Safety and Efficacy of Lung Recruitment Maneuvers in Pediatric Post-Operative Cardiac Patients

Renee L. Devor MD^1,2

Harjot K. Bassi MD³

Paul Kang MPH⁴

Tiffany Morandi MD²

Kristi Richardson RT⁵

John J. Nigro MD^2,6

Christine Tenaglia RT⁵

Chasity Wellnitz RN, BSN, MPH⁶

Brigham C. Willis MD^1,2,7

¹Division of Cardiac Critical Care, Phoenix Children’s Hospital, Phoenix, Arizona

²Department of Child Health, University of Arizona College of Medicine, Phoenix, Arizona

³Division of Critical Care, Phoenix Children’s Hospital, Phoenix, Arizona

⁴Department of Epidemiology and Biostatistics, University of Arizona College of Medicine, Phoenix, Arizona

⁵Department of Respiratory Therapy, Phoenix Children’s Hospital, Phoenix, Arizona

⁶Division of Cardiology, Phoenix Children’s Hospital, Phoenix, Arizona

⁷Department of Pediatrics, Creighton University School of Medicine, Phoenix, Arizona

Abstract

Background: Recruitment maneuvers are a dynamic process of transient increases in transpulmonary pressure intended to open unstable airless alveoli. Due to concerns regarding the hemodynamic consequences of recruitment maneuvers in children with heart disease, these maneuvers have not been widely utilized in this population. The objective of this study was to demonstrate the safety and efficacy of lung recruitment maneuvers in post-operative pediatric cardiac patients. We hypothesized that multiple recruitment maneuvers are physiologically beneficial and hemodynamically tolerated in children with congenital cardiac disease. 

Methods: Retrospective chart review was conducted of post-operative cardiac surgical subjects who received recruitment maneuvers, as well as a matched control group who did not, at a Cardiac ICU in a quaternary care free-standing children’s hospital. Repetitive lung recruitment maneuvers using incremental positive end-expiratory pressure were performed. Hemodynamic and respiratory physiologic variables were recorded.

Results: Sixty-one post-operative cardiac subjects had a total of 435 lung recruitment maneuvers. Assessment of hemodynamic tolerability demonstrated no change in MAP, HR, or CVP during or after the maneuvers. There was a 28% increase in dynamic compliance following recruitment maneuvers (p <0.01, 95% CI). Specific outcomes in the 59 matched control subjects demonstrated no significant difference in length of mechanical ventilation (p = 0.26), length of hospital stay (p = 0.28), mortality (p = 0.58) or difference in occurrence of pneumothorax (p = 0.26). 

Conclusions: Post-operative pediatric cardiac surgical subjects tolerated repeated lung recruitment maneuvers without significant hemodynamic changes. The maneuvers successfully improved dynamic compliance without any adverse effects.

Introduction

Mechanical ventilation is a common therapy used for pediatric patients in the intensive care unit and is frequently used for children with congenital cardiac disease following surgical repair. However, it is well known that mechanical ventilation can induce lung injury or worsen preexisting lung disease (1-3). In patients with congenital cardiac disease, it is crucial to protect the lung from injury and optimize ventilation and oxygenation due to their underlying hemodynamic and physiologic fragility (4, 5). Post-operatively, several factors including general anesthesia, cardiopulmonary bypass, atelectasis, and hypoxemia can contribute to lung dysfunction, which may lead to prolonged mechanical ventilation (6). Children with such prolonged ventilation are at a higher risk for poor overall outcome due to a variety of ventilator-associated morbidities (7, 8). Therefore, it is of practical value to protect the lungs and reduce the length of time mechanical ventilation is required.

Alveolar injury can be caused by the repetitive opening and closing of alveoli when inadequate positive end-expiratory pressure (PEEP) is provided and this can generate shear stress within the alveoli and promote injury (9-10). Lung recruitment maneuvers have been defined as transient increases in the transpulmonary pressure used to open recruitable collapsed alveoli and increase end expiratory lung volume (11-13). Recruitment maneuvers are often considered useful in patients, especially those with acute respiratory distress syndrome (ARDS), to potentially decrease ventilator-induced lung injury by improving oxygenation and lung compliance while reducing the risk of atelectrauma by re-opening and stabilizing collapsed alveoli (11,13-18).

Increased intrathoracic pressure can affect right and left ventricular preload due to decreased venous return, changed right ventricular afterload, and altered biventricular compliance (4,10,14,19-21). This may lead to decreased stroke volume leading to short periods of hypotension, bradycardia, and impaired cardiac output, which is of significant concern in patients with congenital cardiac disease (14). Many patients with congenital cardiac disease must undergo surgical procedures which lead to lung collapse after induction of general anesthesia and during mechanical ventilation (15,22). In those patients undergoing cardiac surgery with cardiopulmonary bypass, significant atelectasis occurs which impairs right ventricular (RV) function. However, lung recruitments using positive pressure have been shown to re-expand collapsed alveoli and improve RV function (23-26). There is a theoretical risk of developing barotrauma leading to pneumomediastinum or pneumothorax during a recruitment; however this is likely less a risk in cardiac surgical patients with relatively healthy lungs (10,27,28).

These cardiopulmonary interactions and hemodynamic concerns limit the willingness of many clinicians to perform positive-pressure recruitment maneuvers in patients with underlying cardiac pathology, making studies involving this population uncommon. One study (29) evaluated the use of a recruitment maneuver performed in twenty pediatric patients with congenital cardiac disease who underwent surgical repair. A single recruitment maneuver was performed shortly after coming off of cardiopulmonary bypass and repeated once in the intensive care unit. Although this study was able to demonstrate an improvement in oxygenation, dynamic lung compliance, arterial to end-tidal CO₂ gradient, and end expiratory lung volume, it excluded patients with residual intracardiac lesions following surgery, patients with valvular regurgitation, or respiratory failure defined as FiO2 >0.8. Due to the relatively small number of patients included in this study, as well as their protocol prescribing only two recruitment maneuvers performed per patient, it is difficult to ascertain the overall long-term safety and potential benefits that repeated lung recruitments may provide.

