Myocardial Ischemia

Ischemic heart disease is a state of repeating mid-section agony or distress that happens when a part of the heart does not get enough blood. This condition happens regularly amid effort or energy, when the heart requires more noteworthy blood stream. Ischemic heart disease, likewise called coronary illness, is regular in the United States and is a main source of death around the world. Ischemic coronary illness creates when cholesterol particles in the blood start to collect on the dividers of the corridors that supply blood to the heart. Inevitably, stores called plaques may shape. These stores limit the supply routes and in the end obstruct the stream of blood. This lessening in bloodstream decreases the measure of oxygen supplied to the heart muscle. The signs and indications of ischemic heart disease may grow gradually as corridors bit by bit get to be blocked, or they may happen rapidly if a course all of a sudden gets to be blocked. A few individuals with ischemic heart disease have no side effects by any means, while others may have serious midsection torment (angina) and shortness of breath that can represent a danger of

The most common physiological process leading to a myocardial infarction is the occlusion of coronary arteries by a process known as atherosclerosis. In fact, atherosclerosis is present in more than 90% of persons with coronary heart disease.1

Systolic heart failure is characterized by enlarged ventricles that are unable to fully contract to pump enough blood into circulation to adequately perfuse tissues. The enlargement in ventricles is due to an increased end-systolic volume. If the heart is not able to sufficiently pump the expected volume of blood with each contraction, which in a normal healthy heart is 50-60%, there will be a residual volume left in the heart after every pump (Heart Healthy Women, 2012). With the next period of filling, the heart will receive the same amount of blood volume from the atria combined with that residual volume from the previous contraction. This causes the ventricles to have to dilate to accommodate this increase in volume. The dilation causes the walls of the ventricles to stretch and become thin and weak. Also the myocardium, the muscle layer of the heart, will stretch and not be able to adequately make a full and forceful enough contraction to push blood from the ventricles (Lehne, 2010).

Cardiogenic shock, according to Werden et al. (2012), is the most common cause of death from an acute myocardial infarction (AMI) and has a chance of mortality from thirty percent to eighty percent. Infarction-related cardiogenic shock (ICS) complicates approximately five to ten percent of acute myocardial infarctions (AMI) and remains the leading cause of death in patients hospitalized from an AMI (Kolte et al., 2014). Kolte et al. (2014) also states that the incidence of cardiogenic shock is higher in patients over the age of seventy-five, and has higher prevalence in women, Caucasians, Asians, and Pacific islanders. This paper will discuss the pathophysiology, clinical manifestations, tools used to diagnose, and therapeutic management of cardiogenic shock.

Cardiogenic shock is results from damage to the heart such as a heart attack. In cardiogenic shock the heart is damaged and unable to supply a sufficient amount of blood to the body and the body cells do not receive enough oxygen (Huether & Mccance, 2012). Symptoms of cardiogenic shock are chest pain or pressure, coma, decreased urination, fast breathing, fast pulse, heavy sweating and moist skin, lightheadedness, loss of alertness and ability to concentrate, restlessness, agitation, confusion, shortness of break, skin that feels cool to touch, pale skin color or blotchy skin, and/or weak pulse (Dugdale, Cardiogenic Shock, 2012). Treatment of cardiogenic shock includes medications to increase blood pressure sucj as dobutamine, dopamine, milirione, and more. Urgent treatment includes electrical shock therapy (defibrillation or cardio version), implanting a temporary pacemaker and medications given through the vein, pain medicine, oxygen, fluids, and blood or blood products (Dugdale, Cardiogenic Shock, 2012). Cardiogenic shock

The relationship between coronary supply and myocardial demand is a very sensitive and an imbalance between them can cause a major concern in the body. If the coronary supply is less than the myocardial demand, the heart can suffer a severe spasm. The spasm cuts off the blood flow through the artery causing the heart to fail (Ischemic Heart Disease, n.d.). In contrast, if the myocardial demand exceeds the coronary supply, the heart fails once again. This is due to impaired cardiac pumping the heart experiences, an oxygen deficit of over 20 minutes causes the heart to essentially fail (Myocardial infarction) and a deficit of oxygen under 20 minutes leads to

Hemodynamic Changes: Contractility is influential in cardiac output and can be compromised due to myocardial infarction, ischemia, cardiomyopathy, and increased cardiac workload, to name a few. Inflammatory, immune, and neurohumoral changes can mediate ventricular remodeling, which will alter myocardial cellular structure resulting in myocardial dilation and further dysfunction of myocyte contractility over time. The decreased contractility will result decreased stroke volume and increased left ventricular end-diastolic volume, which results in dilation of the heart and increased preload. Increased afterload can be caused by increased pulmonary vascular resistance (PVR). This can result from hypertension or aortic valvular disease. The PVR results in resistance to ventricular emptying, increasing the work load of the LV, thus causing hypertrophy of the myocardium. Sustained elevated afterload results in pathologic hypertrophy, caused by angiotensin II and catecholamines. The increase in cardiac muscle mass causes an increase in the heart’s oxygen and energy demands. Thus, more energy from ATP is needed and when demand is greater than supply, cardiac contractility suffers. Ventricular remodeling continues, further

