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Vasodilatory shock

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Vasodilatory shock
Other namesRefractory vasodilatory shock, refractory shock, irreversible shock, vasogenic shock, or vasoplegic shock.
SpecialtyEmergency medicine
ComplicationsMultiple organ dysfunction
PreventionEarly recognition and rapid treatment initiation for any types of shock.
PrognosisHigher than 50% mortality rate within a month[1][dubious – discuss]

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.[2] 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.[3][4][5][6]

Treatment typically involves uses of vasopressor, inotropes, fluid boluses, and introduction of resuscitation.[4] In case vasodilatory shock fails to respond to high doses of vasopressors (defined as ≥ 0.5 mg/kg/min norepinephrine-equivalent dose[7]), meaning it's vasopressor-resistant and advances to being called refractory vasodilatory shock or simply refractory shock.[4][8] Adjunctive therapies include angiotensin II, hydrocortisone, thiamine, catecolamines, ascorbic acid and combinations of thereof.[4][9][10]

Signs and symptoms

See also: Cardiogenic shock § Signs and symptoms, Shock (circulatory) § Signs and symptoms, and Hypovolemic shock § 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

[3]

Cause

A bacterial infection in the bloodstream,[11] a severe allergic reaction (anaphylaxis), systemic inflammatory response syndrome,[12] or damage to the nervous system (brain and nerves) may cause vasodilatory shock.[3][12][13] Besides, nearly all kinds of distributive shock such as septic shock, neurogenic shock, anaphylactic shock, drug and toxin-induced shock, endocrine shock can turn out into rafractory vasodilatory shock when the original shock becomes more severe.[14][2][15][16][17][4]

The most common cause of vasodilatory shock is sepsis.[5] Except sepsis, other causes comprise severe acute pancreatitis, post cardiopulmonary bypass vasoplegia and other triggers for a systemic inflammatory response syndrome.[18][19][20][21] Low serum calcium values might take a role in vasodilatory shock.[17]

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.[22] Nevertheless, in vasodilatory shock, peripheral vascular smooth muscle finds it difficult to constrict.[22] In refractory vasodilatory shock, peripheral vascular smooth muscle even finds itself poorly respond to therapy with vasopressor drugs.[22]

Vasopressin deficiency may play an important role in vasodilatory shock.[23] In refractory vasodilatory shock, the patient have both vasopressin secretion deficit as well as an advanced resistance to vasopressin-induced blood pressure changes.[23] Some hypothesized that patients with vasopressin deficiency including a decrease in baroreceptor stimulation appear to suffer from impaired autonomic reflexes.[23] 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.[23]

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.[24]

[5][6]

Diagnosis

See also: Shock index

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]

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

[15][25][26][27]

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.[24]

The initial treatment aiming at restoring effective blood pressure in patients suffering 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]

[4][28][29]

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]

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.[24]

Epidemiology

Observational studies suggest that, about 6% to 7% of critically ill people may end up developing refractory shock.[33][34]

Prognosis

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].

References

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  2. ^ a b Vincent, Jean-Louis; De Backer, Daniel (2013-10-31). Finfer, Simon R.; Vincent, Jean-Louis (eds.). "Circulatory Shock". The New England Journal of Medicine. 369 (18): 1726–1734. doi:10.1056/nejmra1208943. ISSN 0028-4793. PMID 24171518.
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  7. ^ Bassi, Estevão; Park, Marcelo; Azevedo, Luciano Cesar Pontes (2013). "Therapeutic Strategies for High-Dose Vasopressor-Dependent Shock". Critical Care Research and Practice. 2013: 1–10. doi:10.1155/2013/654708. ISSN 2090-1305. PMC 3787628. PMID 24151551.{{cite journal}}: CS1 maint: unflagged free DOI (link)
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  17. ^ a b c d Minisola, Salvatore; Cipriani, Cristiana; Colangelo, Luciano; Biamonte, Federica; Pepe, Jessica (2019). "Serum Calcium Values and Refractory Vasodilatory Shock". Chest. 155 (1): 242. doi:10.1016/j.chest.2018.08.1066. ISSN 0012-3692. PMID 30616730.
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  19. ^ Hirai, S (2003). "Systemic inflammatory response syndrome after cardiac surgery under cardiopulmonary bypass". Annals of Thoracic and Cardiovascular Surgery. 9 (6): 365–70. ISSN 1341-1098. PMID 15003097.
  20. ^ Herget-Rosenthal, S.; Saner, F.; Chawla, L. S. (2008-02-20). "Approach to Hemodynamic Shock and Vasopressors". Clinical Journal of the American Society of Nephrology. 3 (2): 546–553. doi:10.2215/cjn.01820407. ISSN 1555-9041. PMC 6631076. PMID 18256381.
  21. ^ a b c Vallabhajosyula, S.; Jentzer, J. C.; Khanna, A. K. (2018). "Vasodilatory Shock in the ICU: Perils, Pitfalls and Therapeutic Options". Annual Update in Intensive Care and Emergency Medicine 2018. Cham: Springer International Publishing. pp. 99–111. doi:10.1007/978-3-319-73670-9_9. ISBN 978-3-319-73669-3. ISSN 2191-5709.
  22. ^ a b c Landry, Donald W.; Oliver, Juan A. (2001-08-23). Epstein, Franklin H. (ed.). "The Pathogenesis of Vasodilatory Shock". New England Journal of Medicine. 345 (8): 588–595. doi:10.1056/nejmra002709. ISSN 0028-4793. PMID 11529214.
  23. ^ a b c d Silverstein, Deborah C. (2009). "Vasopressin". Small Animal Critical Care Medicine. Elsevier. pp. 759–762. doi:10.1016/b978-1-4160-2591-7.10177-8. ISBN 978-1-4160-2591-7.
  24. ^ a b c d e f "Advances in Vasodilatory Shock: Emerging Data to Address Current Challenges". Medscape Education. Retrieved 2019-02-08. {{cite web}}: Unknown parameter |authors= ignored (help)
  25. ^ Annane, Djillali; Vignon, Philippe; Renault, Alain; Bollaert, Pierre-Edouard; Charpentier, Claire; Martin, Claude; Troché, Gilles; Ricard, Jean-Damien; Nitenberg, Gérard; Papazian, Laurent; Azoulay, Elie; Bellissant, Eric (2007). "Norepinephrine plus dobutamine versus epinephrine alone for management of septic shock: a randomised trial". The Lancet. 370 (9588): 676–684. doi:10.1016/s0140-6736(07)61344-0. ISSN 0140-6736. PMID 17720019.
  26. ^ Myburgh, JA; Higgins, A; Jovanovska, A; Lipman, J; Ramakrishnan, N; Santamaria, J (2008). "A comparison of epinephrine and norepinephrine in critically ill patients". Intensive Care Medicine. 34 (12): 2226–34. doi:10.1007/s00134-008-1219-0. ISSN 0342-4642. PMID 18654759.
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  28. ^ Levy, Bruno; Fritz, Caroline; Tahon, Elsa; Jacquot, Audrey; Auchet, Thomas; Kimmoun, Antoine (2018-02-27). "Vasoplegia treatments: the past, the present, and the future". Critical Care. 22 (1): 52. doi:10.1186/s13054-018-1967-3. ISSN 1364-8535. PMC 6389278. PMID 29486781.{{cite journal}}: CS1 maint: unflagged free DOI (link)
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