Cardiogenic Shock Chest

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[ Shock CHEST Critical Care Review ] 56

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The Management of Cardiogenic Shock 61
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Q33
From Diagnosis to Devices 63
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10 A Narrative Review 65
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12 Q1 67
Q34 Fatimah A. Alkhunaizi, MD; Nikolhaus Smith; Samuel B. Brusca; and David Furfaro, MD
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Cardiogenic shock (CS) is a heterogenous syndrome broadly characterized by inadequate 70
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cardiac output leading to tissue hypoperfusion and multisystem organ dysfunction that carries
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an ongoing high mortality burden. The management of CS has advanced rapidly, especially with
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the incorporation of temporary mechanical circulatory support (tMCS) devices. A thorough
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20 understanding of how to approach a patient with CS and to select appropriate monitoring and
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21 treatment paradigms is essential in modern ICUs. Timely characterization of CS severity and 76
22 hemodynamics is necessary to optimize outcomes, and this may be performed best by multi- 77
23 disciplinary shock-focused teams. In this article, we provide a review of CS aimed to inform both 78
24 the cardiology-trained and non-cardiology-trained intensivist provider. We briefly describe the 79
25 causes, pathophysiologic features, diagnosis, and severity staging of CS, focusing on gathering 80
26 key information that is necessary for making management decisions. We go on to provide a 81
27 more detailed review of CS management principles and practical applications, with a focus on 82
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tMCS. Medical management focuses on appropriate medication therapy to optimize perfusion— 83
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by enhancing contractility and minimizing afterload—and to facilitate decongestion. For more
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severe CS, or for patients with decompensating hemodynamic status despite medical therapy,
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initiation of the appropriate tMCS increasingly is common. We discuss the most common de-
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33 vices currently used for patients with CS—phenotyping patients as having left ventricular fail-
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34 ure, right ventricular failure, or biventricular failure—and highlight key available data and 89
35 particular points of consideration that inform tMCS device selection. Finally, we highlight core 90
36 components of sedation and respiratory failure management for patients with CS. 91
37 CHEST Critical Care 2024; -(-):100071 92
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39 KEY WORDS: cardiogenic shock; cardiogenic shock severity classification; mechanical 94
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Q6 circulatory support 95
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46 ABBREVIATIONS: AMI = acute myocardial infarction; AMI-CS = Department of Medicine, University of California San Francisco, 101
47 cardiogenic shock resulting from acute myocardial infarction; CS = San Francisco, CA; and the Division of Pulmonary, Critical Care, 102
48 cardiogenic shock; ECMO = extracorporeal membrane oxygenation; and Sleep Medicine (D. F.), Department of Medicine, Beth Israel 103
HF = heart failure; HF-CS = cardiogenic shock resulting from heart Deaconess Medical Center, Boston, MA.
49 failure; IABP = intra-aortic balloon pump; LA = left atrium; LV = left 104
CORRESPONDENCE TO: David Furfaro, MD; email: dfurfaro@bidmc. Q4
50 ventricle; MAP = mean arterial pressure; PA = pulmonary artery; harvard.edu 105
51 PAC = pulmonary artery catheter; PCI = percutaneous coronary Copyright Ó 2024 The Authors. Published by Elsevier Inc under li- 106
intervention; PVR = pulmonary vascular resistance; RA = right atrium;
52 cense from the American College of Chest Physicians. This is an open 107
RV = right ventricle; SCAI = Society of Cardiovascular Angiography
access article under the CC BY-NC-ND license (http://
53 and Interventions; tMCS = temporary mechanical circulatory support creativecommons.org/licenses/by-nc-nd/4.0/). 108
54 Q3 AFFILIATIONS: From the Division of Cardiology (F. A. A.),
DOI: https://doi.org/10.1016/j.chstcc.2024.100071 109
Department of Medicine, Columbia University Irving Medical
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Center, New York, NY; the Division of Cardiology (S. B. B.),
chestcc.org 1
REV 5.6.0 DTD CHSTCC100071_proof 25 April 2024 6:07 pm EO: CHEST-CRITCARE-

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Q7 Clinical Question Key Points 166
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A 42-year-old woman whose toddler recently received a 1. CS is defined by impaired cardiac output (CO)
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diagnosis of Coxsackie A virus demonstrated upper resulting in hypotension, clinical or laboratory evi-
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respiratory symptoms and was in the ICU with dence of end-organ hypoperfusion, or both; SCAI
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cardiogenic shock (CS). The echocardiogram revealed classifications should be used in the evaluation of a 171
117 normal left ventricular volume, global hypokinesis patient with CS to standardize language, to help with 172
118 (ejection fraction, 15%), and severe right ventricular prognostication, and to identify appropriate treatment 173
119 dysfunction. A pulmonary artery catheter was placed and pathways. 174
120 showed a right atrial pressure of 24 mm Hg, pulmonary 2. Multidisciplinary shock teams and experienced 175
121 artery pressure of 68/35/46 mm Hg, and pulmonary regional care centers can enhance the recognition and 176
122 capillary wedge pressure of 32 mm Hg, with a CO of 2.8 L/ initial management of patients with CS and can 177
123 min and a cardiac index of 1.6 L/min/m2. Despite 178
improve outcomes.
124 inopressor support, she shows rising lactate and persistent 179
3. Pulmonary artery catheters provide valuable hemo-
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hypoxia and is becoming more encephalopathic with dynamic information during CS, informing shock
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frequent episodes of nonsustained ventricular tachycardia. phenotypes and allowing for the monitoring of
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128 treatment response; increasing evidence suggests 183
What is the next best step in her management? clinical benefit when used early in the course of dis-
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130 A. Place an Impella 5.5 ease and in severe shock. 185
131 B. Place an intra-aortic balloon pump (IABP) 4. Medical management of CS should focus on reversing 186
132 C. Cannulate for venoarterial extracorporeal membrane the underlying cause and using pharmacologic agents 187
133 oxygenation (ECMO) to optimize perfusion and to reduce congestion; when 188
134 D. Place an Impella CP vasoactive agents are inadequate to restore systemic 189
135 perfusion, mechanical circulatory support should be 190
136 Answer: C, Venoarterial ECMO 191
considered.
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The patient demonstrated severe CS likely secondary to 5. The method of temporary mechanical circulatory
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myocarditis with evidence of biventricular failure based support should be selected based on the type of
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on echocardiography and right heart catheterization support that is necessary (ie, left ventricular, right
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findings. She demonstrated Society of Cardiovascular ventricular, biventricular), the anticipated amount of 196
142 Angiography and Interventions (SCAI) stage C shock at necessary CO support, the need for oxygenation, the 197
143 presentation and deteriorated to SCAI stage D shock feasibility and safety of placement, and the potential 198
144 given the inadequate response to medical therapy. At this for patient-specific complications. 199
145 stage, temporary mechanical circulatory support (tMCS) 200
146 is warranted based on the worsening clinical status, 201
147 young age, and absence of contraindications to therapy. Introduction 202
148 The selection of the appropriate tMCS device is CS is a state of inadequate CO that results in tissue 203
149 hypoperfusion, pulmonary and venous congestion, and 204
dependent on the acuity of the presentation, the type of
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hemodynamic support required, and local comfort and often multisystem organ dysfunction.1 CS is a
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expertise. In this situation, the patient required heterogenous syndrome, with variable causes,
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biventricular support and additional oxygenation hemodynamic profiles, and clinical presentations.
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support, making venoarterial ECMO the only appropriate Despite notable advances in treatment, mortality 209
155 choice listed. Impella CP, Impella 5.5, and IABP all remains unacceptably high, with figures ranging from 210
156 provide left ventricle (LV)-only support and do not 30% to 60%.2-4 It is increasingly important for all critical 211
157 provide additional oxygenation, making them inadequate care providers to be familiar with the management of CS 212
158 support devices in this case (choices A, B, and C are and options for mechanical circulatory support. In this 213
159 incorrect). Given the severe LV dysfunction, she requires review, we summarize the basic pathophysiologic 214
160 close monitoring for need of LV venting, and after a principles of CS and its diagnosis, as well as provide a 215
161 period of stabilization, she may warrant transition to a more extensive discussion of contemporary CS 216
162 management, with a particular emphasis on reviewing 217
more sustainable tMCS option as a bridge to recovery,
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durable mechanical support, or heart transplantation. options for tMCS.
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2 CHEST Critical Care Review [ -#- CHEST Critical Care - 2024 ]

