The 68 patients underwent a total of 94 temporary MCS procedures. Twenty-two patients underwent more than one temporary MCS bridging—6 patients with AMI and 16 with ESHF. Twenty-five of the 68 patients suffered complications that required surgical intervention. Two vascular complications led to below-knee amputations, both in patients on VA-ECMO support. Three patients with ESHF (none in the AMI group) suffered severe pulmonary oedema, who required LV decompression. There were no lower limb amputations related to Impella. Twenty, nine, and seven patients were bridged to transplantation, LVAD and recovery respectively. Thirty-five (27 and 8 patients with ESHF and AMI, respectively) of the 68 patients died (including 2 post-transplant and 1 post-LVAD).
To our knowledge, this is the first study to characterize the phenotype of patients with cardiogenic shock based on the aetiology. This study has shown that patients with cardiogenic shock due to ESHF have a phenotype that was distinct from AMI. First, patients with ESHF had lower Hb, which resulted in lower DO2 compared with AMI. Anaemia is well recognized in patients with chronic HF (17), and has been attributed to a number of different causes. Hemodilution may be contributory in a significant proportion of patients (18), and may be relevant in our patients in light of the higher filling pressures and hyponatremia. Other possible causes include antagonism of the renin–angiotensin system (19) (angiotensin II has direct stimulatory effect on bone marrow erythrocyte precursors (20)), coexisting chronic renal impairment (21), and activation of pro-inflammatory cytokines in HF (22) (with consequent inhibition of erythropoiesis (23)).
Third, there were notable differences in base deficits and acidemia between patients with ESHF and AMI. Chloride as a strong anion is a determinant of acid–base balance. Hypochloremia relative to total cations increases strong ion difference with resultant alkalosis and compensated for the accumulation of unmeasured anions, resulting in more modest base deficits and acidemia. Hypochloremia in patients with ESHF in this study is consistent with other reports of patients with advanced HF and likely to be multifactorial (30, 31). Hypochloremia may have a direct pathophysiological role in the modulation of the cardiorenal axis and congestion in HF, as chloride suppresses plasma renin activity via direct action on the macular densa (32), and decreases the availability of both sodium–potassium–chloride cotransporter and sodium chloride cotransporter (33). However, hypochloremia may also be a marker of neurohormonal activation, water retention, and diuretic therapy. Arterial “underfilling” triggers sympathetic activation, renin–angiotensin system, and nonosmotic release of arginine vasopressin, with consequent alteration in renal hemodynamics and water retention (34). In addition, loop diuretics inhibit the sodium-potassium-chloride cotransporter and reduce reabsorption of sodium and chloride, which contributes to hypochloremia (35).
There are a number of notable limitations to this study. First, this is a single-center study with a relatively small number of highly selected patients. Nonetheless, the current study is one of the largest series of meticulously characterized patients with cardiogenic shock due to ESHF. Second, this was not a prospective or randomized study of the timing and/or the modality of MCS. Future studies should evaluate the use of MCS based on the ΔPCO2/C(a-v)O2 ratio. Third, we included only “surgical” complications. Other complications such as bleeding that did not require intervention or infections treated with antimicrobial therapy were not included. Therefore, the impact of these complications on outcome could not be determined.
1. Lim HS, Howell N, Ranasinghe A. Extracorporeal life support physiological concepts and clinical outcomes. J Card Fail
23 2: 181–196, 2017.
2. Morelli A, Ertmer C, Westphal M, Rehberg S, Kampmeier T, Ligges S, Orecchioni A, D’Ippoliti F, Raffone C, Venditti M, et al. Effect of heart rate control with esmolol on hemodynamic and clinical outcomes in patients with septic shock: a randomized clinical trial. JAMA
310 16: 1683–1691, 2013.
3. Hutcheon DE, Vincent ME, Sandhu RS. Renal electrolyte excretion pattern in response to bumetanide in healthy volunteers. J Clin Pharmacol
21 (11–12 pt 2):604–609, 1981.
4. Atkinson TM, Ohman EM, O’Neill WW, Rab T, Cigarroa JE. A practical approach to mechanical circulatory support
in patients undergoing percutaneous coronary intervention. An interventional perspective. JACC Cardiovasc Interv
9 9: 871–873, 2016.
