anatomy myocardial infarction

7/29/2019 Anatomy Myocardial Infarction

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Anatomy & Physiology

The heart is responsible for pumping the blood to every cell in the body. It is alsoresponsible for pumping blood to the lungs, where the blood gives up carbon dioxideand takes on oxygen. In the systemic circuit, blood leaves the heart through the aorta,goes to all the organs of the body through the systemic arteries, and then returns to theheart through the systemic veins.The heart is no different from any other organ. It must have its own source ofoxygenated blood. The heart is supplied by its own set of blood vessels. These are thecoronary arteries. There are two main ones with two major branches each. They arisefrom the aorta right after it leaves the heart. The coronary arteries eventually branch into

capillary beds that course throughout the heart walls and supply the heart muscle withoxygenated blood. The coronary veins return blood from the heart muscle, but insteadof emptying into another larger vein, they empty directly into the right atrium.

Coronary circulation is the circulation of blood in the blood vessels of the heart muscle(the myocardium). The vessels that deliver oxygen-rich blood to the myocardium areknown as coronary arteries. The vessels that remove the deoxygenated blood from theheart muscle are known as coronary veins.The coronary arteries are classified as "end circulation", since they represent the onlysource of blood supply to the myocardium: there is very little redundant blood supply,which is why blockage of these vessels can be so critical.
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Definition of the Case

Myocardial infarction (MI)or acute myocardial infarction (AMI), commonly known

as a heart attack , is the interruption ofblood supply to part of the heart, causing heart

cells to die. This is most commonly due to occlusion (blockage) of a coronary arteryfollowing the rupture of a vulnerable atherosclerotic plaque, which is an unstable

collection oflipids (fatty acids) and white blood cells (especially macrophages) in the

wall of an artery. The resulting ischemia (restriction in blood supply) and oxygen

shortage, if left untreated for a sufficient period of time, can cause damage or death

(infarction) of heart muscle tissue (myocardium).

There are two basic types of acute myocardial infarction:

Transmural: associated with atherosclerosis involving major coronary artery. It can be

subclassified into anterior, posterior, or inferior. Transmural infarcts extend through the

whole thickness of the heart muscle and are usually a result of complete occlusion of

the area's blood supply.Subendocardial/Nontransmural: involving a small area in the subendocardial wall of

the left ventricle, ventricular septum, or papillary muscles. Subendocardial infarcts are

thought to be a result of locally decreased blood supply, possibly from a narrowing of

the coronary arteries. The subendocardial area is farthest from the heart's blood supply

and is more susceptible to this type of pathology.

Most myocardial infarctions are anterior or inferior but may affect the posterior wall of

the left ventricle to cause a posterior myocardial infarction.

Clinically, an acute myocardial infarction refers to two subtypes ofacute coronary

syndrome, namely ST elevation MI (STEMI) versus anon-ST elevation MI (non-

STEMI) based on ECG changes which are most frequently (but not always) a

manifestation of coronary artery disease.

Classification of Myocardial Infarction:

Type 1 - Spontaneous myocardial infarction related to ischaemia due to aprimary coronary event such as plaque erosion and/or rupture, fissuring, ordissection
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Type 2 - Myocardial infarction secondary to ischaemia due to either increasedoxygen demand or decreased supply, e.g. coronary artery spasm, coronaryembolism, anemia, arrhythmias, hypertension, or hypotension

Type 3 - Sudden unexpected cardiac death, including cardiac arrest, often withsymptoms suggestive of myocardial ischaemia, accompanied by presumably

new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronaryartery by angiography and/or at autopsy, but death occurring before bloodsamples could be obtained, or at a time before the appearance of cardiacbiomarkers in the blood

Type 4 - Associated with coronary angioplasty or stents:o Type 4a - Myocardial infarction associated with PCIo Type 4b - Myocardial infarction associated with stent thrombosis as

documented by angiography or at autopsy Type 5 - Myocardial infarction associated with CABG

General Signs and Symptoms

The onset of symptoms in myocardial infarction (MI) is usually gradual, over severalminutes, and rarely instantaneous.

Classical symptoms of acute myocardial infarction include:

Sudden chest pain- a sensation of tightness, pressure, or squeezing. Chest

pain due to ischemia (a lack of blood and hence oxygen supply) of the heart

muscle is termed angina pectoris. Pain radiates most often to the left arm or left

side of the neck, but may also radiate to the lowerjaw, neck, right arm, back, and

epigastrium, where it may mimic heartburn.

Pain zones in myocardial infarction (dark red = most typical area, light red = otherpossible areas, view of the chest).

Levine's sign- patient localizes the chest pain by clenching their fist over the

sternum, has classically been thought to be predictive of cardiac chest pain.
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Shortness of breath (dyspnea) - occurs when the damage to the heart limits

the output of the left ventricle, causing left ventricular failure and consequent

pulmonary edema.

Diaphoresis

Weakness

Light-headedness

Nausea

Vomiting

Palpitations

Sweating

Anxiety

Loss of consciousness(due to inadequate cerebral perfusion and cardiogenic

shock)

Sudden death(frequently due to the development of ventricular fibrillation) can

occur in myocardial infarctions.

An MI may occur at any time of the day, but most appear to be clustered around the

early hours of the morning, are associated with demanding physical activity, or both.

Women may experience fewer typical symptoms than men, most commonly shortness

of breath, weakness, a feeling of indigestion, and fatigue.

Approximately one quarter of all myocardial infarctions are silent, without chest pain or

other symptoms. These cases can be discovered later on electrocardiograms, using

blood enzyme tests or at autopsy without a prior history of related complaints.

A silent course is more common in the elderly, in patients with diabetes mellitus andafterheart transplantation, probably because the donorheart is not connected to nerves

of the host. In diabetics, differences in pain threshold, autonomic neuropathy, and

psychological factors have been cited as possible explanations for the lack of

symptoms.

Approximately half of all MI patients have experienced warning symptoms such as chest

pain prior to the infarction.
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Physiology

NON-MODIFIABLE:Gender (female)Age (61 yrs. old) Family History ofheart disease

MODIFIABLE: Hypertension DM Diet hi h fat

S/sx: HR & BPDysrhythmia

Ruptured AtheroscleroticPlaque

S/sx:Pain

Arterial Spasm & ThrombusFormation(Occlusion of Coronary Artery)

Activation of SNS(Release of Catecholamine)

Blood supply & O2(myocardium)

Anaerobic Metabolism

Contractility & pumpingabilit

Metabolic Acidosis

S/sx: Light-headednessDyspnea Urinary outputSOB Pale skin

Blood flow to BodyCirculation(Lungs, Kidney, Brain, &Digestive System)

anatomy myocardial infarction

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