221 Part I: Principles of Cardiogenic Shock pericardium, or valves (Table 1). Historically, most 276
222 cases of CS have been precipitated by AMI.16,17 277
223 Definition, Classification of Severity, and Clinical 278
Phenotyping However, the epidemiologic features of CS have
224 279
shifted in recent decades such that decompensated
225 Clinical trials and society guidelines use varying 280
heart failure (HF) has overtaken AMI as the leading
226 definitions of CS, but most rely on clinical criteria, 281
cause.4 In addition, recognition of mixed cardiogenic-
227 namely impaired CO resulting in hypotension 282
228
distributive shock as a particularly high-risk clinical 283
(systolic BP of < 90 mm Hg or need for vasopressors
229 entity has been growing.4 284
or mechanical support) as well as clinical or
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laboratory evidence of end-organ hypoperfusion.5-8 Although the inciting causes of CS may differ, the
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Commonly referenced hemodynamic criteria include resultant pathophysiologic features of CS center
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cardiac index of # 2.2 L/min/m2 and elevated around reduced CO leading to inadequate tissue
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234 intracardiac filling pressures with pulmonary capillary perfusion. This triggers a cycle of maladaptive and 289
235 wedge pressure of > 15 mm Hg.9 Nonclassical unsustainable compensatory hemodynamic changes, 290
236 presentations increasingly have been recognized, including increased systemic vascular resistance and 291
237 including normotensive CS, which is associated with fluid retention, which further decrease stroke volume 292
238 similarly high mortality, and right ventricular- and propagates myocardial ischemia, leading to death 293
239 predominant CS.1,10 if the cycle is not interrupted.1,16 CS, especially after 294
240 AMI, also can produce profound systemic 295
241 To standardize the language surrounding CS, and for 296
inflammation leading to pathologic vasodilation and
242 prognostication, the SCAI proposed a CS classification 297
capillary leakage as opposed to, or after,
243 scheme in 2019.11 The SCAI classification uses physical 298
vasoconstriction, which can exacerbate the deleterious
244 examination findings, hemodynamic parameters, and 299
hemometabolic cascade and lead to worsening
245 biochemical markers to categorize patients into five 300
multiorgan failure.18
246 stages of shock severity (SCAI stages A through E). SCAI 301
247 stage A refers to patients with no signs or symptoms of 302
248 CS but who are at risk of CS developing because of 303
249
Part II: Initial Evaluation 304
underlying cardiac pathologic features. SCAI stage B
250 The initial evaluation of patients with CS should focus 305
refers to patients who are beginning to show signs of CS,
251 on identification of end-organ hypoperfusion and 306
such as tachycardia or relative hypotension, but without
252 categorization of severity based on the SCAI 307
253
end-organ hypoperfusion. SCAI stage C defines patients 308
classification system. A careful assessment and focused
254 with classic CS who show clinical evidence of end-organ 309
history to identify precipitating factors is essential,
255 hypoperfusion requiring pharmacologic or mechanical 310
because certain underlying causes can alter the initial
256 support, or both. SCAI stage D refers to patients with CS 311
course of management and the selection of appropriate
257 whose condition is deteriorating despite initiation of 312
tMCS devices significantly.
258 therapy. Finally, SCAI stage E refers to patients with CS 313
259 in extremis with refractory shock who are at impending The bedside physical examination provides an 314
260 risk of death (Fig 1).12 Importantly, the SCAI stages are important clinical assessment of perfusion and 315
261 dynamic and were designed purposefully to allow congestion. Common signs of hypoperfusion (so-called 316
262 cold profile) include altered mental status, oliguria, 317
patient movement between classes as interventions are
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applied. The SCAI stages are associated with mortality and cool extremities. Hemodynamically, low output
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across various cohorts with CS, including those with often manifests as relative hypotension (commonly
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acute myocardial infarction (AMI) and without with narrow pulse pressure) and compensatory
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267 AMI.2,13,14 Biochemical phenotypes of CS (eg, tachycardia. Common signs of congestion (so-called 322
268 noncongested, cardiorenal, and cardiometabolic shock) wet profile) include tachypnea, pulmonary edema, 323
269 also have been defined and validated to risk-stratify jugular venous distention, and peripheral edema. 324
270 patients further within the SCAI staging system.15 Although the presence of these signs can be helpful, 325
271 their absence does not exclude CS, which can present 326
272 Cause and Pathophysiologic Features with a so-called cold and dry profile (euvolemic CS) 327
273 The causes of CS can be classified according to the or with a so-called warm and wet profile (vasodilatory 328
274 site of initial insult: myocardium, conduction system, CS or mixed shock).1 329
275 330
chestcc.org 3

331 386
A
332 EXTREMIS 387
333 (A) Modifier: A patient with refractory shock or actual/impending 388
334 CA with concern for circulatory collapse. 389
anoxic brain injury
335 DETERIORATING 390
336 391
A patient who has clinical evidence of shock that worsens or
337 392
fails to improve despite escalation of therapy.
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CLASSIC
339 394
340 A patient who has clinical evidence of hypoperfusion 395
that initially requires pharmacologic or mechanical support.
341 Hypotension is usually present. 396
BEGINNING
342 397
343 A patient who has clinical evidence of hemodynamic 398
344 instability (including hypotension, tachycardia or abnormal 399
systemic hemodynamics) without hypoperfusion.
345 AT RISK 400
346 401
A hemodynamically stable patient who is NOT
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experiencing signs or symptoms of CS, but is at risk
348 for its development (i.e. large AMI or decompensated HF). 403
349 404
350 B 405
351 Chronic cardiovascular disease 406
Acute cardiovascular event
352 SCAI shock stage not applicable 407
353 408
354 Recovery Hemodynamically stable 409
SCAI shock stage A
355 410
RECOVERY PATHWAYS Loss of compensation DETERIORATION PATHWAYS
356 411
357 Hemodynamically unstable 412
358 SCAI shock stage B 413
359 Normalization of perfusion Loss of compensation Acute catastrophic event (i.e., 414
360 metrics while on support (MCS Hypoperfusion = Shock prolonged CA) arrives in Stage 415
361 or pharmacologic) improves to SCAI shock stage C E. All others must stop at least 416
Stage C. If remains normal transiently in Stage C for first
362 Deterioration 417
with removal of support, then intervention.
363 improves to Stage B or A. Failure to stabilize with initial Tx 418
364 SCAI shock stage D 419
365 Deterioration 420
web 4C=FPO
366 421
Extremis / refractory shock
367 SCAI shock stage E 422
368 423
369 Figure 1 – A, B, Diagrams showing SCAI shock classification pyramid (A) and the dynamic evolution of cardiogenic shock and progression or Q26
424
recovery through SCAI shock stages (B). AMI ¼ acute myocardial infarction; CA ¼ cardiac arrest; CS ¼ cardiogenic shock; HF ¼ heart failure;
370 425
MCS ¼ mechanical circulatory support; SCAI ¼ Society for Cardiovascular Angiography and Interventions. (Reproduced with permission from Q35
371 Naidu et al.12) 426
Q27 Q28
372 427
373 428
374 429
Noninvasive testing initially should include ECG, chest baseline lactate and subsequent trend are strong
375 430
radiography, and a complete transthoracic predictors of mortality at every SCAI stage.11,20-24
376 431
377
echocardiography. Point-of-care ultrasound also is used 432
378 commonly to identify CS cause and complicating 433
Part III: Management
379 factors, such as valvular disease, while awaiting formal 434
380 echocardiography.19 Laboratory testing provides Early Recognition, Regionalized Systems of Care, 435
381 additional information about end-organ dysfunction. All and Shock Teams 436
382 patients should undergo arterial blood gas, baseline A critical element of successful CS management is early 437
383 lactic acid, complete metabolic panel, complete blood recognition. Efforts to reverse the underlying cause and 438
384 count, and cardiac biomarker testing. Lactic acidosis is to restore tissue perfusion rapidly should take place 439
385 440
an important marker of tissue hypoxia, and both the urgently to prevent the deterioration of CS from a