5. Mekontso-Dessap A, Castelain V, Anguel N, Bahloul M, Schauvliege F, Richard C, Teboul JL. Combination of venoarterial PCO2 difference with arteriovenous O2 content difference to detect anaerobic metabolism in patients. Intensive Care Med
28 3: 272–277, 2002.
6. Mallat J, Lemyze M, Meddour M, Pepy F, Gasan G, Barrailler S, Durville E, Temime J, Vangrunderbeeck N, Tronchon L, et al. Ratios of central venous-to-arterial carbon dioxide content or tension to arteriovenous oxygen content are better markers of global anaerobic metabolism than lactate in septic shock patients. Ann Intensive Care
6: 10–18, 2016.
7. Lim HS. The effect of Impella CP on cardiopulmonary physiology during venoarterial extracorporeal membrane oxygenation support. Artif Organs
41 12: 1109–1112, 2017.
8. Wernovsky G, Wypij D, Jonas RA, Mayer JE Jr, Hanley FL, Hickey PR, Walsh AZ, Chang AC, Castaneda AR, Newburger JW, et al. Postoperative course and hemodynamic profile after the arterial switch operation in neonates and infants. A comparison of low-flow cardiopulmonary bypass and circulatory arrest. Circulation
92 8: 2226–2235, 1995.
9. Lim HS, Zaphiriou A. Sodium nitroprusside in patients with mixed pulmonary hypertension and left heart disease: hemodynamic predictors of response and prognostic implications. J Card Fail
22 2: 117–124, 2016.
10. Fincke R, Hochman JS, Lowe AM, Menon V, Slater JM, Webb JG, LeJemtel TH. Cotter G SHOCK Investigators. Cardiac power is the strongest hemodynamic correlated of mortality in cardiogenic shock
: a report from the SHOCK Trial Registry. J Am Coll Cardiol
44 2: 340–348, 2004.
11. Severinghaus JW. Simple, accurate equations for human blood oxygen dissociation computations. J Appl Physiol
46 3: 599–602, 1979.
12. Teboul JL, Scheeren T. Understanding the Haldane effect. Intensive Care Med
43 1: 91–93, 2017.
13. Jakob SM, Groeneveld ABJ, Teboul JL. Venous–arterial CO2 to arterial–venous O2 difference ratio as a resuscitation target in shock states? Intensive Care Med
41 5: 936–938, 2015.
14. Dres M, Monnet X, Teboul JL. Hemodynamic management of cardiovascular failure by using PCO2 venous-arterial difference. J Clin Monit Comput
26 5: 367–374, 2012.
15. Gilfix BM, Bique M, Magder S. A physical chemical approach to the analysis of acid-base balance in the clinical setting. J Crit Care
8 4: 187–197, 1993.
16. Fencl V, Leith DE. Stewart's quantitative acid-base chemistry: applications in biology and medicine. Respir Physiol
91 1: 1–16, 1993.
17. Ezekowitz JA, McAlister FA, Armstrong PW. Anemia is common in heart failure
and is associated with poor outcomes: insights from a cohort of 12 065 patients with new-onset heart failure
107 2: 223–225, 2003.
18. Androne AS, Katz SD, Lund L, LaManca J, Hudaihed A, Hryniewicz K, Mancini DM. Hemodilution is common in patients with advanced heart failure
107 2: 226–229, 2003.
19. Ishani A, Weinhandl E, Zhao Z, Gilbertson DT, Collins AJ, Yusuf S, Herzog CA. Angiotensin-converting enzyme inhibitor as a risk factor for the development of anemia, and the impact of incident anemia on mortality in patients with left ventricular dysfunction. J Am Coll Cardiol
45 3: 391–399, 2005.
20. Mrug M, Stopka T, Julian BA, Prchal JF, Prchal JT. Angiotensin II stimulates proliferation of normal early erythroid progenitors. J Clin Invest
100 9: 2310–2314, 1997.