In this study, we aimed to investigate the safety and efficacy of increment-decrement recruitment maneuvers in a larger pediatric patient population following surgery for congenital cardiac disease, hypothesizing that multiple recruitment maneuvers are physiologically beneficial and hemodynamically tolerated in these patients. The safety of these maneuvers was evaluated by examining changes in mean arterial pressure (MAP), heart rate (HR), and central venous pressure (CVP) before, during, and after the recruitment maneuvers. The efficacy of the recruitment maneuvers was determined by changes in oxygenation index (OI) and dynamic lung compliance (Cdyn) following recruitment. To further evaluate the safety of repetitive recruitment we reviewed specific clinical outcomes that included length of mechanical ventilation, length of hospital stay (LOS), mortality and occurrence of pneumothorax and compared to a control group.

Materials and Methods

This study was reviewed and approved by the Institutional Review Board at Phoenix Children’s Hospital. Subjects who received lung recruitment maneuvers post-operatively, as identified in the electronic medical record, in the Phoenix Children’s Hospital cardiac intensive care unit, a quaternary referral center, from July 2011 through June 2012 following implementation of a lung recruitment protocol, were included in the study. Further inclusion criteria included subjects from 0-18 years of age who were admitted immediately after having open heart surgery with both single- and two-ventricle physiology and who remained on invasive mechanical ventilation. All subjects were mechanically ventilated with Servo-I ventilators (Maquet Critical Care, Solna, Sweden). Subjects with a tracheostomy or who were receiving extracorporeal membrane oxygenation (ECMO) support were excluded from the analysis. A comparison group of consecutive control subjects who did not receive recruitment maneuvers was selected in the following year from July 2012 to June 2013 following an institutional hiatus of the maneuvers during which time quality data was reviewed and the safety of the protocol was assessed. Recruitment maneuvers have subsequently been reinstated and are now standard care in our post-operative cardiac patients on invasive mechanical ventilation.

During the study period, lung recruitment maneuvers were a new standard of care implemented at our institution in the cardiac intensive care unit. They were performed by either the respiratory therapist or attending physician. Most patients had twice daily recruitment maneuvers unless more were clinically indicated based on chest x-ray findings or lung mechanics. The patients may also have fewer recruitment maneuvers if they were hemodynamically unstable, having other procedures, if there was ongoing resuscitation or at the discretion of the attending physician.

The recruitment maneuver was performed in pressure control mode regardless of the subject’s baseline mode of ventilation. Initial settings were adjusted to achieve a tidal volume of 6mL/kg. PEEP was increased from baseline by 1-2 cmH₂O increments while maintaining a fixed inspiratory driving pressure (PIP-PEEP) with each increase sustained for one-minute intervals until either the tidal volume (V_T) or dynamic compliance (Cdyn) declined (Figure 1).

Figure 1. Lung recruitment maneuver: recruitment maneuver protocol courtesy of Boriosi et al. (11). Each horizontal bar represents an incremental increase of PEEP by 2 cm H₂O in one-minute increments from baseline PEEP.

The recruitment maneuver was terminated if the mean airway pressure surpassed 28 cm H₂O. V_T and Cdyn were documented with each increase in PEEP. Once the critical opening pressure was identified, PEEP was decreased in a step-wise manner in one-minute 1-2 cmH₂O decrements to the critical closing pressure identified by a decrease in V_T or Cdyn. Following this point, the PEEP was again increased to the identified critical opening pressure for one minute. It was then brought back down to 2 cmH₂O above the critical closing pressure (i.e. “optimal PEEP” level demonstrated by improved compliance and increased tidal volume with less ventilating pressure). The subject was then placed back on their original mode of ventilatory support with the PEEP adjusted to the optimal level, as determined during the recruitment maneuver in order to maintain the newly recruited areas of the lungs open.

Data Collected: A database was generated with 61 subjects who had lung recruitment maneuvers, and a convenience sample of 59 matched control subjects were selected from our Society for Thoracic Surgeons (STS) database. Demographic data was collected including age, body surface area, associated anomalies or chromosomal abnormalities, cardiac diagnosis, and type of surgical procedure. Clinical outcomes data collected included length of mechanical ventilation, length of hospital stay, mortality, and occurrence of pneumothorax.

Hemodynamic variables including MAP, HR, and CVP were monitored and recorded by the bedside nurse and/or respiratory therapist. For each variable, the two hourly vital sign measurements prior to the start of the maneuver, two measurements during, and the first two hourly measurements following the maneuver were included for analysis. In an attempt to minimize error and to provide a more accurate representation of the subject’s status at the time of interest, the two vital sign measurements in each category were averaged as physiologic variables are dynamic. The respiratory physiologic variables monitored were dynamic compliance and oxygenation index. In order to further investigate the clinical effects of potentially decreased cardiac output, we reviewed the changes in inotropic and vasopressor support before, during, and after the performance of each recruitment maneuver.