Q30
441 hemodynamic problem to a potentially irreversible 496
CS is a heterogeneous condition with varying causes. It is helpful to categorize CS based on the driving pathologic feature, but it is important to recognize that multiple interacting pathologic drivers are common.
Unstable supraventricular
442 hemometabolic process.25,26 497
Ventricular arrhythmia
Tachycardia mediated
443 498
◦ Sinus dysfunction
444 Conduction As soon as CS has been recognized, continuous 499
◦ AV node block
cardiomyopathy
445 assessment of illness acuity and appropriate repeat 500
446 triaging is another crucial aspect of early management. 501
Bradycardia
AMI ¼ acute myocardial infarction; AV ¼ atrioventricular; CM ¼ cardiomyopathy; CS ¼ cardiogenic shock; LV ¼ left ventricle; LVFWR ¼ left ventricular free wall rupture; RV ¼ right ventricle.
447 arrhythmia Patients treated at institutions with higher CS case 502
448 volumes and more contemporary CS management 503
449 strategies have lower mortality, highlighting the impact 504
450 505
of experience and expertise.27 As such, establishing
451 506
regional systems of care and expedited transfer protocols
452 507
Mechanical valve
between smaller community hospitals and high-volume

◦ Cord rupture
Aortic stenosis
Mitral stenosis
Acute valvular
453 508
◦ Endocarditis
regurgitation
regurgitation
CS centers within a hub-and-spoke model is
◦ Dissection
Valvular
thrombosis
454 509
455 recommended to improve CS outcomes.1,28 510
Mitral
456 In addition to regional care networks, institutional 511

457 512
multidisciplinary shock teams have the potential to
458 513
enhance the quality of early CS management
459 514
significantly.10,29,30 Shock teams typically consist of an
460 515
tamponade
pericarditis
Pericardial
Constrictive
461
advanced HF cardiologist, interventional cardiologist, 516
cardiothoracic surgeon, and intensivist. In prospective
Cardiac
462 517
463 observational studies, use of a standardized shock team 518
464 and local treatment algorithms that focus on rapid 519
465 identification of CS, invasive hemodynamic monitoring, 520
Hypertrophic CM
Nonischemic CM
Postcardiotomy
466 521
Peripartum CM
and early, appropriate escalation to tMCS result in

Restrictive CM
septal rupture
Ischemic CM
467 improved survival.10,31 522

Myocarditis
Ventricular
Stress CM
468 523
LV
LVFWR
469 Hemodynamic Assessment and Monitoring 524

AMI
470 525
Initial noninvasive assessments, specifically Doppler
471 526

echocardiography, can be used to estimate

472 527
hemodynamic parameters and have been shown to
Chronic thromboembolic pulmo-
Pulmonary arterial hypertension
473 528
Myocardial
474
correlate well with those obtained invasively.32 Several 529
Acute pulmonary embolism
475 echocardiographic parameters have been shown to be 530

476 associated with higher hospital mortality in patients with 531
477 CS at each SCAI stage, including LV ejection fraction, 532
nary hypertension
RV
478 stroke volume index, cardiac index, cardiac power 533

479 output, and E to e0 ratio.33 The LV outflow tract 534
Q8
480 velocity-time integral is a surrogate measure of stroke 535
RV AMI
481 volume and has been shown to be a predictor of in- 536

482 34,35 537
hospital mortality in CS. These relatively easily
483
obtained measurements may aid in prognostication and 538
484 539
] Common Causes of CS
risk stratification of patients with CS and can be

CS resulting from decompensated
485 540
performed during point-of-care ultrasound as well as
486 541
during formal echocardiography. Another noninvasive 542
CS resulting from an acute
487
488 tool that is being adopted increasingly in the care of 543
489 patients with CS is lung ultrasound. Lung ultrasound 544
chronic disease
490 can be used to assess for B-lines that, in the setting of 545
491 CS, reflect pulmonary vascular congestion and elevated 546
492 left atrium (LA) pressures.36 This is superior to chest 547
insult
493 radiography in patients with chronic HF, which lacks 548

Variable
TABLE 1
494 sensitivity in detecting pulmonary edema, and is less 549

495 36 550
invasive than pulmonary artery catheters (PACs).
chestcc.org 5

551 Notably, other pulmonary pathologic features also may CS remains an area of active investigation.46 Urgent 606
552 result in B-lines on lung ultrasound, and clinical context revascularization also should be considered in high-risk 607
553 608
must be taken into consideration in interpreting this patients with non-ST-segment elevation myocardial
554 609
finding. infarction as well as in patients with known ischemic
555 610
cardiomyopathy who have progressive shock or
556 Invasive hemodynamic monitoring with PAC provides 611
refractory arrhythmia.47
557 direct information about biventricular filling pressures, 612
558 PA pressures, and CO, allowing for the calculation of Many other causes of CS may warrant specific 613
559 vascular resistances. These hemodynamic parameters interventions to address the underlying process. For 614
560 615
are useful prognostically and are paramount for clinical example, acute myocarditis requires prompt
561 616
decision-making for patients with CS. The usefulness of immunosuppression, hemodynamically unstable
562 617
PACs has been debated based on prior studies bradyarrhythmias require pacing, unstable
563 618
564
demonstrating lack of benefit in various clinical tachyarrhythmias require pharmacologic or electrical 619
565 contexts, including broad populations of critically ill cardioversion, acute valvular disease may require 620
566 patients and in acute decompensated HF without emergent percutaneous or surgical valvular repair or 621
567 shock.37,38 replacement, tamponade requires pericardiocentesis or 622
568 pericardial window, and high-risk pulmonary embolism 623
Recently, however, evidence to support the clinical benefit
569 may require thrombolysis or thrombectomy. 624
of PAC-derived hemodynamic data in guiding CS
570 625
571
treatment has been growing, especially in the setting of Mixed cardiogenic-septic shock can be caused either by 626
572 tMCS.39-41 An early knowledge of CO and filling sepsis-induced cardiomyopathy or by an HF 627
573 pressures allows providers to select the appropriate exacerbation in a patient with sepsis with preexisting 628
574 device(s), and the continuous feedback allows for fine- cardiomyopathy, and it poses unique treatment 629
575 tuning of treatment decisions. In a large multicenter challenges.48 Although antimicrobial therapy and 630
576 registry of patients with CS, hemodynamic profiling with achieving infection source control are of utmost 631
577 PAC before tMCS was associated with improved importance in all patients, the challenges arise primarily 632
578 outcomes, including mortality, particularly in advanced regarding fluid balance. Rapid fluid resuscitation is a 633
579 stages of shock.39 In an observational study of patients cornerstone of sepsis management, but it may be 634
580 635
with CS resulting from HF (HF-CS), PAC use was detrimental in a patient with decompensated HF and
581 636
associated with decreased hospital mortality, particularly impending CS. In these patients, careful monitoring of
582 637
when performed early.42 A randomized trial of patients respiratory status and fluid balance is crucial, as well as
583 638
584
with CS currently is underway to assess the impact of the ongoing reassessment of the relative contribution of 639
Q9
585 early PAC on in-hospital mortality.43 From a safety septic vs cardiogenic shock to the patient’s 640
586 standpoint, PAC use can be associated with a small hemodynamics.49 641
587 incidence of complications related to central venous 642
588 access, infection, catheter manipulation, and Medical Management and Treatment Targets 643
589 misinterpretation of the data.44 However, clinical trial and Medical management of CS is focused on rapidly 644
590 registry data show that the complication rates are low (< restoring tissue perfusion and beginning the process 645
591 5%), especially when PAC insertion and management are of decongestion to mitigate end-organ damage 646
592 647
performed by experienced operators and centers, (Fig 2).1,2,10,12,50-54 Treatment targets in CS are not
593 648
highlighting the need for procedural expertise.41,45 defined clearly in guideline recommendations because of
594 649
limited data and may vary based on the underlying cause
595 Treating the Underlying Cause 650
of CS.1,55,56 Generally speaking, hemodynamic targets
596 651
597
Early identification of the underlying cause of CS is include achieving a perfusing mean arterial pressure 652
598 crucial, because certain causes may require specific (MAP) and normalization of cardiac index (> 2.2 L/ 653
599 medical or interventional therapies, or both. In CS min/m2) and filling pressures (right atrial pressure, # 654
600 resulting from AMI (AMI-CS), emergent 10-12 mm Hg; PA diastolic pressure, # 20 mm Hg; 655
601 revascularization of the occluded coronary artery pulmonary capillary wedge pressure, # 15- 656
602 significantly improves survival, as was demonstrated 18 mm Hg).55,57 Notably, although a MAP target of > 657
603
Q10 first in the landmark SHOCK trial.9 Although early 65 mm Hg is recommended in septic shock, a lower 658
604 revascularization is essential, the optimal MAP may be adequate in CS, particularly in the 659
605 660
revascularization strategy for nonculprit lesions in AMI- presence of pathologic features that may be exacerbated

