Septic shock is a common cause for admission to the intensive care unit (ICU).1–3 It is defined by a systemic inflammatory response syndrome (SIRS) coupled with complex hemodynamic failure. By traditional definition, the term sepsis implies the presence of infection. In this chapter, the term sepsis will be used in a more inclusive way. Septic shock follows the activation of the inflammatory response at the systemic level, most commonly as a result of infection, but on occasion due to other initiating factors. The molecular pathophysiology of sepsis is complex, and beyond the scope of this chapter. However, the clinical presentation is well known to the frontline intensivist. Hemodynamic failure is a dominant feature of septic shock, so that echocardiography has a major application in the bedside management of the condition.4 This chapter will review the use of echocardiography in characterizing and managing the cardiovascular dysfunction associated with septic shock.
The pathophysiological consequences of sepsis include hypovolemia, left ventricular (LV), systolic, and diastolic dysfunction, and right ventricular (RV) systolic dysfunction. Echocardiography allows the intensivist to identify these processes, to monitor their progression, and to direct therapeutic interventions.
Absolute hypovolemia is defined as a reduction of total circulating blood volume. Absolute intravascular hypovolemia is common in septic shock on initial presentation and requires prompt correction; there are several causes that depend on the underlying disease process. They may include the following:
Insensible losses (e.g., skin and respiratory) augmented by fever, sweating, and hyperventilation.
Gastrointestinal losses (e.g., diarrhea and vomiting)
Third-space losses (e.g., pancreatitis, burns, soft tissue injury, capillary leak, low oncotic pressure, ascites, pleural effusion)
Lack of fluid intake (e.g., mental status change, physical weakness, inadequate volume resuscitation when in hospital)
Relative hypovolemia is caused by an abnormal distribution of blood volume between the peripheral and central compartments. Relative hypovolemia is common in septic shock and may persist as a manifestation following initial volume resuscitation. The total blood volume may be normal, but the distribution of the blood volume is away from the central vascular compartment. The vasodilatation arises from failure of peripheral vasoconstrictor mechanisms with an inappropriate activation of vasodilator mechanisms.
Whether hypovolemia is absolute, relative, or combined, its effect is the same. Significant central hypovolemia reduces venous return to the heart, preload, stroke volume (SV), mean arterial pressure, and cardiac output. Volume resuscitation benefits the patient with septic shock by increasing venous return, preload, stroke volume, cardiac output, arterial blood pressure (systolic, mean, and pulse pressure), and tissue oxygen delivery. Identification and correction of hypovolemia is a major goal in the treatment of septic shock.
Left Ventricular Systolic Dysfunction and Septic Shock
Myocardial contractile dysfunction occurs in septic shock. Both experimental and clinical studies have demonstrated the presence of circulating substances that depress myocardial function in septic shock through a variety of mechanisms. Myocardial edema,5 cardiomyocyte apoptosis,6 cytokine effects ...