21. Dries DL, Exner DV, Domanski MJ, Greenberg B, Stevenson LW. The prognostic implications of renal insufficiency in asymptomatic and symptomatic patients with left ventricular systolic dysfunction. J Am Coll Cardiol
35 3: 681–689, 2000.
22. Rauchhaus M, Doehner W, Francis DP, Davos C, Kemp M, Liebenthal C, Niebauer J, Hooper J, Volk HD, Coats AJ, et al. Plasma cytokine parameters and mortality in patients with chronic heart failure
102 25: 3060–3067, 2000.
23. Iversen PO, Woldbaek PR, Tonnessen T, Christensen G. Decreased hematopoiesis in bone marrow of mice with congestive heart failure
. Am J Physiol Regul Integr Comp Physiol
282 1:R166–172, 2002.
24. Metcalfe J, Dhindsa DS, Edwards MJ, Mourdjinis A. Decreased affinity of blood for oxygen in patients with low-output heart failure
. Circ Res
25 1: 47–51, 1969.
25. Bersin RM, Kwasman M, Lau D, Klinski C, Tanaka K, Khorrami P, DeMarco T, Wolfe C, Chatterjee K. Importance of oxygen-hemoglobin binding to oxygen transport in congestive heart failure
. Br Heart J
70 5: 443–447, 1993.
26. Vallet B, Teboul JL, Cain S, Curtis S. Venoarterial CO2 difference during regional ischemic or hypoxic hypoxia. J Appl Physiol
89 4: 1317–1321, 2000.
27. Mallat J, Lemyze M, Meddour M, Pepy F, Gasan G, Barrailler S, Durville E, Temime J, Vangrunderbeeck N, Tronchon L, et al. Ratios of central venous-to-arterial carbon dioxide content or tension to arteriovenous oxygen content are better markers of global anaerobic metabolism than lactate in septic shock patients. Ann Intensive Care
6 1: 10–18, 2016.
28. Garcia-Alvarez M, Marik P, Bellomo R. Stress hyperlactataemia: present understanding and controversy. Lancet Diabetes Endocrinol
2 4: 339–347, 2014.
29. James JH, Luchette FA, McCarter FD, Fischer JE. Lactate is an unreliable indicator of tissue hypoxia in injury or sepsis. Lancet
345 9177: 505–508, 1999.
30. Grodin JL, Simon J, Hachamovitch R, Wu Y, Jackson G, Halkar M, Starling RC, Testani JM, Tang WH. Prognostic role of serum chloride levels in acute decompensated heart failure
. J Am Coll Cardiol
66 6: 659–666, 2015.
31. Grodin JL, Verbrugge FH, Ellis SG, Mullens W, Testani JM, Tang WH. Importance of abnormal chloride homeostasis in stable chronic heart failure
. Circ Heart Fail
9 1:e002453, 2016.
32. Lorenz JN, Kotchen TA, Ott CE. Effect of Na and Cl infusion on loop function and plasma renin activity in rats. Am J Physiol
258 (5 pt 2):F1328–F1335, 1990.
33. Ponce-Coria J, San-Cristobal P, Kahle KT, Vazquez N, Pacheco-Alvarez D, de Los Heros P, Juárez P, Muñoz E, Michel G, Bobadilla NA, et al. Regulation of NKCC2 by a chloride-sensing mechanism involving the WNK3 and SPAK kinases. Proc Natl Acad Sci USA
105 24: 8458–8463, 2008.
34. Schrier RW, Abraham WT. Hormones and hemodynamics in heart failure
. N Engl J Med
341 8: 577–585, 1999.
35. Ellison DH. The physiologic basis of diuretic synergism: its role in treating diuretic resistance. Ann Intern Med
114 10: 886–894, 1991.
36. Musa T, Chue C, Lim HS. Mechanical circulatory support
for decompensated heart failure
. Curr Heart Fail Rep
14 5: 365–375, 2017.
37. Jeger RV, Lowe AM, Buller CE, Pfisterer ME, Dzavik V, Webb JG, Hochman JS, Jorde UP. Investigators SHOCK. Hemodynamic parameters are prognostically important in cardiogenic shock
but similar following early revascularization or initial medical stabilization: a report from the SHOCK trial. Chest
132 6: 1794–1803, 2007.