBP > 180mm Hg,DBP > 110 mmHg,aortic dissection,active internal bleeding.

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Relative --- pregnancy,hemorrhagicdiabetic retinopathy,active peptic ulcer disease,severe HTN ,allergic reactions .<5 days- 2yrs.,trauma within 2-4 weeks,major surgery within 3 weeks,traumatic CPR ,current use of anticoagulants INR >2-3.Antithrombotic agentsGoal is to maintain the patency of the infarct related artery in conjunction with reperfusion related strategies.UFH --- 60 U/kg followed by infusion of 12 U/kg/hrThe APTT should be 1.5 – 2 times the control value.LMWH – enoxaparin 30 mg IV bolus –1mg/kg every 12 hrs---ASSENT 3 trial. Decreased the death at day 30 compared to UFH –EXTRACT trial OASIS 6 trial – fondaparinux given at dose of 2.5 mg /day reduced death and reinfarction .no benefit in patients udergoing PCI –catheter thrombosis..Use antacids and an H2 blocker as prophylactically

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Asessment of reperfusionEarlycessation of pain

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The resolution ofthe ST segment elevation at 90 min.

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50% resolution ofST elevation can occur even without reperfusion –still a strong predictor of better outcome.

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Reinfarction – recurrenceof pain and ST segment elevation –angio and PCI. General measuresActivity :

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Bed rest forthe first 12 hrs.

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Diet :

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Clear liquids forthe first 12 hrs .

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Fibre but lowin sodium diet

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Bowels:

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Stool softeners arerecommended

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Sedation:

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Lorazepam ,oxazepam,diazepam 3.Analgesics– morphineVery effective analgesic for pain assosciated STEMIReduces sympathetically mediated arteriolar and venous constrictionReduces arterial pressure and cardiac output.Dose – 2- 8 mg repeated in 5-15 min.Hypotension and bradycardia – atropine 0.6mg4.b blockers:If HR > 60 /min,BP > 100 mm Hg SBPMetoprolol 5 mg every 2-5 min ,3 doses.5.nitrates:Should not be given in inferior wall MI –causes hypotension and bradycardia.If waxing and waning of pain ,systole > 100 mm Hg --- IV NTG. 5µg --- 200 µg /min

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6.oxygen:

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By face mask/nasalprongs

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2-4 lit /min

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7.ACEI /ARBs:

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The benefits inEF < 40% ,presence of left heart failure .

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SAVE ,AIRE,SMILE ,TRACE,GISI–III,ISIS 4 ---short and long term benefits

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CURE trial clopidogrel75 mg/day to be given along with aspirin for 1 year in MI patients. At discharge Aspirin

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Clopdiogrel

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H2 blockers

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ACEI /ARBS

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Stress testing –seefor ST segment depression during submximal exercise –positive send him for angiography---revascualrization.TIMI grading Thrombolysis in myocardial infarction

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Grade 0 –completeocclusion of the infarct related artery.

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Grade 1 –some penetration of the contrast material beyond the point of obstruction,but without the perfusion of the distal coronary bed.

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Grade 2 –perfusion of the entire infarct vessel into the distal bed but with flow that is delayed compared with that of the normal artery.

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Grade 3 –full perfusion of the infarct vessel with normal flow. GRACE scoreGlobal Registry of Acute Coronary Events (GRACE) Hospital Discharge Risk Score Accurately Predicts Long-Term Mortality Post Acute Coronary Syndrome

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ComplicationsPost infarction ischemia

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RVMI

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VPCs

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AF

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AFL

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AIVR

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Sinus bradycardia

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Pericarditis

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Septum rupture

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Cardiogenic shockArryhthmiasAutonomic nervoussystem imbalance.

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Electrolyte disturbances

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Ischemia

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Slowed conduction inzones of ischemic myocardium

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1. Sinus bradycardia—50%CASES

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2.PVCs

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3.VT

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4.VF

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5.AIVR

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6.AF AFLPericarditisPericardial frictionRUB and pericardial pain are frequently encountered in patients with MI.

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Pain radiating toeither trapezius muscle is typical.

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Rub -heard within24 hrs or as late as 2 weeks…most commonly on second or third day.

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Audible along theleft sternal border or at the point of maximal impulse.

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Anticoagulants should bestopped.Lets have a look at the ECGs

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Acute Inferior wallMI

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Acute Inferolateral MI

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Acute InferoPosterior MyocardialInfarction

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RIGHT SIDED LEADS

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Acute Inferior MIwith RVMI

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Acute Inferolateral MIwith 2:1 AVblock

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Acute inferior wallMI and complete AV block

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Take home messageInferiorwall MI presents with nausea and abdominal pain also.Inferior wall in 30-50% cases is assosciated with RV MI.Take right sided V4R in all the patients with IWMI.Presence of RVMI increases the mortality of the patients.IV fluids and inotropes,pacing play a equally contributing role in the management of patients on presentation.Recurrence of IWMI at the same site is more than in the anterior wall MI.Triad of raised JVP ,hypotension and clear lungs think of RVMI.PWMI in case of R wave in V1 with upright T wave and R/S ratio >1 V1 and V2..take leads V7-9.

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ReferencesBraunwald – 7th editionAn Introduction to electrocardiography ---Schamroth ,7 thedMarriott’s practical electrocardiography –GalenBasic and bedside electrocardiography –Romulo.F.BaltazarCMDT 2009HARRISON’S 17 thedhttp://www.ncbi.nlm.nih.gov/pmc/articleswww.ecglibrary.comwww.netterimages.comwww.medscape.comwww.americanjournalofcaridology.com

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Thank you

Inferior myocardial infarction

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Inferior myocardial infarction