Sepsis affects the cardiovascular system through multiple mechanisms, and these disorders often result in tissue hypoperfusion.
Tissue hypoperfusion is often present in overt shock, but it can also be present in patients without apparent shock physiology.
If left untreated, tissue hypoperfusion contributes to the development of multiple organ dysfunction and ultimately death. Therefore, the clinician must understand the pathophysiology, recognition, and treatment of sepsis-induced hypoperfusion.
Sepsis-induced tissue hypoperfusion leads to an inadequate supply of oxygen and nutrients to the tissues.
Indicator of tissue hypoperfusion
The clinical parameters used to assess hypovolemia each lack a certain degree of sensitivity and specificity. Indicators that reflect metabolic processes may have more potential to recognize subtle changes.
Nurses caring for trauma patients may find baseline deficit monitoring to be valuable in determining whether the patient continues to be hypoperfused.
Shock is defined as any disease state that leads to hypoperfusion of tissues and an inadequate supply of oxygen (O2) to meet metabolic needs. It is a complex phenomenon that involves both hemodynamic and inflammatory components.
Shock is classified as cardiogenic (pump failure) or due to decreased venous return (due to hypovolemia or vasodilation).
Cardiogenic shock occurs with left ventricular (LV) and right ventricular (RV) failure (possibly due to myocardial infarction or ischemia ), arrhythmia, valve dysfunction, pericardial tamponade, and pulmonary embolism.
Hypovolemia is the result of bleeding or dehydration. Vasodilation can be caused by sepsis, anaphylaxis, neurogenic insult, and burns.
Other shock causes include adrenal insufficiency, carbon monoxide poisoning, and severe thyroid disease. Early treatment of shock is necessary to prevent multisystem organ failure.
Sepsis is associated with cardiovascular changes that can lead to the development of tissue hypoperfusion. Early recognition of sepsis and tissue hypoperfusion is essential to implement adequate hemodynamic support and prevent irreversible organ damage.
Endpoints for resuscitation must be defined, and invasive hemodynamic monitoring is generally required. Targets for hemodynamic optimization should include intravascular volume, blood pressure, and cardiac output.
Therapeutic interventions aimed at optimizing hemodynamics in patients with sepsis include aggressive fluid resuscitation, vasopressor agents, inotropic agents, and in selected cases, blood product transfusions.
Sepsis-induced tissue hypoperfusion
Even with restoring adequate blood pressure and average or supranormal cardiac output, signs of tissue hypoperfusion may persist.
This is often referred to as ‘distributive shock’ and may be related to regional (splanchnic, mesenteric, and renal) or microvascular poor blood flow distribution and a cellular inability to use oxygen despite adequate oxygen supply (hypoxia cytotoxic).
Whether these abnormalities are present at the onset of sepsis or represent a progression of events is unknown. However, it is believed that early intervention with aggressive hemodynamic support may limit the damage of sepsis-induced tissue hypoperfusion and limit or prevent the development of endothelial injury.
Septic shock, defined as sepsis with hypotension refractory (mean systolic blood pressure <90 mmHg, arterial pressure <60 mmHg, or a fall of ≥40 mmHg from baseline pressures), despite the administration of fluids, has been used traditionally for conceptualizing the clinical syndrome of persistent tissue hypoperfusion induced by sepsis.
Blood pressure alone is unlikely to be sufficient to identify the presence or absence of tissue hypoperfusion in patients with sepsis; patients with sepsis-induced hypoperfusion may have normal blood pressures.
Therefore, it is important to recognize other signs indicative of tissue hypoperfusion. Tissue hypoperfusion markers can be classified into global hypoperfusion indices and regional hypoperfusion indices.
A recent International Conference on Definitions of Sepsis recommended expanding the diagnostic criteria for sepsis.
Many of these criteria, including altered mental status, organ dysfunction parameters, acute oliguria, hyperlactatemia (> 3 mmol / L), and decreased capillary filling or motility, suggest the presence of tissue hypoperfusion.