SHOCK, Vol. 50, No. 2, pp.

167–172, 2018

CARDIOGENIC SHOCK DUE TO END-STAGE HEART FAILURE AND ACUTE

MYOCARDIAL INFARCTION: CHARACTERISTICS AND OUTCOME OF
TEMPORARY MECHANICAL CIRCULATORY SUPPORT

Hoong Sern Lim and Neil Howell

University Hospital Birmingham, Edgbaston, Birmingham, UK

Received 22 Jul 2017; first review completed 7 Sep 2017; accepted in final form 27 Oct 2017

ABSTRACT—Background: Mechanical circulatory support (MCS) is increasingly used in cardiogenic shock, but outcomes
may differ between patients with acute myocardial infarction (AMI) or end-stage heart failure (ESHF). This study aimed to
describe the characteristics of patients with cardiogenic shock due to AMI and ESHF. Methods: Single-center study of
consecutive patients with cardiogenic shock due to AMI (n ¼ 26) and ESHF (n ¼ 42) who underwent MCS (extracorporeal life
support, Impella or temporary ventricular assist devices). Arterial and venous O2 content and CO2 tension (PCO2), O2-
hemoglobin affinity (P50) were measured. Veno-arterial difference in PCO2/arterio-venous difference in O2 content ratio was
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derived. Acid–base balance was characterized by the Gilfix method. MCS-related complications that required intervention or
surgery were collected. Results: Patients with ESHF had lower ejection fraction, higher right and left-sided filling pressures,
pulmonary artery pressure and vascular resistance, lower oxygen delivery (DO2) compared with AMI, which was not fully
compensated by the increased hemoglobin P50. As a result, patients with ESHF had higher veno-arterial difference in PCO2
relative to arterio-venous difference in O2 content. Despite greater anerobic metabolism, patients with ESHF had less severe
metabolic acidosis and base deficit compared with AMI, predominantly due to differences in strong ions. Conclusion: The
cardiogenic shock phenotype in ESHF was distinct from AMI, characterized by higher filling and pulmonary artery pressures,
lower DO2, greater anaerobic metabolism but less severe metabolic acidosis.
KEYWORDS—Cardiogenic shock, heart failure, mechanical circulatory support