661 716
Monitoring
Initial Cardiogenic Shock Management
662 1. Exam for perfusion, congestion
717
663 1: Identify: Persistent CI < 2.2 L/min/m2 with adequate or elevated filling pressures* 2. Serial serum lactates 718
2a. Define SCAI 3. Serial TTE
664 Stage 2b: Phenotype by PAC placement 4. Hemodynamics by PA-C 719
665 RV Dominant CS
720
LV CS, BiV CS without PAH Metrics to Monitor & PAC Correlates
666 PCW > 15 mmHg, CPO < 0.6 W,
PAPi < 2, CVP > 15, PCW < 15 721
667 PVR < 2.0 WU No Pre-capillary PH With pre-capillary PH 1. Thermodilution CI 722
PVR < 2.0 WU PVR ≥ 2.0 WU - Fick CI by ScVO2
668 2. CVP 723
669 3. Choose Vasoactive agent based on MAP - JVP by physical exam 724
- IVC assessed by POCUS
670 SCAI ≥ C - CVP by CVC 725
671 Pure Vasodilators: Nitroprusside, Hypertensive Inhaled, Oral, or 3. PCW 726
Nitroglycerin#, MAP > 90 or IV Pulmonary - E/e’ ratio on Echocardiography
672 Nicardipine SVR > 1200 Vasodilators - Rales on exam 727
Inodilator - Congestion on CXR
673 and 728
Inodilator
674 729
Normotensive Treatment Goals
675 MAP 65-80 or
730
Inodilators: Milrinone, Dobutamine**
676 SVR 800-1200 1. Optimize organ perfusion 731
- MAP > 65 mmHg
677 Inhaled, Oral, or - Cl > 2.2 L/min/m2
732
IV Pulmonary
678 Vasodilators
- Lactate clearance in 24 hours 733
Inodilator + norepinephrine, vasopressin - UOP > 30 cc/hr
679 or
Inodilator + and 734
Hypotensive Vasopressor Inodilator + 2. Renal/Hepatic Decongestion
680 Inopressor: Epinephrine**,
MAP < 65 or Vasopressin^ or - CVP < 15 735
norepinephrine, - Normalize Cr and LFTs
Inopressor Norepinephrine
681 dopamine
or - Reduce pulmonary and 736
682 Inopressor peripheral edema 737
3. Optimize cardiac performance
683 - Septum midline on TTE 738
684 739
685 4. Continuous close monitoring for refractory Cardiogenic Shock (SCAI D or E, or 740
failing treatment goals) Refractory Shock
686 741
web 4C=FPO
SCAI D or E
1. Persistent Cl < 2.2 L/min/m2
687 Multi-Disciplinary Shock Team Assessment for tMCS 2. Persistent lactate > 2.2 mmol/L 742
688 743
689 Figure 2 – Flowchart showing medical management of cardiogenic shock. This management algorithm represents the expert opinions of the authors and 744
690 is informed by trial data and society guidelines.1,2,10,12,50-54 No singular approach to treating CS exists, and this is meant to serve as a guide, not the 745
only definitive approach. Key components in the management of CS include early recognition, SCAI staging, and phenotyping by PAC. Early treatments
691 for CS prioritize prompt resolution of organ hypoperfusion using vasoactive agents with close monitoring for deterioration. Vasoactive agent use is 746
692 tailored to an individual patient based on the hemodynamic phenotype. Please see Table 2 for more information on vasoactive agents. BiV ¼ 747
693 biventricular; CI ¼ cardiac index; CS ¼ cardiogenic shock; CVP ¼ central venous pressure; LFT ¼ lung function test; LV ¼ left ventricle; MAP ¼ mean 748
arterial pressure; PAC ¼ pulmonary artery catheter; PAPi ¼ pulmonary artery pulsatility index; PCWP ¼ pulmonary capillary wedge pressure; PH ¼
694 pulmonary hypertension; PVR ¼ pulmonary vascular resistance; RV ¼ right ventricle; SCAI ¼ Society for Cardiovascular Angiography and In- 749
695 terventions; SVR ¼ systemic vascular resistance; tMCS ¼ temporary mechanical circulatory support; TTE ¼ transthoracic echocardiography; WU ¼ 750
696 Wood unit. aPatients who are hypovolemic and have inadequate preload can have low CI and a high SVR mimicking CS. Patients should show 751
adequate filling pressures and be resuscitated as needed before proceeding with CS diagnosis. bNitroglycerin provides more venous than arterial
697 vasodilation and often is used in patients with volume overload, acute coronary syndrome, or both. cIn CS resulting from acute myocardial infarction, 752
698 inotropes can increase myocardial oxygen demand and increase or provoke ischemia. These agents should be used with caution and in expert centers. 753
d
699 Evidence exists that vasopressin has more impact on SVR than PVR, but norepinephrine often is used also in patients with pulmonary arterial 754
hypertension in shock given the larger titratable range and also a favorable SVR to PVR impact. Q29
700 755
701 756
702 by excess afterload, such as severe mitral varieties: vasopressors, inopressors, inodilators, and 757
703 regurgitation.55,58 Clinical targets include restoration of vasodilators (Table 2).60 Nearly all of these medications 758
704 baseline mental status, improved urine output and contribute to increased myocardial oxygen consumption 759
705 respiratory status, and relief of congestion symptoms.55 and may provoke atrial or ventricular arrhythmias, 760
706 Biochemical targets include improvement in markers of which can be detrimental in CS.61 Thus, although the 761
707 762
end-organ perfusion, including serum creatinine, liver value of these medications cannot be overstated in the
708 763
enzymes, and particularly lactate.55 Indeed, lactate acute management of CS, their use ideally should be
709 764
should be monitored every 1 to 4 h until normalization, limited to the lowest doses necessary and for the shortest
710 765
711
given the association between lack of lactate clearance duration possible. 766
712 and mortality in CS.1,59 767
Inopressors are the preferred first-line agents in
713 768
Early use of vasoactive agents is recommended to hypotensive patients because they increase MAP and
714 769
optimize perfusion in CS. These agents are of four provide inotropic support. Several expert consensus
715 770
chestcc.org 7

825
824
823
822
821
820
819
818
817
816
815
814
813
812
811
810
809
808
807
806
805
804
803
802
801
800
799
798
797
796
795
794
793
792
791
790
789
788
787
786
785
784
783
782
781
780
779
778
777
776
775
774
773
772
771
8 CHEST Critical Care Review
TABLE 2 ] Vasoactive Agents Used in CS

