Jump to content

Vasodilatory shock

From Wikipedia, the free encyclopedia
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 will not 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, catecholamines, ascorbic acid and combinations of thereof.[4][9][10]

Signs and symptoms

[edit]
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

[edit]

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 refractory 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

[edit]

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]

Vasodilatory shock is often involved with the dysfunction of physiologic compensatory mechanisms such as the sympathetic nervous system, vasopressin arginine system and renin-angiotensin aldosterone system.[24]

[5][6]

Diagnosis

[edit]
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

[edit]

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]

[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

[edit]

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

Prognosis

[edit]

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

[edit]
  1. ^ a b Auchet, Thomas; Regnier, Marie-Alix; Girerd, Nicolas; Levy, Bruno (2017-04-20). "Outcome of patients with septic shock and high-dose vasopressor therapy". Annals of Intensive Care. 7 (1): 43. doi:10.1186/s13613-017-0261-x. ISSN 2110-5820. PMC 5397393. PMID 28425079.
  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. S2CID 6900105.
  3. ^ a b c "National Heart, Lung, and Blood Institute (NHLBI)". Cardiogenic Shock. Retrieved 2019-02-07. Public Domain This article incorporates text from this source, which is in the public domain.
  4. ^ a b c d e f g Jentzer, Jacob C.; Vallabhajosyula, Saraschandra; Khanna, Ashish K.; Chawla, Lakhmir S.; Busse, Laurence W.; Kashani, Kianoush B. (2018). "Management of Refractory Vasodilatory Shock". Chest. 154 (2): 416–426. doi:10.1016/j.chest.2017.12.021. ISSN 0012-3692. PMID 29329694. S2CID 206678750.
  5. ^ a b c Gkisioti, S; Mentzelopoulos, SD (2011). "Vasogenic shock physiology". Open Access Emergency Medicine. 3: 1–6. doi:10.2147/OAEM.S10388. ISSN 1179-1500. PMC 4753960. PMID 27147845.
  6. ^ a b c d Lambden, Simon; Creagh-Brown, Ben C.; Hunt, Julie; Summers, Charlotte; Forni, Lui G. (2018-07-06). "Definitions and pathophysiology of vasoplegic shock". Critical Care. 22 (1): 174. doi:10.1186/s13054-018-2102-1. ISSN 1364-8535. PMC 6035427. PMID 29980217.
  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.
  8. ^ Masarwa, Reem; Paret, Gideon; Perlman, Amichai; Reif, Shimon; Raccah, Bruria Hirsh; Matok, Ilan (2017-01-05). "Role of vasopressin and terlipressin in refractory shock compared to conventional therapy in the neonatal and pediatric population: a systematic review, meta-analysis, and trial sequential analysis". Critical Care. 21 (1): 1. doi:10.1186/s13054-016-1589-6. ISSN 1364-8535. PMC 5217634. PMID 28057037.
  9. ^ Khanna, Ashish; English, Shane W.; Wang, Xueyuan S.; Ham, Kealy; Tumlin, James; Szerlip, Harold; Busse, Laurence W.; Altaweel, Laith; Albertson, Timothy E.; Mackey, Caleb; McCurdy, Michael T.; Boldt, David W.; Chock, Stefan; Young, Paul J.; Krell, Kenneth; Wunderink, Richard G.; Ostermann, Marlies; Murugan, Raghavan; Gong, Michelle N.; Panwar, Rakshit; Hästbacka, Johanna; Favory, Raphael; Venkatesh, Balasubramanian; Thompson, B. Taylor; Bellomo, Rinaldo; Jensen, Jeffrey; Kroll, Stew; Chawla, Lakhmir S.; Tidmarsh, George F.; Deane, Adam M. (2017-08-03). "Angiotensin II for the Treatment of Vasodilatory Shock" (PDF). The New England Journal of Medicine. 377 (5): 419–430. doi:10.1056/nejmoa1704154. ISSN 0028-4793. PMID 28528561.
  10. ^ Dünser, M.; Wenzel, V.; Mayr, A. J.; Hasibeder, W. R. (2002-08-01). "Arginin-Vasopressin im vasodilatatorischen Schock". Der Anaesthesist (in German). 51 (8): 650–659. doi:10.1007/s00101-002-0349-y. ISSN 0003-2417. PMID 12391525. S2CID 33545204.
  11. ^ Singer, Mervyn; Deutschman, Clifford S.; Seymour, Christopher Warren; Shankar-Hari, Manu; Annane, Djillali; Bauer, Michael; Bellomo, Rinaldo; Bernard, Gordon R.; Chiche, Jean-Daniel; Coopersmith, Craig M.; Hotchkiss, Richard S.; Levy, Mitchell M.; Marshall, John C.; Martin, Greg S.; Opal, Steven M.; Rubenfeld, Gordon D.; van der Poll, Tom; Vincent, Jean-Louis; Angus, Derek C. (2016-02-23). "The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)". JAMA. 315 (8): 801–10. doi:10.1001/jama.2016.0287. ISSN 0098-7484. PMC 4968574. PMID 26903338.
