Myocardial Infarction And Depression a Review Article Text

Jonathan Friesen - Writing Coach

Whereas myocardial depression was previously considered a preterminal event, it is now clear that cardiac dysfunction as evidenced by biventricular dilatation and reduced ejection fraction is present in most patients with severe sepsis and septic shock. Myocardial depression exists despite a fluid resuscitation dependent hyperdynamic state that typically persists in septic shock patients until death or recovery. Myocardial dysfunction does not appear to be due to myocardial hypoperfusion but due to circulating depressant factors, including the cytokines tumor necrosis factor alpha and il 1 x003b2. At a cellular level, reduced myocardial contractility seems to be induced by both nitric oxide dependent and nitric oxide independent mechanisms.

How Is Academic Writing Different From Other Types of Writing

The present paper reviews both the clinical manifestations and the molecular/cellular mechanisms of sepsis induced myocardial depression. keywords: contractility, cytokine, heart, myocardial depression, nitric oxide sepsis and septic shock have been recognized as an increasingly serious clinical problem, accounting for substantial morbidity and mortality. The past four decades have seen the age adjusted mortality of sepsis increase from 0.5 to 7 per 100,0 episodes despite major advances in the understanding of its pathophysiology 1 . The incidence of severe sepsis in the united states today is estimated at 750,0 cases per year, resulting in 215,0 deaths annually 2 .

The majority of these sepsis patients die of refractory hypotension and of cardiovascular collapse. Endo toxin or another microbiologic element induces the release of local and systemic inflammatory mediators, especially tumor necrosis factor alpha tnf x003b1 and il 1 x003b2 , from monocytes/macrophages and other cells 4 . These cytokines stimulate polymorphonuclear leukocytes, macrophages and endothelial cells to release a number of downstream inflammatory mediators, including platelet activating factor and nitric oxide no , further amplifying the inflammatory response. Several anti inflammatory mediators are also released as part of this amplification cascade namely, il 10, transforming growth factor beta and il 1 receptor antagonist.

The relative contribution of these cytokines will determine the severity of the septic episode. If the inflammatory reaction is particularly intense, homeostasis of the cardiovascular system will be disrupted, leading to septic shock. One of the manifestations of cardiovascular dysfunction in septic shock is myocardial depression.

The present article reviews the clinical manifestations of cardiac dysfunction in sepsis, from the point of view of both the right and left ventricle, as well as cardiovascular prognostic factors in sepsis and septic shock. We will also review the potential pathophysiologic processes responsible for myocardial depression in sepsis, from the perspective of organ physiology and molecular biology. Our understanding of the cardiovascular manifestations of septic shock has evolved over the years, as new techniques to assess cardiovascular performance have become available. Before the introduction of the pulmonary artery catheter pac , two distinct cardiovascular clinical presentations of septic shock were described: a high cardiac output co state, associated with warm, dry skin and a bounding pulse despite hypotension warm shock and a low co state, associated with hypotension, cold, clammy skin and a thready pulse cold shock 5 . 6 , in a 1966 study, described these two clinical pictures as different stages of septic shock: patients were believed to initially experience a hyperdynamic phase warm shock , and then to either recover or progress to hypodynamic shock cold shock and death. This view was reinforced by other clinical studies 5 ,7 that correlated survival with high cardiac index ci.

Global Warming Essay Malayalam

Only a few studies hinted at the relationship between volume status, the ci and outcome 8 ,9 . All these studies that supported the concept of terminal cold shock suffered from the fact that they used central venous pressure cvp as the best available estimate of left ventricular end diastolic volume and adequacy of resuscitation. Evidence accumulated over the past 40 years shows that cvp, as a reflection of right ventricular preload, is a poor estimate of left ventricular preload in critically ill patients, and particularly in sepsis 10 . The introduction of the pac which could measure pulmonary artery wedge pressure as a more accurate estimate of left ventricular preload has allowed for better definition of the cardiovascular dysfunction in septic shock and has improved volume resuscitation.