INTRODUCTION oxygen (O2) content difference (5, 6) may be a more reliable

Temporary mechanical circulatory support (MCS) such as
Impella, veno-arteral extracorporeal membrane oxygenation
(VA-ECMO), and surgical temporary ventricular assist devices
are increasingly used to bridge patients with cardiogenic shock
to recovery, transplantation or durable left ventricular assist
devices (LVAD). However, outcomes are highly variable in part
due to variability in patient selection (1). Hemodynamic and
metabolic differences between patients with cardiogenic shock
of different aetiology, such as acute myocardial infarction
(AMI) and end-stage chronic heart failure (ESHF) due to an
underlying ischemic or nonischemic cardiomyopathy may
contribute to the variability in outcomes, as the chronicity in
the latter may allow the development of compensatory mecha-
nisms in the face of long-standing low cardiac output; ubiqui-
tous use of neurohormonal antagonists in ESHF may blunt the
response to shock (2); and chronic high dose diuretic therapy
also contributes to metabolic abnormalities (3), which may be
absent in AMI. However, there are limited data on the cardio-
genic shock phenotype based on the aetiology (ESHF and
AMI). Therefore, the objective of this study was to characterize
patients with cardiogenic shock due to ESHF and AMI. Hemo-
dynamic and metabolic (lactate) parameters are often used as
surrogates of hypoperfusion (4), but the ratio of veno-arterial
carbon dioxide tension (PCO2) difference to arteriovenous
Address reprint requests to Hoong Sern Lim, MD, Queen Elizabeth Hospital
Birmingham, University Hospital Birmingham NHS Foundation Trust, Edgbaston,
Birmingham, UK. E-mail: sern.lim@uhb.nhs.uk
The authors report no conflicts of interest.
DOI: 10.1097/SHK.0000000000001052
Copyright ß 2017 by the Shock Society
measure of anaerobic metabolism, although this parameter has
not been studied in cardiogenic shock. Hence, we aimed to
characterize these metabolic metabolic parameters that are
typically associated with anaerobic metabolism in patients with
cardiogenic shock due to ESHF and AMI.
METHODS
Study design and patient population
This single-center study included consecutive patients with severe cardio-
genic shock due to AMI or ESHF, who underwent MCS from January 2012 to
January 2016. The following patients were included: cardiogenic shock fol-
lowing acute myocardial infarction with or without ST-segment elevation (AMI
group); and cardiogenic shock in patients with established heart failure and
reduced left ventricular ejection fraction (LVEF) (an end-stage cardiomyopathy
or ESHF group). The following patients were excluded from this study: patients
with mechanical complication from AMI, cardiogenic shock of other aetiology
and/or MCS for other indications (e.g., post-cardiotomy or post-transplant graft
dysfunction) (Fig. 1).
In our institution, MCS are used in patients with cardiogenic shock to bridge
patients to decision, candidacy or in some cases to directly bridge to heart
transplantation or LVAD following multidisciplinary team discussion. Patients
with worsening cardiogenic shock with mean arterial blood pressure of <60
mm Hg, end-organ hypoperfusion, cardiac index of less than 2.0 Lmin1m2
and right atrial and pulmonary-capillary occlusion pressure of at least 10 mm
Hg and 20 mm Hg respectively despite escalating inotropes/vasopressors would
be considered for MCS. Vascular access for Impella CP and/or VA-ECMO was
obtained via the femoral vessels in all cases, with a distal perfusion cannula
routinely inserted with VA-ECMO as previously described (7). Surgical MCS
were achieved by sternotomy and direct cannulation of the right atrium and
pulmonary artery (right ventricular support), and LV and aorta (LV support).
The inotrope score was used to quantify support from vasoactive drugs
(Inotrope score¼ doses of dopamine þ dobutamine in mgkg1min1 þ [(epi-
nephrine þ norepinephrine þ isoproterenol in mgkg1min1)  100] þ [milri-
none mgkg1min1  15]) (8). Specific MCS-related complications that were
evaluated in this study included (ischemic or hemorrhagic) strokes and compli-
cations that required surgical/procedural interventions: bleeding requiring
reopening or wound exploration, device failure, surgical/percutaneous venting
of the LV due to severe pulmonary oedema, vascular complications that required

