Critical Care Archives - Cardionerds

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In this webinar, the CardioNerds collaborated with the Cardiogenic Shock Working Group (CSWG) to discuss LV unloading and the updated AMI guidelines, which upgraded transvalvular flow pumps to a Class 2A recommendation in AMI shock.

Dr. Rachel Goodman and Dr. Gurleen Kaur from CardioNerds were joined by Dr. Navin Kapur (Tufts Medical Center), Dr. Shashank Sinha (INOVA Fairfax Hospital), and Dr. Rachna Kataria (Brown University) from the CSWG.

Together, they explore a case of an older woman who presented with inferior STEMI and was found to have complete occlusion of an anomalous single coronary artery originating from the right coronary cusp and supplying the entire left ventricle. She was treated with DES to the anomalous RCA. Her course was complicated by AMI shock with re-occlusion of the DES, which was treated with thrombectomy and balloon angioplasty. An IABP was placed. After transfer to a tertiary care center, a pulmonary artery catheter revealed a CI of 0.96. With worsening shock, rising lactate, and end organ dysfunction, the team proceeded with VA-ECMO and Impella CP for LV unloading. Her lactate subsequently normalized.

Produced by CardioNerds in collaboration with the Cardiogenic Shock Working Group.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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CardioNerds Co-Founder, Dr. Amit Goyal, along with Series Co-Chairs, Dr. Yoav Karpenshif and Dr. Eunice Dugan, and episode Lead, Dr. Sean Dikdan, had the opportunity to expand their knowledge on the topic of ventricular tachycardia and electrical storm from esteemed faculty expert, Dr. Janice Chyou.

Electrical storm (ES) is a life-threatening arrhythmia syndrome. It is characterized by frequently occurring bouts of unstable cardiac arrythmias. It typically occurs in patients with susceptible substrate, either myocardial scar or a genetic predisposition. The adrenergic input of the sympathetic nervous system can perpetuate arrythmia. In the acute setting, identifying reversible triggers, such as ischemia, electrolyte imbalances, and heart failure, is important. Treatment is complex and varies based on previous treatments received and the presence of intra-cardiac devices. Many options are available to treat ES, including medications, intubation and sedation, procedures and surgeries targeting the autonomic nervous system, and catheter ablation to modulate the myocardial substrate. A multidisciplinary team of cardiologists, intensivists, electrophysiologists, surgeons, and more are necessary to manage this complex disease.

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.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Pearls • Notes • References • Production Team

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Pearls and Quotes – Management of Ventricular Tachycardia and Electrical Storm 1. Electrical storm is defined as 3 or more episodes of VF, sustained VT, or appropriate ICD shocks within 24 hours. It occurs more commonly in ischemic compared to non-ischemic cardiomyopathy, and it is associated with a poor prognosis and high cardiovascular mortality. 2. The classic triad of electrical storm is a trigger, a myocardial susceptible substrate, and autonomic input perpetuating the storm. 3. Triggers for electrical storm include ischemia, heart failure, electrolyte abnormalities, hypoxia, drug-related arrhythmogenicity, and thyrotoxicosis. A thorough evaluation of possible triggers is necessary for each patient, but it is uncommonly found. The evaluation may include laboratory studies, genetic testing, advanced imaging, or invasive testing. 4. Acute treatment options involve acute resuscitation, pharmacotherapy with antiarrhythmics and beta-blockers, device interrogation and possible reprogramming, and sedation. Subacute treatment involves autonomic modulation and catheter ablation. Surgical treatments include sympathectomies and, ultimately, heart transplant. 5. Catheter ablation is safe and effective for the treatment of electrical storm. In select patients, hemodynamic peri-procedural hemodynamic support should be considered.

Show notes – Management of Ventricular Tachycardia and Electrical Storm Simple diagram of the classic “triad” of ES (see reference 10).

Treatment algorithm provided by the 2017 AHA/ACC/HRS guidelines (see reference 1).

1. Define electrical storm.

Electrical storm (ES), also called “arrhythmic storm” or “VT storm” refers to a state of cardiac instability associated with 3 or more episodes of VF, sustained VT, or appropriate ICD shocks within 24 hours. Sustained VT refers to 30 seconds of VT or hemodynamically unstable VT requiring termination in < 30 seconds. Incessant VT refers to continued, sustained hemodynamically stable VT that lasts longer than one hour. VT is incessant or recurrent when it recurs promptly despite repeated intervention for termination.1,2

In patients with ICDs for secondary prevention, ES is estimated to occur in 10-28% of patients.3–5 This incidence is much lower in patients who have ICDs implanted for primary prevention in whom the incidence has been estimated as low as 4% at 20 months of follow up.6 ES occurs at similar rates in patients with ischemic or non-ischemic cardiomyopathy.7

ES is associated with a poor prognosis and high cardiovascular mortality. The three-month mortality in patients with an episode of ES has been estimated at up to 18 times higher than in patients without any VT.6 Risk factors for the development of ES include male sex, advanced age, low left ventricular ejection fraction, use of class 1A antiarrhythmic drugs, and the presence of cardiovascular comorbidities.8,9

2. Evaluate the cause of VT storm (e.g., evaluation for ischemia, sarcoidosis , etc)

The classic triad of ES is a trigger, a substrate susceptible to ES, and autonomic input perpetuating the storm.10 Potential triggers are varied and typically include myocardial ischemia, decompensated heart failure, electrolyte abnormalities, hypoxia, drug-related arrhythmogenicity, and thyrotoxicosis.4,11 A clear trigger is often not found (only 13% of the time by some estimates).12 Searching for a trigger should not delay management decisions in the acute setting.

Structural heart disease unrelated to ischemia such as congenital heart disease and infiltrative cardiomyopathies can serve as the substrate for ES. Conditions related to genetic causes such as long QT syndrome or catecholaminergic polymorphic VT may be a rare etiology. These conditions represent an electrophysiologic substrate as opposed to a structural substrate.13

3. Choose an initial management strategy for patients with electrical storm in the CCU.

Treatment of ES is complex. The initial steps in management involve resuscitation, pharmacotherapy, device interrogation and reprogramming, and sedation. ACLS should be used in patients with pulseless VT or VF.

Patients with and without cardioverter-defibrillators may be treated differently. Defibrillations from an implanted device accentuate sympathetic tone and may perpetuate further arrhythmia.

Once a patient is stabilized, more advanced therapies involving autonomic modulation or catheter ablation (CA) can be utilized. In the patient with ischemia, emergent revascularization should be pursued. The need for mechanical circulatory support (MCS) should be determined. Inotropes and many vasopressors are sympathetic agonists and may worsen the arrhythmia by accentuating adrenergic tone, and so the benefits of improved hemodynamics need to be weighed against the risk of worsening electrical instability.

Initial pharmacotherapy in ES includes an antiarrhythmic drug and a beta blocker. Typically loading the patient with IV amiodarone and administering a non-selective beta blocker like propranolol is done. This combination has been shown in ES patients to have superior freedom of arrhythmia compared to using metoprolol.14 Propranolol’s superiority may also be due to its ability to cross the blood-brain barrier. Lidocaine has improved efficacy in ischemic VT.15,16 Procainamide has been shown to be useful in patients with hemodynamically stable VT.17

4. Identify predisposing conditions that should be managed to help treat electrical storm such as ischemia and AHF.

Identifying and managing specific triggers is an important initial step in the management of ES. Hypoxia on vital signs or evidence of decompensated HF on exam (with JVD, edema, crackles on auscultation) can implicate volume overload; this can be managed with diuresis.

Ischemic ECG changes on the 12-lead ECG when the patient’s ventricular arrhythmia is broken, can suggest myocardial ischemia. If ischemia is believed to be the trigger, urgent revascularization should be pursued while resuscitation is underway.

Blood work should include screening for electrolyte abnormalities and thyroid disease. Carefully screening the patient’s medication list and checking a digoxin level (when appropriate) can help detect drug-induced arrhythmia.

Once out of the acute setting, genetic testing may be important in patients without structural disease for determining an etiology. Idiopathic VT, Brugada syndrome, long QT syndrome, short QT syndrome, early repolarization syndrome, catecholaminergic polymorphic VT, arrhythmogenic right ventricular cardiomyopathy, and cardiac sarcoidosis are potential etiologies that may be related to ES.10

5. Recognize when to use general anesthesia to aid in the stabilization of electrical storm and incessant VT.

Intubation and deep sedation are immediate next steps to minimize the sympathetic drive contributing to the arrhythmia. This treatment is very effective at terminating arrythmia and preventing immediate recurrence.18,19 This step is used in the acute setting for ES that persists despite pharmacotherapy. Note that propofol is a negative inotrope with the potential to worsen heart failure in decompensated patients and precipitate shock.

In addition to breaking the sympathetic cycle that drives this pathophysiology, sedation mitigates some of the psychological stress that repeated ICD shocks can cause in patients.20

6. Describe considerations specific to patients with implanted ICDs.

If a patient with an ICD presents with ES, the device should be interrogated. It is important to confirm the shocks are appropriate. Inappropriate shocks can occur in up to 40% of patients with an ICD; causes may include atrial arrythmia, oversensing, and lead fracture.21,22 Inappropriate ICD shocks are associated with a worse outcome.

