الفهرس 
Patients and methodsOnly 14 pages are availabe for public view
 |  | from | 120 |  |  |
| | | from | 120 | | |
Abstract
According to the Surviving Sepsis Campaign, a patient with sepsis has an infection and then has organ failure as a result of their body’s dysregulated response to the infection (SSC). Septic shock is a subtype of sepsis characterised by high mortality rates associated with serious underlying metabolic, circulatory, and cellular problems.
Septic shock is characterised by persistent fluid-unresponsive hypotension, persistently high blood lactate levels (over 2 mmol/l) despite adequate volume resuscitation, and the need of vasopressors to maintain a mean arterial pressure (MAP) greater than 65 mm Hg.
The SSC ensured that patients who remained hypotensive after the first fluid resuscitation received the one-hour bundle, which includes rapid commencing fluid resuscitation, empiric antibiotic medication, and the use of vasopressors, within one hour after sepsis diagnosis.
It may be difficult for some critically ill patients to gradually reduce their use of intravenous (IV) vasopressors, even after they recover. Patients who fulfil the criteria for intensive care unit discharge cannot be discharged due to the fact that they are continually administered low-dose intravenous vasopressors, which cause their blood pressure to stay dangerously low.
Patients run the risk of tachyphylaxis, peripheral limb and visceral ischemia, increased healthcare costs, longer intensive care unit stays, disorientation, infections that are resistant to treatment, and mortality if they are not adequately weaned off IV vasopressors. To achieve target blood pressure goals (MAP) of 65 mm Hg or above and serum lactate levels below 2 mmol/l, it is recommended to utilise vasopressors at the lowest effective dosage for the shortest duration necessary.
The FDA has authorised the oral drug midodrine for the treatment of symptomatic hypotension. The active metabolite desglymidodrine is an alpha-1 adrenergic agonist. Desglymidodrine has no effect on the central nervous system or the heart, but it does raise vascular tone by binding to alpha-adrenergic receptors in the blood vessels. Retention of urine, itching, paresthesia, and piloerection are the most often reported side effects. A systolic blood pressure of 200 mm Hg or higher is known as spine hypertension, and it was the most severe side effect of midodrine. Midodrine may cause a reduction in heart rate as a defensive mechanism.
Patients experiencing neurogenic orthostatic hypotension exhibited a dose-dependent rise in systolic blood pressure (SBP), with an average elevation of 34 mm Hb, after an hour of treatment with a single oral dose of 10 mg of midodrine.
A similar study found that 171 individuals with neurogenic orthostatic hypotension had a 21.8 mm Hg rise in systolic blood pressure (SBP) after three weeks of taking 10 mg of midodrine three times daily compared to a placebo.
Patients with orthostatic hypotension are helped to wean off IV vasopressor infusions by midodrine, which has a predictable pharmacological response and favourable sympathomimetic effects. This is done off-label.