Vasodilatory shock

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Vasodilatory shock
Other namesRefractory vasodilatory shock, refractory shock, irreversible shock, vasogenic shock, or vasoplegic shock.
Specialty Emergency medicine
Complications Multiple organ dysfunction
PreventionEarly recognition and rapid treatment initiation for any types of shock.
Prognosis Higher 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]

Contents

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

[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 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

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

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]

DrugDoseNorepiniphrine equivalent
Epinephrine0.1 μg/Kg/min0.1 μg/Kg/min
Dopamine15 μg/Kg/min0.1 μg/Kg/min
Norepinephrine0.1 μg/Kg/min0.1 μg/Kg/min
Phenylephrine1 μg/Kg/min0.1 μg/Kg/min
Vasopressin0.04 U/Kg/min0.1 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 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

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 ].

Related Research Articles

<span class="mw-page-title-main">Shock (circulatory)</span> Medical condition of insufficient blood flow

Shock is the state of insufficient blood flow to the tissues of the body as a result of problems with the circulatory system. Initial symptoms of shock may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest, as complications worsen.

<span class="mw-page-title-main">Sepsis</span> Life-threatening organ dysfunction triggered by infection

Sepsis is a potentially life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs.

<span class="mw-page-title-main">Vasopressin</span> Mammalian hormone released from the pituitary gland

Human vasopressin, also called antidiuretic hormone (ADH), arginine vasopressin (AVP) or argipressin, is a hormone synthesized from the AVP gene as a peptide prohormone in neurons in the hypothalamus, and is converted to AVP. It then travels down the axon terminating in the posterior pituitary, and is released from vesicles into the circulation in response to extracellular fluid hypertonicity (hyperosmolality). AVP has two primary functions. First, it increases the amount of solute-free water reabsorbed back into the circulation from the filtrate in the kidney tubules of the nephrons. Second, AVP constricts arterioles, which increases peripheral vascular resistance and raises arterial blood pressure.

<span class="mw-page-title-main">Fluid replacement</span>

Fluid replacement or fluid resuscitation is the medical practice of replenishing bodily fluid lost through sweating, bleeding, fluid shifts or other pathologic processes. Fluids can be replaced with oral rehydration therapy (drinking), intravenous therapy, rectally such as with a Murphy drip, or by hypodermoclysis, the direct injection of fluid into the subcutaneous tissue. Fluids administered by the oral and hypodermic routes are absorbed more slowly than those given intravenously.

<span class="mw-page-title-main">Septic shock</span> Dangerously low blood pressure due to damage from an organ infection

Septic shock is a potentially fatal medical condition that occurs when sepsis, which is organ injury or damage in response to infection, leads to dangerously low blood pressure and abnormalities in cellular metabolism. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) defines septic shock as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone. Patients with septic shock can be clinically identified by requiring a vasopressor to maintain a mean arterial pressure of 65 mm Hg or greater and having serum lactate level greater than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia. This combination is associated with hospital mortality rates greater than 40%.

<span class="mw-page-title-main">Hypotension</span> Abnormally low blood pressure

Hypotension is low blood pressure. Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood. Blood pressure is indicated by two numbers, the systolic blood pressure and the diastolic blood pressure, which are the maximum and minimum blood pressures, respectively. A systolic blood pressure of less than 90 millimeters of mercury (mmHg) or diastolic of less than 60 mmHg is generally considered to be hypotension. Different numbers apply to children. However, in practice, blood pressure is considered too low only if noticeable symptoms are present.

In immunology, systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole body. It is the body's response to an infectious or noninfectious insult. Although the definition of SIRS refers to it as an "inflammatory" response, it actually has pro- and anti-inflammatory components.

Multiple organ dysfunction syndrome (MODS) is altered organ function in an acutely ill patient requiring medical intervention to achieve homeostasis.

Hyperchloremia is an electrolyte disturbance in which there is an elevated level of chloride ions in the blood. The normal serum range for chloride is 96 to 106 mEq/L, therefore chloride levels at or above 110 mEq/L usually indicate kidney dysfunction as it is a regulator of chloride concentration. As of now there are no specific symptoms of hyperchloremia; however, it can be influenced by multiple abnormalities that cause a loss of electrolyte-free fluid, loss of hypotonic fluid, or increased administration of sodium chloride. These abnormalities are caused by diarrhea, vomiting, increased sodium chloride intake, renal dysfunction, diuretic use, and diabetes. Hyperchloremia should not be mistaken for hyperchloremic metabolic acidosis as hyperchloremic metabolic acidosis is characterized by two major changes: a decrease in blood pH and bicarbonate levels, as well as an increase in blood chloride levels. Instead those with hyperchloremic metabolic acidosis are usually predisposed to hyperchloremia.

An induced coma – also known as a medically induced coma (MIC), barbiturate-induced coma, or drug-induced coma – is a temporary coma brought on by a controlled dose of an anesthetic drug, often a barbiturate such as pentobarbital or thiopental. Other intravenous anesthetic drugs such as midazolam or propofol may be used.