Overdrive pacing is a possible therapy to prevent ES. If the ES is hemodynamically stable, then the ICD therapies may be disabled manually or with the use of a magnet.

If anti-tachycardia pacing (ATP) treats the ventricular arrythmia effectively, adjusting these settings and increasing the use of ATP can mitigate unnecessary shocks in the future.23

7. Understand the role of catheter ablation in the management of electrical storm.

Research has shown an excellent response of ES to catheter ablation (CA). CA has a class 1 indication in patients with ES due to anti-arrhythmic drug refractory VA in both ischemic and nonischemic cardiomyopathy.2

Treatment of an initial episode of ES with CA has shown a reduction in all-cause mortality compared to other modalities.24 At nearly 1-2 years of follow up, nearly 90% of patients with ES that undergo CA are free from further ES, and roughly two-thirds of these patients are free from any ventricular arrythmia (VA) recurrence.25,26

CA is also relatively safe in this setting, with procedure-related mortality estimated to be less than 1%.27 Rapid transfer to an experienced catheter ablation capable facility is important in all critically ill patients with ES.

8. Consider when it may be appropriate to use mechanical support such as IABP, pVAD and ECMO.

Mechanical circulatory support (MCS) may be necessary to maintain adequate perfusion when the patient is suffering from cardiogenic shock due to unstable arrhythmia.

Patients with high risk for hemodynamic decompensation during CA can be preemptively supported with MCS. This practice has been shown to improve mortality compared to rescue or no MCS. 28,29 The PAAINESD score may be useful in identifying high risk patients. This score assigns numerical values to the following risk factors: pulmonary disease, age over 60 years, general anesthesia, ischemic cardiomyopathy, NYHA class III or IV, LV EF < 25%, VT storm, and diabetes mellitus. 2,28

An intra-aortic balloon pump may be sufficient but requires the patient to have enough adequate forward flow to generate a pulse. Extracorporeal membrane oxygenation (ECMO) has been studied and shows good long-term outcomes.29 Guidelines have a IIa recommendation for hemodynamic support with ECMO or a temporary LVAD during CA in select patients. 2

9. Discuss other strategies such as sympathectomies (stellate ganglion block vs. surgical), stereotactic radio ablation, and transplant for refractory cases.

There are several therapies available to treat ES that specifically target the autonomic nervous system (ANS).30 While sedation is used for this purpose acutely, other interventions seek to mitigate sympathetic activity in the subacute or chronic setting. These include stellate ganglion blockade (SGB), thoracic epidural anesthesia (TEA), cardiac sympathetic denervation (CSD), and renal artery sympathetic denervation (RSD).

Percutaneous SBG involves an injection of anesthetic directly into the stellate ganglia with or without ultrasound guidance. This is a temporizing measure that can be performed in the acute or subacute setting. It has shown complete suppression of VA in 50% of patients for the subsequent 48 hours.31

TEA involves the percutaneous administration of a local anesthetic directly into the thoracic epidural space. This is also a temporary treatment best used as a bridge to definitive treatment, such as CA or surgical denervation. In ES patients with a failed CA TEA can reduce VA up to 80% in most patients.32

CSD is a surgical measure that offers a more permanent solution. It can be useful in refractory ES that has not responded to multiple treatments. CSD has achieved 80% event-free survival up to 2 years.33 Guidelines recommend CSD in ES when beta-blockade, anti-arrhythmic drugs, and CA are deemed ineffective with a class IIb recommendation.1

RSD functions similarly but has the added benefit of being non-surgical and directly reducing catecholamine secretion.

Cardiac transplantation would be indicated in a patient that has unrelenting ES despite these aggressive measures. Patients with MCS and life-threatening arrhythmias qualify as status 1 for OHT.34 Whereas VT/VF without MCS by itself would qualify a patient as status 2.

References 1. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Circulation 2018;138(13):e272–391. 2. Cronin EM, Bogun FM, Maury P, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias. Europace 2019;21(8):1143–4. 3. Exner D v, Pinski SL, Wyse DG, et al. Electrical Storm Presages Nonsudden Death The Antiarrhythmics Versus Implantable Defibrillators (AVID) Trial. Circulation [Internet] 2001;103:2066–71. Available from: http://www.circulationaha.org 4. Credner SC, Klingenheben T, Mauss O, Sticherling C, Hohnloser SH. Electrical Storm in Patients With Transvenous Implantable Cardioverter-Defibrillators Incidence, Management and Prognostic Implications. J Am Coll Cardiol 1998;32(7):1909–15. 5. Bänsch D, Böcker D, Brunn J, Weber M, Breithardt G, Block M. Clusters of Ventricular Tachycardias Signify Impaired Survival in Patients With Idiopathic Dilated Cardiomyopathy and Implantable Cardioverter Defibrillators. J Am Coll Cardiol 2000;36(2):566–73. 6. Sesselberg HW, Moss AJ, McNitt S, et al. Ventricular arrhythmia storms in postinfarction patients with implantable defibrillators for primary prevention indications: A MADIT-II substudy. Heart Rhythm 2007;4(11):1395–402. 7. Streitner F, Kuschyk J, Dietrich C, et al. Comparison of ventricular tachyarrhythmia characteristics in patients with idiopathic dilated or ischemic cardiomyopathy and defibrillators implanted for primary prevention. Clin Cardiol 2011;34(10):604–9. 8. Vergara P, Tung R, Vaseghi M, et al. Successful ventricular tachycardia ablation in patients with electrical storm reduces recurrences and improves survival. Heart Rhythm 2018;15(1):48–55. 9. Emkanjoo Z, Alihasani N, Alizadeh A, et al. Electrical Storm in Patients with Implantable Cardioverter-Defibrillators Can It Be Forecast? Tex Heart Inst J 2009;36(6):563–7. 10. Kowlgi GN, Cha YM. Management of ventricular electrical storm: A contemporary appraisal. Europace 2020;22(12):1768–80. 11. Muser D, Liang J, Santangeli P. Electrical Storm in Patients with Implantable Cardioverter-defibrillators: A Practical Overview. J Innov Card Rhythm Manag 2017;8(10):2853–61. 12. Stefan H. Hohnloser, Hussein R. Al-Khalidi, Craig M. Pratt, et al. Electrical storm in patients with an implantable defibrillator: incidence, features, and preventive therapy: insights from a randomized trial. Eur Heart J 2006;27(24):3027–32. 13. Geraghty L, Santangeli P, Tedrow UB, Shivkumar K, Kumar S. Contemporary Management of Electrical Storm. Heart Lung Circ 2019;28(1):123–33. 14. Chatzidou S, Kontogiannis C, Tsilimigras DI, et al. Propranolol Versus Metoprolol for Treatment of Electrical Storm in Patients With Implantable Cardioverter-Defibrillator. J Am Coll Cardiol 2018;71(17):1897–906. 15. MacMahon S, Collins R, Peto R, Koster RW, Yusuf S, MacMahon M. Effects of Prophylactic Lidocaine in Suspected Acute Myocardial Infarction. J Am Med Assoc [Internet] 1988;260(13):1910–6. Available from: https://jamanetwork.com/ 16. Collinsworth KA, Kalman SM, Harrison DC. The Clinical Pharmacology of Lidocaine as an Antiarrhythymic Drug. Circulation [Internet] 1974;50(6):1217–30. Available from: http://ahajournals.org 17. Ortiz M, Martin A, Arribas F, et al. Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: The PROCAMIO study. Eur Heart J 2017;38(17):1329–35. 18. Martins RP, Urien JM, Barbarot N, et al. Effectiveness of Deep Sedation for Patients With Intractable Electrical Storm Refractory to Antiarrhythmic Drugs. Circulation 2020;142(16):1599–601. 19. Bundgaard JS, Jacobsen PK, Grand J, et al. Deep sedation as temporary bridge to definitive treatment of ventricular arrhythmia storm. Eur Heart J Acute Cardiovasc Care 2020;9(6):657–64. 20. Passman R, Subacius H, Ruo B, et al. Implantable Cardioverter Defibrillators and Quality of Life Results From the Defibrillators in Nonischemic Cardiomyopathy Treatment Evaluation Study. Journal of the American Medical Association Internal Medicine [Internet] 2007;167(20):2226–32. Available from: https://jamanetwork.com/ 21. Powell BD, Saxon LA, Boehmer JP, et al. Survival after shock therapy in implantable cardioverter-defibrillator and cardiac resynchronization therapy-defibrillator recipients according to rhythm shocked: The altitude survival by rhythm study. J Am Coll Cardiol 2013;62(18):1674–9. 22. van Rees JB, Borleffs CJW, de Bie MK, et al. Inappropriate implantable cardioverter-defibrillator shocks: Incidence, predictors, and impact on mortality. J Am Coll Cardiol 2011;57(5):556–62. 23. Wathen MS, DeGroot PJ, Sweeney MO, et al. Prospective randomized multicenter trial of empirical antitachycardia pacing versus shocks for spontaneous rapid ventricular tachycardia in patients with implantable cardioverter-defibrillators: Pacing fast ventricular tachycardia reduces shock therapies (PainFREE Rx II) trial results. Circulation 2004;110(17):2591–6. 24. Morawski S, Pruszkowska P, Sredniawa B, Lenarczyk R, Kalarus Z. Long-term outcome of catheter ablation and other form of therapy for electrical storm in patients with implantable cardioverter-defibrillators. Journal of Interventional Cardiac Electrophysiology 2017;50(3):227–34. 25. Carbucicchio C, Santamaria M, Trevisi N, et al. Catheter ablation for the treatment of electrical storm in patients with implantable cardioverter-defibrillators : Short-and long-term outcomes in a prospective single-center study. Circulation 2008;117(4):462–9. 26. Deneke T, Shin DI, Lawo T, et al. Catheter ablation of electrical storm in a collaborative hospital network. American Journal of Cardiology 2011;108(2):233–9. 27. Nayyar S, Ganesan AN, Brooks AG, Sullivan T, Roberts-Thomson KC, Sanders P. Venturing into ventricular arrhythmia storm: A systematic review and meta-analysis. Eur Heart J 2013;34(8):560–9. 28. Mariani S, Napp LC, lo Coco V, et al. Mechanical circulatory support for life-threatening arrhythmia: A systematic review. Int J Cardiol 2020;308:42–9. 29. Baratto F, Pappalardo F, Oloriz T, et al. Extracorporeal Membrane Oxygenation for Hemodynamic Support of Ventricular Tachycardia Ablation. Circ Arrhythm Electrophysiol 2016;9(12). 30. Zhu C, Hanna P, Rajendran PS, Shivkumar K. Neuromodulation for Ventricular Tachycardia and Atrial Fibrillation: A Clinical Scenario-Based Review. JACC Clin Electrophysiol 2019;5(8):881–96. 31. Fudim M, Qadri YJ, Waldron NH, et al. Stellate Ganglion Blockade for the Treatment of Refractory Ventricular Arrhythmias. JACC Clin Electrophysiol 2020;6(5):562–71. 32. Bourke T, Vaseghi M, Michowitz Y, et al. Neuraxial modulation for refractory ventricular arrhythmias: Value of thoracic epidural anesthesia and surgical left cardiac sympathetic denervation. Circulation 2010;121(21):2255–62. 33. Li J, Liu Y, Yang F, et al. Video-Assisted Thoracoscopic Left Cardiac Sympathetic Denervation: A Reliable Minimally Invasive Approach for Congenital Long-QT Syndrome. Annals of Thoracic Surgery 2008;86(6):1955–8. 34. Stevenson LW, Kormos RL, Young JB, Kirklin JK, Hunt SA. Major advantages and critical challenge for the proposed United States heart allocation system. Journal of Heart and Lung Transplantation 2016;35(5):547–9.

