Patterns Of Septic Shock In Man—a Detailed Study Of 56 Patients

MacLean, Lloyd D.; Mulligan, William G.; McLean, A. Peter H.; Duff, John

doi:10.1097/00000658-196710000-00004

Cited by 347 publications

(101 citation statements)

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“…This was observed in the initial phase of hospitalization due to septic shock. In contrast, "cold shock" seemed to be related to low cardiac output and was correlated with the later clinical stages of septic shock before patients succumbed to sepsis (1)(2)(3). Based on these findings, it was concluded that patients during septic shock initially encountered an early hyperdynamic phase from which they either recovered or declined into a hypodynamic phase associated with myocardial depression, heart failure, and death (4).…”

Section: Introductionmentioning

confidence: 99%

Molecular Events in the Cardiomyopathy of Sepsis

Flierl

Rittirsch

Huber‐Lang

et al. 2008

Mol Med

108

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Septic cardiomyopathy is a well-described complication of severe sepsis and septic shock. However, the interplay of its underlying mechanisms remains enigmatic. Consequently, we constantly add to our pathophysiological understanding of septic cardiomyopathy. Various cardiosuppressive mediators have been discovered, as have multiple molecular mechanisms (alterations of myocardial calcium homeostasis, mitochondrial dysfunction, and myocardial apoptosis) that may be involved in myocardial dysfunction during sepsis. Finally, the detrimental roles of nitric oxide and peroxynitrite have been unraveled. Here, we describe our present understanding of systemic, supracellular, and cellular molecular mechanisms involved in sepsis-induced myocardial suppression. SYSTEMIC, SUPRACELLULAR MECHANISMS Decreased Coronary Blood FlowOne of the first suggestions was that reduced coronary perfusion in the septic heart might be responsible for a setting of global cardiac ischemia. This hypothesis was soon abandoned after direct measurements of coronary blood flow were obtained, showing no reduced, but rather increased, coronary blood flow (22,23). In later studies, however, increased levels of plasma troponin were observed and correlated with the severity of myocardial depression during sepsis and septic shock (24). Myocardial necrosis could not be observed in patients who died from septic shock (3,25), however, raising the question whether increases in troponin were due to cytokine-induced, transient increases in cardiomyocyte membrane permeability to troponin. To date, this remains to be determined. Alterations of MicrovasculatureThere is now increasing evidence that sepsis and septic shock leads to changes of the myocardial microvasculature. In a canine model of endotoxemia, maldistribution of heterogeneous coronary blood flow has been reported (26). These findings might be caused by endothelial swelling and nonocclusive intravascular fibrin deposits in the microvasculature (27). In parallel, activated cardiomyocytes from septic mice promoted transendothelial migration and activation of circulating neutrophils into the interstitium (28) where these cells may augment the sepsis-induced intracardial inflammation, and contribute to an increased vascular leakage, which has been described to also impair cardiac function and compliance secondary to myocardial edema (29,30). Yet, studies have failed to confirm cellular hypoxia in a murine sepsis model (31). Cardiosuppressing Circulating Proinflammatory MediatorsAnother hypothesis suggested circulating myocardium-depressing factors as the cause of septic cardiomyopathy (32). Parrillo et al. (33) confirmed the existence of a cardiodepressant substance by incubating isolated rat cardiomyocytes with serum obtained from septic shock patients, leading to decreased amplitude and velocity of cardiomyocyte shortening. Levels of cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and the complement anaphylatoxin, C5a, are known to be elevated in the circulation during sepsis an...

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Section: Introductionmentioning

confidence: 99%

Molecular Events in the Cardiomyopathy of Sepsis

Flierl

Rittirsch

Huber‐Lang

et al. 2008

Mol Med

108

View full text Add to dashboard Cite

show abstract

“…McLean et al described a further two patterns. One group resembled the hyperdynamic patients but were markedly acidaemic, and probably represented an early phase of the transition between hyperdynamic and hypodynamic shock [107]. The other group were patients who were hypodynamic with acidaemia and low CVPs but who did not respond to fluid resuscitation, and represented a preterminal phase of late shock [107].…”

Section: Clinical Haemodynamicsmentioning

confidence: 99%

“…One group resembled the hyperdynamic patients but were markedly acidaemic, and probably represented an early phase of the transition between hyperdynamic and hypodynamic shock [107]. The other group were patients who were hypodynamic with acidaemia and low CVPs but who did not respond to fluid resuscitation, and represented a preterminal phase of late shock [107]. The effect on the clinical presentation of pre-existing comorbidities, particularly age and heart disease, was also acknowledged [112,115,116].…”

Section: Clinical Haemodynamicsmentioning

confidence: 99%

“…In the period 1963±1970, techniques for assessing preload underwent a significant evolution from measurement of plasma volume using radioisotopes [104,107,113,128,129] to the measurement of intravascular pressures. This initially involved pressure measurement in the external jugular vein [129] or a central vein using a brachial catheter [104,130].…”

Section: Clinical Haemodynamicsmentioning

confidence: 99%

“…This initially involved pressure measurement in the external jugular vein [129] or a central vein using a brachial catheter [104,130]. Only later was a properly verified right atrial pressure measured using a long catheter inserted in an upper limb vein [105, 110±113, 131], femoral vein [128], or central vein [107,114]. This move away from circulating volume to right ventricular filling pressure reflected increased clinical appreciation and application of Starling's Law of the heart, permitting an ever more`aggressive' [108] approach to resuscitation with intravenous fluids.…”

Section: Clinical Haemodynamicsmentioning

confidence: 99%

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