<span class="mw-page-title-main">Neurogenic shock</span> Insufficient blood flow due to autonomic nervous system damage

Neurogenic shock is a distributive type of shock resulting in hypotension, often with bradycardia, caused by disruption of autonomic nervous system pathways. It can occur after damage to the central nervous system, such as spinal cord injury and traumatic brain injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting from loss of sympathetic tone, which in turn causes blood pooling within the extremities rather than being available to circulate throughout the body. The slowed heart rate results from a vagal response unopposed by a sympathetic nervous system (SNS) response. Such cardiovascular instability is exacerbated by hypoxia, or treatment with endotracheal or endobronchial suction used to prevent pulmonary aspiration.

<span class="mw-page-title-main">Terlipressin</span> Chemical compound

Terlipressin, sold under the brand name Terlivaz among others, is an analogue of vasopressin used as a vasoactive drug in the management of low blood pressure. It has been found to be effective when norepinephrine does not help. Terlipressin is a vasopressin receptor agonist.

Distributive shock is a medical condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate supply of blood to the body's tissues and organs. It is one of four categories of shock, a condition where there is not enough oxygen-carrying blood to meet the metabolic needs of the cells which make up the body's tissues and organs. Distributive shock is different from the other three categories of shock in that it occurs even though the output of the heart is at or above a normal level. The most common cause is sepsis leading to a type of distributive shock called septic shock, a condition that can be fatal.

The Surviving Sepsis Campaign (SSC) is a global initiative to bring together professional organizations in reducing mortality from sepsis. The purpose of the SSC is to create an international collaborative effort to improve the treatment of sepsis and reduce the high mortality rate associated with the condition. The Surviving Sepsis Campaign and the Institute for Healthcare Improvement have teamed up to achieve a 25 percent reduction in sepsis mortality by 2009. The guidelines were updated in 2016 and again in 2021.

Critical illness–related corticosteroid insufficiency is a form of adrenal insufficiency in critically ill patients who have blood corticosteroid levels which are inadequate for the severe stress response they experience. Combined with decreased glucocorticoid receptor sensitivity and tissue response to corticosteroids, this adrenal insufficiency constitutes a negative prognostic factor for intensive care patients.

<span class="mw-page-title-main">Tricyclic antidepressant overdose</span> Medical condition

Tricyclic antidepressant overdose is poisoning caused by excessive medication of the tricyclic antidepressant (TCA) type. Symptoms may include elevated body temperature, blurred vision, dilated pupils, sleepiness, confusion, seizures, rapid heart rate, and cardiac arrest. If symptoms have not occurred within six hours of exposure they are unlikely to occur.

<span class="mw-page-title-main">Norepinephrine (medication)</span> Therapeutic use of norepinephrine

Norepinephrine, also known as noradrenaline, is a medication used to treat people with very low blood pressure. It is the typical medication used in sepsis if low blood pressure does not improve following intravenous fluids. It is the same molecule as the hormone and neurotransmitter norepinephrine. It is given by slow injection into a vein.

<span class="mw-page-title-main">Dopamine (medication)</span> Hormone used as a medication

Dopamine, sold under the brandname Intropin among others, is a medication most commonly used in the treatment of very low blood pressure, a slow heart rate that is causing symptoms, and, if epinephrine is not available, cardiac arrest. In newborn babies it continues to be the preferred treatment for very low blood pressure. In children epinephrine or norepinephrine is generally preferred while in adults norepinephrine is generally preferred for very low blood pressure. It is given intravenously or intraosseously as a continuous infusion. Effects typically begin within five minutes. Doses are then increased to effect.

<span class="mw-page-title-main">Vasopressin (medication)</span> Chemical compound

Vasopressin infusions are in use for septic shock patients not responding to fluid resuscitation or infusions of catecholamines to increase the blood pressure while sparing the use of catecholamines. These argipressins have much shorter elimination half-life than synthetic non-arginine vasopresines with much longer elimination half-life of many hours. Further, argipressins act on V1a, V1b, and V2 receptors which consequently lead to higher eGFR and lower vascular resistance in the lungs. A number of injectable arginine vasopressins are in clinical use in the United States and the European Union. Pitressin among others, is a medication most commonly used in the treatment of frequent urination, increased thirst, and dehydration such as that resulting from diabetes insipidus, which causes increased and diluted urine. It is used to treat abdominal distension following some surgeries, and in stomach roentgenography. Vasopressin is a hormone that affects the kidneys and reduces urine flow.

<span class="mw-page-title-main">Angiotensin II (medication)</span> Treatment for low blood pressure

Angiotensin II is a medication that is used to treat hypotension resulting from septic shock or other distributive shock. It is a synthetic vasoconstrictor peptide that is identical to human hormone angiotensin II and is marketed under the brand name Giapreza. The Food and Drug Administration approved the use of angiotensin II in December 2017 to treat low blood pressure resulting from septic shock.

References

  1. 1 2 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. 1 2 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. 1 2 3 "National Heart, Lung, and Blood Institute (NHLBI)". Cardiogenic Shock. Retrieved 2019-02-07.PD-icon.svg This article incorporates text from this source, which is in the public domain .
  4. 1 2 3 4 5 6 7 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. 1 2 3 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. 1 2 3 4 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. 1 2 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. 1 2 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. 1 2 3 4 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. 1 2 3 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. 1 2 3 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. 1 2 3 4 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. 1 2 3 4 5 6 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.
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