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The practice of critical care cardiology relies on the use of invasive hemodynamics, mechanical ventilation, mechanical circulatory support, and other advanced techniques to help our patients recover from critical cardiac illnesses. To facilitate these interventions, it is essential to have a broad understanding of how sedation and analgesia keep our patients comfortable and safe throughout their time in the CICU. In this episode, series co-chair, Dr. Yoav Karpenshif, and CardioNerds co-founder, Dr. Daniel Ambinder, are joined by Dr. Natalie Tapaskar, cardiology fellow and CardioNerds FIT Ambassador from Stanford, and faculty expert, Dr. Chris Domenico, to discuss sedation in the cardiac ICU. Notes were drafted by Dr. Natalie Tapaskar. Audio editing by CardioNerds academy intern, Anusha Gandhi.

We discuss the use of analgesics and sedative medications in the cardiac ICU. We dissect three cases of VT storm, heart failure associated cardiogenic shock, and cardiac arrest. We assess the hemodynamic, arrhythmic, and metabolic effects of opioids and sedatives and delve into the altered pharmacokinetics of these drugs during targeted temperature management. Most importantly, we highlight the use of structured pain and sedation scoring systems and discuss the recognition and management of ICU delirium both from a pharmacologic and non-pharmacologic standpoint.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Pearls • Notes • References • Production Team

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Pearls and Quotes – Sedation in the Cardiac ICU with Dr. Christopher Domenico1. Think about analgesia and sedation as separate entities with management of analgesia first and sedation second. Frequent re-assessment of needs should be performed to reduce ICU delirium and improve long-term outcomes. 2. Fentanyl is generally a good starting point for analgesia in the ICU since it is fast on/fast off, but can stick around for a long time the longer it is used. The choice of bolus or continuous infusion opioids depends on the clinical scenario and personal/institutional preference. Remember to administer bolus doses that are 50-100% of the hourly continuous infusion dose to reach steady state faster. 3. When managing refractory VT storm with sedative agents (propofol, benzodiazepines and/or dexmedetomidine), you should target the deepest level of sedation necessary to suppress sympathetic drive. 4. For cardiogenic shock patients, the choice of sedative agent is a nuanced decision. Think about etomidate first for intubation as it has the least cardiovascular and hemodynamic impact. And remember the propofol trifecta: negative inotropy, direct vasodilation, and bradycardia! 5. Pharmacokinetics are disrupted during targeted temperature management, thus be weary of overly sedating patients due to reduced drug clearance.