6. Demand Ischemia- is when someone is not receiving enough oxygen in their blood. If there is not enough oxygen going into the blood stream, then not enough oxygen is going out to the rest of the body. It affects the heart first which causes the heart attack.

disease. Myocardium is the heart muscles. It's getting it's oxygen and nutrients through the coronary

Sudden cardiac death (SCD) is one of big medical challenges that threaten our life and it is left over very tragic memories among family’s members(Adabag et al., 2010). Clinically, it is firstly associated with stopping the activity of cardiac muscular tissue, thereafter turning off the blood pump and finally permanent damage of brain tissue(Go et al., 2014). Despite the lack of having a clear definition of SCD, the most acceptable description is that the sudden cardiac death is unexpected death that can be happened within 60 minutes from the symptoms being appeared and approved by witnesses, or it may be occurred during a period of 24 hours in a person who has clearly been found in a healthy condition when the death is not witnessed(Uchmanowicz et al., 2015). According the definition above, around 35-40% of the total cases of SCD are happened out of hospital which is namely known, Out of hospital sudden cardiac death (OHSCD((Basso et al., 2010). Cardiac arrhythmia resulted from myocardial infarction is classified to be the most important causes leading to the OHSCD. However, other causes like Angina pectoris, unspecified

arteries totally blocked181. Damage is reversible for approximately 20-30 minutes after complete obstruction of blood flow; thereafter myocardial cell death ensues and progresses as time passes182-184. Therefore, complete and sustained restoration of blood flow must be as prompt as possible to ensure maximum salvage of functional myocardium, a principle expressed in the maxim “time is muscle”185. This is achieved with reperfusion therapy, which is based on invasive reopening of the afflicted coronary artery with primary PCI, or non-invasive breaking up of the responsible blood clot with a thrombolytic drug186. Patients without ST-elevation are said to suffer from NSTEMI and tend not to have full occlusion of a coronary artery187. If there is evidence of myocardial cell death they are considered to have a NSTEMI; otherwise they are classified as suffering from unstable angina188. Their management is based on the estimation of their risk for adverse events. Patients at low risk can be adequately treated with medical therapy, in many ways similar to the one used for STEMI189-190. Those at moderate to high-risk benefit from an early invasive strategy, which includes coronary angiography, and if necessary, revascularization with

What oxidative phosphorylation does occur is shifted to β-oxidation through AMPK-mediated reductions in malonyl CoA [26, 27]. Deregulation of FA substrate selection has implications for subsequent reperfusion injury. During ischemia plasma concentrations of FAs increase, and remain elevated up-to 24 h following re-oxidation [2]. Catecholamines are released in response to tissue injury, which also act to increase circulating FAs [77]. Deregulation of the rate-limiting step of mitochondrial FA uptake increases myocardial capacity for FAO when oxygen restored [78], leading to a FA predominated oxidative recovery in reperfused myocardium. FA-derived acetyl CoA also down-regulates glucose-oxidative pathways which contributes to an FAO-dominated recovery. FAO is less energy efficient than glucose oxidation at generating contractile force per oxygen unit consumed [8]. It requires approximately 10% more oxygen per unit of ATP produced than glucose oxidation [5]. Instead of being used for contractile function, FA-derived ATP is used to re-establish ion homeostasis, which was disrupted by FA and glycolytic metabolites [79]. With prolonged ischemia the accumulation of FA metabolites and the metabolic by-products of anaerobic glycolysis lead to metabolic

Myocardial Infarction (MI); heart attack affected Circulatory system, the sudden passing of heart muscle due to limited stream of oxygenated blood to the heart muscle; characterized by strongly chest pain, sweating, shortness of breath, or some of the time none of these symptoms. Myocardial areas of dead tissue, superior known as heart attack happen when there are interferences within the blood supplies to the heart and pumps blood from the heart to other vital organs. The heart is an exceedingly specialized muscle whose work is to pump life-sustaining blood to all parts of the body. Its activity includes creating weight to impel blood through arriving and leaving channels veins and arteries that must keep up that weight

Myocardial infarction is the technical name for a heart attack, is the damage and death of heart muscle from the sudden blockage of a coronary artery by a blood clot. Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen. Blockage of a coronary artery deprives the heart muscle of blood and oxygen, causing injury to the heart muscle. Injury to the heart muscle causes chest pain and chest pressure sensation. If blood flow is not restored to the heart muscle within 20 to 40 minutes, irreversible death of the heart muscle will begin to occur. Muscle continues to die for six to eight hours at which time the heart attack usually is "complete." The dead heart muscle is eventually replaced by scar tissue.

Free radicals are thought to play an important role in the pathogenesis of reperfusion abnormalities including myocardial stunning, irreversible injury, and reperfusion arrhythmias. Free radical accumulation has been measured in ischemic and reperfused myocardium directly using techniques such as electron paramagnetic resonance spectroscopy and tissue chemiluminescence and indirectly using biochemical assays of lipid per oxidation products. In Ischemia free radicals are generated in myocytes, vascular endothelium, and leukocytes. Injury to processes involved in regulation of the intracellular Ca2+ concentration may be a common mechanism underlying both free radical- induced and reperfusion abnormalities.