Sepsis is a life-threatening medical emergency representing the body’s overwhelming and dysregulated response to an infection. Instead of fighting only the invading pathogen, the immune system begins to injure the body’s own tissues and organs. This systemic dysfunction often results in hypotension, defined as abnormally low blood pressure, typically a systolic reading below 90 millimeters of mercury (mmHg). This condition is caused by a complex biological cascade involving excessive immune signaling and profound physical changes to the circulatory system.
The Immune System’s Inflammatory Trigger
When an infection begins, the body releases signaling molecules to mobilize its defenses, a process that becomes dangerously excessive during sepsis. This out-of-control response involves the massive, systemic release of inflammatory proteins called cytokines. These mediators, including Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α), normally coordinate the immune response. Their widespread and excessive release, often called a “cytokine storm,” initiates a destructive, body-wide cascade.
These signals travel through the bloodstream, transforming a localized infection into a systemic problem. The cytokine storm is the primary upstream cause that triggers physical changes in the blood vessels, primarily targeting the endothelium, the delicate layer of cells lining all blood vessels.
Vascular Changes: Loss of Blood Vessel Resistance
The excessive inflammatory signals directly attack the smooth muscle surrounding the blood vessels, causing them to relax and widen dramatically. This process is known as vasodilation. The widespread vasodilation causes a significant drop in Systemic Vascular Resistance (SVR), which is the force the heart must overcome to push blood through the body. SVR acts as the body’s primary mechanism for maintaining blood pressure; if resistance drops, the pressure inside the vessels falls sharply. This is the central reason for septic hypotension, as the vessels can no longer constrict sufficiently to maintain adequate pressure.
The blood vessels essentially become too large for the volume of blood they contain, leading to a state called distributive shock. Simultaneously, the cytokine storm damages the endothelium, leading to increased capillary permeability. The vessel walls, normally a tight barrier, become “leaky,” allowing fluid to seep out of the blood and into the surrounding tissues. This capillary leakage reduces the effective circulating blood volume, meaning less fluid remains in the vessels to maintain pressure. The combination of vastly reduced SVR and lower blood volume circulating in a dilated system causes the profound drop in blood pressure seen in sepsis.
Sepsis Impact on Cardiac Pumping
While the loss of vessel resistance is the main driver of early septic hypotension, the heart is also directly compromised by systemic inflammation. Sepsis can induce sepsis-induced cardiomyopathy, where the heart muscle becomes less efficient at pumping blood. The inflammatory mediators that cause vasodilation also negatively affect the heart’s contractility.
This leads to a decreased Cardiac Output (CO), which is the volume of blood the heart pumps per minute. The heart is unable to compensate for the dramatically lowered SVR by increasing its output, further worsening the low blood pressure. The direct injury to the heart muscle contributes to circulatory failure. Therefore, the severity of septic hypotension stems from the combined failure of the vascular system to maintain resistance and the heart’s inability to maintain output.
The Progression to Septic Shock
When hypotension persists despite medical intervention, the patient progresses to the most severe state: septic shock. Septic shock is defined as sepsis with persistently low blood pressure, requiring vasopressors to keep the mean arterial pressure above a safe threshold. This profound hypotension means blood pressure is too low to adequately perfuse, or deliver blood to, the body’s tissues.
When tissues are starved of oxygen and nutrients due to inadequate blood flow, they experience cellular hypoxia and begin to fail. This tissue hypoperfusion is responsible for the rapid development of multi-organ dysfunction syndrome. Consequences include acute kidney injury due to insufficient blood reaching the kidneys, and respiratory failure. The resulting damage can quickly become irreversible, demonstrating why septic hypotension is a direct and life-threatening medical emergency.