Show notes – Sedation in the Cardiac ICU with Dr. Christopher Domenico * How do we initiate analgesics and sedatives? + Analgesia first and sedation second! * Analgesia: think about how to reduce a patient’s pain + Everyone has a different pain tolerance and critically ill patients can have moderate to severe pain at baseline. + Metrics to assess pain include self-reported scales, behavioral scales, facial expressions, extremity movement, compliance with the ventilator, tachycardia, tachypnea, and hypertension. * Sedation: think about how to reduce a patient’s agitation or anxiety + The target depth of sedation depends on the clinical scenario. - For example, a patient with a femoral balloon pump may need more sedation if agitation is causing excessive lower extremity movement and thus a higher risk of device dislodgement. + Use the Richmond Agitation and Sedation Scale (RASS) for titrating sedation leve. - -5 – Unarousable. No response to voice or physical stimuli - -4 – Deep sedation. No response to voice, but movement or eye opening to physical stimulation - -3 – Moderate sedation. Movement or eye-opening to voice - -2 – Light sedation. Briefly awakens to voice - -1 – Drowsy. Not fully alert, but has sustained awakening to voice - 0 – Alert and calm - +1 – Restless. Anxious, apprehensive, but not aggressive - +2 – Agitated. Frequent non-purposeful movement, fights vent - +3 – Very agitated. Pulls or removes tubes/catheters - +4 – Combative. Violent, immediate danger to staff * What are the different opioid options and when should we use them? + Break down opioids into 3 groups (as per Dr. Domenico): - Group 1 (morphine, hydromorphone, fentanyl) for pain management in the ICU. * Onset of action: Fentanyl is the quickest on/off (30 seconds-2 minutes), but is highly lipophilic, redistributing in fatty tissues after ~30 minutes. The longer you use fentanyl, the longer it will stick around – i.e. “context-sensitive half-time.” Morphine and Hydromorphone have an onset from 5-15 minutes. * Half-life: All 3 are similar at 2-4 hours. (Fentanyl can be even higher the longer it is used). * Metabolism: Morphine is metabolized by the liver, but has active metabolites that are renally cleared; thus, be cautious with high doses in renal impairment. Fentanyl is metabolized by the CYP system thus it accumulates in hepatic dysfunction. - Group 2 (remifentanil and sufentanil) generally for use in the operating room. * Onset of action: Both are very quick on/off ranging from 1-3 minutes. * Half-life: Remifentanil’s is 3-10 minutes, whereas sufentanil’s is 2-3 hours. * Metabolism: Remifentanil demonstrates no accumulation in hepatic or renal impairment, thus is a good choice in these scenarios. Beware of the rare possibility of serotonin syndrome with both these agents. - Group 3 (methadone) as a bridge to wean off from long term infusions of other opioids. * Onset of action: 1-20 minutes when given intravenously, but 3-5 days when given orally. * Half-life: Ranges from 8-60 hours. * Metabolism: Hepatic, exercise caution with dysfunction. Also monitor for QT prolongation. * Should we administer opioids as boluses or continuous infusions? + There is no strong data to guide bolus versus continuous infusion dosing of opioids and the choice is often left up to personal/institutional preference. Small studies in emergency department patients suggest there is less ICU delirium post-intubation with bolus dosing over continuous infusions of opioids. + Generally, think about starting with bolus dosing to assess a patient’s true needs, but patients may require continuous infusions if they are receiving frequent boluses. + When increasing the rate of a continuous infusion, one can reach steady state faster by administering bolus doses at 50-100% of the hourly dose of the infusion. * How should we use analgesics and sedatives for management of arrhythmias, specifically VT storm? + The main goal in refractory VT storm is to sedate the patient as deeply as necessary to suppress their sympathetic drive. Generally, the choice of sedative agent is less important than the level of sedation achieved. - Propofol, benzodiazepines, and dexmedetomidine can all decrease sympathetic drive. - Propofol has some anti-arrhythmic effects via autonomic nervous system modulation. - Dexmedetomidine may increase the arrhythmogenic threshold. - Benzodiazepines have no direct effect on the conduction system. + Opioids have GABA agonist properties and thus have some anti-arrhythmic properties. However, opioids alone are rarely effective in managing malignant arrhythmias unless pain is the main trigger for the arrhythmia. + In some animal studies, fentanyl and morphine are thought to increase the ventricular fibrillation threshold, but this is not validated with hard outcomes in clinical trials. * What sedatives are safe to use for intubation in cardiogenic shock? + Induction: Etomidate, ketamine, and propofol are common agents used for induction of sedation peri-intubation. - Etomidate – has minimal cardiovascular/hemodynamic effects and should be considered first for induction in cardiogenic shock. Can lead to adrenal insufficiency. - Ketamine – is a direct vasoconstrictor (including coronary arteries) and results in hypertension and tachycardia. It should be avoided in patients with ACS. It may have a direct myocardial depressant effect, so its use is avoided in prolonged shock states. - Propofol – has a plethora of properties-sedative, hypnotic, amnestic, antiemetic, and anticonvulsant, but importantly has NO ANALGESIC properties. Remember its hemodynamic trifecta: negative inotropy, direct vasodilation, and bradycardia. It is also highly lipophilic, with a long half-life with extended infusions- i.e. “context-sensitive half-time”. Don’t forget to check triglyceride levels at baseline and at regular intervals while on a continuous infusion. + Maintenance: Propofol, benzodiazepines, and dexmedetomidine can be used for maintenance of sedation post-intubation. - Benzodiazepines * Also have a plethora of properties- sedative, amnestic, anticonvulsant, anxiolytic, and hypnotic but NO ANALGESIC properties. * Midazolam is quicker on/off (2-5 minutes) compared to lorazepam. Midazolam can accumulate in renal dysfunction. Think about polyethylene toxicity when patients on lorazepam at high doses for extended periods of time develop metabolic acidosis. * In general, benzodiazepines use is associated with increased ventilator time, ICU delirium, and ICU length of stay. - Dexmedetomidine * Is an alpha 2 agonist and thus monitor for hypotension and bradycardia with ongoing use. It does not cause respiratory depression. It generally does not result in deep sedation (less than -2) and is not very effective for acute management of agitation. Consider its use for patients that require mild sedation during extubation. * What are general principles of analgesia and sedation during targeted temperature management? + Always assess baseline pain and RASS prior to medication initiation. Once the need for analgesia and sedation is established, these medications should be started prior to initiating cooling protocols. + Consider using the lowest effective doses of medications to increase the ability to perform accurate neuro-prognostication. + Pharmacokinetics are disrupted during TTM, including absorption, distribution, metabolism, and excretion. These properties may vary among drugs of the same class. - In hypothermia, there is a general decrease in global drug perfusion as there is shunting of blood away from non-vital organs and intra-vascular volume of distribution is reduced. Drug clearance may be reduced, thus be cautious of over-sedation. - Serum creatinine may not be a reliable indicator of renal function during TTM as there is a decrease in creatinine synthesis and secretion. + Remember that hypothermia can cause hypomagnesemia, check and replete often! * How should we manage shivering? + Shivering increases baseline metabolic activity and is associated with decreased brain tissue oxygenation and can lead to worsening hypoxic brain injury. + Assess shivering using the bedside shivering assessment scale (BSAS). + Use the Columbia anti-shivering protocol to achieve shiver control with the least sedating regimen. + There is limited data on opioids versus neuromuscular blockade for shivering, both strategies may be effective. Generally, neuromuscular blockade is considered after other strategies have failed. * How do we assess and treat ICU delirium? + Delirium should be assessed frequently using metrics such as the Confusion Assessment Method (CAM-ICU) or the Intensive Care Delirium Screening checklist (ICDSC). - CAM-ICU assesses for acute changes or fluctuation in mental status, inattention, altered level of consciousness, and disorganized thinking. + There is not a lot of data on the use of antipsychotics to treat ICU delirium. - Haloperidol is most often used even though data is limited. - Quetiapine has some positive data in small studies. Try to start with 15 mg q12 hours and titrate up to reach a target dose of 200 mg q12 hours as needed. Be cautious of hypertension and QT prolongation. - Very few patients will require antipsychotics once they leave the hospital, unless they have a pre-existing indication. + Non-pharmacologic methods should always be used such as sleep hygiene, freedom from lines/catheters, early mobilization, avoidance of constipation, and providing glasses/hearing aids as needed. * What strategies can be used to limit analgesia and sedation and why is that important? + Constant re-evaluation of the need for analgesia and sedation is paramount to reducing ventilator time, ICU delirium, and ICU and hospital length of stay. + Ask yourself if the RASS goal is the same today as it was yesterday. Re-evaluate often. + Take sedation vacations! Spontaneous breathing and spontaneous awakening trials should be performed at least daily if it is safe for the patient. + Consider re-introduction of home medications when appropriate, such as gabapentin for neuropathic pain or prior psychiatric medications.

References 1. Riker RR, Gagnon DJ, May T, Seder DB, Fraser GL. Analgesia, sedation, and neuromuscular blockade during targeted temperature management after cardiac arrest. Best Practice & Research Clinical Anaesthesiology. 2015;29(4):435-450. doi:10.1016/j.bpa.2015.09.006 2. Zakaria S, Kwong HJ, Sevransky JE, Williams MS, Chandra-Strobos N. Editor’s Choice-The cardiovascular implications of sedatives in the cardiac intensive care unit. European Heart Journal: Acute Cardiovascular Care. 2018;7(7):671-683. doi:10.1177/2048872617695231 3. Schenone A, Chen K, Andress K, Militello M, Cho L. Editor’s Choice- Sedation in the coronary intensive care unit: An adapted algorithm for critically ill cardiovascular patient. European Heart Journal: Acute Cardiovascular Care. 2019;8(2):167-175. doi:10.1177/2048872617753797 4. Van Diepen S, Katz JN, Albert NM, et al. Contemporary Management of Cardiogenic Shock: A Scientific Statement from the American Heart Association. Circulation. 2017;136(16):e232-e268. doi:10.1161/CIR.0000000000000525

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CardioNerds (Amit and Dan) join Dr. Maria Pabon (cardiology fellow), Dr. Kevin Bersell (cardiology fellow), Dr. Saad Sultan Ghumman (interventional cardiology fellow), and Dr. Rhanderson Cardoso (cardiovascular imaging fellow) from Brigham and Women’s Hospital. Together, they explore a complex case of STEMI that was further complicated by ventricular free wall rupture. Additionally, Dr. Ajar Kochar, Program Director for Interventional Cardiology at Brigham and Women’s Hospital, provides an insightful “ECPR” segment, adding a unique perspective to the case. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah.

This is the case of a patient who presented with STEMI and was found to have a moderate pericardial effusion with echogenic material within the pericardial space concerning for thrombus. Urgent CTA/CT surgery was engaged due to concern for dissection, but no evidence of dissection, rupture or intramural hematoma was found. The patient underwent an urgent pericardiocentesis which yielded 350cc of hemorrhagic fluid, leading to an improvement in hemodynamic status. A coronary angiogram was performed which showed a 100% thrombotic occlusion of OM 1, the culprit lesion for the STEMI. Due to the possibility of a delayed STEMI and high suspicion for mechanical complication of MI, aspirin and IV cangrelor were chosen as the preferred antiplatelet strategy. However, cangrelor was held and cardiac surgery was consulted, as LV free wall rupture was suspected. The patient underwent urgent repair of the LV free wall rupture, with an uneventful post-op recovery and discharge on day 8 to cardiac rehab.

CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ).

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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Case MediaPearls – When Infarction Brings the Walls Down – Brigham and Women’s Hospital1. In the era of primary PCI, mechanical complications of MI are relatively rare. 2. Timely recognition using multi-modality imaging and prompt surgical intervention can result in favorable outcomes. 3. An approach that involves a Heart Team can be advantageous in optimizing outcomes in such complex cases.

Show Notes – When Infarction Brings the Walls Down – Brigham and Women’s Hospital1. Incidence of post AMI LV free wall rupture: * 0.1-1% 2. Risk factors for LV Free wall Rupture: * Older age * Female sex * Prior HTN * 1st lateral or Anterior Wall MI 3. Protective factors towards free wall rupture: * LV hypertrophy * CHF * Hx of prior infarcts * Chronic ischemic heart disease * Early use of beta blockers post MI * Timely intervention 4. Incidence of Mortality associated with mechanical rupture related to AMI: * 8-10% 5. When to suspect a mechanical complication of AMI: * AMI with shock/hypotension * New murmur * New pericardial effusion > 10mm on bedside echo 6. Other etiologies that can cause free wall rupture: * Trauma * Cardiac infection * Aortic dissection * Cardiac tumors * Infiltrative diseases * Iatrogenic from PCI or surgical procedures

References – When Infarction Brings the Walls Down – Brigham and Women’s Hospital1. Varghese S, Ohlow MA. Left ventricular free wall rupture in myocardial infarction: A retrospective analysis from a single tertiary center. JRSM Cardiovasc Dis. 2019 Jan-Dec;8:2048004019896692. doi: 10.1177/2048004019896692. PMID: 31970072. 2. Pineda-De Paz, D.O., Hernández-del Rio, J.E., González-Padilla, C. et al. Left ventricular free-wall rupture, a potentially lethal mechanical complication of acute myocardial infarction: an unusual and illustrative case report. BMC Cardiovasc Disord 19, 80 (2019). https://doi.org/10.1186/s12872-019-1063-x 3. Yip HK, Wu CJ, Chang HW, Wang CP, Cheng CI, Chua S, Chen MC. Cardiac rupture complicating acute myocardial infarction in the direct percutaneous coronary intervention reperfusion era. Chest 2003;124:565–71. doi: 10.1378/chest.124.2.565. PMID: 12907558. 4. Sutherland FW, Guell FJ, Pathi VL, Naik SK. Postinfarction ventricular free wall rupture: strategies for diagnosis and treatment. Ann Thorac Surg 1996;61:1281–5. doi: 10.1016/0003-4975(95)00953-6. PMID: 8627055. 5. Meta-analysis of corticosteroid treatment in acute myocardial infarction. Am J Cardiol 2003;91:1055–9. doi: 10.1016/S0002-9149(03)00216-4. PMID: 12745097.

