NR 567 Week 4 Septic Shock Vasopressor Write-Up Example

Vasoactive Support Write-Up: Norepinephrine at 0.28 Micrograms per Kilogram per Minute Holding a Mean Arterial Pressure of 65, the Vasopressin and Hydrocortisone Added to It, and the Conditions for Coming Down

Student Name

College of Nursing, Chamberlain University

NR 567: Advanced Pharmacology for the Adult Gerontology Acute Care Nurse Practitioner

Instructor Name

Month Day, Year

Vasoactive Support Write-Up: Norepinephrine at 0.28 Micrograms per Kilogram per Minute Holding a Mean Arterial Pressure of 65, the Vasopressin and Hydrocortisone Added to It, and the Conditions for Coming Down

The Number Being Held

On day 2, the composite patient from this course, a 66-year-old in septic shock from severe pneumonia, depends on norepinephrine running at 0.28 mcg/kg/min for a mean pressure of 65. At 92 kg, that is about 26 mcg per minute. The requirement has risen over 12 hours despite about 5 liters of crystalloid. Lactate is 4.1 mmol/L, the patient is anuric and now on continuous hemodiafiltration, the extremities are cool and mottled at the knees, and capillary refill is four seconds.

The target of 65 mm Hg reflects guidance for septic shock (Evans et al., 2021). A higher target of 80 to 85 did not improve survival in a large trial and caused more atrial fibrillation, although patients with chronic hypertension needed less renal replacement therapy at the higher target. This patient had well-controlled hypertension, so 65 is chosen, with a review if kidney perfusion appears pressure-dependent.

Name the Physiology

The shock is vasodilatory. Sepsis has caused profound loss of vascular tone, and cardiac output is preserved on a bedside echocardiogram, with a hyperdynamic left ventricle and no right ventricular failure. The agents therefore follow from the need to restore tone, not to increase contractility. An inotrope such as dobutamine would be added only if the echocardiogram later showed myocardial depression with persistent poor perfusion.

The First Agent

Norepinephrine is the first-line vasopressor in septic shock (Evans et al., 2021). It acts mainly on alpha-1 receptors to constrict vessels, with some beta-1 effect that supports cardiac output. It is continued.

The Second Agent

Rather than continuing to escalate norepinephrine, vasopressin is added at a fixed rate of 0.03 units per minute. The sepsis guideline suggests bringing vasopressin in once norepinephrine climbs into the range of a quarter to half a microgram per kilogram per minute (Evans et al., 2021). Vasopressin works through V1 receptors, independent of the catecholamine receptors that become less responsive in septic shock, and patients are often relatively deficient in it. In a large trial, vasopressin added to norepinephrine did not reduce overall mortality, but it reduced the norepinephrine dose required and appeared to benefit patients with less severe shock (Russell et al., 2008). Vasopressin is not titrated upward beyond 0.03 units per minute because higher doses cause digital, mesenteric and cardiac ischemia.

Vasopressin does not need to be adjusted for kidney failure or for the hemodiafiltration, and its effect fades within about 20 minutes of stopping, which keeps it easy to remove once the shock resolves.

Hydrocortisone

Because the norepinephrine requirement has stayed at or above a quarter of a microgram per kilogram per minute for over four hours, hydrocortisone is added, 50 mg into the vein every six hours (Evans et al., 2021). In a large trial, hydrocortisone did not lower 90-day mortality in septic shock but led to faster resolution of shock and shorter time on mechanical ventilation (Venkatesh et al., 2018). The aim here is to shorten the time on vasopressors. Glucose will rise, and the insulin infusion protocol is started for glucose above 180 mg/dL.

Delivery and Monitoring

Norepinephrine and vasopressin run through a central venous catheter in the internal jugular vein, each on its own lumen with no other infusions, so that boluses of other drugs cannot push vasopressor through the line. An arterial line in the radial artery gives continuous pressure. Peripheral norepinephrine was used briefly in the emergency department through a large forearm cannula, and the site is checked for extravasation. The nurse records mean arterial pressure every 15 minutes, checks the fingers and toes for ischemia every hour while vasopressin runs, and reports a rise in lactate, new arrhythmia or ischemic changes.