Statistical Analysis: Subject demographic and clinical characteristics between the control and recruitment maneuver groups were reported as medians, interquartile ranges (IQR) for continuous variables and frequencies, percentages for categorical variables. The Wilcoxon Rank Sum was used to compare the continuous variables; while Chi-squared/Fisher’s Exact Tests were used to compare the categorical variables.  The Linear Mixed Model was used to ascertain trends in hemodynamic outcomes (mean arterial pressure, heart rate, and central venous pressure) across three timepoints (before, during and after the recruitment maneuver).  If the overall trend showed statistical significance, the Wilcoxon Signed Rank Test was used to ascertain differences via multiple comparisons followed by the Bonferroni adjustment for multiple comparisons.  Before and after differences in physiological outcomes (oxygenation index and dynamic compliance) were assessed using the Wilcoxon Signed Rank.  All p-values were 2-sided and p<0.05 was considered statistically significant. All data analyses were conducted using STATA version 14 (STATACorp; College Station, TX).  

Results

A total of 61 subjects underwent lung recruitment from June 2011 to June 2012 (Table 1) accounting for a total of 439 recruitment maneuvers during this time.

Table 1. Comparison of subjects receiving recruitment maneuvers versus controls.

Recruitment was initiated in the post-operative period once deemed safe by the primary intensivist. The maneuvers were performed as frequently as every two hours but, on average, subjects in the cohort received 2 recruitment maneuvers per ventilator day. Both groups had similar congenital heart disease diagnoses with an average Society of Thoracic Surgeons-European Association for Cardiothoracic Surgery Congenital Heart Surgery Mortality Score of 3 in each group covering a variety of anatomical defects and surgical procedures performed. Subjects with residual intracardiac lesions on intraoperative transesophageal echocardiogram were included in the study.

Hemodynamics: All 61 subjects tolerated the maneuvers with no hemodynamic instability defined as hypotension, need for fluid bolus during the recruitment, bradycardia, or dysrhythmias. No subject had any of the maneuvers discontinued prematurely. We found no significant difference in the MAP (p = 0.13, 95% CI) (Figure 2a) or HR (p = 0.74, 95% CI) (Figure 2b) during the time intervals measured.

Figure 2. Hemodynamics: comparison of hemodynamic measurements before, during, and after the recruitment maneuvers. There was no significant change in MAP (Fig 2a), HR (2b), or CVP (2c) during or after the maneuvers. Boxplot with whiskers with minimum/maximum 1.5 IQR.

Due to the transient increase in intrathoracic pressure that theoretically results in a decrease in venous return and therefore cardiac output, CVP was monitored throughout the recruitments. The CVP measurement did not show a significant change with the recruitment maneuver (p = 0.79, 95% CI) (Figure 2c).

In order to further investigate the clinical effects of potentially decreased cardiac output, we reviewed the changes in inotropic and vasopressor support surrounding the performance of the recruitment maneuvers. All infusion rates of epinephrine, norepinephrine, vasopressin, dopamine, milrinone, and calcium were documented prior to, during, and after lung recruitments. Of the 439 recruitment maneuvers performed, 84% were performed without any change in inotropic support during or within 1 hour after completion of the maneuver. Inotropic support was decreased after the recruitment in 12% of maneuvers. Only 3% of maneuvers required an increase in support. No subjects had any significant hypotension requiring fluid bolus administration during or immediately after the maneuvers.

Efficacy: The efficacy of recruitment maneuvers on lung function was determined by measuring changes in the OI and Cdyn before and after recruitment. There was no statistically or clinically significant change in the OI with a median OI before recruitment of 7.3 (IQR 4.1-12.6) and after 7.7 (IQR 4.6-12.6) (p = 0.96, 95% CI) (Figure 3a).

Figure 3. Efficacy: comparison of physiologic measures used to assess efficacy of the recruitment maneuvers. No significant change was demonstrated in the OI before and after recruitment (3a). There was a significant increase in Cdyn by an average of 28% immediately after the maneuvers (3b). Boxplot with whiskers with minimum/maximum 1.5 IQR.

Of the 439 maneuvers, 83% resulted in a measurable improvement of the Cdyn with all 61 of the subjects demonstrating an increase at least once over the course of the interventions. The Cdyn increased from 0.45 ml/cmH₂O/kg (IQR 0.37-0.57) to 0.58 ml/cmH₂O/kg (IQR 0.47-0.75) afterwards (p < 0.001, 95% CI). (Figure 3b). The duration of improved Cdyn was an average of 8 hours +/- 11.4 hours. Subjects continued to show improvement with repeated efforts.

Clinical Outcomes. All subjects included in this study were on invasive mechanical ventilation support on return from cardiac surgery for a minimum of 24 hours. As shown in Table 2, there was no significant difference in the number of ventilator days between the recruitment maneuver and control groups (p = 0.26, 95% CI).

Table 2. Clinical outcomes.

There was also no difference in the occurrence of extubation failure requiring reintubation between both groups (p = 0.52). There was no difference in hospital LOS with the RM group staying 17.5 days (10.5 – 27) and control group 15 days (9.5 – 23) (p = 0.28, 95% CI) or in the rate of in-hospital mortality (p = 0.58, 95% CI). Despite the theoretical concern for development of pneumothorax with recruitment maneuvers, there was no significant difference in the occurrence between the two groups (p = 0.26, 95% CI).

Discussion

Our results suggest that lung recruitment maneuvers are well tolerated in the pediatric post-operative cardiac patient population both with and without residual intracardiac shunts, and may be repeated for the duration of their time requiring invasive mechanical ventilation. Despite being at high risk of hemodynamic instability shortly after surgery, especially following complex repair and prolonged cardiopulmonary bypass time, our subjects did not require significant preload optimization or escalation of inotropic support during the maneuvers. We were also able to demonstrate that there was an improvement in dynamic lung compliance following the maneuver. Not only were these maneuvers tolerated from a hemodynamic standpoint, but there were no adverse outcomes when compared to control subjects with no difference in the length of mechanical ventilation, LOS, mortality, or the occurrence of pneumothorax.