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It’s another session of CardioNerds Rounds! In these rounds, Dr. Karan Desai (Formerly FIT at University of Maryland Medical Center and currently faculty at Johns Hopkins School of Medicine) joins Dr. Dan Burkhoff (Director of Heart Failure, Hemodynamics and MCS Research at the Cardiovascular Research Foundation) to discuss mechanical circulatory support options through the lens of pressure-volume loops! Dr. Burkhoff is the author of Harvi, an interactive simulation-based application for teaching and researching many aspects of ventricular hemodynamics. Don’t miss this wonderfully nerdy episode with a world-renowned expert in hemodynamics and MCS! Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes.

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Show notes – Hemodynamics and Mechanical Circulatory SupportCase Synopsis:

Case Synopsis
We focused on one case during these rounds. A man in his mid-50s presented to his local community hospital with 3 days of chest pain, nausea, and vomiting. He appeared ill in the emergency room with HR in the 150s, BP 90/70s and ECG demonstrating inferior ST elevations. He was taken emergently to the catheterization lab and received overlapping stents to his right coronary artery. Over the next 24 hours, he developed a new harsh systolic murmur heard throughout his precordium and progressed to cardiogenic shock. Echocardiogram demonstrated a large basal inferoseptum ventricular septal rupture. From this point, we discussed the hemodynamics of VSR and MCS options.

**Case Takeaways****

Dr. Burkhoff took us through the hemodynamics of VSR with pressure-volume loops to better understand the pathology and impact of various MCS options. Of note, there are no MCS devices specifically approved to treat acute ventricular septal rupture.
In regards to the acute hemodynamic effects of a VSR (an abrupt left to right shunt), there are several aspects to note. First, the effective LV afterload is reduced; however, there is less “forward flow” as well and as a consequence, decreased left-sided cardiac output (“Qs”) and blood pressure. At the same time, flow through the pulmonary artery increases (the “Qp”). Additionally, due to the abrupt shunt flow, there is increased RV “loading” with increasing central venous pressure and pulmonary artery pressure.
The hemodynamic priorities in treating patients with cardiogenic shock and VSR are to normalize blood pressure, cardiac output, and oxygen delivery, while attempting to minimize shunt flow to allow healing. However, medications and MCS are unlikely to completely normalize hemodynamics. For instance, if the patient was placed on peripheral VA ECMO, while total CO and BP may increase, flow across the VSR could also increase at high ECMO flows (e.g., by introducing more LV afterload).
In patients with persistent cardiogenic shock and VSR, short-term MCS to divert flow away from the shunt can be an effective strategy. LV-to-aorta or LA-to-arterial MCS may provide the best single-device hemodynamic profiles by decreasing shunt flow, reducing pulmonary capillary wedge pressure, and improving blood pressure.
Surgical and percutaneous VSD repair are the definitive treatment options. If able to stabilize patients and pursue delayed repair, it may lead to better outcomes by allowing for better tissue substrate for a more effective repair.

Enjoy this ACC.org Expert Analysis by Goyal and Menon to learn more about post-myocardial infarction ventricular septal rupture.

References 1. Pahuja M, Schrage B, Westermann D et al. Hemodynamic Effects of Mechanical Circulatory Support Devices in Ventricular Septal Defect. Circ Heart Fail. 2019 Jul;12(7):e005981. doi: 10.1161/CIRCHEARTFAILURE.119.005981. 2. TEACH Videos via Harvi.Org: https://harvi.org/book/data/00%20-%20TeachVideos/TeachVideos.html

Production TeamKaran Desai, MDNatalie Stokes, MDAmit Goyal, MDDaniel Ambinder, MD

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Renal replacement therapy (RRT) is routinely utilized in the CICU. Series co-chairs Dr. Eunice Dugan and Dr Karan Desai along with CardioNerds Co-founder Dr. Daniel Ambinder were joined by FIT lead and CardioNerds Ambassador from University of Washington, Dr. Tomio Tran. Our episode expert is world-renowned nephrologist Dr. Joel Topf. Dr. Topf is Medical Director of Research at St. Clair Nephrology, and editor of the Handbook of Critical Care Nephrology. In this episode, we describe a case of cardiogenic shock due to acute myocardial infarction resulting in renal failure, ultimately requiring continuous RRT (CRRT). We discuss the most common causes of AKI within the cardiac ICU, indications for initiating RRT, evidence on the timing of RRT, different modes of RRT, basic management of the RRT circuit, and how to transition patients off of RRT during renal recovery. Episode notes were drafted by Dr. Tomio Tran. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

This episode is made possible with support from Glass.Health – The first digital notebook designed for doctors. Follow @GlassHealthHQ for the latest product updates!

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Pearls and Quotes – Approach to Renal Replacement Therapy in the CICU 1. Do not commit “Renalism” – withholding lifesaving treatments from patients with renal impairment due to fear of causing renal injury. Shared decision making is key. 2. In the ICU, most of the time, AKI is caused by ATN due to adverse hemodynamics. Nephrologists can help determine the cause if the patient has an atypical presentation. 3. Late dialysis initiation is non-inferior to early dialysis initiation. Early initiation may lead to higher rates of prolonged time on dialysis. 4. Slow low efficiency daily diafiltration (SLEDD) vs CRRT are equivalent in terms of outcomes and are the preferred methods among patients with hypotension. Intermittent Hemodialysis (iHD) can be used once patients are hemodynamically stable. 5. A “Furosemide Stress Test” can be used to test intact renal function or renal recovery by challenging the nephron to make urine.

Show notes – Approach to Renal Replacement Therapy in the CICU What are the risk factors and differential for AKI in the CICU?

Start by using the pre-renal vs intrinsic renal vs post-renal framework. Additional considerations in cardiac patients include contrast induced nephropathy, pigment nephropathy, cardiorenal syndrome. Enjoy Episode 262. Management of Cardiorenal Syndrome in the CICU.
In the ICU setting, intrinsic renal injury due to ATN is among the most common etiology of AKI.
Many risk factors for AKI are not modifiable in the ICU. Optimize renal function by avoiding nephrotoxins, minimizing contrast usage, and keeping the MAP >65-75 mmHg.
Contrast nephropathy as an etiology is questionable and may be a marker of a sicker patient population. Avoid “Renalism” – providing substandard care to patients with renal disease due to fear of worsening renal function.
Most etiologies are treated with supportive care.

What is the approach to timing of renal replacement therapy initiation?

Definitions for early vs late vs very late initiation of RRT:
- Early – Worsening AKI without indications for RRT
- Late – Worsening AKI with relative indications for RRT
- Very late – Worsening AKI with strict indications for RRT
Late initiation is noninferior in terms of mortality; early initiation is associated with higher rates of prolonged/permanent RRT.1,2,3
Very late initiation associated with worse outcomes.4 In general, start RRT if there are absolute indications (“AEIOU) or the patient is anuric with a high BUN (~140) as delaying RRT much further is associated with worse outcomes.
“Furosemide Stress Test” (FST) can be used to predict RRT need.5
- 1 mg/kg IV for diuretic naive, 1.5 mg/kg IV if on diuretic
- Goal = 200 cc urine over 1-2 hours

For the non-nephrologists, what are options for RRT acutely and how do they work?

There are two principles of RRT:
- Convection – movement of solutes through semipermeable membrane using pressure
  - Ultrafiltration – volume removal using convection; fluid is then replaced to prevent hypovolemia
    - Fluid removed has the same composition of the plasma
    - Negative fluid balance is the difference between volume removed and replacement fluid; goal usually 25-250 cc/hour
- Diffusion – movement of solutes from high to low concentration
  - Dialysate runs countercurrent through semipermeable membrane
  - Typical dialysate composition – normal sodium, magnesium, low potassium, no creatinine, no BUN, high bicarbonate
  - Does not remove fluid
There are 3 types of RRT: iHD (intermittent hemodialysis), CRRT (continuous renal replacement therapy), SLEDD (slow low efficiency daily diafiltration)
- None have been shown to be superior in normotensive patients
- iHD can remove potassium and toxins more quickly
- SLEDD and CRRT are equivalent and preferred for hypotensive patients.6
  - SLEDD is less labor intensive
  - Institutions usually have a preference of one modality over another
- Peritoneal dialysis has been used in the ICU in some specialized centers, but is not common.
There are 3 methods of CRRT:
- Continuous hemodialysis
  - Removes fluid by diffusion
  - Uses dialysate, no replacement fluid
  - Removes small-medium sized molecules
- Continuous hemofiltration
  - Removes fluid by convection
  - No dialysate, needs replacement fluid
  - Removes large sized molecules
- Continuous hemodiafiltration
  - Removes fluid by diffusion and convection
  - Uses dialysate and replacement fluid

What should non-nephrologists understand about daily management of patients on CVVH?

