Cardiac Preconditioning

Cardiogenic shock is a frequently fatal complication that occurs when the heart cannot pump an adequate amount of blood in order to perfuse tissues. This hypoperfusion causes multiple organ dysfunction and damage which classifies cardiogenic shock a medical emergency. In the past, cardiogenic shock had a poor prognosis. However, currently approximately half of the people that go into cardiogenic shock survive (National Heart, Lung, and Blood Institute [NHLBI], 2011).

Futterman LG, Lemberg L. The Significance of Hypothermia in Preserving Ischemic Myocardium. Amer J Crit Care 13: 79-84, 2004. Web. 29 June 2015.

Our cardiac muscle remains unaffected in those with Malignant Hyperthermia because this condition is within the skeletal muscles. Here, the brain sends electrical signals that eventually reach the calcium pump and cause a domino effect. There are minimal proven theories about Malignant Hyperthermia’s effect on the cardiac muscle by professionals; however, what is known, is that during a Malignant Hyperthermia crisis, there are increased abnormal heart rhythms frequent in this disorder. These arrhythmias are often attributed to the damage made directly to the cardiac muscle.

Dugdale, D. (2012, June 22). Cardiogenic Shock. U.S National Library of Medicine. Retrieved November 23, 2013, from http://www.nlm.nih.gov/medlineplus/ency/article/000185.htm

These stated facts very well implicate an imperative need to investigate promising alternative treatment strategies as well preventive measures. Impairment in cardiac functions, organ (heart) failure or trigger of compensatory mechanisms (hypertrophy, neurohumoral system activation, autokrine, paracrine stimulation, etc) are the result of loss in cardiac myocytes predominantly due to myocardial infarction (Zimmermann and Eschenhagen, 2003). In addition to the traditional treatment of

Camp Cardiac offers a variety of skills and experiences which will expose me to numerous career choices in the field of medicine and the diligence of surgeons and other doctors. I am interested in going into surgery, specifically cardiothoracic surgery and I believe this camp will give me the experience I need to understand what I will be getting myself into and getting an idea of what I will be doing in the future. I am open to other careers in the medical field to such as a physician and and nurse practitioner so what is nice about this program is that it will expose me to other careers as well. I am also interested in talking to the medical students about how they got into medical school and what it takes to reach their level.

American Heart Association (AHA) estimates that nearly 700 Americans die each day of sudden cardiac arrest (MI), or 250,000 every year, as many as 50,000 lives could be saved each year if certain critical interventions were made. (Freeman , 50) A patient who receives early life support measures and defibrillation within one to five minutes of arrest is much more likely to live and to retain normal brain function. The brain is often at a serious risk for irreparable brain damage related to anoxia and many other co-morbidities that are associated with cardiac arrest (MI). When a perfusing cardiac rhythm returns after a heart attack, the most important objective is to preserve brain function. The AHA and the Advanced Life Support Task Force of

Clearly differentiate the pathophysiology of angina and myocardial infarction, including signs and symptoms. (5 marks)

- Lilly et al, Pathophysiology of Heart Disease, 5th Ed., Lippincott Williams & Wilkins, 2011.

I am conducting biomedical research in the laboratory of cardiac physiology under the mentorship of Dr. Elizabeth Murphy. Cardiovascular disease is the major cause of death in the US; therefore, a better understanding of the mechanisms regulating cardiomyocyte death in ischemia and reperfusion injury are important. Mitochondrial calcium plays a crucial role in the normal functioning of many processes, including the regulation of cardiac biochemical pathways and mediating ischemia-reperfusion injury. The uptake of calcium into the mitochondrial matrix is regulated by the mitochondrial calcium uniporter (MCU). An endogenous enzyme, Ca2+ Calmodulin Dependent Kinase II (CaMKII) has shown to regulate cell death and have increased activity during

Next we have Cardiac tamponade [which is caused by blunt or penetrating trauma or a few medical conditions such as cancer or autoimmune dieses] which is a serious condition where the blood accumulates in the pericardial sac [the sack around the heart]. While there is no definitive treatment on a basic level and ALS provider can relieve fluid with a needle in a risky but necessary procedure the last form of cardiogenic shock is a pulmonary embolism. A pulmonary embolism is when there is a blood clot blocking the flow of the pulmonary veins leading to obstructive shock and causing heart failure. Interesting enough to mention is the fact that one of the more common causes to cardiogenic shock is damage to the heart muscle however just because you have a heart attack does not necessarily mean you have had caridogenic

The heart was given two minutes to recover. Thirty seconds of baseline data was recorded again. Finally, atropine and acetylcholine were the last chemicals applied to the heart via a syringe. Approximately three drops were added. After about thirty seconds, the frog was given two minutes to recover with ringer’s

We acknowledge several limitations of this study. First, we used only one liver ischemic intervention protocol, i.e. three cycles of 5 min ischemia/5 min reperfusion; thus, it remains unknown whether other liver stimuli strategies can produce cardioprotection. Second, we did not use all three liver ischemic conditioned hearts for immunohistochemical analysis. Rather, we used only RPre+RPost treated hearts, to prove the concept that liver conditioning can inhibit apoptosis in the myocardium. Thus, it remains unknown whether RPre or RPost alone can affect apoptotic protein expression after I/R injury. In addition, the mechanisms by which remote liver conditioning enhance cytoprotective actions seem to be related to MAPK signaling pathways, since

Meis1 is a key regulatory protein for cardiac differentiation during embryonic development and using siRNA against Mesi1 can increase the proliferation of cardiomyocytes about threefold [145]. Additionally, siRNA administration against PLB, a key regulator of cardiac Ca2+ homeostasis, can improve cardiac function in heart failure. It was suggested from this study that down-regulation of PLB can enhance the activity of sarcoplasmic reticulum Ca2+ pump (SERCA2a) and therefore can improve the cardiac function [149-151]. Another strategy for heart regeneration is targeting the inflammatory reactions in infarcted area of myocardium. Reactive oxygen species (ROS) are the key factors in inflammatory reactions and provoking heart regeneration (i.e. cardiomyocytes apoptosis, fibroblast proliferation and myocyte hypertrophy). NADPH (Nicotinamide adenine dinucleotide phosphate) oxidase is a major source for superoxide production in infarcted myocardium that contains a catalytic subunit, Nox2

Myocardial infarction (MI) is the leading causes of mortality and morbidity in the world. Ischemic heart disease, where the oxygen supply to the myocardium is restricted, is a common cause of an MI. Myocardial injury results in loss of cardiomyocytes (cardiac muscle cells) due to apoptosis, and the development of necrotic myocardium, eventually leading to heart failure. The formation of the necrotic myocardium causes an inflammatory response and recruitment of myofibroblasts, resulting in the formation of scar tissue and decreased function. Current treatment (excluding heart transplantation) aims to prevent further loss of cardiomyocytes, but cannot