a.

Congestive renal failure

Is a circulatory congestion due to myocardial dysfunction. Myocardial infarction interferes
with myocardial function because it leads to reduced contractility, causing abnormal wall
movement and altering the heart's heart rate. With reduced left ventricular ability to empty
away, the bulk stability decreases so that the remaining volume of the ventricle increases.
As a result the left heart pressure increases. This raised pressure is channeled back into the
pulmonary veins. When the hydrostatic pressure in the lung capillaries exceeds the
vascular oncotic pressure the transudation process occurs into the interstitial space. When
this pressure is still increasing again, lung udema from fluid permeation into the alveolis
until left heart failure occurs. Left heart failure can progress to right heart failure due to
increased vascular pressure of the lung causing the right ventricle to burden.

b. Cardiogenic shock
It is caused by real left ventricular dysfunction after a massive infarction, usually
about a liftie of 40% of the left ventricle. An irreversibly progressive evolutionary
hemodynamic vicious circle arises:
Decreased peripheral perfusion
Decrease in coronary perfusion
Increased lung congestion

c. Papillary muscle dysfunction

Ischemic dysfunction or rupture of papillary muscle necrosis interferes with the
function of the mitralis valve, allowing the eversion of the valve leaf into the atrium
during systolic. The incompentency of the valve results in retrograde flow from the left
ventricle into the left atrium with two due to reduced flow to the aorta and increased
congestion in the left atrium and pulmonary veins. The volume of the regulatory flow
depends on the degree of disturbance in the papillary muscle.

d. Ventricular septum depress

Intercellular septal necrosis may cause septal wall rupture resulting in ventricular
septal depression. Because the septum obtains a double blood flow from the artery that
runs down on the anterior and posterior surfaces of the interventricular sulcus, the septal
rupture shows a severe coronary artery disease affecting more than one artery. Rupture
forms the second outlet of the left ventricle. In each ventricular contraction the flow is
 split in two through the aorta and through the ventricular septal defect. Since left heart
pressure is greater than the right heart, the blood will experience a shunt through the defect
from left to right, from larger regions of pressure to smaller areas of pressure. The blood
that can be transferred to the right of the heart is large enough so that the amount of blood
released by the aorta becomes reduced. As a result, cardiac output is greatly reduced with
increased right ventricular and congestion work.

e. Heart rupture
Rupture of the free ventricular wall of the heart may occur early in the course of
infarction during the necrotic tissue removal phase prior to scarring. The thin necrotic
walls are ruptured causing massive bleeding into the relatively inelastic pericardium sacs
that can not develop. A pericardial sac filled with blood pressing the heart will give rise to
a heart tanponade. This heart's tanponade will reduce the venous flow and cardiac output.

f. Thromboembolism
Endothelial necrosis of the ventricles will make the endothelial surface become coarse that
predisposes to thrombus formation. Fractions of intracardiac mural thrombus may be
released and systemic embolization occurs. The second area that has the potential to form
a thrombus is the venous system. Vein embolization will cause embolism in the lungs.

g. Pericarditis
A transmural infarction can make the epicardium layer directly contact with the
pericardium to become large, stimulating the pericardium surface and causing an
inflammatory reaction, occasionally pericardial effusion or fluid accumulation between the
two layers.

h. Dressler Syndrome
Post myocardial infarction syndrome is a benign inflammatory response accompanied by
pain in the pleuropericardial. It is thought that this syndrome is a hypersensitivity reaction
to a necrotic myocardium.

i. Arrhythmias
Arrhythmias arise due to electrophysiological changes in myocardial cells. This
electrophysiological change manifests as a change in the form of an action potential ie a
recording of a graph of electrical activity of a cell