CICU clinicians should frequently communicate fluid balance and hemodialysis goals with nephrology and nurses
The circuit has 2 pumps: 1 to pull fluid, another to push fluid back
- Monitor daily pressure trends as deviations may implicate issues with the access
- Look at I/Os on the circuit to determine fluid balance
Ask RN if filter is clotting off because this can cause blood loss anemia due to the amount of blood lost when the circuit needs to be changed
Electrolyte management:
- After 1-2 days of normalizing hyperkalemia, try to keep potassium steady using a 4 K bath
- CRRT can drop phosphorous precipitously, which may cause cardiac myocyte dysfunction; add Na-Phos if necessary.
Very important: frequent line checks to identify infections. If the line is in for several days and begin considering a switch to a tunneled dialysis catheter, especially if longer-term RRT is expected.

How does the CICU team monitor for native renal recovery and initiate cardiovascular GDMT?

The CICU team should assess daily trends in urine output. Patients may spontaneously make more urine especially as critical illness resolves. Consider trialing diuretics (FST) to assess recovery. Once hemodynamics improves, transition to iHD if there is still a persistent indication for RRT. Temporary dialysis lines are infection prone; consider exchanging for a tunneled iHD line if in place >1 week.
Many GDMT medications, often crucial for CV optimization, are considered nephrotoxic and may increase serum potassium. Therefore, it is important to be thoughtful about timing of initiation.
Consider initiating GDMT when the Cr is trending towards baseline. Cr is “cosmetic”, and the team should tolerate some Cr increases with life-saving GDMT. Please note that trends in potassium levels is more important than Cr with “nephrotoxic” CV meds.
There may be a role for gastrointestinal potassium binders to facilitate GDMT optimization, but the clinical safety and efficacy remains unanswered (trials are underway).
It is crucial for patients to get back on GDMT for improved long term cardiac outcomes.

References 1. Gaudry S, Hajage D, Schortgen F, et al. Initiation strategies for renal-replacement therapy in the intensive care unit. New England Journal of Medicine. 2016;375(2):122-133. 2. STARRT-AKI Investigators, Canadian Critical Care Trials Group, Australian and New Zealand Intensive Care Society Clinical Trials Group, et al. Timing of initiation of renal-replacement therapy in acute kidney injury. N Engl J Med. 2020;383(3):240-251. 3. Zarbock A, Kellum JA, Schmidt C, et al. Effect of early vs delayed initiation of renal replacement therapy on mortality in critically ill patients with acute kidney injury: the elain randomized clinical trial. JAMA. 2016;315(20):2190. 4. Gaudry S, Hajage D, Martin-Lefevre L, et al. Comparison of two delayed strategies for renal replacement therapy initiation for severe acute kidney injury (AKIKI 2): a multicentre, open-label, randomised, controlled trial. The Lancet. 2021;397(10281):1293-1300. 5. Chawla LS, Davison DL, Brasha-Mitchell E, et al. Development and standardization of a furosemide stress test to predict the severity of acute kidney injury. Crit Care. 2013;17(5):R207. 6. Rabindranath K, Adams J, Macleod AM, Muirhead N. Intermittent versus continuous renal replacement therapy for acute renal failure in adults. Cochrane Database Syst Rev. 2007;(3):CD003773.

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The Cardiorenal Syndrome is commonly encountered, and frequently misunderstood. Join the CardioNerds team as we discuss the complex interplay between the heart and kidneys with Dr. Elliott Miller (Assistant Professor of Medicine at Yale University School of Medicine and Associate Medical Director of the Cardiac Intensive Care Unit of Yale New Haven Hospital), and Dr. Nayan Arora (Clinical Assistant Professor of Medicine and Nephrologist at the University of Washington Medical Center). We are hosted by FIT lead Dr. Matthew Delfiner (Cardiology Fellow at Temple University), Cardiac Critical Care Series Co-Chairs Dr. Mark Belkin (AHFTC faculty at University of Chicago) and Dr. Karan Desai (Cardiologist at Johns Hopkins Hospital), and CardioNerds Co-Found Dr. Dan Ambinder. In this episode we discuss the definition and pathophysiology of the cardiorenal syndrome, explore strategies for initial diuresis and diuretic resistance, and management of the common heart failure medications in this setting. Show notes were developed by Dr. Matthew Delfiner. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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Pearls and Quotes – Management of Cardiorenal Syndrome in the CICU 1. Cardiorenal syndrome (CRS) represents a range of clinical entities in which there is both heart and kidney dysfunction, and can be driven by one, or both, of the organs. 2. CRS is caused by reduced renal perfusion, elevated renal congestion, or a combination of the two. Treatment therefore focuses on increasing perfusion, by optimizing cardiac output and mean arterial pressure, and reducing congestion through diuresis. 3. Patients should be monitored for an adequate response to the initial diuretic dose within 2 hours of administration. If the response is inadequate, the loop diuretic dose should be doubled. 4. Diuretic resistance can be managed via sequential nephron blockade, most commonly with thiazide diuretics, but also with amiloride, high-dose spironolactone, or acetazolamide, as these target different regions of the nephron. 5. In cases of refractory diuretic resistance, hypertonic saline can be considered with the help of an experienced clinician. 6. Continuation or cessation of renin-angiotensin-aldosterone system (RAAS) inhibitors in the setting of CRS should be made on a case-by-case basis.

Show notes – Management of Cardiorenal Syndrome in the CICU 1. Cardiorenal syndrome (CRS) is a collection of signs/symptoms that indicate injury to both the heart and kidneys. Organ dysfunction in one can drive dysfunction in the other. Cardiorenal syndrome can be categorized as:

Type 1 – Acute heart failure causing acute kidney injury
Type 2 – Chronic heart failure causing chronic kidney injury
Type 3 – Acute kidney injury causing acute heart failure
Type 4 – Chronic kidney injury causing chronic heart failure
Type 5 – Co-development of heart and kidney injury by another systemic process.

These categories can be helpful for education, discussion, and research purposes, but they do not usually enter clinical practice on a regular basis since different categories of cardiorenal syndrome are not necessarily treated differently.

CRS is caused by either reduced renal perfusion, elevated renal congestion, or a combination of the two. When dealing with CRS, note that:
CRS can be caused by poor kidney perfusion, though is mostly driven by low renal perfusion pressure.
Renal perfusion pressure is the gradient between renal arteries and renal veins, which can be approximated by mean arterial pressure (MAP) minus central venous pressure (CVP)
CRS can therefore be treated by reducing CVP (i.e. with diuresis) or increasing MAP or cardiac output
Renal decongestion is achieved primarily through diuresis.
For diuretic “naïve” patients, furosemide 40 mg IV is a reasonable starting dose
For patients already on diuretics prior to admission, increasing their home dose by 2.5x (administered intravenously) usually achieves an adequate initial response
Patients should be reassessed 1-2 hours after their initial diuretics dose. If the patient has not made 200 mL of urine, the loop diuretic dose should be doubled.
Diuretic dose and urine output have a logarithmic relationship, meaning doubling the dose does not double the urine output. Once you reach a certain dose threshold, you won’t necessarily increase the quantity of diuresis, but rather you will increase the duration of diuresis.
It is okay if creatinine rises with diuresis, to a degree.
Creatinine elevation with decongestion is more a sign of hemoconcentration and is paradoxically associated with better outcomes.
However, if the creatinine rises by more than 30-50% and you are not seeing clinical evidence of decongestion, then that is likely a poor prognostic sign.
There are multiple ways to manage diuretic resistance.
Diuretic resistance is often due to a variety of mechanisms including increased sodium reabsorption and hypertrophy of the distal convoluted tubule. Sequential nephron blockade can be considered, most commonly with a thiazide diuretic in addition to a loop diuretic, after the loop diuretic dose is sufficiently optimized.
Patients with diuretic resistance may also have increased sodium reabsorption in the proximal tubule, so acetazolamide may be helpful in certain cases. Check out the CardioNerds Journal Club on the ADVOR trial!
Amiloride and high doses of spironolactone can be used to target the collecting ducts.
Finally, hypertonic saline has been used to address persistent diuretic resistance in certain cases, though should be done with an experienced clinician.
Decisions regarding cessation versus continuation of renin-angiotensin-aldosterone system (RAAS) inhibitors in the setting of CRS should be made on a case-by-case basis.
RAAS inhibitors may not specifically cause harm, but they may make it difficult to discern whether a change in creatinine related to their use versus worsening renal function.
On the other hand, there is an increased likelihood that RAAS inhibitors are not resumed when they are held in CRS, which is associated with worse outcomes. Therefore, it is imperative that there is a plan made to resume these medications if they are held.

