Vasodilatory shock
Vasodilatory shock, vasogenic shock, or vasoplegic shock is a medical emergency belonging to shock along with cardiogenic shock, septic shock, allergen-induced shock and hypovolemic shock. When the blood vessels suddenly relax, it results in vasodilation. In vasodilatory shock, the blood vessels are too relaxed leading to extreme vasodilation and blood pressure drops and blood flow becomes very low. Without enough blood pressure, blood and oxygen won’t be pushed to reach the body’s organs. If vasodilatory shock lasts more than a few minutes, the lack of oxygen starts to damage the body’s organs. Vasodilatory shock like other types of shock should be treated quickly, otherwise it can cause permanent organ damage or death as a result of multiple organ dysfunction.
Treatment typically involves uses of vasopressor, inotropes, fluid boluses, and introduction of resuscitation. In case vasodilatory shock fails to respond to high doses of vasopressors, meaning it's vasopressor-resistant and advances to being called refractory vasodilatory shock or simply refractory shock. Adjunctive therapies include angiotensin II, hydrocortisone, thiamine, catecolamines, ascorbic acid and combinations of thereof.
Signs and symptoms
- Confusion or lack of alertness
- Loss of consciousness
- A sudden and ongoing rapid heartbeat
- Sweating
- Pale skin
- A weak pulse
- Rapid breathing
- Decreased or no urine output
- Cool hands and feet
Cause
The most common cause of vasodilatory shock is sepsis. Except sepsis, other causes comprise severe acute pancreatitis, post cardiopulmonary bypass vasoplegia and other triggers for a systemic inflammatory response syndrome. Low serum calcium values might take a role in vasodilatory shock.
Pathophysiology
In case of cardiogenic shock or acute hemorrhagic shock resulted from heart failure or from a large volume of blood loss, respectively, body deals with which by constricting peripheral vessels for the sake of reversing low arterial pressure that causes inadequate tissue perfusion. Nevertheless, in vasodilatory shock, peripheral vascular smooth muscle finds it difficult to constrict. In refractory vasodilatory shock, peripheral vascular smooth muscle even finds itself poorly respond to therapy with vasopressor drugs.Vasopressin deficiency may play an important role in vasodilatory shock. In refractory vasodilatory shock, the patient have both vasopressin secretion deficit as well as an advanced resistance to vasopressin-induced blood pressure changes. Some hypothesized that patients with vasopressin deficiency including a decrease in baroreceptor stimulation appear to suffer from impaired autonomic reflexes. They also argued that tonic may be inhibited by atrial stretch receptors and vasopressin release may be inhibited by nitric oxide or high circulating levels of norepinephrine.
Often, vasodilatory shock is contributed by the dysfunction of the physiologic compensatory mechanisms such as sympathetic nervous system, vasopressin arginine system, and the renin-angiotensin aldosterone system.
Diagnosis
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.| Drug | Dose | Norepiniphrine equivalent |
| Epinephrine | 0.1 μg/Kg/min | 0.1 μg/Kg/min |
| Dopamine | 15 μg/Kg/min | 0.1 μg/Kg/min |
| Norepinephrine | 0.1 μg/Kg/min | 0.1 μg/Kg/min |
| Phenylephrine | 1 μg/Kg/min | 0.1 μg/Kg/min |
| Vasopressin | 0.04 U/Kg/min | 0.1 μg/Kg/min |
Management
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.The initial treatment aiming at restoring effective blood pressure in patients suffering refractory shock typically starts with
introducing norepinephrine and dopamine. Vasopressin comes as the second-line agent.
However, high-dose therapy is linked to excessive coronary, splanchnic vasoconstriction, and hypercoagulation. Excessive vasoconstriction can cause cardiac output reduction or even fatal heart complication particularly in those with weak myocardial function.
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, 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.
A successful treatment requires leveraging the respective unique contributions of a multi-disciplinary team not only critical care doctors and often, infectious disease specialists but also respiratory therapy, nursing, pharmacy and others in collaboration.