Assessing Fluid Before Adding Drug

Before each increase in norepinephrine, the team stops to ask whether this patient needs more fluid or more vascular tone. The patient has already received about 5 liters, has visible edema and needs increasing oxygen. A passive leg raise with cardiac output measured by echocardiography is the test used: if stroke volume rises by more than about 10%, a 500 mL balanced crystalloid bolus is given; if not, more fluid will only add to lung water, and vasopressor support is the right tool. The sepsis guideline prefers tests of how the heart responds to a fluid challenge over single readings such as central venous pressure (Evans et al., 2021). The result of each test is charted with the decision it led to. Documenting this check each time prevents both under-resuscitation and the opposite error of reaching for more drug when the problem is volume.

What Is Reducing the Requirement

The requirement will fall when the underlying causes improve, and the write-up names them. First, antibiotics: vancomycin, cefepime and azithromycin began within an hour of arrival, and cultures were taken before the first dose. Second, fluid: further boluses are given only when a passive leg raise or pulse pressure variation shows fluid responsiveness, because the patient is already edematous and fluid now risks worsening oxygenation. Third, hydrocortisone. Fourth, correction of acidosis and electrolytes through the hemodiafiltration. Sedation is kept as light as safe, because deep sedation lowers vascular tone and raises the vasopressor need.

The Exit Criteria

The infusions do not run indefinitely. The criteria for starting to come down are: mean arterial pressure at or above 65 mm Hg for at least four hours without an increase in dose; lactate falling and below 2 mmol/L, or falling by at least half; capillary refill under three seconds with mottling resolved; and the patient responding appropriately when sedation is lightened. Urine output cannot be used while the patient is anuric on dialysis, which is why the other markers carry more weight.

When those criteria hold, norepinephrine is reduced by about 0.02 to 0.05 mcg/kg/min every 30 to 60 minutes while the pressure holds. Vasopressin is stopped after norepinephrine has been weaned to a low dose, around 0.05 to 0.1 mcg/kg/min, because stopping vasopressin first has been associated with more hypotension in observational studies. Hydrocortisone is stopped or tapered once vasopressors are off.

The Trigger to Escalate Again

If mean arterial pressure falls below 65 for more than 15 minutes during the wean, or lactate rises again, the last reduction is reversed, and the provider is called to look for a new cause: a new infection source, bleeding or a cardiac problem.

References

Evans, L., Rhodes, A., Alhazzani, W., Antonelli, M., Coopersmith, C. M., French, C., Machado, F. R., Mcintyre, L., Ostermann, M., Prescott, H. C., Schorr, C., Simpson, S., Wiersinga, W. J., Alshamsi, F., Angus, D. C., Arabi, Y., Azevedo, L., Beale, R., Beilman, G., . . . Levy, M. (2021). Surviving Sepsis Campaign: International guidelines for management of sepsis and septic shock 2021. Critical Care Medicine, 49(11), e1063-e1143. https://doi.org/10.1097/CCM.0000000000005337

Russell, J. A., Walley, K. R., Singer, J., Gordon, A. C., Hébert, P. C., Cooper, D. J., Holmes, C. L., Mehta, S., Granton, J. T., Storms, M. M., Cook, D. J., Presneill, J. J., & Ayers, D. (2008). Vasopressin versus norepinephrine infusion in patients with septic shock. New England Journal of Medicine, 358(9), 877-887. https://doi.org/10.1056/NEJMoa067373

Venkatesh, B., Finfer, S., Cohen, J., Rajbhandari, D., Arabi, Y., Bellomo, R., Billot, L., Correa, M., Glass, P., Harward, M., Joyce, C., Li, Q., McArthur, C., Perner, A., Rhodes, A., Thompson, K., Webb, S., & Myburgh, J. (2018). Adjunctive glucocorticoid therapy in patients with septic shock. New England Journal of Medicine, 378(9), 797-808. https://doi.org/10.1056/NEJMoa1705835