Consequences and complications of MI 1. Cardiac arrhythmias i. May be the conduction system is effected like sa node or AV node ii.

Reperfusion to ischemic cells leads to entry of Na & Ca ions inside leading to swelling and rapid threshold leading to the excessive impulses leading to tachy arrythemia. iii. So, there will be sinus bradycardia and nodal block. These 2 are more important and commonly due to posterior inferior MIs. ( mean right coronary artery is involved) iv. Ventricular tachycardia and ventricular fibrillation 2. Contractile dysfunction i. Infracted cell do not contract well which may affect stroke volume and cardiac output and may be lead to pulmonary edema. Or pump failure. ii. If very sever and acute pump failure i.e global failure, patient develop cardiogenic shok. 3. Cardiac rupture syndromes (3-7th day) i. Coagulative necrosis is here and there is no fibrosis , its more vulnerable ii. 2 types , a. Free wall rupture (most commeon in anterior wall mi , very catastrophic) and blood goes into pericardial sack leading to condition called as hemo pericardium. Increase accumulation leads to compression of both ventricles. Due to which , i. there will be no venous return, leading to increase JVP. ii. No csrdisc output by left heart i.e low b.p . iii. Distant heart sounds are heard. Like they are coming from distant. This phenomenon in which all 3 are seen are called as cardiac temponade b. Rupture of septum ( left to right shunt) c. Papillary muscle dysfunction (bcoz papillary mscles normally control mitral wall , if endocardium where it is attached are infracted , then pappilary muscle will soften and rupture leading to mitral regurgitation.) so papillary muscles dysfunction will occur dur to, i. Rupture ii. Ischemic dysfunction iii. Fibrosis iv. Left ventricular dilatation 4. Pericarditis(only occurs if transmural infarct is there, does not occurs in sub endo cardial) i. Localize (during acute phase)i.e neutrophils coming to infarct also attacked the pericardium. ii. Immunological reaction (after few weeks) pericarditis + pleuritis >>> deresslers syndrome 5. MI expansion >>> infarct becomes expanded and looks that its balloons out. 6. MI extension >>> artery near to MI area become occulosive and area of MI extends, this is called as MI extension

7. Left ventricular aneurysm>>>> it is scaar formation after somedays in MI expansion(now it is called aneurysms) , due to this thrombus formation occurs, and arrythemia is also there plus decrese in cardiac output and left ventricular failure. 8. Thrombus formation i. Thrombus within left ventricle >>> systemic thrombo embolism ii. DVT (pulmonary thrombo embolism due to bed rest) 9. Chronic ischemic heart disease and CCF >>>> progressive left ventricular failure. So, ** 1. Large infarction has , i. More risk of rupture ii. Arrythemia 2. anterior wall MI makes i. easily aneurysms ii. expands easily iii Makes thrombi easily 3. posterior MI and inferior MI i. especially associated with SA nodal and AV nodal complication bcoz of their supply by right coronary artery. 4. sub endocardial MI They usually dont develop, i. ii. iii. Pericarditis Aneurysms Do not rupture

HOW TO PREVENT M.I 1. Primary prevention Some1 who has never developed the athero sclerosis and we r trying to reduce b.p, diabetes, cholesterol control, no smoking, regular exercise. (main purpose is modification before the occurrence of MI) 2. 2ndary prevention Doing prevention for the re occurrence of MI i.r, to prevent an another attack of MI.