  12. ^ a b Williams, Felicia N; Herndon, David N; Hawkins, Hal K; Lee, Jong O; Cox, Robert A; Kulp, Gabriela A; Finnerty, Celeste C; Chinkes, David L; Jeschke, Marc G (2009). "The leading causes of death after burn injury in a single pediatric burn center". Critical Care. 13 (6): R183. doi:10.1186/cc8170. ISSN 1364-8535. PMC 2811947. PMID 19919684.
  13. ^ Banks, Peter A; Bollen, Thomas L; Dervenis, Christos; Gooszen, Hein G; Johnson, Colin D; Sarr, Michael G; Tsiotos, Gregory G; Vege, Santhi Swaroop (January 2013). "Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus". Gut. 62 (1): 102–111. doi:10.1136/gutjnl-2012-302779. hdl:11336/29220. ISSN 0017-5749. PMID 23100216.
  14. ^ "Definition, classification, etiology, and pathophysiology of shock in adults". UpToDate. Retrieved 2019-02-07.
  15. ^ a b De Backer, Daniel; Biston, Patrick; Devriendt, Jacques; Madl, Christian; Chochrad, Didier; Aldecoa, Cesar; Brasseur, Alexandre; Defrance, Pierre; Gottignies, Philippe; Vincent, Jean-Louis (2010-03-04). "Comparison of Dopamine and Norepinephrine in the Treatment of Shock". The New England Journal of Medicine. 362 (9): 779–789. doi:10.1056/nejmoa0907118. ISSN 0028-4793. PMID 20200382. S2CID 2208904.
  16. ^ Kheng, Cheah P; Rahman, Nik H (2012-07-24). "The use of end-tidal carbon dioxide monitoring in patients with hypotension in the emergency department". International Journal of Emergency Medicine. 5 (1): 31. doi:10.1186/1865-1380-5-31. ISSN 1865-1380. PMC 3585511. PMID 22828152.
  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.
  18. ^ Sablotzki, Armin; Friedrich, Ivar; Mühling, Jörg; Dehne, Marius G; Spillner, Jan; Silber, Rolf E; Czeslik, Elke (2002). "The systemic inflammatory response syndrome following cardiac surgery: different expression of proinflammatory cytokines and procalcitonin in patients with and without multiorgan dysfunctions". Perfusion. 17 (2): 103–109. doi:10.1177/026765910201700206. ISSN 0267-6591. PMID 11958300. S2CID 208361755.
  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 Timothy E. Albertson. "Advances in Vasodilatory Shock: Emerging Data to Address Current Challenges". Medscape Education. Retrieved 2019-02-08.
  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. S2CID 25225709.
  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. S2CID 27732980.
  27. ^ Wakefield, Brett J.; Sacha, Gretchen L.; Khanna, Ashish K. (2018). "Vasodilatory shock in the ICU and the role of angiotensin II". Current Opinion in Critical Care. 24 (4): 277–285. doi:10.1097/mcc.0000000000000517. ISSN 1070-5295. PMID 29877879. S2CID 46959811.
  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.
  29. ^ Bansal, Beena; Bansal, Manish; Bajpai, Pankaj; Garewal, Hardeep Kaur (2014). "Hypocalcemic Cardiomyopathy—Different Mechanisms in Adult and Pediatric Cases". The Journal of Clinical Endocrinology and Metabolism. 99 (8): 2627–2632. doi:10.1210/jc.2013-3352. ISSN 0021-972X. PMID 24840807.
  30. ^ Ballane, Ghada T; Sfeir, Jad G; Dakik, Habib A; Brown, Edward M; El-Hajj Fuleihan, Ghada (2012). "Use of recombinant human parathyroid hormone in hypocalcemic cardiomyopathy". European Journal of Endocrinology. 166 (6): 1113–1120. doi:10.1530/eje-11-1094. ISSN 0804-4643. PMID 22430263.
  31. ^ Pepe, Jessica; Cipriani, Cristiana; Sonato, Chiara; Raimo, Orlando; Biamonte, Federica; Minisola, Salvatore (2017). "Cardiovascular manifestations of primary hyperparathyroidism: a narrative review". European Journal of Endocrinology. 177 (6): R297–R308. doi:10.1530/eje-17-0485. ISSN 0804-4643. PMID 28864535.
  32. ^ Benbenishty, Julie; Weissman, Charles; Sprung, Charles L.; Brodsky-Israeli, Mali; Weiss, Yoram (2011). "Characteristics of patients receiving vasopressors". Heart & Lung. 40 (3): 247–252. doi:10.1016/j.hrtlng.2010.04.007. ISSN 0147-9563. PMID 20630594.
  33. ^ Jenkins, CR; Gomersall, CD; Leung, P; Joynt, GM (2009). "Outcome of patients receiving high dose vasopressor therapy: a retrospective cohort study". Anaesthesia and Intensive Care. 37 (2): 286–9. doi:10.1177/0310057X0903700212. ISSN 0310-057X. PMID 19400494.
  34. ^ Maheshwari, Kamal; Nathanson, Brian H.; Munson, Sibyl H.; Khangulov, Victor; Stevens, Mitali; Badani, Hussain; Khanna, Ashish K.; Sessler, Daniel I. (2018). "The relationship between ICU hypotension and in-hospital mortality and morbidity in septic patients". Intensive Care Medicine. 44 (6): 857–867. doi:10.1007/s00134-018-5218-5. ISSN 0342-4642. PMC 6013508. PMID 29872882.
Retrieved from "https://en.wikipedia.org/w/index.php?title=Vasodilatory_shock&oldid=1193784096"