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Communications to the Editor |

Cardiogenic Shock : Nothing Has Changed FREE TO VIEW

Aaron Joffe, DO
Author and Funding Information

Affiliations: St. Franicis Medical Center, Honolulu, HI,  *Erasme University Hospital, Brussels, Belgium

Correspondence to: Aaron Joffe, DO, Staff Intensivist, St. Franicis Medical Center, 2230 Liliha St, Honolulu, HI 96817; e-mail: doctrj@pol.net



Chest. 2004;126(2):652-653. doi:10.1378/chest.126.2.652
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To the Editor:

In the November 2003 issue of CHEST, Lim and colleagues1suggest that some patients initially presenting with cardiogenic shock actually succumb to a form of distributive shock. The idea of altered gut permeability and bacterial translocation in cardiogenic shock is not new. Brunkhorst et al2 reported patients presenting with cardiogenic shock surviving > 12 h were found to have elevated levels of procalcitonin, neopterin, tumor necrosis factor-α, interleukin-6, and C-reactive protein, suggesting exposure to bacterial endotoxin presumed to be of gut origin. However, evidence for this phenomenon in the patients reported by Lim et al1 is lacking and is not supported by the hemodynamic data. Using data presented in Table 2 of the article by Lim et al,1 stroke volume index and left ventricular stroke work index can be calculated. In addition, interpretation of the hemodynamic data within a “per-beat” rather than traditional “per-minute” framework using stroke systemic vascular resistance index in place of systemic vascular resistance index allows a more accurate assessment of the state of vasoactivity as the cardiac index used in the systemic vascular resistance index equation already includes chronotropic compensation by the heart rate.3The true nature of shock in both the low and normalized cardiac index groups is shown in Table 1 , and they are the same. All patients are hypodynamic (low stroke volume index), hypocontractile (low left ventricular stroke work index), and vasoconstricted (high stroke systemic vascular resistance index), a state compatible with progressive failure of the left ventricular pump. Not surprisingly, the younger normalized cardiac index group was better chronotropically compensated achieving heart rates of 5 to 17% in excess of their older low cardiac index counterparts. Both groups, however, achieved similar percentages of their age-predicted maximum heart rate, suggesting chronotropic competence appropriate for their age (Table 1). Although the difference in heart rate between groups did not reach statistical significance, the difference is clinically significant as elevated heart rate engenders proportional increases in cardiac index given a constant stroke volume index. Other than cardiac index, no other measure of myocardial function was returned to even near normal despite maximal therapy. Thus, it would appear both the low and normalized cardiac index groups represent one group exhibiting a narrow spectrum of hemodynamic derangements within the same clinical entity, cardiogenic shock, and succumb to the so-called downward spiral after all. Any thought to the contrary would be real “hubris”4 indeed.

Table Graphic Jump Location
Table 1. Hemodynamics in Nonsurvivors With Low and Normalized Cardiac Index*
* 

LVSWI = left ventricular stroke work index; SSVRI = stroke systemic vascular resistance index.

Lim, N, Dubois, MJ, De Backer, D, et al (2003) Do all nonsurvivors of cardiogenic shock die with a low cardiac index?Chest124,1885-1891. [CrossRef] [PubMed]
 
Brunkhorst, FM, Clark, AL, Forycki, ZF, et al Pyrexia, procalcitonin, immune activation and survival in cardiogenic shock: the potential importance of bacterial translocation.Int J Cardiol1999;72,3-10. [CrossRef] [PubMed]
 
Scardo, J, Kiser, R, Dillon, A, et al Hemodynamic comparison of mild and severe preeclampsia: concept of stroke systemic vascular resistance index.J Matern Fetal Med1996;5,268-272. [CrossRef] [PubMed]
 
Puri, VK Cardiogenic shock: what has changed?Chest2003;124,1634-1636. [CrossRef] [PubMed]
 
To the Editor:

We thank Dr. Joffe for his comments on our article. Although interesting, the concept of single-beat analysis should be regarded with caution. We strongly disagree with Dr. Joffe’s hypothesis suggesting that most of the differences can be explained by differences in heart rate. Indeed, this would imply that stroke volume was lower or equal, but surely not higher, in the high cardiac index group. However, we observed just the reverse: stroke index decreased over time by 9% in the low cardiac index group, while it increased by 38% in the normalized cardiac index group. In addition, heart rate decreased over time in the normalized cardiac index group, while it was stable in the low cardiac index group. Finally, the stroke systemic vascular resistance index, a parameter of doubtful value, proposed by Dr. Joffe (Table 1 of his letter) was stable in the low cardiac index group but decreased by 33% in the normalized cardiac index group. Altogether, these data are in accordance with the observation that 9 of the 23 nonsurvivors acquired hyperdynamic shock, excluding pump failure as the primary cause of death. Other mechanisms, including endotoxin and cytokine release, and excessive nitric oxide release leading to peroxinitrite formation may also explain why these patients present pronounced microcirculatory alterations,12 which are more severe in nonsurviving than in surviving patients,2 and are remarkably similar to those observed in patients with septic shock.12

References
Kirschenbaum, LA, Astiz, ME, Rackow, EC, et al Microvascular response in patients with cardiogenic shock.Crit Care Med2000;28,1290-1294. [CrossRef] [PubMed]
 
De Backer, D, Creteur, J, Dubois, MJ, et al Microvascular alterations in patients with acute severe heart failure and cardiogenic shock.Am Heart J2004;147,91-99. [CrossRef] [PubMed]
 

Figures

Tables

Table Graphic Jump Location
Table 1. Hemodynamics in Nonsurvivors With Low and Normalized Cardiac Index*
* 

LVSWI = left ventricular stroke work index; SSVRI = stroke systemic vascular resistance index.

References

Lim, N, Dubois, MJ, De Backer, D, et al (2003) Do all nonsurvivors of cardiogenic shock die with a low cardiac index?Chest124,1885-1891. [CrossRef] [PubMed]
 
Brunkhorst, FM, Clark, AL, Forycki, ZF, et al Pyrexia, procalcitonin, immune activation and survival in cardiogenic shock: the potential importance of bacterial translocation.Int J Cardiol1999;72,3-10. [CrossRef] [PubMed]
 
Scardo, J, Kiser, R, Dillon, A, et al Hemodynamic comparison of mild and severe preeclampsia: concept of stroke systemic vascular resistance index.J Matern Fetal Med1996;5,268-272. [CrossRef] [PubMed]
 
Puri, VK Cardiogenic shock: what has changed?Chest2003;124,1634-1636. [CrossRef] [PubMed]
 
Kirschenbaum, LA, Astiz, ME, Rackow, EC, et al Microvascular response in patients with cardiogenic shock.Crit Care Med2000;28,1290-1294. [CrossRef] [PubMed]
 
De Backer, D, Creteur, J, Dubois, MJ, et al Microvascular alterations in patients with acute severe heart failure and cardiogenic shock.Am Heart J2004;147,91-99. [CrossRef] [PubMed]
 
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