Dissertation Comique Theatre

Several studies have shown that adequately resuscitated septic shock patients consistently manifest a hyperdynamic circulatory state with high co and low systemic vascular resistance svr 11 ,12 . In contrast to previous belief, this hyperdynamic state usually persists until death in nonsurvivors fig. Despite the strong evidence characterizing sepsis as a hyperdynamic state, studies that examined myocardial performance still showed left ventricular dysfunction illustrated by decreased left ventricular stroke work index in properly resuscitated septic patients 15 . The depression in the frank x02013 starling curve demonstrated in these studies, however, could be explained by either a change in myocardial contractility or compliance.

The mean x0b1 sem cardiac index plotted against time for all patients, survivors, and nonsurvivors. The difference between the . the development of portable radionuclide cineangiography and its application to critically ill patients has further improved our understanding of cardiovascular dysfunction in septic shock, by allowing differentiation between impaired contractility and impaired compliance. Frank x02013 starling ventricular performance relationship for each of the three patient groups. Data points plotted represent the mean prevolume and postvolume infusion values of end diastolic volume index edvi and left ventricular stroke work index . left ventricular diastolic function in septic shock is not as clearly defined. The dilatation of the left ventricle 16 and the lack of discordance between pulmonary artery wedge pressure pawp and left ventricular end diastolic volume 17 both argue against significant diastolic dysfunction in sepsis.

More recent studies using echocardiography, however, have demonstrated slower left ventricular filling 20 and aberrant left ventricular relaxation 21 ,22 in septic patients, suggesting that impaired compliance may significantly contribute to myocardial depression in sepsis. A number of studies have documented right ventricular systolic dysfunction in volume resuscitated septic patients, as evidenced by decreased right ventricular ejection fraction rvef and right ventricular dilation 24 ,25 ,26 ,27 . 26 also showed that right ventricular dysfunction occurred independently of pulmonary vascular resistance and pulmonary artery pressure, suggesting that increased right ventricular afterload could not be the dominant cause of right ventricular depression in septic shock. 26 further demonstrated a close temporal parallel between right ventricular and left ventricular dysfunction in sepsis. In their study, survivors experienced significant right ventricular dilation and decreased rvef and right ventricular stroke work index, all of which returned to normal within 7 x02013 14 days fig. Nonsurvivors had moderate right ventricular dilation and a marginally decreased rvef, neither of which improved throughout their illness.

Serial changes in right ventricular ejection fraction and end diastolic volume index during septic shock in humans. a mean initial and final right ventricular ejection fractions for survivors closed circles, p x03c 0.001 and nonsurvivors open . there is also evidence of right ventricular diastolic dysfunction in septic patients. 24 noticed a lack of correlation between right atrial pressure and right ventricular end diastolic volume, suggesting altered right ventricular compliance.

Amherst College Admission Essays

25 similarly identified a subgroup of patients who failed to exhibit an increased right ventricular end diastolic volume index in response to volume loading, despite a rise in cvp. However, the relative contribution of systolic and diastolic dysfunction to right ventricular depression in sepsis remains largely unknown. Early studies of cardiovascular dysfunction in septic shock suggested that a low or decreasing ci invariably carried a poor prognosis 5 ,6 ,7 ,8 . As previously discussed, these studies relied on cvp measurements to assess volume status. It is now known that cvp is a poor reflection of left ventricular preload in critical illness and cannot accurately determine adequacy of resuscitation. Introduction of the pac showed that adequately volume resuscitated septic shock patients as measured by pawp predictably exhibited a high ci and low svr, including nonsurvivors 11 ,12 . Recognition of the significant post resuscitation peripheral vasodilation low svr in septic shock led to the theory that peripheral vascular failure could be a major determinant of mortality in septic shock.

Process Essay About Friendship