In the cases of
cardiogenic shock resulting from
heart failure or acute
hemorrhagic shock caused by a large volume of
blood loss, the body constricts peripheral vessels to reverse the low arterial pressure that causes inadequate tissue perfusion.[22] With vasodilatory shock, it is difficult for the peripheral vascular smooth muscle to constrict.[22] In refractory vasodilatory shock, peripheral vascular smooth muscle responds poorly to therapy with vasopressor drugs.[22]
Vasopressin deficiency may play an important role in vasodilatory shock.[23] In refractory vasodilatory shock, the patient has both vasopressin secretion deficit and an advanced resistance to vasopressin-induced blood-pressure changes.[23] Some have hypothesized that patients with vasopressin deficiency, including a decrease in baroreceptor stimulation, appear to have impaired autonomic reflexes.[23]Tone may be inhibited by
atrial stretch receptors and vasopressin release may be inhibited by
nitric oxide or high circulating levels of
norepinephrine.[23]
The definition of refractory shock or vasodilatory shock varies. In 2018, the American College of Chest Physician stated that it is presents if there is an inadequate response to high-dose vasopressor therapy defined as ≥ 0.5 mg/kg/min norepinephrine-equivalent dose.[4]
Reversing the underlying causes of vasodilatory shock, stabilizing
hemodynamic, preventing renal,
myocardial, and other organs from injuries due to hypoperfusion and hypoxia, and taking necessary measures to safeguard against complications including
venous thromboembolism are served as the top priorities during the treatment.[24]
The initial treatment aiming at restoring effective blood pressure in patients that have refractory shock typically starts with introducing norepinephrine and dopamine.[24] Vasopressin comes as the second-line agent.[24]
However, high-dose therapy is linked to excessive coronary, splanchnic vasoconstriction, and hypercoagulation.[6] Excessive vasoconstriction can cause cardiac output reduction or even fatal heart complication particularly in those with weak
myocardial function.[6]
In those whose vasodilatory shock is caused by hypocalcemic cardiomyopathy in the context of dilated
cardiomyopathy with documented both reduced heart ejection fraction and contractile performance,[17] the uses of calcium and active
vitamin D or
recombinant human parathyroid hormone treatment are viable since there were many successful cases reported while given the physiological role of calcium on muscle contraction.[17][30][31][32]
Early recognition and rapid treatment initiation are crucial to saving life.[24] If vasodilatory shock being left untreated, even brief
hypotensive periods can result in
myocardial and
renal injury.[21][35] It can also increased
mortality in the
critically ill.[21] Refractory shock has an all-cause mortality rate greater than 50% within a month[1][dubious –
discuss].
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^Jentzer, Jacob C.; Coons, James C.; Link, Christopher B.; Schmidhofer, Mark (May 2015). "Pharmacotherapy Update on the Use of Vasopressors and Inotropes in the Intensive Care Unit". Journal of Cardiovascular Pharmacology and Therapeutics. 20 (3): 249–260.
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