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]
Pathophysiologyedit
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]
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].
Referencesedit
^ abAuchet, 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. PMC5397393. PMID 28425079.
^ abVincent, 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.
^ abc"National Heart, Lung, and Blood Institute (NHLBI)". Cardiogenic Shock. Retrieved 2019-02-07. This article incorporates text from this source, which is in the public domain.
^ abcdLambden, 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. PMC6035427. PMID 29980217.
^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. PMC3787628. PMID 24151551.
^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. PMC5217634. PMID 28057037.
^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.
^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.
^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. PMC4968574. PMID 26903338.
^ abWilliams, 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. PMC2811947. PMID 19919684.
^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.
^"Definition, classification, etiology, and pathophysiology of shock in adults". UpToDate. Retrieved 2019-02-07.
^ abDe 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.
^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. PMC3585511. PMID 22828152.
^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.
^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.
^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. PMC6631076. PMID 18256381.
^ abcVallabhajosyula, 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.
^ abcLandry, 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.
^ abcdSilverstein, 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.
^ abcdefTimothy E. Albertson. "Advances in Vasodilatory Shock: Emerging Data to Address Current Challenges". Medscape Education. Retrieved 2019-02-08.
^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.
^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.
^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. doi:10.1177/1074248414559838. ISSN 1074-2484. PMID 25432872. S2CID 26047546.
^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.
^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. PMC6389278. PMID 29486781.
^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.
^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.
^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.