References * Jentzer, Bihorac, Brusca et al. “Contemporary Management of Severee Acute Kidney Injury and Refractory Cardiorenal Syndrome: JACC Council Perspectives.” J Am Coll Cardiol. 2020 Sep, 76 (9) 1084-1101. https://www.jacc.org/doi/abs/10.1016/j.jacc.2020.06.070 * Rangaswami J., Bhalla V., Blair J.E.A., et al. “Cardiorenal syndrome: classification, pathophysiology, diagnosis, and treatment strategies: a scientific statement from the American Heart Association”. Circulation 2019;139:e840-e878: https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000000664 * Jentzer J.C., Chawla L.S. “A clinical approach to the acute cardiorenal syndrome”. Crit Care Clin 2015; 31:685-703. https://www.criticalcare.theclinics.com/article/S0749-0704(15)00048-2/abstract

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This episode is focused on Palliative Care and Shared Decision-Making in the CICU. In this episode, we learn about how the principles of palliative care and shared decision-making apply to our patients across the spectrum of cardiovascular care, especially in the cardiac intensive care unit. We discuss pivotal trials of specialty palliative care and decision aids in cardiology and how they might inform our practice to enhance patient quality of life and improve goal-concordant care. Finally, we discuss practical tips and communication strategies for how to engage patients about end-of-life decisions and topics that can be utilized from outpatient to inpatient to critical care settings.

“We need to help patients hope for the best and plan for the worst as time goes on.”

Dr. Larry Allen

Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai, along with CardioNerds Co-founder Amit Goyal are joined by FIT lead, Dr. Sarah Chuzi. Dr. Chuzi is a Chicagoan and completed her internal medicine residency, cardiology fellowship, AHFTC fellowship and is now Assistant Professor at Northwestern University. Our episode expert is a true national leader in shared decision-making and palliative care in heart failure – Dr. Larry Allen, Medical Director of Advanced Heart Failure and the Co-Director of the Colorado Program for Patient-Centered Decisions at the University of Colorado School of Medicine. Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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Pearls and Quotes – Palliative Care and Shared Decision-Making in the CICU1. “Much of what we do in cardiology is thinking about how to make people feel better (not just improving cardiac function or length of life). So, on a day-to-day basis we are really providing primary palliative care.” – Dr. Larry Allen

“Risk models in cardiology can only be so accurate… While risk models can give us some grounding, we also need to embrace the concept of uncertainty, and help patients understand that there are a variety of things that might happen to them, suggest some things they might plan for, and continue to iteratively come back to the patient and reevaluate what their options are.” – Dr. Larry Allen
“Our goal is to help people live happy, healthy, full lives. But, everyone dies. So understanding that death is a part of life and understanding how to help them make those transitions is critical” – Dr. Larry Allen
“Having good deaths is a part of good healthcare. We can’t ignore that. We can’t fight against it. We should embrace it. And we have the opportunity to do that.” – Dr. Larry Allen
We should still keep in mind the concept of medical futility and determining what options are reasonable for patients. Part of shared decision-making includes discussing what interventions would not be feasible or helpful with patients and families

Show notes – Palliative Care and Shared Decision-Making in the CICUNotes drafted by Dr. Sarah Chuzi.

1. How are the basic principles of palliative care relevant to cardiology, and can you define the key concepts of shared decision-making, primary palliative care, specialty (or secondary) palliative care, and hospice care?

Throughout medicine, we confront the concepts of symptom control, difficult medical decision-making, and end-of-life. These are the principles of palliative care and they apply very easily across the spectrum of cardiology.
Shared decision-making is a meeting between two experts – the patient and the clinician. The patient is the expert in what’s important to them and their hopes, fears, values, goals, and preferences. The clinician is the expert in the medical aspects of care, including care that is not possible, care that might be high value, and the potential trade-offs and range of outcomes involved in a medical decision.
Palliative care is defined by the WHO – as care that deals with patient symptoms and quality of life. Increasingly, the terms primary and secondary palliative care are used. Primary palliative care is care provided by a general clinician (or cardiologist), while secondary palliative care is provided by a board-certified palliative care clinician.
Hospice care is really a health insurance benefit that provides a certain group of services (e.g. nurses, equipment) for patients who have terminal illness and less than 6 months to live.

2. What have we learned from existing trials looking at specialty palliative care in heart failure?

A few large trials (CASA, ENABLE, SWAP-HF, PAL-HF) of specialty palliative care interventions in heart failure have shown mixed results.
One of the reasons for this is the heterogeneity in patient and caregiver adjustment/symptoms at baseline.
Future trials will need to determine which patients and caregivers are really in need of interventions or assistance surrounding some of these issues.

3. What are some strategies trainees can use to help elucidate a patient’s goals and values and engage in shared decision-making in high intensity, critical care situations?

Trying to determine (from the patient or family) whether the patient is a medical maximizer or minimizer can be helpful; i.e., what is his preference for aggressiveness of care.
Obtaining collateral from a patient’s power of attorney/next of kin/proxy about prior discussions regarding goals and values is valuable.
We should still keep in mind the concept of medical futility and determining what options are reasonable for patients. Part of shared decision-making includes discussing what interventions would not feasible or helpful with patients and families.

4. What is the role of decision aids in the process of deciding whether to pursue LVAD implantation?

Decision aids are unique from educational materials in that decision aids discuss alternative treatment options, including what life might be like if a certain treatment option is not pursued. Decision aids encourage patients to reflect on their values and then try to map the decisions in the context of their values.
The research group at the University of Colorado developed a decision aid to help patients and their families determine whether an LVAD would be an appropriate medical intervention for them. The decision aid is available online (patientdecisionaid.org) and includes a 26-minute video and an 8-page pamphlet. Currently, they are being disseminated nationally in a large implementation trial. The DECIDE-LVAD trial demonstrated that this decision aid improved values-choice concordance for patients considering LVAD therapy.

5. What are the benefits of hospice for patients with cardiac disease and how does hospice fall short?

It’s important to understand what hospice will and will not cover. The hospice benefit is a fixed payment per day. So, it’s important to consider what treatments might be covered and to discuss this with patients and families.
For patients with advanced cardiac disease, coverage of inotropes is a common issue that we encounter. It’s important to prepare patients for the fact that inotropes may not be accepted in a given hospice program.
Additionally, sometimes clinicians struggle with how to continue to provide care for patients who enter hospice as we try to navigate how to stay involved in their care while respecting their wishes to be at home and not necessarily come to clinic.

References – Palliative Care and Shared Decision-Making in the CICURogers JG, Patel CB, Mentz RJ, et al. The palliative care in heart failure (PAL-HF) randomized, controlled clinical trial. 2017. J Am Coll Cardiol, 70(3): 331-341.

Allen LA, Mcilvennan CK, Thompson JS, et al. Effectiveness of an intervention supporting shared decision making for destination therapy left ventricular assist device: the DECIDE-LVAD randomized clinical trial. 2018. JAMA Intern Med, 178(4): 520-529.

Warraich HJ, Patel CB, Kochar A, Rogers JG, Patel MR. Incorporating shared decision making and palliative care into cardiogenic shock pathways. 2010. J Am Coll Cardiol, 74(4): 501-502.

Chuzi S, Khan SS, Pak ES. Primary palliative care education in advanced heart failure and transplant cardiology fellowships. 2021. J Am Coll Cardiol, 77(4): 501-505.

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In this episode, we discuss the utility of veno-arterial extra-corporeal membrane oxygenation (VA-ECMO) for the temporary management of biventricular failure and cardiogenic shock requiring full cardiopulmonary support. Here, we define the types of ECMO and describe the unique physiology of this mechanical circulatory support platform, as well as review the potential complications and management strategies. Most notably, we highlight indications for and contraindications to the use of VA-ECMO and review the importance of patient selection. Lastly, we discuss de-escalation and de-cannulation strategies for patients on VA-ECMO as a bridge to recovery.

Join Dr. Amit Goyal (CardioNerds Cofounder and FIT at Cleveland Clinic), Dr. Yoav Karpenshif (Series Co-chair and FIT at University of Pennsylvania), and Dr. Megan Burke (Episode FIT Lead and FIT at University of Pennsylvania) as they learn about how to care for some of our sickest patients from Dr. Ann Gage, interventional and critical care cardiologist at Centennial Heart. At the beginning of the episode, enjoy a message from the very first CardioNerds Scholar, Dr. Katie Vaughan (Chief Resident and soon Cardiology Fellow at BIDMC). Episode notes were developed by Dr. Megan Burke. Audio editing by CardioNerds Academy Intern, Hirsh Elhence.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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Pearls and Quotes – Biventricular Failure and the Use of VA-ECMO 1. Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a form of temporary mechanical circulatory support that can do the work of both the heart and lungs. 2. The ECMO circuit is a narcissist, i.e. cannulas are named in reference to the circuit and not the patient (“inflow” vs “outflow”). 3. The decision to utilize ECMO should be made by a multidisciplinary shock team and patient selection is KEY! 4. ECMO physiology rule #1: VA-ECMO increases LV afterload 5. Patients on VA-ECMO should be monitored with a PA catheter and an arterial line in the right arm

Show notes – Biventricular Failure and the Use of VA-ECMO Notes drafted by Dr. Megan Burke.