167
Copyright © 2017 by the Shock Society. Unauthorized reproduction of this article is prohibited.
168 SHOCK VOL. 50, No. 2
FIG. 1. Study patients.
surgery including amputation and hemolysis resulting in renal failure that required
device manipulation/removal.
Pulmonary artery catheter studies
Pulmonary artery catheters were used routinely in all patients with cardio-
genic shock under consideration for MCS. Pulmonary hemodynamic data
including right atrial (RAP), pulmonary artery systolic (PASP), diastolic
(PADP) and mean (mPAP), and pulmonary artery occlusion (PAOP) pressures
were measured as previously described (9). Cardiac output was taken as the
mean of three thermodilution measurements and indexed for BSA (cardiac
index, CI). Cardiac power index was calculated as the product of mean arterial
blood pressure and CI divided by 451 (10). Pulmonary vascular resistance
(PVR) was calculated as the ratio of transpulmonary gradient and CO.
Pulmonary capacitance (PCap) was the stroke volume divided by pulmonary
pulse pressure.
Blood gas analyses oxygen delivery
Immediately before or after completion of thermodilution measurements,
arterial and mixed venous blood samples were drawn together at the same time
for the determination of arterial oxygen tension (PaO2), arterial carbon dioxide
tension (PaCO2), mixed venous oxygen (PvO2) and carbon dioxide tension
(PvCO2), arterial (SaO2) and mixed venous oxygen saturation (SvO2). Hemo-
globin (Hb) concentration was also measured. Oxygen–hemoglobin affinity
was expressed as the oxygen tension at which blood is 50% saturated with
oxygen (P50). The P50 was calculated from the measured oxygen saturation and
oxygen tension of mixed venous blood by the Severinghaus method (11).
The following parameters were derived from these measurements:
 Arterial blood oxygen content: CaO2¼(1.34SaO2Hb)þ
(0.003PaO2)
 Mixed venous blood oxygen content: CvO2¼(1.34
SvO2Hb)þ(0.003PvO2)
 Arterial-venous oxygen content difference: C(a-v)O2¼
CaO2 –CvO2
 Oxygen delivery: DO2¼cardiac output  CaO2
 Oxygen extraction ratio: O2ER¼(CaO2 –CvO2)/CaO2
 Carbon dioxide tension difference: DPCO2¼PvCO2 –PaCO2
Copyright © 2017 by the Shock Society. Unauthorized reproduction of this article is prohibited.
LIM AND HOWELL
Global O2 consumption (VO2) reduces under conditions of tissue hypoxia,
which results in corresponding reduction in aerobic CO2 production. However,
anaerobic CO2 production continues mostly through buffering of excess protons
by bicarbonate ions. Thus, total CO2 production (VCO2) is reduced to a lesser
extent compared to the reduction in O2 consumption, resulting in an increase in
the VCO2/VO2 ratio under hypoxic conditions. According to the Fick equation,
VO2 is the product of CO and arterio-venous O2 content difference (C(a-v)O2),
and VCO2 similarly is the product of CO and veno-arterial CO2 content
difference (C(v-a)CO2). Hence, the VCO2/VO2 ratio can be expressed as the
ratio of C(v-a)CO2/C(a-v)O2. CO2 content has a curvilinear relationship to CO2
tension (PCO2), and this relationship is affected by O2 saturation (Haldane
effect) and acidosis (12). CO2 content is further increased at low flow states due
to the phenomenon of CO2 stagnation. At higher CO2 content, the CO2 content–
PCO2 relationship flattens, resulting in greater PCO2 per unit change in CO2
content. In this study, we used CO2 tension difference (DPCO2) as a surrogate
for C(v-a)CO2, as: CO2 tension is linearly related to CO2 content over the
physiological range (steep part of the CO2 dissociation curve), DPCO2 is greater
at low output states, and calculation of CO2 content is cumbersome and more
susceptible to error (13). By extension the ratio of DPCO2/C(a-v)O2 ratio was
used as a marker of global anaerobic metabolism (14).
Acid–base quantification
We quantified the metabolic acid–base disorder in cardiogenic shock using
the base-excess (BE) method described by Gilfix et al. (15), which was based on
the fundamental principles of Stewart physicochemical model (16). In brief, the
physicochemical model identified strong ions, weak acids, and partial pressure
of CO2 as the three independent determinants of acid–base disorders. Accord-
ingly, the Gilfix method proposed that non-respiratory acid–base disturbances
may be attributed to: changes in strong ions due to free water deficit or excess
(determined by changes in sodium concentration) and changes in chloride (Cl)
concentration; changes in protein charges (mainly albumin); and presence of
organic unmeasured anions. Hence,
BEmeas ¼ BEfw þ BECl þ BEalb þ BEXA
where BEmeas is the measured BE;
BEfw is the free water-related BE ¼ 0.3  ([Na]-140);
BECl is the chloride-related BE ¼ 102-corrected Cl;
(corrected Cl ¼ (140/[Na])  [Cl])
BEalb is the albumin-related BE ¼ 0.34  (42-[Albumin])
SHOCK AUGUST 2018
Statistical analysis
Continuous variables are reported as mean  standard deviation (SD) or median
(interquartile range, IQR) and categorical variables as proportions. Characteristics of
the 2 groups of patients (AMI and ESHF) were compared by t test or Mann–
Whitney
U test for parametric and non-parametric data respectively. Fisher exact test was
used for categorical variables. All statistical analyses were performed using R
(version 3.1.1) and a two-sided P value of <0.05 was considered statistically
significant.
RESULTS
This study included 68 patients (26 AMI and 42 ESHF) with
cardiogenic shock who underwent MCS. Of the 42 patients with
ESHF, 12 and 30 patients had underlying ischemic and non-
ischemic dilated cardiomyopathy respectively. The causes of the
nonischemic cardiomyopathy were idiopathic in the majority
(28/30) and chemotherapy-related in the remaining 2 patients.
The median duration of heart failure was 19 (17–23) months. All
the patients with AMI underwent percutaneous revascularization
to the left anterior descending artery, and additional intervention
to the left main stem in three patients and at least one other
coronary artery in eight patients. Patients with ESHF had lower
LVEF but no significant difference in CI or cardiac power index
compared with patients with AMI (Table 1). Right and left-sided
filling pressures and pulmonary artery pressures were higher in
patients with ESHF compared with AMI (Fig. 2), resulting
in higher pulmonary vascular resistance (3.72  0.52 vs
2.23  0.23 WU, P < 0.001) and lower pulmonary capacitance
CARDIOGENIC SHOCK OUTCOME 169
(1.33  0.20 vs 2.18  0.28 mL/mm Hg, P < 0.001). A greater
proportion of patients with ESHF were supported with biven-
tricular assist devices.
There were also differences in acid–base balance due to
differences in strong ions, albumin, and unmeasured anions
between patients with ESHF and AMI (Table 2). Patients with
cardiogenic shock due to ESHF had greater ‘‘dilutional acido-
sis’’ (excess-free water) and unmeasured anions, which were
balanced by hypochloremic alkalosis and hypoalbuminemia,
resulting in relatively modest acidemia. In contrast, patients
with cardiogenic shock due to AMI had greater acidemia driven
largely by unmeasured anions (Fig. 3).
Oxygen delivery, DPCO2/C(a-v)O2 ratio, and clinical
outcomes
Global oxygen delivery, DO2 was lower in patients with ESHF
due to lower Hb. The lower DO2 in ESHF was partly compen-
sated by greater O2 extraction, facilitated by the higher P50
(Table 3). DO2 was inversely related to P50 (r ¼ 0.563,
P < 0.001) in patients with ESHF. The veno-arterial PCO2
difference was greater in patients with ESHF, primarily due to
higher venous PCO2. The higher PCO2 gradient, coupled with
greater O2 extraction, resulted in significantly higher DPCO2/
C(a-v)O2 ratio in patients with ESHF compared with AMI. The
DPCO2/C(a-v)O2 ratio correlated with lactate (r ¼ 0.290,
P ¼ 0.016) and inversely with DO2 (r ¼ 0.550, P < 0.001),
but no significant correlation with cardiac power index.