Advocacy for the optimization of oxygenation and ventilation through the use of an “open lung” strategy, especially in the treatment of ARDS, has been present in the critical care literature for decades. Multiple reports have described the importance of lung recruitment with high inspiratory pressures in addition to the appropriate PEEP above closing pressures to maintain optimal gas exchange and minimize hypercapnia (30). Recruitment maneuvers are recommended in the protective ventilation strategy in adult post-operative patients who have undergone cardiac surgery with significant benefits as compared to traditional ventilation (31,32). To our knowledge, there is very limited data on the use of lung recruitment maneuvers in the pediatric cardiac patient population with the majority of the pediatric literature focusing on the use of these maneuvers in patients with ARDS. Scohy et al. (29) previously evaluated the use of recruitment maneuvers in subjects undergoing surgery for congenital cardiac disease but excluded several key subgroups of these subjects and did not evaluate the continued use of recruitment maneuvers over the entire course of mechanical ventilation. Amorim et al. (6) assessed the tolerance of recruitment maneuvers in a small population of infants who were prone to pulmonary arterial hypertension and excessive pulmonary circulation just after skin closure for open heart surgery. In general, data on the safety of these maneuvers in pediatric patients is very limited.

The efficacy of lung recruitment maneuvers in patients with ARDS remains controversial with some studies suggesting an improvement in oxygenation and dynamic or static compliance (1,11,20,21,33-35), some demonstrating brief or no improvement (36,37), and others that show improvement but suggest that the deleterious hemodynamic effects may outweigh the benefits (14). In children with ARDS, a staircase recruitment strategy has been described to improve oxygenation with increasing PaO_2. In order to sustain improved oxygenation, the PEEP must be set above the critical closing pressure of the lung following recruitment (11,21,38,39). Boriosi et al. (11) further described that a “re-recruitment” maneuver that was performed at critical opening pressures for a short period of time improved the PaO₂/FiO₂ ratio for up to 12 hours and OI for up to four hours following the recruitment maneuver. In our study, we were not able to demonstrate an improvement in the OI. However, we did demonstrate a significant improvement in Cdyn of 29% following completion of each recruitment which was sustained for eight hours. The lack of improvement in oxygenation may be secondary to less primary lung injury in our patient population, or due to the common presence of residual intracardiac shunts. The increase in Cdyn may be a clinically significant change for some patients and could help reduce the time on invasive mechanical ventilation.

The overall goal of recruitment maneuvers is to open atelectatic alveoli, increase end expiratory lung volume, and improve gas exchange. However, as discussed, generation of high intrathoracic pressures during the maneuvers can theoretically result in hemodynamic instability (4,10,14,20,21). Currently, there is no specific non-invasive monitoring that is the best indicator for hemodynamic assessment during recruitment maneuvers, with vital sign changes serving as a surrogate marker for the safety of the recruitment maneuver (40). In our study, there was no change in MAP, HR, or CVP from baseline, during, or after the maneuvers indicating that they were well tolerated from a hemodynamic standpoint with 97% of the recruitment maneuvers using the same or less inotropic support and no subject required fluid bolus administration for hypotension during any of the maneuvers.

The occurrence of barotrauma, including pneumomediastinum and pneumothorax, has been reported with the intermittent increase in peak airway inspiratory pressures (10,27,28). In our study, there was no significant difference in the occurrence of pneumothorax between the two groups. With the preponderance of studies on recruitment maneuvers being performed in the adult ARDS patient population, there is limited data on pediatric outcomes in mortality and duration of mechanical ventilation. A Cochrane review performed by Hodgson et al. (41) demonstrated no reduction in mortality or length of mechanical ventilation following recruitment maneuvers in adult ARDS patients. In our study, we demonstrated similar findings in that there was no difference in mortality, length of mechanical ventilation, or LOS in pediatric post-operative congenital cardiac patients with or without the maneuvers.

There were several limitations to our study. This was a single-center, retrospective study that involved a small pediatric cardiac population. Our assessment of cardiac output was dependent on measurements of MAP and CVP. We also did not investigate the occurrence of hypercapnia during the recruitment maneuvers. Overdistension of open alveoli can occur resulting in an increase in pulmonary vascular resistance and a decrease in blood flow to the alveoli, thereby increasing dead space ventilation (21). There are a number of studies demonstrating that throughout recruitment maneuvers there is an increase in PaCO₂, with a potential need to titrate the respiratory rate on the ventilator in order to maintain constant minute ventilation throughout the maneuver, as this development of hypercapnia during the maneuvers may result in adverse effects (11,34,36,41). A multifaceted approach to monitoring the effectiveness as well as any negative consequences of these maneuvers including end-expiratory lung volumes, dead space ventilation, pulmonary compliance, volumetric capnography as well as bedside ultrasound would be beneficial (40). This study was conducted prior to our institution utilizing volumetric CO₂ analysis to monitor physiologic gas exchange as well as dead-space ventilation during mechanical ventilation.

Conclusion

Overall, our study demonstrated that pediatric post-operative cardiac subjects, having a wide variety of cardiopulmonary physiology, tolerated repeated recruitment maneuvers without significant hemodynamic changes or adverse outcomes. As has been the case in many previous studies, we did not find any significant improvement in oxygenation, length of mechanical ventilation, or length of stay. However, as recruitment maneuvers have been shown to be an integral part of lung protection strategies and to benefit adults following open heart surgery, it is possible that our pediatric post-operative cardiac patients could benefit from the integration of recruitment maneuvers into ventilator management strategies while on invasive mechanical ventilation. Future prospective studies need to be conducted to further evaluate the potential benefit and utility of lung recruitment maneuvers in pediatric patients without significant lung disease.

