Cardiogenic shock classification
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammad Salih, MD. João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3]
Overview
The Society for Cardiovascular Angiography and Intervention (SCAI) developed an expert consensus statement, endorsed by multiple relevant societies, proposing a novel CS classification scheme, which categorizes patients with or at risk of CS into worsening stages of hemodynamic compromise for the purposes of facilitating patient care and research. The SCAI CS classification consensus statement describes 5 stages of CS, each of which may have an “A” modifier signifying the occurrence of cardiac arrest (CA). This classification schema was developed based on expert consensus opinion and its ability to discriminate among levels of mortality risk in critically ill patients remains to be established. The goal of this study was to examine the construct validity of the SCAI CS staging schema by demonstrating the ability of a simple functional classification of SCAI shock stages at the time of cardiac intensive care unit (CICU) admission to predict mortality in CICU patients.The purpose of the classification schema is to assist in clear communication among clinicians and researchers regarding the patient’s current clinical status, recognizing that CS encompasses a spectrum, including those at high risk of developing shock from myocardial dysfunction to those who develop hemodynamic collapse and cardiac arrest. The CS classification schema includes five stages of shock labeled A through E. The authors categorized patients in three domains, including laboratory findings, physical exams findings, and hemodynamics. When cardiac arrest has occurred the modifier (A) is added to stage classification (i.e. stage CA).
Classification
- Here is a brief description of each stage, including the domains of patient characteristics that you can expect to find when your patient is each stage.[1][2]
Stage A or “At Risk”
- Patient identified at risk of developing, but is not yet displaying signs or symptoms of CS
- Diagnoses such as non-ST elevated myocardial infarction, ST elevated myocardial infarction (especially in the anterior wall distribution or large infarcts), and decompensated heart failure (both systolic and diastolic)
- Physical exam, laboratory, and hemodynamics are within normal limits.
Stage B or “Beginning CS”
- Also referred to as pre-shock or compensated shock
- Patient with relative hypotension (SBP < 90 mm Hg or mean arterial pressure [MAP] < 60 mm Hg or drop in MAP of > 30 mm Hg from baseline) or tachycardia (pulse > 100 bpm) without hypoperfusion
- Physical exam findings may include elevated jugular vein distension (JVP), rales in lung fields, warm skin with strong distal pulses, normal mentation
- Laboratory findings may include normal lactate, minimal renal function impairment, and elevated brain natriuretic peptide (BNP)
- Hemodynamic findings include relative hypotension, tachycardia, normal cardiac index (≥ 2.2 L/min/m2) and pulmonary arterial (PA) oxygen saturation ≥ 65%.
Stage C or “Classic CS”
- Patient with hypotension and signs of hypoperfusion that require various interventions (inotropes, pressor, mechanical support, or extracorporeal membrane oxygenation [ECMO])
- Physical exam findings may include distressed/panicked appearance, ashen/mottled/ dusky skin color, extensive rales in lung fields, cold/clammy skin temperature, altered mentation, decreased urine output (< 30 mL/h)
- Laboratory findings may include lactate ≥ 2 mmol/L, decreased renal function (creatinine doubling or > 50% drop in glomerular filtration rate [GFR])
- Hemodynamic findings may include SBP <90 mm Hg or MAP < 60 mm Hg or drop in MAP > 30 mm Hg from baseline and devices/medications utilized to maintain adequate SBP, *cardiac index < 2.2 L/min/m2, pulmonary artery capillary wedge pressure (PCWP) > 15 mm Hg, cardiac power output ≤ 0.6 W/m2.
Stage D or “Deteriorating or Doom CS”
- Patient who fail to stabilize after at least 30 minutes of initial treatment methods
- Treatment efforts are escalated, including the addition of multiple pressors; mechanical circulatory support may be initiated
- Physical exam, laboratory, and hemodynamic findings are similar to those found in stage C, but deteriorating.
Stage E or “Extremis”
- Patient with circulatory collapse, possibly with cardiac arrest with ongoing cardiopulmonary resuscitation (CPR) and/or ECMO
- Patient requires multiple interventions (mechanical ventilation, defibrillation) and assistance from multiple clinicians
- Physical exam findings may include near pulselessness, severe hypotension, lethal cardiac disturbances (pulseless electrical activity [PEA], ventricular tachycardia, ventricular fibrillation)
- Laboratory findings may include lactate ≥ 5 mmol/L and pH ≤ 7
- Hemodynamic findings include no SBP without resuscitation, PEA or ventricular arrythmias, hypotension despite maximum medical interventions.
In cardiogenic shock, the root abnormality is the inability of the heart to pump out enough blood to maintain normal organ perfusion and blood pressure. However, this failure may be due to different factors, which allow us to classify cardiogenic shock into two categories:[3][4][5]
- Intrinsic - this includes the conditions affecting the heart or the structures that allow it to function properly. In this category, the affected structures may be: the myocardial muscle, responsible to pump out the blood; the heart valves allowing the blood in and out of the heart chambers; the conduction system, responsible for the transmission of the electrical signals that allow the myocardium to contract in a coordinated fashion or, a combination of the previous. Examples of such factors are: myocardial infarction, mitral regurgitation and electrolyte imbalances.
- Compressive - this includes the conditions in which an otherwise "healthy heart" is prevented from working properly and pumping the blood through the vascular system, by a mechanism not related to it. The degree of impact that an extrinsic factor must have on the heart will depend on the overall "health status" of this last one. An "healthy heart" might take a more aggressive outside influence without compromising its function, while a heart already weakened by another disease, such as atherosclerosis, might fail more promptly. An example of such factor is cardiac tamponade.
Often times both factors are affecting the heart's ability to perform its function, at which times it might be hard to identify clearly the underlying mechanism of the cardiogenic shock.[6]
References
- ↑ . doi:10.1016/j.jacc.2019.07.07. Missing or empty
|title=(help) - ↑ van Diepen, Sean; Katz, Jason N.; Albert, Nancy M.; Henry, Timothy D.; Jacobs, Alice K.; Kapur, Navin K.; Kilic, Ahmet; Menon, Venu; Ohman, E. Magnus; Sweitzer, Nancy K.; Thiele, Holger; Washam, Jeffrey B.; Cohen, Mauricio G. (2017). "Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association". Circulation. 136 (16). doi:10.1161/CIR.0000000000000525. ISSN 0009-7322.
- ↑ Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
- ↑ Myers, Jeffrey (2002). Principles of pathophysiology and emergency medical care. Albany: Delmar/Thomson Learning. ISBN 978-0766825482.
- ↑ Kheng CP, Rahman NH (July 2012). "The use of end-tidal carbon dioxide monitoring in patients with hypotension in the emergency department". Int J Emerg Med. 5 (1): 31. doi:10.1186/1865-1380-5-31. PMC 3585511. PMID 22828152.
- ↑ Myers, Jeffrey (2002). Principles of pathophysiology and emergency medical care. Albany: Delmar/Thomson Learning. ISBN 978-0766825482.