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Cardiogenic shock (CS) remains a complex, multifactorial syndrome associated with significant morbidity and mortality. The CardioNerds Critical Care Cardiology Series tackles this important syndrome in a series of several episodes including: LV-predominant Shock, RV-predominant Shock, and Bi-ventricular Shock.
In this episode, we review the definitions, pathophysiology, evaluation, and contemporary management, including use of inotropes and mechanical circulatory support, of left ventricular (LV) predominant CS. Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai along with CardioNerds Co-founders Dr. Amit Goyal and Dr. Daniel Ambinder were joined by FIT lead, Dr. Vanessa Blumer, the recipient of the AHA 2021 Laennec Fellow in Training Clinician Award and currently pursuing Advanced Heart Failure and Transplant fellowship at the Cleveland Clinic. Our episode expert is Dr. Shashank Sinha, an Advanced Heart Failure, Mechanical Circulatory Support, and Cardiac Transplant cardiologist, Medical Director of the Cardiac Intensive Care Unit, and Director of the Cardiovascular Critical Care Research Program at INOVA Fairfax Hospital. His illustrious career accomplishments include being a Steering Committee member and site Principal Investigator for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network. Audio editing by CardioNerds academy intern, Anusha Gandhi.
The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif.
Pearls • Notes • References • Production Team
Pearls and Quotes – LV Predominant Cardiogenic Shock
- LV-CS is complex! It is important to recognize that the pathophysiology of heart failure-related cardiogenic shock (HF-CS) is distinct from that of acute myocardial infarction (AMI-CS), and also crucial to differentiate between LV-dominant, right ventricular (RV)-dominant and biventricular (BiV)-shock.
- The SCAI SHOCK Stage Classification provides a unified and standardized vocabulary when assessing severity of CS, and facilitates communication about the diagnosis, presentation, and evolving nature of CS.
- Norepinephrine is considered the initial vasopressor of choice in most CS patients; the initial inotrope choice is a bit more nuanced!
- When considering mechanical circulatory support (MCS) for LV shock, high-quality data to guide therapy is lacking but one must always consider “the right patient, for the right device, at the right time” and remember that “pumps pump blood, decisions save lives”.
- Multidisciplinary, team-based care is paramount to improving survival of the critically ill patient with CS.
Show notes – LV Predominant Cardiogenic Shock
Notes drafted by Dr. Vanessa Blumer.
1. What tools do you use to define LV CS?
- CS is a hemodynamically complex and multifactorial syndrome, one of the most common indications for admission to a cardiac intensive care unit, with short-term mortality ranging from 35-50%.
- It is defined by systemic hypoperfusion and tissue hypoxia due to a primary cardiac insult or dysfunction.
- Clinical criteria used to define CS typically include evidence of hypotension (classically defined as SBP < 90 mmHg for 30 minutes and/or use of vasopressors, inotropes, or MCS to maintain systolic blood pressure > 90 mmHg) AND evidence of end-organ hypoperfusion (for example, serum lactic acid > 2 mmol/L, acute kidney injury, acute liver injury, altered mental status) in the setting of acute coronary syndrome or acute decompensated heart failure.
- Laboratory markers, including serum lactic acid, liver function tests, kidney function, and biomarkers including troponin and natriuretic peptides may be helpful. An echocardiogram is an excellent point of care tool to help demonstrate and confirm evidence of LV systolic dysfunction and/or valvular abnormalities. Finally, a right heart catheterization (demonstrating an abnormally low cardiac output and index with elevated filling pressures) may be useful in facilitating the diagnosis and subsequent management.
2. How do HF-CS and AMI-CS lead to different phenotypes?
- It is important to recognize that HF-CS is now the predominant cause of CS, accounting for more than half of all CS.
- AMI-CS is characterized by an abrupt presentation due to a primary myocardial ischemic insult leading to necrosis (occurring in 5-10% of AMI patients) and can occur after STEMI or NSTEMI. The canonical clinical course is hypotension due to primary myocardial dysfunction leading to hypoperfusion with congestion as a later clinical or hemodynamic finding.
- Conversely, a patient with heart failure related shock commonly presents with acutely decompensated heart failure and congestion, leading to hypoperfusion, and culminating in hypotension.
3. How do you distinguish LV-dominant, RV-dominant and BiV shock?
- LV predominant CS is characterized by high pulmonary capillary wedge pressure (PCWP) and normal or reduced central venous pressure (CVP) in the setting of reduced cardiac output (CO).
- RV dominant CS is characterized by elevated CVP, normal to low PCWP, and normal to reduced CO.
- BiV shock is characterized by hypotension, elevated CVP, normal or elevated PCWP, and reduced CO.
4. What is the current role for inotropes, vasodilators, and vasopressors in the management of LV CS?
- The Acute Cardiovascular Care Association of the European Society of Cardiology published a position statement for the diagnosis and treatment of patients with AMI complicated by CS in 2020. According to this, vasopressors (norepinephrine preferable over dopamine) in the presence of persistent hypotension received a Level of IIb/B recommendation. Intravenous inotropes to increase cardiac output received a IIb/C recommendation.
- Based on the available evidence and its accompanying limitations, norepinephrine is considered the initial vasopressor of choice in most CS patients.
5. When should we consider management with temporary mechanical circulatory support (t-MCS) devices and how should one strategize device selection?
- Initiation or escalation of t-MCS largely depends on matching the right device to the right patient at the right time. Because the risk and number of complications increases with duration and type of MCS, these decisions are complex, nuanced, and must consider operator and institutional expertise.
- When considering type of device (IABP, Impella, ECMO), SCAI Staging and phenotyping (AMI vs HF CS) are absolutely critical.
6. What are treatment goals when following patients with LV CS?
- Optimize preload, afterload, and contractility
- Perform serial reassessment (≤ q 6hr) of hemodynamics & end-organ perfusion
- Aim for timely and tailored treatment escalation/de-escalation
- Assess for LV and RV recovery (wean t-MCS, vasopressors and inotropes as able
- Early identification of worsening shock:
- Rising Lactate
- Increasing pressor requirement
- Worsening end-organ function
- CPO < 0.6 and/or PAPi < 1
- RA > 15 and/or PCWP > 15