Acknowledgements

We would like to thank the staff of the Pediatric Cardiovascular Intensive Care Unit at Phoenix Children’s Hospital for their assistance and support in this study. We would also like to acknowledge the work of Juan P Boriosi, MD and his colleagues for use of their recruitment protocol and RM diagram (Figure 1) in our study.

Contributions: Renee L. Devor MD^1,4,5,6, Harjot K. Bassi, MD^1-6, Paul Kang MPH⁴, Tiffany Morandi MD^1-3, Kristi Richardson RT^2,3, John J. Nigro MD², Christine Tenaglia RT^2,3, Chasity Wellnitz RN, BSN, MPH^2,4, and Brigham C. Willis MD^3,6

¹Literature search, ²Data collection, ³Study Design, ⁴Analysis of data, ⁵Manuscript preparation, ⁶Review of manuscript

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40. Godet T, Constantin JM, Jaber S, Futier E. How to monitor a recruitment maneuver at the bedside. Curr Opin Crit Care 2015;21(3):253-8. [CrossRef] [PubMed]
41. Hodgson C, Keating JL, Holland AE, Davies AR, Smirneos L, Bradley SJ, et al. Recruitment manoeuvres for adults with acute lung injury receiving mechanical ventilation. Cochrane Database Syst Rev 2009(2):Cd006667. [CrossRef] [PubMed]

Cite as: Devor RL, Bassi HK, Kang P, Morandi T, Richardson K, Nigro JJ, Tenaglia C, Wellnitz C, Willis BC. Safety and efficacy of lung recruitment maneuvers in pediatric post-operative cardiac patients. Southwest J Pulm Crit Care. 2020;20(1):16-28. doi: https://doi.org/10.13175/swjpcc068-19 PDF 

January 2020 Critical Care Case of the Month: A Code Post Lung Needle Biopsy

Sarika Savajiyani MD and Clement U. Singarajah MBBS

 Phoenix VA Medical Center

Phoenix, AZ USA

A 67-year-old man with a history of stage IIA rectal adenocarcinoma post neoadjuvant chemoradiation presented with a near code event after elective CT guided biopsy of an enlarging left lower lobe lung nodule. The patient became bradycardic and profoundly hypotensive immediately after the CT guided biopsy with the following vital signs: Systolic BP < 90 mmHg, HR 40/min sinus bradycardia, SpO₂ on 100% oxygen non rebreather was 90%. Telemetry and EKG showed ST elevation in the anterior leads. He complained of vague arm and leg weakness and tingling, but did not lose consciousness or suffer a cardiac arrest. 

A CT scan was performed about 2-3 minutes after the patient deteriorated (Figure 1).

Figure 1. A-E: Representative images from CT scan in soft tissue windows. Lower: Video of CT scan in soft tissue windows.

What radiographic finding likely explains the patient’s clinical deterioration?  (Click on the correct answer to be directed to the second of six pages)

1. Arterial air embolism
2. Pneumothorax
3. Pulmonary edema
4. Pulmonary Embolism
5. Venous air embolism

Cite as: Savajiyani S, Singarajah CU. January 2020 critical care case of the month: a code post lung needle biopsy. Southwest J Pulm Crit Care. 2020;20(1):1-6. doi: https://doi.org/10.13175/swjpcc042-19 PDF

October 2019 Critical Care Case of the Month: Running Naked in the Park

Spencer Jasper MD

Matthew Adams DO

Jonathan Boyd MD

Jeremiah Garrison MD

Janet Campion MD

The University of Arizona College of Medicine

Tucson, AZ USA

History of Present Illness

A 34-year-old man with a history of IV drug abuse was brought into emergency department by EMS and Tucson Police Department after complaints of naked man running and behaving erratically in a park. On arrival to emergency department patient was acting aggressively towards staff, spitting and attempting to bite. The ER staff attempted multiple times to sedate the patient with benzodiazepines, however, due to continued aggressive behavior, ongoing encephalopathy and the need for increased sedation, the patient was intubated for airway protection.

The patient was febrile (40.6° C), tachycardic (122) and hypertensive (143/86). On physical exam patient was not cooperative, was diaphoretic, cachectic, with reactive constrictive pupils, track marks in antecubital fossa bilaterally. No clonus or hypertonicity. During intubation, there was noted to be nuchal rigidity.

He was then admitted to the medical ICU. Drug intoxication from possible methamphetamines was the presumptive diagnosis of encephalopathy but given nuchal rigidity and fevers there was concern for other etiologies.

Physical Exam

• Vitals: T 40.6 °C, HR: 122, RR: 22, BP: 143/86, SpO2: 97% WT: 55 kg
• General: Intubated and sedated, cachectic
• Eye: Pupils constricted but reactive to light
• HEENT: Normocephalic, atraumatic
• Neck: Stiff, non-tender, no carotid bruits, no JVD, no lymphadenopathy
• Lungs: Clear to auscultation, non-labored respiration
• Heart: Normal rate, regular rhythm, no murmur, gallop or peripheral edema
• Abdomen: Soft, non-tender, non-distended, normal bowel sounds, no masses
• Skin: Skin is warm, dry and pink, multiple abrasions on the lower extremities bilaterally, track marks noted in the antecubital fossa bilaterally. Large abrasion with bruising around the right knee and erythema and welts on the right shin. Erythematous area on the dorsal surface of the right hand
• Neurologic: Nonfocal prior to intubation, no clonus or hypertonicity noted

Drug overdose/intoxication was presumptive diagnosis for his acute encephalopathy. Based on physical exam and vitals, what other etiologies should be considered? (click on the correct answer to be directed to the second of seven pages)

