In Myocardial Infarction, inadequate coronary blood flow rapidly results in

myocardial ischemia in the affected area. The location and extent of the infarct
determine the effects on the cardial function. Ischemia depress cardiac function and
triggers autonomic nervous system responses that exaxerbate the imbalance
between myocardial oxygen supply and demand. Persistent ischemia results in
tissue necrosis and scar tissue formation, with permanent loss of mrocardial
contractility in the affected area. Cardiac output from decreased myocardial
contractility and pumping capacity.

Although heart disease is most often caused by atherosclerosis of coronary arteries,

other phenomena decrease blood flow to the heart includes:
>Vasospasm (sudden constriction or narrowing) of a coronary artery
>Myocardial trauma from internal or external forces
>Structural disease
>Congenital anomalies
>Decreased oxygen supply (acute blood loss, anemia, low blood pressure)
>Increase demand for oxygen

Myocardial Ischemia

Narrowing and obstructing

blood flow
Non-modifiable
risk factors
Modifiable risk factors
>may
result in infarction
>Family/Genetics
>cell
death
-(+)Hypertension

>(+)High blood cholesterol

Decreased myocardial oxygen
level
supply

-(+)Diabetes Mellitus

Cellular Hypoxia

>Age (Increasing age)

>Environment

-74 years old

>Gender(heart disease occurs
3 times more often in men
than in premenopausal
women)
-Female
>Race(higher incidence of
heart disease in african
americans than in caucasians)
-Filipino

>(-)Cigarette smoking,
Tobacco use

Altered cell membrane-(+)second hand smoke

integrity
>(+)Hypertension
Decreased myocardial>(+)Diabetes Mellitus
contractility
>(+)Lack of estrogen in
women
Decreased cardiac output
>(+)Physical Inactivity
>(+)Obesity
Decreased arterial pressure
>Illnesses/Inflammatory
response
-(+) past history exposure of
Stimulation of baroreceptors
infections

Atherosclerosis begins as
fatty streaks, lipids that are
Stimulation
of sympathetic
deposited
in the
intima of
receptors
the arterial wall
Lipid core may
grow

Causing to
rupture and
hemorrhage

Formation
of peripheral
deposits
Increased
called atheromas/plaques
vasoconstriction

StableIncreased
thick
heart rate
plaque

Increased afterload
Protrude into the lumen of
the vessel

Increased diastolic filling

Resist the stress
from blood flow and
vessel movement

Myocardial oxygen demand

Thrombus or
embolus develop

Increased myocardial
contractility

Narrowing and obstructing

blood flow

Decreased myocardial
tissue perfusion

Atherosclerosis involves a normally patent artery (A.) and an inflammatory response

whereby smooth muscle cells proliferate within the blood vessel to form a fibrous
cap. (B.) The proliferation results in deposits, called atheromas or plaques, which
protrude into the lumen of the vessel, narrowing it and obstructing blood flow. If the
cap ruptures and hemorrhages into the plaque (C.) A thrombus (D.) may develop
and obstruct blood flow further.

The anatomic structure of the coronary arteries makes them particularly susceptible
to the mechanism of atherosclerosis. The many angles and curves of the coronary
arteries contribute to the vessels susceptibility to atheromatous plaques.