TABLE 1. Baseline characteristics

AMI (n ¼ 26) ESHF (n ¼ 42) P

Age (years) 44  5 40  5 0.223

Males (n, %) 16 (62) 25 (60) 0.869
Body mass index (kg/m2) 25.6  1.6 24.8  1.2 0.419
Atrial fibrillation (n, %) 4 (15) 13 (31) 0.150
Diabetes mellitus (n, %) 6 (23) 6 (14) 0.355
Cardiac arrest (n, %) 7 (27) 7 (17) 0.309
Ventilated (n, %) 13 (50) 13 (31) 0.116
IABP (n, %) 19 (73) 18 (43) 0.015
Furosemide (mg/d) 49  19 168  18 <0.001
Inotrope score 24.0  2.5 22.5  2.2 0.358
Systolic blood pressure (mm Hg) 72  3 75  3 0.267
Mean arterial pressure (mm Hg) 58  3 57  2 0.602
Heart rate (beats/min) 110  4 108  4 0.399
LVEF (%) 25  3 13  2 <0.001
Cardiac index (L/min/m2) 1.87  0.09 1.81  0.08 0.350
Cardiac power index (W/m2) 0.24  0.02 0.23  0.02 0.315
Lactate (mmol/L) 7.1  0.6 6.4  0.5 0.093
Primary support modality (n, %) 0.043
Impella 5 (20) 3 (7)
VA ECMO 13 (50) 17 (40)
ImpellaþECMO 4 (15) 3 (7)
BIVAD 4 (15) 19 (46)
>1 modality (n, %) 6 (23) 16 (38) 0.198
Duration of support (days) 7 (3–19) 16 (7–26) 0.051
Complications (n, %) 7 (27) 18 (43) 0.185
Vascular 4 6
Pulmonary oedema 0 3
Device failure 1 0
Hemolysis 0 2
Bleeding 2 7
BIVAD indicates biventricular assist device; IABP, intra-aortic balloon pump; VA ECMO, veno-arterial extracorporeal membrane oxygenation.