What is ECMO and what are the different types?
Extracorporeal membrane oxygenation (ECMO) is a temporary form of mechanical life support that comes in two flavors: veno-arterial, or “VA” and veno-venous, or “VV.”
VV-ECMO supports extracorporeal gas exchange in the setting of acute respiratory failure
VA-ECMO provides full circulatory support in addition to gas exchange, doing the work of both the heart and lungs.
What are the components and “anatomy” of the VA-ECMO circuit?
The circuit is made up of the following major components:
- Venous (inflow) cannula
- Centrifugal Pump
- Oxygenator (also responsible for CO2 removal)
- Arterial (outflow) cannula
The cannulas are named in reference to the ECMO circuit, not the patient. Dr. Gage suggests that we think of the ECMO circuit (and mechanical circulatory support in general) as narcissistic, i.e. flow is always in reference to the device.
Gas exchange happens in the oxygenator. In the oxygenator blood flows through thin filaments that allow for diffusion of oxygen and carbon dioxide. Gas flows in the opposite direction of blood flow to maximize diffusion through the countercurrent effect. Oxygenation is determined by rate of blood flow through the oxygenator and FiO2 delivered. Carbon dioxide removal is determined by rate of countercurrent gas flow, referred to as the sweep speed.
What are the indications for VA-ECMO?
VA-ECMO is utilized in the setting of severe refractory cardiogenic shock (in the setting of left, right, or biventricular failure) and cardiac arrest. It is a temporary mechanical circulatory support platform, and should be used as a bridge to recovery or a more durable therapy (i.e. durable mechanical support or transplant). Due to lack of randomized data, there are no consensus guidelines for the use of VA-ECMO, and the decision to implement it should be made as part of a multidisciplinary cardiogenic shock team. Common indications include cardiogenic shock, refractory ventricular arrhythmias, massive pulmonary embolism, cardiac arrest, and failure to wean from cardiopulmonary bypass during surgery. The absolute and relative contra-indications to ECMO vary by institution.
Given the high mortality rates for patients on VA-ECMO (hospital mortality is approximately 50%, and 6-month survival is as low as 30%), patient selection is key. There are multiple pre VA-ECMO risk factors independently associated with poor outcomes. These include older age, female sex, higher body mass index, and markers of increased severity of illness including laboratory evidence of end-organ dysfunction and longer duration of mechanical ventilation.
What are the pathophysiological consequences of VA-ECMO and how do we monitor and treat them?
The goal of VA-ECMO is to provide perfusion, however unlike other forms of mechanical circulatory support, it is NOT supporting the heart’s ability to pump blood. In fact, VA-ECMO increases left ventricular afterload, because blood enters the aorta from the outflow cannula somewhere between the aortic root and the diaphragm (depending on cannulation strategy). This creates increased aortic pressure and increased left ventricular volume and afterload, which can lead to pulmonary edema and worsened myocardial demand. In the most extreme cases, the aortic pressure can exceed the left ventricular systolic pressure, thereby preventing blood from ejecting from the LV. This can lead to stasis, thrombus formation, and strokes. For this reason, echocardiography is used frequently to monitor LV ejection. One key marker is the opening of the aortic valve with every beat.
Furthermore, hemodynamic monitoring with a pulmonary artery catheter and a RIGHT radial arterial line is essential for management of patient’s on ECMO.
- The PA catheter allows for an estimation of the filling pressures. Of note, the mixed venous O2 cannot be used to estimate cardiac output when a patient is on VA-ECMO, but low levels still do correlate with poor tissue perfusion and worse outcomes.
- In general, it is essential to have an arterial catheter in a patient on VA-ECMO to monitor for arterial pulsatility, which is a surrogate for the contribution of the patient’s heart to perfusion.
- Specifically, a RIGHT radial arterial line is key in these patients because blood from it originates the brachiocephalic artery, which is the closest branch in the aortic arch to the coronary arteries and great vessels of the aortic arch and therefore best estimates the oxygen content in the coronaries and brain. This is key because when a patient is on peripheral VA-ECMO, oxygenated blood arrives to the heart retrograde from the femoral artery. If the left ventricle retains or regains contractility, the poorly oxygenated blood from the lungs (in patients with concurrent significant respiratory failure) is ejected into the proximal aorta. This can lead to the so called “North-south” or “Harlequin” syndrome, where the head and right upper extremity are relatively hypoxic compared to the rest of the body. Arterial blood gases from a right radial arterial line can forewarn of possible coronary and cerebral hypoxia during LV recovery as this syndrome develops and the “mixing” cloud develops.
For patients with poor ejection, there are various strategies to decompress, or “vent,” the left ventricle. Strategies include use of medicines to reduce afterload and/or improve inotropy, creation of an atrial septal defect to offload the left heart, and use of temporary mechanical circulatory support devices (IABP or percutaneous LVAD) to allow blood to more easily leave the LV.
Treatment of the North-South Syndrome focuses on increasing the oxygenation of blood ejecting from the left ventricle through vent management or adding another venous catheter to pre-oxygenate blood before entering the lungs (VAV-ECMO). Increasing VA-ECMO flow can also shift the mixing zone towards the aortic arch and improve oxygenation, but this will also increase the LV afterload.
Other complications of the ECMO circuit include infection, bleeding, and limb ischemia (due to the large bore vascular access), as well as stroke, hemolysis, and thrombus formation (due to the extracorporeal circuitry).
How is VA-ECMO weaned?
If a patient is on VA-ECMO support as a bridge to recovery, the ability to wean a patient off the circuit relies on invasive hemodynamics, echocardiography, and an assessment of improving end-organ function.
The flow of blood out of the circuit can be gradually weaned down to allow for the patient’s native heart to do more of the work of perfusion. Once the patient is thought to be ready for decannulation it is common to perform a turndown study under echocardiographic guidance, where serial evaluations of biventricular function are done at different flow speeds.
VA-ECMO is usually decannulated in the operating room to allow for surgical repair of the vasculature in the setting of large bore access.

References – Biventricular Failure and the Use of VA-ECMO 1. Papolos AI, Kenigsberg BB, Berg DD, Alviar CL, Bohula E, Burke JA, Carnicelli AP, Chaudhry SP, Drakos S, Gerber DA, Guo J, Horowitz JM, Katz JN, Keeley EC, Metkus TS, Nativi-Nicolau J, Snell JR, Sinha SS, Tymchak WJ, Van Diepen S, Morrow DA, Barnett CF; Critical Care Cardiology Trials Network Investigators. Management and Outcomes of Cardiogenic Shock in Cardiac ICUs With Versus Without Shock Teams. J Am Coll Cardiol. 2021 Sep 28;78(13):1309-1317. doi: 10.1016/j.jacc.2021.07.044. PMID: 34556316. 2. Burkhoff D, Sayer G, Doshi D, Uriel N. Hemodynamics of Mechanical Circulatory Support. J Am Coll Cardiol. 2015;66(23):2663-2674. doi:10.1016/j.jacc.2015.10.017 3. Guglin M, Zucker MJ, Bazan VM, et al. Venoarterial ECMO for Adults: JACC Scientific Expert Panel. J Am Coll Cardiol. 2019;73(6):698-716. doi:10.1016/j.jacc.2018.11.038 4. Keebler ME, Haddad EV, Choi CW, et al. Venoarterial Extracorporeal Membrane Oxygenation in Cardiogenic Shock. JACC Heart Fail. 2018;6(6):503-516. doi:10.1016/j.jchf.2017.11.017 5. Rao P, Khalpey Z, Smith R, Burkhoff D, Kociol RD. Venoarterial Extracorporeal Membrane Oxygenation for Cardiogenic Shock and Cardiac Arrest. Circ Heart Fail. 2018;11(9):e004905. doi:10.1161/CIRCHEARTFAILURE.118.004905 6. Tehrani BN, Truesdell AG, Psotka MA, et al. A Standardized and Comprehensive Approach to the Management of Cardiogenic Shock. JACC Hear Fail. 2020;8(11):879-891. doi:10.1016/j.jchf.2020.09.005 7. Grant C, Richards JB, Frakes M, Cohen J, Wilcox SR. ECMO and Right Ventricular Failure: Review of the Literature. J Intensive Care Med. 2021;36(3):352-360. doi:10.1177/0885066619900503 8. Debaty G, Babaz V, Durand M, et al. Prognostic factors for extracorporeal cardiopulmonary resuscitation recipients following out-of-hospital refractory cardiac arrest. A systematic review and meta-analysis. Resuscitation. 2017;112:1-10. doi:10.1016/j.resuscitation.2016.12.011 9. Russo JJ, Aleksova N, Pitcher I, et al. Left Ventricular Unloading During Extracorporeal Membrane Oxygenation in Patients With Cardiogenic Shock. J Am Coll Cardiol. 2019;73(6):654-662. doi:10.1016/j.jacc.2018.10.085 10. ELSO General Guidelines Extracorporeal Life Support Organization (ELSO) General Guidelines for All ECLS Cases.; 2017. www.elso.org. Accessed April 10, 2021. 11. Su Y, Liu K, Zheng JL, Li X, Zhu DM, Zhang Y, Zhang YJ, Wang CS, Shi TT, Luo Z, Tu GW. Hemodynamic monitoring in patients with venoarterial extracorporeal membrane oxygenation. Ann Transl Med. 2020 Jun;8(12):792. doi: 10.21037/atm.2020.03.186. PMID: 32647717; PMCID: PMC7333156.

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