Receptor Affinity/
Category Agent Target Hemodynamics Special Considerations
Vasopressors Vasopressin V1a, V2 Increases SVR, and thus MAP, through V1a- No chronotropic or inotropic effects
mediated vascular smooth muscle May result in digital ischemia
vasoconstriction
Phenylephrine a-1 Increases SVR, and thus MAP, through a-1 No chronotropic or inotropic effects
mediated vasoconstriction May result in reflex bradycardia
Can be agent of choice in hypotension because of hyper-
trophic obstructive cardiomyopathy
Inopressors Norepinephrine a-1 þþþþ Increases SVR and augments CO by increasing Increased risk of atrial and ventricular arrhythmias Q31
b-1 þþþ HR and contractility

b-2 þþ
Epinephrine a-1 þþþþ Increases SVR and augments CO by increasing Increased risk of atrial and ventricular arrhythmias and lactic
b-1 þþþþ HR and contractility acidosis
b-2 þþ
Dopamine a-1 þþþ Acts in a dose-dependent fashion to increase HR, Increased risk of atrial and ventricular arrhythmias
b-1 þþþ contractility, and SVR at higher doses
b-2 þþ
DA þþþþ
Inodilators Dobutamine b-1 þþþþ Increases contractility and reduces SVR Increased risk of atrial and ventricular arrhythmias
b-2 þþþ Vasodilatory and can lower MAP in patients with mixed
shock
[
Milrinone PDE-3 inhibitor Increases contractility and reduces SVR Caution in patients with worsening renal function resulting
-#- CHEST Critical Care - 2024
from predominant renal excretion

Increased risk of atrial and ventricular arrhythmias
Vasodilators Sodium Generates NO in Promotes both arterial and venous vasodilation; No chronotropic or inotropic effects
nitroprusside circulation reduces ventricular afterload and preload May result in marked hypotension in patients without con-
tractile reserve
Requires close monitoring of thiocyanate toxicity especially
with prolonged use or in patients with renal dysfunction
Nitroglycerin Generates NO in Promotes primarily venous vasodilation and No chronotropic or inotropic effects
circulation reduces ventricular preload
CO ¼ cardiac output; CS ¼ cardiogenic shock; DA ¼ dopamine; HR ¼ heart rate; MAP ¼ mean arterial pressure; NO ¼ nitric oxide; PDE ¼ phosphodiesterase; SVR ¼ systemic vascular resistance; V ¼ vasopressin.
]
880
879
878
877
876
875
874
873
872
871
870
869
868
867
866
865
864
863
862
861
860
859
858
857
856
855
854
853
852
851
850
849
848
847
846
845
844
843
842
841
840
839
838
837
836
835
834
833
832
831
830
829
828
827
826
881 documents recommend norepinephrine as the initial strategy, it frequently is associated with electrolyte 936
882 agent of choice, and a subgroup analysis of patients with disturbances including hypokalemia, hypomagnesemia, 937
883Q11 938
CS enrolled in the SOAP II trial showed that and hyponatremia, and thus electrolytes should be
884 939
norepinephrine was associated with lower rates of death monitored carefully and should be replaced as necessary
885 940
and arrhythmia in CS than dopamine.62 However, no during treatment.71 Volume removal using
886 941
singular approach exists, and often norepinephrine is ultrafiltration should be reserved for patients showing
887 942
888
used concurrently with the inodilator dobutamine for inadequate diuretic response. It should be noted that 943
889 greater b-agonist effect, or epinephrine can be used as data are insufficient regarding ultrafiltration in CS, as 944
890 monotherapy. It should be noted that in a small well as evidence that it is inferior to pharmacotherapy in 945
891 randomized trial comparing norepinephrine with patients with acute decompensated HF.72 946
892 epinephrine in AMI-CS, norepinephrine use was 947
893 associated with lower rates of refractory shock, lower Mechanical Circulatory Support 948
894 lactate levels, and less tachycardia than epinephrine.63 The use of tMCS in the management of CS has 949
895 However, these findings are controversial, and at low 950
expanded rapidly despite a paucity of high-quality
896 951
doses, epinephrine represents a reasonable, primarily evidence to support and guide its routine use.73
897 952
inotropic, agent that may be highly effective and has Although the development of randomized trials using
898 953
been used widely in care after cardiotomy.64,65 tMCS in CS has been challenging, equipoise to use tMCS
899 954
900 In normotensive CS and hypotensive CS stabilized with in patients refractory to medical management remains.74 955
901 pressors, the inodilators dobutamine or milrinone can Multidisciplinary shock teams aid in both patient and 956
902 be used effectively.66 Notably, the MAP should be device selection, ideally achieving at least center-specific 957
903
adequate (with or without vasopressor support) before standardization to the use of these high-intensity, high- 958
904 resource therapies. 959
the initiation of either agent because of their
905 960
vasodilatory properties and difficulty predicting The general role of tMCS is to provide hemodynamic
906 961
907
individual patient responses to therapy. Despite support and end-organ perfusion without increasing 962
908 physiologic and pharmacokinetic differences, a myocardial oxygen demand, serving as a bridge to 963
909 randomized controlled trial comparing dobutamine to recovery, to intervention, or to advanced HF therapies, 964
910 milrinone in patients with CS showed no significant such as durable ventricular assist device or heart 965
911 difference in outcomes, arrhythmias, or hypotension.66 transplantation. Numerous tMCS devices now have 966
912 Commonly, it is the local practice pattern that dictates entered the market, complicating the device decision 967
913 which is initiated and patient-specific factors such as tree (Table 3), but in general, appropriate device 968
914 renal dysfunction (milrinone being primarily renally 969
selection should be made based on a few key
915 cleared). Finally, in normotensive or hypertensive 970
considerations. These include the cause of CS, the type
916 971
patients with CS, vasodilators such as nitroprusside can of support needed (ie, LV, RV, or biventricular); the
917 972
be an effective bridge to guideline-directed therapy.67 amount of anticipated CO augmentation required; the
918 973
919 Vascular congestion is common in both AMI-CS and need for decompression of the LV, RV, or both; the need 974
920 HF-CS and is associated with worse shock severity and for oxygenation support; feasibility and safety of 975
921 increased in-hospital mortality, especially biventricular placement; and patient-specific potential complications. 976
922
congestion.15,57 Persistent congestion at 24 h is Device selection also is dictated often by the local 977
923 expertise and comfort. 978
associated with a worse prognosis, indicating that PAC-
924 979
guided decongestion and relief of renovascular
925 980
congestion should be therapeutic targets in CS.68 LV Predominant Failure
926 981
927
Decongestion can minimize secondary organ 982
dysfunction and can help to enhance perfusion by IABP
928 983
929 optimizing ventricular stroke volume and performance. The most conservative LV-only support device, and the 984
930 Loop diuretics in combination with thiazide or thiazide- most frequently used nationally, is the IABP, which 985
931 like diuretics should be initiated in patients to achieve consists of a conical balloon attached to a peripherally 986
932 sequential nephron blockade synergistically and to inserted catheter. The appropriate position of the IABP 987
933 achieve more effective diuresis.69-71 Of note, although is within the descending aorta, between the renal and the 988
934 sequential nephron blockade can overcome diuretic left subclavian arteries.75 The IABP provides 989
935 990
resistance and can serve as a highly effective therapeutic hemodynamic support through counterpulsation, with
chestcc.org 9