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170 SHOCK VOL. 50, No. 2 LIM AND HOWELL

FIG. 3. Quantification of base excess/deficit in patients with cardio-

genic shock due to ESHF and AMI. BE (alb) indicates base excess due to
changes in albumin; BE (Cl), base excess due to changes in chloride; BE
FIG. 2. Pulmonary hemodynamics in patients with AMI and ESHF. (FW), base excess due to changes in free water; BE (XA), base excess due to
changes in unmeasured anions; BE, base excess.

Clinical outcomes of pro-inflammatory cytokines in HF (22) (with consequent

The 68 patients underwent a total of 94 temporary MCS inhibition of erythropoiesis (23)).
procedures. Twenty-two patients underwent more than one Second, the lower DO2 that was partially compensated by
temporary MCS bridging—6 patients with AMI and 16 with increased O2 extraction. Reduced oxygen–hemoglobin affinity
ESHF. Twenty-five of the 68 patients suffered complications is a recognized compensatory mechanism in HF, facilitated by
that required surgical intervention. Two vascular complications increase in 2,3 diphosphoglycerate (24, 25). However, this
led to below-knee amputations, both in patients on VA-ECMO adaptive response could not fully compensate for the marked
support. Three patients with ESHF (none in the AMI group) reduction in DO2, which was associated with higher DPCO2/
suffered severe pulmonary oedema, who required LV decom- C(a-v)O2 ratio. The higher DPCO2/C(a-v)O2 ratio was, to a
pression. There were no lower limb amputations related to large extent, related to higher PvCO2. The higher PvCO2 is
Impella. Twenty, nine, and seven patients were bridged to likely to be multifactorial. Regional differences in blood flow
transplantation, LVAD and recovery respectively. Thirty-five and perfusion are common in shocked states, and low flow and
(27 and 8 patients with ESHF and AMI, respectively) of the hypoperfused regions may contribute disproportionately to
68 patients died (including 2 post-transplant and 1 post-LVAD). increased CO2 content due to the combination of acidosis,
CO2 stagnation, and the Haldane effect (26). The CO2 content–
PCO2 relationship is relatively flat at higher CO2 content
DISCUSSION
levels, which results in further disproportionate increase in
To our knowledge, this is the first study to characterize the PCO2. Differences in CO2 production may also be contributory
phenotype of patients with cardiogenic shock based on the and cannot be excluded in the absence of direct CO2
aetiology. This study has shown that patients with cardiogenic production measurements.
shock due to ESHF have a phenotype that was distinct from
AMI. First, patients with ESHF had lower Hb, which resulted in TABLE 3. Oxygen and carbon dioxide measurements
lower DO2 compared with AMI. Anaemia is well recognized in AMI (n ¼ 26) ESHF (n ¼ 42) P
patients with chronic HF (17), and has been attributed to a Hemoglobin (g/dL) 13.6  0.2 11.0  0.3 <0.001
number of different causes. Hemodilution may be contributory CaO2 (ml O2/dL) 18.5  0.3 14.9  0.4 <0.001
in a significant proportion of patients (18), and may be relevant DO2 (ml O2/L/min) 642  33 511  23 <0.001
in our patients in light of the higher filling pressures and SvO2 (%) 44.3  2.9 35.6  2.2 <0.001
hyponatremia. Other possible causes include antagonism of CvO2 (ml O2/dL) 8.1  0.5 5.3  0.3 <0.001
DO2 content (mL O2/dL) 10.3  0.6 9.6  0.4 0.071
the renin–angiotensin system (19) (angiotensin II has direct O2 extraction ratio 56  3 64  3 <0.001
stimulatory effect on bone marrow erythrocyte precursors P50 (mm Hg) 27.3  0.4 31.7  0.6 <0.001
(20)), coexisting chronic renal impairment (21), and activation PaCO2 (mm Hg) 38.2  1.5 39.9  1.4 0.098
PvCO2 (mm Hg) 50.6  1.3 55.1  1.2 <0.001
DPCO2 (mm Hg) 12.4  0.4 15.2  0.4 <0.001
TABLE 2. Strong ions and acid–base balance DPCO2 /DO2 content 1.22  0.07 1.61  0.09 <0.001
(mm Hg/ ml O2/dL)
AMI (n ¼ 26) ESHF (n ¼ 42) P
CaO2 indicates arterial oxygen content; DO2, global oxygen delivery;
pH 7.20  0.02 7.32  0.09 <0.001 SvO2, mixed venous oxygen saturation; CvO2, mixed venous oxygen
Na (mmol/L) 137.2  1.0 129.7  1.1 <0.001 content; DO2 content, arterio-venous difference in oxygen content;
Cl (mmol/L) 101.9  1.0 91.9  0.8 <0.001 PaCO2, arterial partial pressure of carbon dioxide; PvCO2, mixed
Albumin (g/L) 35.3  1.5 31.6  0.7 <0.001 venous partial pressure of carbon dioxide; DPCO2, veno-arterial
difference in partial pressure of carbon dioxide; DPCO2 /DO2 content,
BE -9.1  0.8 -4.1  0.6 <0.001
ratio of veno-arterial difference in partial pressure of carbon dioxide and
BE indicates base excess; Cl, chloride; Na, sodium. arterio-venous difference in oxygen content.

