Heart attack,one of the most common cause of death world-wide, is manifested by chest pain, syncope, and shortness of breath. First of all, chest pain is caused by the depletion of energy in the ischemic myocardium. After the extensive done by numerous biologists world-wide, one may be able to conclude that chest pain is a stimulus triggered by the nucleic base adenosine, which constitutes the nucleoside of ATP, ADP, and AMP. After the depletion of the sources of ATP production and consequently the high-energy phosphate bonds, adenosine is released into the bloodstream, and ultimately tirggers action potentials in the adjacent nerve endings. These nerve endings then transmits these impulses as pain. Due to the fact that the internal organs (both thoracic and abdominal) are vaguely represented in the cerebral cortex, the interpretation of the pain may be diffuse and ambiguous. This phenomenom is known as referred pain. Second of all, syncope may result from the hypoperfusion of brain tissues. These nerve tissues may produce symptoms such as confusion or fainting, in severe cases. Third of all, pulmonary edema can result from increased hydrostatic pressure in the lungs. Due to the decreased cardiac output from the left ventricle, all the venous return from the pulmonary veins cannot flow into the left atrium, and have to be stored in the pulmonary veins. Note that even though the outflow of the pulmonary vessels are diminished by the obstruction, the input is no reduced due to the continuous return of venous blood from the periphery. The venous return is pumped from the right atrium into the pulmonary circulation. Due to the fact that the compliance of the pulmonary vessels has not been altered during the course of myocardial infarction (due to its short duration), the hydrostatic pressure greatly increases, and the ultrafiltration of blood plasma occurs. The leakage (medically known as the transudate) flows into the pulmonary interstitium, and ultimately into the pulmonary alveoli. Fluid accumulation in the alveolar sacs can lead to increased required work of breathing, resulting in shortness of breath (dyspnea). If left untreated, the dyspnea can result in death, since the fluid accumulated can interfere with the gas exchange that must occur in order to maintain the proper cellular metabolic reactions. To conclude, heart attacks may be manifested by chest pain, syncope, and shortness of breath.