Anatomy & Physiology

The heart is responsible for pumping the blood to every cell in the body. It is also responsible for pumping blood to the lungs, where the blood gives up carbon dioxide and 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 the heart through the systemic veins. The heart is no different from any other organ. It must have its own source of oxygenated blood. The heart is supplied by its own set of blood vessels. These are the coronary arteries. There are two main ones with two major branches each. They arise from 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 with oxygenated blood. The coronary veins return blood from the heart muscle, but instead of 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 are known as coronary arteries. The vessels that remove the deoxygenated blood from the heart muscle are known as coronary veins. The coronary arteries are classified as "end circulation", since they represent the only source of blood supply to the myocardium: there is very little redundant blood supply, which is why blockage of these vessels can be so critical.

Definition of the Case

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack , is the interruption of blood supply to part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (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 of acute coronary syndrome, namely ST elevation MI (STEMI) versus a non-ST elevation MI (nonSTEMI) 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 a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection

Type 2 - Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension Type 3 - Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood Type 4 - Associated with coronary angioplasty or stents: o Type 4a - Myocardial infarction associated with PCI o 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 several minutes, 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 lower jaw, neck, right arm, back, and epigastrium, where it may mimic heartburn.

Pain zones in myocardial infarction (dark red = most typical area, light red = other possible 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.

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 and after heart transplantation, probably because the donor heart 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.

Physiology

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

MODIFIABLE: Hypertension DM Diet (high fat)

S/sx: HR & BP Dysrhythmia

Ruptured Atherosclerotic Plaque

S/sx: Pain

Arterial Spasm & Thrombus Formation (Occlusion of Coronary Artery)

Activation of SNS (Release of Catecholamine)

Blood supply & O2 (myocardium)

Anaerobic Metabolism

Contractility & pumping ability

Metabolic Acidosis

S/sx: Light-headedness Dyspnea Urinary output SOB Pale skin

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