Copyright © 2017 by the Shock Society. Unauthorized reproduction of this article is prohibited.
SHOCK AUGUST 2018
Based on previous studies (27), higher DPCO2/C(a-v)O2
ratio would suggest greater anaerobic metabolism. The finding
of lower lactate levels in patients with ESHF compared with
AMI may appear inconsistent with this suggestion of greater
anaerobic metabolism. However, lactatemia may not simply
reflect anaerobic glycolysis. Indeed, adrenergic stimulation
with catecholamines and beta-blocker therapy are associated
with increase and decrease in lactatemia respectively (28, 29).
It is possible that neurohormonal antagonists and beta-blocker
use in patients with ESHF may have contributed to the lower
lactatemia in ESHF.
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. Hypo-
chloremia 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 cardi-
orenal 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 activa-
tion, water retention, and diuretic therapy. Arterial ‘‘underfill-
ing’’ 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).
Our approach to MCS in severe cardiogenic shock has previ-
ously been described (36). The pulmonary hemodynamics in
patients with AMI described in our study are comparable to that
reported by the SHOCK trial (37), indicating dominant left
ventricular failure. In contrast, patients with ESHF had more
severe biventricular dysfunction. The more severe right heart
failure is evidenced by the higher right-sided filling pressures,
which may be related to chronic elevation in pulmonary vascular
resistance. As a result, biventricular support modalities were
used more frequently in patients with ESHF. The more invasive
biventricular support may have contributed to the higher inci-
dence of vascular and bleeding complications and the poorer
outcomes in ESHF. In addition, more patients with ESHF
underwent multiple MCS bridging, as none of the patients
demonstrated recovery of cardiac function, unlike some of the
patients with AMI. These differences highlight the complexities
of MCS in patients with ESHF compared with AMI.
Study limitations
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 prospec-
tive or randomized study of the timing and/or the modality of
Copyright © 2017 by the Shock Society. Unauthorized reproduction of this article is prohibited.
CARDIOGENIC SHOCK OUTCOME 171
MCS. Future studies should evaluate the use of MCS based on the
DPCO2/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.
CONCLUSION
Patients with cardiogenic shock due to ESHF have a phe-
notype that is distinct from AMI, characterized by higher filling
and pulmonary artery pressures, lower DO2, partially compen-
sated by higher P50 and more severe anaerobic metabolism but
less severe metabolic acidosis due to hypochloremia. Under-
standing these phenotypic differences may guide intervention
based on the underling aetiology of cardiogenic shock.
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