1. Embolic stroke
2. Heat stroke
3. Hyperthyroidism
4. Meningitis
5. All of the above

Cite as: Jasper S, Adams M, Boyd J, Garrison J, Campion J. October 2019 critical care case of the month: running naked in the park. Southwest J Pulm Crit Care. 2019;19(4):110-8. doi: https://doi.org/10.13175/swjpcc054-19 PDF

Severe Accidental Hypothermia in Phoenix? Active Rewarming Using Thoracic Lavage

Michael Mozer BS¹

Guy Raz, MD²

Ryan Wyatt, MD²

Alexander Toledo, DO, PharmD²

¹University of New England College of Osteopathic Medicine

Biddeford, ME USA

²Department of Emergency Medicine

Maricopa Medical Center, Phoenix, AZ USA

Abstract

Hypothermia can progress quickly and become life threatening if left untreated. Rewarming in the severely hypothermic patient is of critical importance and is achieved with active and passive techniques. Here we present a case of a hypothermic patient with cardiac instability for whom thoracic lavage was ultimately used. We will review the treatment of hypothermia and discuss the technical aspects our approach.

Case Presentation

A 53 year-old male with a past medical history of substance abuse, chronic hepatitis C, and poorly controlled type 2 diabetes mellitus complicated by a recent hospitalization for osteomyelitis was brought to the emergency department after being found lying on a road in a shallow pool of water in the early morning hours of a rainy day in Phoenix, Arizona. The ambient temperature that night was 39 °F (3.9 °C). Emergency Medical Services (EMS) noted a decreased level of consciousness and obtained a finger stick glucose of 15 mg/dl. EMS reported a tympanic membrane temperature of 23.9 °C. En route, the patient was administered 2mg naloxone and 25g dextrose intravenously with no improvement in his mental status. On Emergency Department (ED) arrival, the patient had a GCS of 8 (Eyes 4, Verbal 1, Motor 3) and exhibited intermittent posturing. His foot wound appeared clean and without signs of infection. The initial core temperature recorded was 25.9°C via bladder thermometer, systolic blood pressure was 92/50, and heart rate fluctuated between 50 and 90 beats per minute.

After removing wet clothing, initiation of warmed saline, and placing a forced warm air blanket on the patient, he was intubated for airway protection and vasopressors were initiated. Osborn waves were evident on the initial EKG (Figure 1).

Figure 1. Initial EKG with Osborn Waves (arrows).

A warmed ventilator circuit was initiated with only 0.5 °C increase in temperature in first 30 minutes. Despite these measures, he remained hypotensive and unstable. Significant laboratory findings were a white blood cell count of 25.5 thousand (92% neutrophils), lactic acid of 7.6, potassium of 5.8, serum creatinine of 1.05, glucose of 283, INR of 1.1, and urine drug screen positive for cocaine. Given his recalcitrance to norepinephrine and risk of death secondary to fatal dysrhythmia with temperatures below 28 °C intrathoracic lavage initiated.

The right hemithorax was selected for irrigation because left-sided tube placement can induce ventricular fibrillation in a perfusing patient (1). Using standard sterile technique, two 36 French thoracostomy tubes were placed; the first in the second intercostal space along the mid-clavicular line, and the second in the 5^th intercostal space in the posterior axillary line (1-3). The tips of the thoracostomy tubes were oriented such that the anterior-superior tube was positioned near the right apex and the lateral-inferior tip was positioned low in the thoracic cavity (1,3). To maintain the temperature of the instilled fluid, a fluid warmer system (Level 1; Smiths Medical; Minneapolis, MN) was used and set to 41 °C. A Christmas tree adapter was used to connect the IV tubing to the superior thoracostomy tube, and a water seal chamber was attached to the inferior tube for passive drainage (3). Flow through the system was targeted to maintain steady passive drainage as described in the literature (1-6).

Thoracic cavity lavage with 41 °C saline was performed and the patient was transferred to the medical ICU after 3 hours in the ED. When he was transferred his core temperature was 29 °C and he remained on norepinephrine for hemodynamic instability. After 2 hours of continued rewarming in the MICU, his core temperature was 32 °C. Osborn waves evident on initial EKG were resolved (Figure 2).

Figure 2. Repeat EKG showing resolution of Osborn waves.

The patient left against medical advice from the hospital 4 days later neurologically intact and without sequela.

Discussion

Hypothermia can be clinically classified as mild, moderate or severe (7). Mild hypothermia, defined as core temperatures of 32-35 °C, presents with shivering. Amnesia, dysarthria, ataxia, tachycardia, and tachypnea can also be seen (1). Moderate hypothermia, defined as core temperatures of 28-32 °C, usually can present with or without shivering. Stupor, hypoventilation, paradoxical undressing and non-fatal arrhythmias such as atrial fibrillation and junctional bradycardia may also be seen (1). Patients with severe hypothermia, generally defined as temperatures below 28 °C, can present with coma, areflexia, pulmonary edema, bradycardia, and hypotension (1). There is a significant risk of fatal cardiac dysrhythmias without rapid therapeutic rewarming (1,7,8).

