Sepsis is a life-threatening condition that arises when the body’s response to an infection injures its own tissues and organs. The initial infection, which may start anywhere from the lungs to the urinary tract, triggers a dysregulated response that can lead to rapid organ damage or failure. Monitoring vital signs, particularly blood pressure, is important because changes in pressure are an early signal of illness severity. A dramatic drop in blood pressure signals the progression from severe sepsis to the most dangerous stage, known as septic shock.
Understanding Septic Shock and Blood Pressure Thresholds
The identification of dangerously low blood pressure in sepsis is defined by specific numerical thresholds. Hypotension, or low blood pressure, in a patient with a known or suspected infection is typically identified when the systolic blood pressure drops below 90 mmHg. It is also signaled by a decrease of more than 40 mmHg from a person’s normal baseline blood pressure.
The most critical measurement used to define the severity of circulatory failure is the Mean Arterial Pressure (MAP), which represents the average pressure in a person’s arteries during one cardiac cycle. The primary clinical threshold for intervention is an MAP of less than 65 mmHg.
A pressure below this 65 mmHg threshold indicates a severe lack of blood flow, or perfusion, to the body’s major organs. This insufficient pressure prevents oxygen and nutrients from reaching tissues, which leads to organ dysfunction. This numerical goal is a standardized target, though higher pressures may be targeted in patients with pre-existing conditions like chronic hypertension.
Why Blood Pressure Drops During Sepsis
The drop in blood pressure during sepsis is a complex physiological event driven by the systemic inflammatory response to the infection. One major cause is widespread vasodilation, the dramatic widening of blood vessels throughout the circulatory system. Inflammatory mediators cause this loss of vascular tone, which sharply reduces the total peripheral resistance.
Another contributing factor is capillary leak, where the integrity of the blood vessel walls is compromised. This increased permeability allows fluid to leak out of the bloodstream and into the surrounding tissues. The shift of fluid out of the vessels causes hypovolemia, meaning the circulating blood volume decreases, leading to a fall in pressure.
The infection can also directly affect the heart, leading to sepsis-induced myocardial depression. This means the heart muscle becomes less effective at pumping blood, reducing the amount of blood ejected with each beat. The combined effect of vasodilation, fluid loss from capillary leak, and decreased heart function causes the severe and persistent hypotension seen in septic shock.
The Immediate Clinical Goal for Blood Pressure Management
The immediate medical response to low blood pressure in sepsis is time-critical, as delays in treatment can significantly increase the risk of death. The goal is to quickly restore the Mean Arterial Pressure to at least 65 mmHg to ensure adequate blood flow to the organs. Continuous monitoring of the patient’s blood pressure, often using an arterial line, is required to guide these rapid interventions.
The first line of therapy involves fluid resuscitation, the rapid administration of large volumes of intravenous fluids. This compensates for the reduced circulating volume caused by the capillary leak and fluid loss. Clinicians typically follow guidelines recommending an initial fluid bolus, such as 30 milliliters per kilogram of body weight.
If the blood pressure remains below the 65 mmHg target despite the initial fluid administration, the next step is the introduction of vasopressors. These medications work by constricting the blood vessels, which increases the peripheral resistance. Norepinephrine is the most common medication used for this purpose and is often started early to stabilize circulation.
While 65 mmHg is the general target, patients with chronic high blood pressure may require a slightly higher MAP, sometimes between 75 to 85 mmHg, to prevent injury to organs like the kidneys. Continuous re-evaluation of the patient’s response to both fluids and pressors is necessary to achieve the individualized pressure target.