1045
1044
1043
1042
1041
1040
1039
1038
1037
1036
1035
1034
1033
1032
1031
1030
1029
1028
1027
1026
1025
1024
1023
1022
1021
1020
1019
1018
1017
1016
1015
1014
1013
1012
1011
1010
1009
1008
1007
1006
1005
1004
1003
1002
1001
1000
999
998
997
996
995
994
993
992
991
TABLE 3 ] Summary of Temporary Mechanical Circulatory Support Devices
10 CHEST Critical Care Review
Duration
of Use
(FDA
Device Pump Mechanism Configuration Access Point(s) Lumen Size Approved)a Advantages Limitations
Left-sided support
IABP Counterpulsation Ao Femoral or axillary 7-8 F 9d Ease of placement No oxygenation

artery Low-profile vascular capacity
access Modest cardiac output
Favorable safety profile augmentation and
hemodynamic
support
Poor performance in
arrhythmias
Contraindicated in
severe aortic
regurgitation
Impella CP Axial flow LV to Ao Femoral artery 14 F 14 d Single arterial access No oxygenation
Direct LV support and capacity
decompression Unstable positioning
Frequent hemolysis
Requires AC
Impella 5.5 Axial flow LV to Ao Axillary artery, via 23 F 14 d Single arterial access No oxygenation
graft Direct LV support and capacity
decompression Requires surgical
placement
Requires AC
Right-sided Support
[
-#- CHEST Critical Care - 2024
Impella RP (Flex) Axial flow RA to PA Right IJ or femoral 11 F 14 d Single venous access No oxygenation
vein capacity
Contraindicated with
right sided valvular
disease
IVC or right sided
clots, or IVC filter
Risk of pulmonary
hemorrhage if high
PVR
Requires AC
(Continued)
]
1100
1099
1098
1097
1096
1095
1094
1093
1092
1091
1090
1089
1088
1087
1086
1085
1084
1083
1082
1081
1080
1079
1078
1077
1076
1075
1074
1073
1072
1071
1070
1069
1068
1067
1066
1065
1064
1063
1062
1061
1060
1059
1058
1057
1056
1055
1054
1053
1052
1051
1050
1049
1048
1047
1046
1155
1154
1153
1152
1151
1150
1149
1148
1147
1146
1145
1144
1143
1142
1141
1140
1139
1138
1137
1136
1135
1134
1133
1132
1131
1130
1129
1128
1127
1126
1125
1124
1123
1122
1121
1120
1119
1118
1117
1116
1115
1114
1113
1112
1111
1110
1109
1108
1107
1106
1105
1104
1103
1102
1101
TABLE 3 ] (Continued)
chestcc.org
Duration
of Use
(FDA
Device Pump Mechanism Configuration Access Point(s) Lumen Size Approved)a Advantages Limitations
Centrifugal flow < 24 h Single IJ vein access al- Contraindicated with
Protek Duo RA to PA Right IJ vein 29 F or 31 F

lows patient to remain IJ stenosis or
ambulatory thrombosis
Allows addition of Contraindicated with
oxygenator right-sided valvular
disease
Risk of pulmonary
hemorrhage if high
PVR
Biventricular support
TandemHeart Centrifugal flow LA to Ao or Left-sided support: Inflow: 21F 30 d Allows addition of Need for atrial trans-
RA to PA Femoral vein þ Outflow: 15- oxygenator septal puncture for
femoral artery 19F Provides LV unloading left-sided support
Right-sided support: Limited patient
Bilateral femoral veins mobility
or femoral vein and Requires AC
right IJ vein
Venoarterial ECMO Centrifugal flow RA and IVC Femoral or IJ vein to Varies by 9d Provides gas exchange Frequently causes LV
-Ao femoral artery patient size; Ease of cannulation: can distention and re-
venous be performed at bedside quires secondary de-
cannula, 21- without fluoroscopy vice—LV vent—for
29 F; arterial depending on institu- mechanical unloading
cannula, tional experience Risk of differential
15-21 F Bypasses RV oxygenation (north-
south syndrome)
Contraindicated in
severe peripheral
arterial disease
aortic regurgitation
Requires AC Q32
AC ¼ anticoagulation; Ao ¼ aorta; FDA ¼ Food and Drug Administration; IABP ¼ intraaortic balloon pump; IJ ¼ internal jugular; IVC ¼ inferior vena cava; LA ¼ left atrium; LV ¼ left ventricle; PA ¼ pulmonary artery;
PVR ¼ pulmonary vascular resistance; RA ¼ right atrium; RV ¼ right ventricle; VA-ECMO ¼ venoarterial extracorporeal membrane oxygenation.
a
Although these are the FDA-approved durations, temporary mechanical circulatory support devices commonly are used off-label and courses may extend well beyond these durations.
11
1210
1209
1208
1207
1206
1205
1204
1203
1202
1201
1200
1199
1198
1197
1196
1195
1194
1193
1192
1191
1190
1189
1188
1187
1186
1185
1184
1183
1182
1181
1180
1179
1178
1177
1176
1175
1174
1173
1172
1171
1170
1169
1168
1167
1166
1165
1164
1163
1162
1161
1160
1159
1158
1157
1156
1211 inflation of the balloon during early diastole and It is the opinion of the authors that, given the modest 1266
1212 deflation just before systole, gated by either CO support and high rates of hemolysis and kidney 1267
1213 1268
electrocardiography or a fiber-optic arterial pulse wave injury, the Impella CP is no longer considered to be an
1214 1269
sensor. Inflation increases diastolic BP in the aorta, adequate longitudinal shock device at many shock
1215 1270
augmenting coronary perfusion pressure and MAP, referral centers. Instead, the axillary-placed Impella 5.5,
1216 1271
whereas deflation before systole creates a vacuum effect, which also enables ongoing rehabilitation before heart
1217 1272
1218
thus reducing afterload and improving the myocardial replacement therapy, is preferred for more sustained 1273
1219 oxygen supply to demand ratio.76 The IABP generally support.80-82 1274
1220 provides only a modest increase in carbon monoxide of 1275
In patients with AMI-CS, the Impella was compared
1221 0.5 to 1 L/min, but may be more efficacious in select 1276
with the IABP in the IMPRESS trial, which showed no Q12
1222 patients with decompensated HF.76 Limitations include 1277
mortality benefit for the Impella over the IABP.7
1223 the device’s poor performance in the setting of 1278
1224
However, it is important to note that the trial design 1279
tachyarrhythmias as well as its contraindication in
1225 included patients who had progressed to profound 1280
patients with significant aortic regurgitation.76
1226 hemometabolic CS, with > 90% of patients having 1281
1227 IABP was studied prospectively in patients with AMI-CS experienced cardiac arrest. Observational data show 1282
1228 in the IABP SHOCK II trial and was not associated with inconsistent findings. Although the National 1283
1229 decreased mortality.6 However, observational data in Cardiogenic Shock Initiative touts early deployment of 1284
1230 HF-CS are encouraging, with some patients being the Impella and demonstrated astounding inpatient 1285
1231 identified as so-called super-responders, augmenting the survival rates of > 70%, a propensity-matched cohort 1286
1232 CO significantly and many achieving stabilization 1287
study showed worse mortality with the Impella
1233 1288
without the need for further tMCS escalation.76,77 Given compared with the IABP and increased vascular
1234 1289
the ease of IABP deployment—a viable bedside complications.83,84 Additional randomized controlled
1235 1290
procedure—and lower vascular complication rates trials are underway to assess the efficacy of the Impella
1236 1291
1237
compared with other tMCS devices, the IABP remains a in AMI-CS better.85,86 The lack of randomized data 1292
1238
practical option and is a reasonable first step in the supporting the efficacy and usefulness of the Impella 5.5 1293
1239 management of CS, especially when end-organ function device is notable. 1294
1240 is relatively preserved and hemodynamic collapse is not 1295
Venoarterial ECMO: Venoarterial ECMO provides
1241 imminent.78 1296
cardiopulmonary support to patients in CS, with or
1242 1297
without concomitant respiratory failure.87 Blood is
1243 1298
1244
Percutaneous Ventricular Assist Device: Impella: The removed from the venous circulation via a drainage 1299
1245 Impella (Abiomed, Inc.) is a percutaneously implanted, cannula in the right atrium, circulated via a centrifugal 1300
1246 transvalvular, axial flow pump.79 Axial flow is produced pump through an oxygenator, and then returned to the 1301
1247 by an impeller that traverses the aortic valve and expels arterial system either peripherally via a cannula in the 1302
1248 blood from the LV into the ascending aorta. The two femoral or subclavian artery or, less commonly, centrally 1303
1249 available models for LV support are Impella CP into the aorta. 1304
1250 (providing up to 4 L/min of flow) and Impella 5.5 1305
1251 Hemodynamically, venoarterial ECMO provides 1306
(providing up to 5.5 L/min of flow). The CP is inserted
1252 circulatory support and improved end-organ perfusion 1307
femorally via a 14-F sheath, whereas the 5.5 is inserted
1253 and unloads the RV, but it significantly increases LV 1308
via a 23-F sheath through a surgical axillary cutdown
1254 afterload resulting from retrograde arterial flow.88 In 1309
and graft. Hemodynamically, the Impella directly
1255 cases of severe LV dysfunction, venoarterial ECMO can 1310
unloads the LV and augments CO, reducing wall stress
1256 lead to increased LV pressures, myocardial oxygen 1311
1257
and end-diastolic pressure and volume. Limitations of 1312
demand, pulmonary edema, and potentially LV to LA
1258 the Impella include access site complications resulting 1313
stasis. As such, venoarterial ECMO for LV-predominant
1259 from large-bore cannulation, as well as significant risk 1314
CS often is used in tandem with an LV so-called vent to
1260 for hemolysis (with associated renal failure) and 1315
maintain aortic valve opening, to reduce LV end-
1261 thrombocytopenia, especially with the Impella CP.79 1316
diastolic pressure, and to protect the lungs. Venting
1262 Impella placement requires fluoroscopy and, in the case 1317
1263
strategies commonly include concurrent Impella, IABP, 1318
of the Impella 5.5, surgical cutdown and graft
1264 atrial septostomy, or transeptal LA-RA venous limb 1319
anastomosis; thus, the Impella typically is not an option
1265 drainage.89 Although venting data are sparse, 1320
for emergent bedside placement.