Rewarming in the hypothermic patient is of critical importance and is achieved with passive and/or active techniques. Attempts to limit heat loss are often unsuccessful, especially in the absence of a normal shiver response. It however remains as the first line treatment for hypothermia (8-10). Passive rewarming is attempted by the removal of cold/wet clothing and keeping the patient covered (8-10). Active external rewarming (AER) is the next line of treatment and consist of the use of externally rewarming devices such as warmed blankets, warm environment, forced air warming (Bair Hugger; 3M; Maplewood, MN) or warm hot water bladders placed in the groin and axilla (1,7-10). Active Internal Rewarming (AIR) techniques can be used to achieve more rapid increases in core temperature and are primarily utilized in cases of cardiac instability or if AER is unsuccessful (8). When available, the method of choice for active internal rewarming (AIR) is cardiopulmonary bypass (CPB) or extracorporeal membrane oxygenation (ECMO) as they can achieve the fastest increase in core temperature (9 °C/hr and 6 °C/hr respectively) and provide cardiovascular support (1,8,11,12). Several techniques are described in the literature that can be considered if CPB or ECMO are unavailable. These include esophageal warming devices, endovascular catheters, hemodialysis, and endocavitary lavage (1,2,4-6,13-15). While no randomized controlled trials exist, several case reports and reviews have tried to compare various techniques. These sources to do not seem to favor any particular technique over another but rather reports the rates of temperature rise (1-3,5-7,13-15). Classically, lavage techniques are attempted in the thoracic cavity, the peritoneum, the bladder, the stomach, the esophagus, or the colon. These techniques are generally coupled with warm IV fluids and warming air through the ventilator to limit loss of body heat to iatrogenic procedures during the rewarming attempt (1,7). Thoracic lavage is effective with a reported rewarming rates of 3-6 °C/hr and with excellent outcomes in case reports (1,2,4-6). Here we present a case of a hypothermic patient with cardiac instability where thoracic lavage is used and discuss the technical aspects of this approach.

Our case demonstrates the efficacy of utilizing thoracic cavity lavage for rapid rewarming in patients with severe hypothermia with a pulse and at high risk of fatal cardiac arrhythmia. In multiple case reports, thoracic lavage has been used successfully in hypothermic patients who suffered complete cardiopulmonary collapse requiring CPR (2,4,5). Although warm thoracic lavage is not the treatment of choice in these circumstances, in a facility not equipped with ECMO or CPB and a patient too unstable to transfer, it seemed to us to be the best technique. Gastric, colonic, and bladder lavage offer very minimal heat transfer due to limitations in surface area (2).

Hemodialysis would have required for us to call in a technician and would have required approval by a nephrologist at our institution. Available central venous rewarming catheters require bypass of a failsafe mechanism that does not allow rewarming to be initiated below 30 °C (1). Peritoneal lavage was a plausible choice but does not directly warm the mediastinum (2). While an open mediastinal technique has been used, we did not feel it was appropriate in a patient with a concurrent pulse (1,3). Thoracic lavage is therefore an effective alternative that should be used in cases where CPB and ECMO are unavailable especially in a patient that is hemodynamically unstable and may not survive transfer. The equipment is readily available to any Emergency Medicine or Critical Care physician. In addition, this case exemplifies the positive outcomes that are associated with rapid rewarming in the hypothermic patient with a pulse. We believe our case demonstrates the efficacy of this technique for myocardial protection from hemodynamic collapse, a topic which has not been adequately studied in the literature.

References

1. Brown DJ, Danzl DF. Accidental hypothermia. In: Auerbach PS, ed. Wilderness Medicine. 7th ed. St. Louis: Mosby Inc.; 2017:135-62.
2. Plaisier BR. Thoracic lavage in accidental hypothermia with cardiac arrest--report of a case and review of the literature. Resuscitation. 2005 ;66(1):99-104. [CrossRef] [PubMed]
3. Schiebout JD. Hypothermic Patient Management. In: Reichman EF. eds. Reichman's Emergency Medicine Procedures, 3e New York, NY: McGraw-Hill. Available at: http://accessemergencymedicine.mhmedical.com/content.aspx?bookid=2498&sectionid=201303754 (accessed August 02, 2019).
4. Little G. Accidental hypothermic cardiac arrest and rapid mediastinal warming with pleural lavage: A survivor after 3.5 hours of manual CPR. BMJ Case Reports. July 2017:bcr-2017-220900. [CrossRef] [PubMed]
5. Turtiainen J, Halonen J, Syväoja S, Hakala T. Rewarming a patient with accidental hypothermia and cardiac arrest using thoracic lavage. Ann Thorac Surg. 2014 Jun;97(6):2165-6. [CrossRef] [PubMed]
6. Ellis MM, Welch RD. Severe hypothermia and cardiac arrest successfully treated without external mechanical circulatory support. Am J Emerg Med. 2016;34(9):1913.e5-6. [CrossRef] [PubMed]
7. Tintinalli J, Stapczynski J, Ma O, Yealy D, Meckler G, Cline D. Tintinalli's Emergency Medicine. 8th ed. New York, NY: McGraw-Hill Education; 2016:1743-4.
8. Brugger H, Boyd J, Paal P. Accidental Hypothermia. N Engl J Med. 2012;367(20):1930-8. [CrossRef] [PubMed]
9. Paal P, Gordon L, Strapazzon G, et al. Accidental hypothermia-an update: The content of this review is endorsed by the International Commission for Mountain Emergency Medicine (ICAR MEDCOM). Scand J Trauma Resusc Emerg Med. 2016;24(1):111. [CrossRef] [PubMed]
10. Zafren K, Giesbrecht GG, Danzl DF, et al. Wilderness Medical Society practice guidelines for the out-of-hospital evaluation and treatment of accidental hypothermia: 2014 update. Wilderness Environ Med. 2014 Dec;25(4 Suppl):S66-85. [CrossRef] [PubMed]
11. Schober A, Sterz F, Handler C, et al. Cardiac arrest due to accidental hypothermia-A 20 year review of a rare condition in an urban area. Resuscitation. 2014;85(6):749-56. [CrossRef] [PubMed]
12. Saczkowski RS, Brown DJA, Abu-Laban RB, Fradet G, Schulze CJ, Kuzak ND. Prediction and risk stratification of survival in accidental hypothermia requiring extracorporeal life support: An individual patient data meta-analysis. Resuscitation. 2018;127:51-7.[CrossRef] [PubMed]
13. Primozic KK, Svensek F, Markota A, Sinkovic A. Rewarming after severe accidental hypothermia using the esophageal heat transfer device: a case report. Ther Hypothermia Temp Manag. 2018 Mar;8(1):62-4. [CrossRef] [PubMed]
14. Murakami T, Yoshida T, Kurokochi A, et al. Accidental hypothermia treated by hemodialysis in the acute phase: three case reports and a review of the literature. Intern Med. 2019 Jun 7. [CrossRef]
15. Klein LR, Huelster J, Adil U, et al. Endovascular rewarming in the emergency department for moderate to severe accidental hypothermia. Am J Emerg Med. 2017 Nov;35(11):1624-9. [CrossRef] [PubMed]

