Hemodynamic and Metabolic Studies on Shock Associated With Gram Negative Bacteremia

The haemodynamics of human septic shock*

“…In contrast, the`hyperdynamic' group had larger circulating volumes, had been in shock for shorter periods of time [105], and had tended to survive [116]. This was the pattern seen in prospectively studied patients who became bacteraemic immediately following urological procedures [117,118].…”

“…Many workers came to the view that the hyperdynamic circulation was a feature of early shock that became hypodynamic with time and hypovolaemia [107±109, 116,117,119,120]. This view was supported by clinical observations and the fact that many hypodynamic patients would respond to a fluid challenge by a decrease in SVR and an increase in CI [115,121], and that death appeared to be associated with metabolic acidaemia [108,116,120,122,123] and a low cardiac output [110,111,116,120].`The confusion in the literature over sepsis presenting as a hyperdynamic or hypodynamic cardiac state and as a low or high resistance vascular state may result from comparing patients who were at different points in their septic episode' [124]. McLean et al described a further two patterns.…”

“…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]. It later emerged that those who survived the episode of shock subsequently died of multiple organ failure [125,126], which was the consequence of inadequate or maldistributed organ perfusion' [127].…”

“…Postoperative respiratory failure was well described in the early 1960s [37±39] and the acute respiratory distress syndrome was first described in 1967 [135]. Whether these respiratory problems were in part caused by the change in fluid management is not clear, but it is evident that respiratory failure (`shock lung' [106,116]) and the need for mechanical ventilation [108,116] were both associated with an increased risk of death.…”

Myocardial Failure With Altered Response to Adrenaline in Endotoxin Shock

“…Recent reports have identified a subsequent phase of shock, following the early compensatory period, when myocardial performance begins to falter or fail altogether (Solis & Downing, 1966;Goodyer, 1967;Siegel, Greenspan & Del Guercio, 1967;Cavanagh et al, 1970;Bell & Thal, 1970;Cann, Stevenson, Fiallos & Thal, 1972;Hinshaw et al, 1972c;Hinshaw, Archer, Black, Greenfield & Guenter, 1973;Parratt, 1973;Nishijima, Weil, Shubin & Cavanilles, 1973;Hinshaw, Archer, Black, Elkins, Brown & Greenfield, 1974a;Parratt & Winslow, 1974;Greenfield, Jackson, Elkins, Coalson & Hinshaw, 1974) in both animal endotoxic studies and clinical septic shock. The observed myocardial dysfunction in not merely a preterminal event and is not necessarily associated with systemic hypotension, acidemia, or depressed oxygen delivery (Hinshaw et al, 1972c(Hinshaw et al, , 1973Hinshaw, Archer, Spitzer, Black, Peyton & Greenfield, 1974b), and does not appear to be due to the release of a myocardial depressant factor (Hinshaw, Greenfield, Owen, Archer & Guenter, 1972b;Hinshaw et al, 1974a).…”