1321 mechanical unloading may be associated with improved selected patients with AMI-CS, and especially those 1376
1322 survival compared with venoarterial ECMO alone.90,91 whose disease is refractory to medical management 1377
1323 1378
However, a recent randomized controlled trial showed alone.95 Finally, the trial results are limited in their
1324 1379
that early unloading was not superior to a rescue generalizability and should not be taken to apply to all
1325 1380
strategy, so upfront venting may not be necessary for all patients with CS, such as those with HF-CS.
1326 1381
patients.92 One particular challenge in the management
1327 TandemHeart: TandemHeart (LivaNova, Inc.) is a 1382
1328
of venoarterial ECMO is maintaining the delicate 1383
percutaneously placed extracorporeal centrifugal pump
1329 balance between the need to vent the LV, which outputs 1384
that uses a 21-F transeptal inflow cannula—blood is
1330 relatively deoxygenated blood in the setting of 1385
removed from the LA—and either a 15-F or 17-F arterial
1331 respiratory failure, and the need to circulate oxygenated 1386
return cannula in the aorta to deliver 4 to 6 L/min of
1332 blood provided by the ECMO circuit. The location 1387
flow.96 This allows for circulatory support with
1333 where this blood mixes within the aorta, known as the 1388
concomitant LV unloading, but without RA drainage,
1334 mixing cloud, is of particular clinical importance to 1389
1335
thus providing minimal RV support. Right-sided 1390
avoid differential oxygenation of tissue beds (ie, north-
1336 configurations with RA drainage and PA return can be 1391
south syndrome).
1337 used as well. One limitation of this device is the 1392
1338 Results of the first randomized controlled trial for requirement for transeptal puncture, which is a 1393
1339 venoarterial ECMO in patients with AMI-CS who were technically challenging process requiring specific 1394
1340 planned for revascularization were published in 2023 interventional cardiology expertise. 1395
1341Q13 (ECLS-Shock).93 Four hundred patients with AMI-CS 1396
1342
LV Failure Device Selection: The choice of tMCS device 1397
were randomized to early tMCS support with
1343 in LV-predominant shock is dictated by the cause and 1398
venoarterial ECMO (with predefined criteria for LV
1344 severity of CS, rapidity of progression, the presence of 1399
venting) or medical management alone. The patients
1345 concurrent respiratory failure, and perhaps most 1400
enrolled in ECLS-Shock were critically ill, with a median
1346 significantly, by local expertise and comfort. Indeed, in 1401
1347
lactate of 6.9 mM, 78% having received CPR before 1402
the absence of high-quality data or recognized
1348 enrollment, and 50% categorized as having SCAI stage D 1403
guidelines, device selection is driven by expert opinion.
1349 or E disease. Death resulting from any cause at 30 days 1404
The following represents one approach, supported by
1350 was not different between the two study groups, and 1405
the authors.
1351 both bleeding and peripheral ischemia were more 1406
1352 prevalent in the venoarterial ECMO group. As stated, no clear mortality benefit to Impella CP over 1407
1353 IABP has been shown in randomized trials, and an 1408
1354
Overall, the results of ECLS-Shock suggest that 1409
association with increased vascular complications
1355 nonselective early use of venoarterial ECMO should not 1410
exists.97 With this in mind, IABP often is the device of
1356 be standard first-line care in AMI-CS. However, a 1411
choice in the absence of profound hemometabolic
1357 number of questions remain to be answered, and it can 1412
shock.77 In these cases, the IABP is selected with the aim
1358 be argued that venoarterial ECMO has never been 1413
of providing sufficient CO and perfusion support while
1359 considered (nor should it be) a first-line therapy to begin 1414
also avoiding larger devices with higher-risk profiles.76,83
1360 with. Within the trial protocol, patients in the treatment 1415
1361
However, Impella CP inarguably provides substantially 1416
arm were not assessed for alternative methods of tMCS
1362 more CO support and LV unloading compared with 1417
that may have been more appropriate on an individual
1363 IABP, can be placed under fluoroscopy similarly, and 1418
patient basis. Additionally, only 5.8% of patients
1364 has been used with astounding success in some national 1419
supported with venoarterial ECMO received mechanical
1365 shock registries.83 When placed for AMI-CS, the Impella 1420
LV unloading, which may have impacted the efficacy of
1366 CP typically is considered a short-term support device 1421
1367
the intervention on reducing LV demand and filling 1422
with the aim of stabilizing a patient until they can be
1368 pressures. The trial population was both generally 1423
weaned off the Impella CP or the device can be upgraded
1369 elderly and severely ill, with 78% having experienced a 1424
to a more sustainable LV support device.86 In practice,
1370 cardiac arrest. In considering translatability to a real- 1425
the Impella CP often is placed at referring centers as a
1371 world cohort of patients with AMI-CS, > 60% would 1426
means of patient stabilization until they can be
1372 not have met eligibility for the trial, so there may be 1427
transferred to a hub shock center. In the setting of
1373 populations in which venoarterial ECMO could be 1428
1374
profound hemometabolic shock or progressive shock 1429
expected more reasonably to alter outcomes.94
1375 despite IABP or Impella CP, full LV support can be 1430
Venoarterial ECMO should be reserved for carefully
chestcc.org 13

