Bacterial Septic Shock

Abstract

Summary Septic shock is an increasingly common disorder that produces profound dysfunction of multiple organ systems and is lethal in approximately 50 per cent of patients. Early deaths are usually caused by refractory hypotension with a low systemic vascular resistance (SVR). Deaths occurring later are usually caused by sepsis-induced multiple organ system failure syndrome. A distinct pattern of hemodynamic change occurs during septic shock. Within the first 2 to 3 days, the LV dilates, LVEF decreases, and alterations on the Frank-Starling and end-systolic pressure plots show LV dysfunction. CO usually increases or remains normal, whereas SVR decreases or remains normal. This maintenance of CO and SV in the setting of LV dysfunction is probably related to changes in diastolic function. During septic shock, the LV dilates without increasing pressure, and SV and CO either remain unchanged or increase via the Frank-Starling mechanism. Occasionally, patients with septic shock have low CO and concomitant hypotension, but this is uncommon and occurs only in patients with severe cardiac deficiency and combined septic and cardiogenic shock. In surviving patients, these cardiovascular changes reverse to normal in 7 to 10 days. Because we have also found an identical sequence of hemodynamic change in our canine model, this response may be common for all large mammals. The pathophysiology of septic shock is complex and still not completely understood. It is believed that multiple bacterial toxins (not necessarily endotoxin) release host mediators (for example, MDS, TNF, IL-1, IL-2, complement, eicosanoids) that produce shock and death. The chemical nature of these mediators and their role in infection is still undergoing investigation. Treatment of patients with septic shock is often optimized by immediate referral to the intensive care unit. Patients should receive broad-spectrum antibiotics, and intra-arterial and pulmonary artery catheters to help guide resuscitative therapy with fluids and pressors. Initially patients should be given volume resuscitation. However, if hypotension persists after adequate volume resuscitation, patients should be given pressor agents selected for their effects on peripheral resistance, contractility, and HR. At the NIH medical intensive care unit, we use the following algorithm to treat patients in septic shock. We correct all laboratory abnormalities including anemia, acidosis, hypoalbuminemia, and hypoxia. We administer crystalloid as initial resuscitative therapy to increase preload while simultaneously measuring serial hemodynamic variables (PCWP, CVP, SVR, CO, and MAP). If PCWP is greater than or equal to 15 and hypotension persists, we administer a vasopressor. Initially we administer dopamine in low doses (1 to 10 µg per kg per minute) to preserve renal blood flow. If hypotension persists with dopamine in doses greater than 20 µg per kg per minute, we add norepinephrine and turn dopamine down to 1 to 2 µg per kg per minute to avoid adverse effects of dopamine in high doses (tachycardia and atrial arrhythmias). In patients with cardiac arrhythmias, we use phenylephrine instead of norepinephrine because of its predominant alpha-adrenergic agonist effects. In the rare circumstances of patients with low CO despite adequate preload, we administer epinephrine for its potent beta- and alpha-adrenergic effects.