1431 provided by venoarterial ECMO or the Impella 5.5. The hypertension. Reinfusion into a noncompliant 1486
1432 decision between these two devices often is determined pulmonary circulation can impact the amount of 1487
1433 1488
by the perceived risk of subsequent RV failure after generated flow negatively as well as lead to
1434 1489
Impella 5.5 placement (akin to RV failure after durable complications such as pulmonary hemorrhage, and in
1435 1490
LV assist device placement), the need for oxygenation, these cases, venoarterial ECMO is the preferred
1436 1491
and the urgency of cannulation.81 Venoarterial ECMO tMCS.103 Although reports have indicated that these
1437 1492
1438
can be placed readily at the bedside, and thus often is devices can be used successfully with elevated PVR, RA- 1493
1439 preferred when a patient is in extremis. However, the PA flow devices are best suited to situations of primary 1494
1440 Impella 5.5 is preferable for long-term support because it RV failure, including RV AMI, RV failure after heart 1495
1441 allows for ongoing rehabilitation. If necessary, a patient transplant, or LV assist device implantation.104,105 1496
1442 can be cannulated to venoarterial ECMO emergently, 1497
1443 with the Impella 5.5 subsequently placed as a venting Biventricular Failure 1498
1444 strategy and venoarterial ECMO as an exit strategy. 1499
AMI-CS as well as various forms of CS not owing to
1445 1500
AMI can result in biventricular failure, which is
1446 1501
RV Predominant Failure associated with worse mortality than isolated LV
1447 1502
Several tMCS options are available for RV-predominant failure.106,107 When selecting a tMCS strategy for the
1448 1503
1449
CS, although they are fewer and less well studied patient with biventricular failure, it is important to 1504
1450 compared with those used for LV-predominant CS.98 consider the hemodynamic impact of the selected device 1505
1451 Venoarterial ECMO often is the most reliable and on both left-side and right-side circulation. Options for 1506
1452 readily available device because it bypasses the biventricular support include venoarterial ECMO, 1507
1453 dysfunctional RV, dramatically decreasing RV preload biventricular extracorporeal centrifugal pumps such as 1508
1454 without increasing RV afterload. In addition to the TandemHeart or Protek Duo, the biventricular 1509
1455 venoarterial ECMO, RV-only support can be provided Impella (BiPella), or the LV Impella plus Protek Duo.108 1510
1456 with a right-sided Impella device called the Impella RP, As in other cases, the decision here is driven largely by 1511
1457 1512
as well as the Protek Duo cannula (LivaNova), which institutional preference and comfort, with venoarterial
1458 1513
can function in line with the TandemHeart pump or an ECMO—often requiring an LV vent—being the simplest
1459 1514
ECMO circuit.99 The Impella RP aspirates blood from and most rapidly deployed option.
1460 1515
the RA and expels it into the PA, using an axial
1461 Respiratory Failure and Sedation in CS 1516
1462
transvalvular impeller similar to other Impella 1517
1463 devices.100 The Protek Duo is a dual-lumen cannula that Respiratory failure is common in CS because of elevated
1518
1464 also aspirates blood from the RA and ejects it into the left-sided filling pressures resulting in pulmonary 1519
1465 PA. However, unlike the Impella, blood is removed from vascular congestion and cardiogenic pulmonary edema. 1520
1466 the body via a centrifugal pump before reinfusion, Respiratory support for patients with CS is aimed at 1521
1467 allowing for flexibility of pump types as well as the minimizing hypoxemia, correcting respiratory acidosis 1522
1468 insertion of an oxygenator.101 Both the Protek Duo and, and hypercapnia, and minimizing the work of breathing 1523
1469 more recently, the novel Impella RP flex can be placed and high catecholamine states.109 Noninvasive 1524
1470 ventilatory support with high-flow nasal cannula or 1525
via internal jugular access, thus eliminating the need for
1471 bilevel positive pressure ventilation should be attempted; 1526
femoral access and allowing for patient mobilization.
1472 1527
however, in more severe CS with progressive acidosis,
1473 RV Failure Device Selection 1528
altered mental status, and hemodynamic instability,
1474 1529
Venoarterial ECMO often is the device of choice in invasive mechanical ventilation often is required.110
1475 1530
patients with RV-predominant failure, when escalation Positive pressure ventilation, either via noninvasive or
1476 1531
1477
to tMCS is needed rapidly. If oxygenation is a concern, invasive strategies, can impact CO and myocardial 1532
1478 then only venoarterial ECMO or the Protek Duo in line oxygen demand significantly, and the specific impact 1533
1479 with an oxygenator are feasible choices.102 The other depends largely on the relative RV and LV 1534
1480 main determinant of RV support selection concerns the dysfunction.111 Broadly, high transpulmonary pressures, 1535
1481 status of RV afterload and pulmonary vascular either at end expiration (positive end-expiratory 1536
1482 resistance (PVR). Minimal data are available to support pressure) or with inspiration, lead to increased PVR and 1537
1483 the use of RA-PA flow devices in the setting of severely to increased RV afterload.110 In the same circumstances, 1538
1484 elevated PVR and increased RV afterload, such as in the LV experiences decreased preload and filling and 1539
1485 1540
acute PE or long-standing pulmonary arterial decreased afterload because of reflex vasodilation and

1541 decreased transmural pressures, resulting in decreased 5. Thiele H, Akin I, Sandri M, et al. PCI Strategies in patients with 1596
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1558 associated with improved outcomes as compared with was endorsed by the American College of Cardiology (ACC), the 1613
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shock severity on short-term survival in patients with cardiogenic
1568 the severity of shock. This is achieved best with a shock. Eur Heart J Acute Cardiovasc Care. 2021;10(6):604-612. 1623
1569 combination of noninvasive and invasive hemodynamic 15. Zweck E, Thayer KL, Helgestad OKL, et al. Phenotyping 1624
1570 cardiogenic shock. J Am Heart Assoc. 2021;10(14):e020085. 1625
testing and multidisciplinary discussion. As soon as a
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1572 1627
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1574
decongestion and initiation of tMCS for patients with 2020;22(4):664-672. 1629
1575 severe or worsening CS. 18. Thiele H, Ohman EM, Desch S, Eitel I, de Waha S. Management of 1630
1576 cardiogenic shock. Eur Heart J. 2015;36(20):1223-1230. 1631
1577Q15 19. Yoshida T, Yoshida T, Noma H, Nomura T, Suzuki A, Mihara T. 1632
Q16 Financial/Nonfinancial Disclosures Diagnostic accuracy of point-of-care ultrasound for shock: a
1578 systematic review and meta-analysis. Crit Care. 2023;27(1):200. 1633
Q17
None declared.
1579 20. Jentzer JC, Kashani KB, Wiley BM, et al. Laboratory markers of 1634
1580 acidosis and mortality in cardiogenic shock: developing a definition 1635
Acknowledgments of hemometabolic shock. Shock. 2022;57(1):31-40.
1581 1636
Author contributions: F. A. A., N. S., S. B. B., and D. F. were all 21. Jentzer JC, Schrage B, Patel PC, et al. Association between the
1582 involved in the preparation, research, writing, and editing of this 1637
acidemia, lactic acidosis, and shock severity with outcomes in
1583 manuscript. F. A. A. developed the first draft of the manuscript. All patients with cardiogenic shock. J Am Heart Assoc. 2022;11(9): 1638
authors reviewed and edited the final version of the manuscript. e024932.
1584 1639
1585 22. Fuernau G. Lactate and other biomarkers as treatment target in 1640
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1

[ Shock CHEST Critical Care Review ] 56

REV 5.6.0 DTD CHSTCC100071_proof 25 April 2024 6:07 pm EO: CHEST-CRITCARE-

2 CHEST Critical Care Review [ -#- CHEST Critical Care - 2024 ]

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4 CHEST Critical Care Review [ -#- CHEST Critical Care - 2024 ]

between smaller community hospitals and high-volume

456 In addition to regional care networks, institutional 511

and early, appropriate escalation to tMCS result in

467 improved survival.10,31 522

469 Hemodynamic Assessment and Monitoring 524

echocardiography, can be used to estimate

475 echocardiographic parameters have been shown to be 530

478 stroke volume index, cardiac index, cardiac power 533

481 volume and has been shown to be a predictor of in- 536

risk stratiﬁcation of patients with CS and can be

493 radiography in patients with chronic HF, which lacks 548

494 sensitivity in detecting pulmonary edema, and is less 549

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6 CHEST Critical Care Review [ -#- CHEST Critical Care - 2024 ]

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TABLE 2 ] Vasoactive Agents Used in CS

b-1 þþþ HR and contractility

from predominant renal excretion

REV 5.6.0 DTD CHSTCC100071_proof 25 April 2024 6:07 pm EO: CHEST-CRITCARE-

IABP Counterpulsation Ao Femoral or axillary 7-8 F 9d Ease of placement No oxygenation

Protek Duo RA to PA Right IJ vein 29 F or 31 F

12 CHEST Critical Care Review [ -#- CHEST Critical Care - 2024 ]

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14 CHEST Critical Care Review [ -#- CHEST Critical Care - 2024 ]

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16 CHEST Critical Care Review [ -#- CHEST Critical Care - 2024 ]

REV 5.6.0 DTD CHSTCC100071_proof 25 April 2024 6:07 pm EO: CHEST-CRITCARE-

18 CHEST Critical Care Review [ -#- CHEST Critical Care - 2024 ]

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