Cite as: Mozer M, Raz G, Wyatt R, Toledo A. Severe accidental hypothermia in Phoenix? Active rewarming using thoracic lavage. Southwest J Pulm Crit Care. 2019;19(2):79-83. doi: https://doi.org/10.13175/swjpcc038-19 PDF 

Left Ventricular Assist Devices: A Brief Overview

Bhargavi Gali MD

Department of Anesthesiology and Perioperative Medicine

Division of Critical Care Medicine

Mayo Clinic Minnesota

Rochester, MN, USA

Introduction

Second and third generation left ventricular assist devices (LVAD) have been increasingly utilized as both a bridge to transplantation and as destination therapy (in patients who are not considered transplant candidates) for advanced heart failure. Currently approximately 2500 LVADs are implanted yearly, with an estimated one year survival of >80% (1). Almost half of these patients undergo implantation as destination therapy. A recent systematic review and meta-analysis found no difference in one-year mortality between patients undergoing heart transplantation in comparison with patients undergoing LVAD placement (2).

Early LVADs were pulsatile pumps, but had multiple limitations including duration of device function, and requirement for a large external lead that increased risk of infection. Currently utilized second and third generation devices are continuous flow (first generation were pulsatile flow). Second generation devices have axial pumps (HeartMate II®). The third generation LVADs ((HeartMate III®), HVAD®) are also continuous flow, with centrifugal pumps, which are thought to decrease possibility of thrombus formation and increase pump duration in comparison to the second generation axial pumps. It is also felt that a lack of mechanical bearings contributes to this effect.

LVADs support circulation by either replacing or supplementing cardiac output. Blood is drained from the left ventricle with inflow cannula in the left ventricular apex to the pump, and blood is returned to the ascending aorta via the outflow cannula (3) (Figure 1).

Figure 1. Third generation Left Ventricular Assist Device. Heartware System ™. Continuous flow left ventricular assist device (LVAD) configuration. One of the third generation LVADs is the HeartWare System. With this device the inflow cannula is integrated into the pump. The pump is attached to the heart in the pericardial space, with the outflow cannula in the aorta. A driveline connects the device to the control unit. This control unit is attached to the two batteries. (Figure used with permission from Medtronic).

The device assists the left ventricle by the action of the axial (second generation) or centrifugal (third generation) pump that rotates at a very high speed and ejects the blood into the aorta via the outflow cannula. A tunneled driveline connects the pump to the external controller that operates the pump function. The controller connects to the power source via two cables, which can be battery or module-powered.

LVADs offload volume from the left ventricle, and decrease left ventricular work. Pulmonary pressures and the trans pulmonary gradients are also decreased by the reduced volume in the left ventricle (4). End organ perfusion is improved secondary to enhanced arterial blood pressure and micro perfusion.

There are four main parameters of pump function:

• Pump speed: the speed at which the LVAD rotors spin, and is programmed. Measured in RPM.
• Pump power: the wattage needed to maintain speed and flow, which is the energy needed to run the pump. Measured in Watts.
• Pump flow: estimate of the cardiac output, which is the blood returned to the ascending aorta, and is based on pump speed and power. Measure in L/min
• Pulsatility index (PI): a calculated value that indicates assistance the pump provides, in relation to intrinsic left ventricular A higher number indicates higher left ventricular contribution to pulsatile flow.

The cardiac output of currently utilized LVADs is directly related to pump speed and inversely related to the pressure gradient across the pump. As the pump speed is fixed, right ventricular failure can decrease the volume of blood transmitted to the pump and decrease LVAD flow (3, 4). With right ventricular failure, inotropic support may be needed to improve the LVAD pump flow. High afterload, such as may be seen with an increase in systemic vascular resistance can decrease pump flow.

Complications

Adverse events occur in more than 70% of LVAD patients in the first year (5). These complications include infections, bleeding, stroke, and LVAD thrombosis. More than 50% of patients are readmitted within the first 6 months after LVAD implantation (6).

Driveline infections are the most commonly reported LVAD infection, and are the most likely to respond to treatment (7). Pump pocket infections may require debridement plus/minus antibiotic bead placement. Bloodstream infections are less commonly reported, and more difficult to treat, and many patients are placed on chronic suppressive antibiotic therapy (7). There is a possible association between stroke and bloodstream infection, reported in some studies. Patients who were younger and had a higher body mass index were noted to have a higher incidence of LVAD infections.

Gastrointestinal bleeding is a major cause of nonsurgical bleeding, reported in almost 30% of patients after LVAD placement (1). Patients may develop acquired von Willebrand factor deficiency secondary to high shear forces in the LVAD that lead to breakdown of von Willebrand protein (6). Antithrombotic therapy is commonly instituted after LVAD implantation which also increases risk of bleeding. A high incidence of arteriovenous malformations is reported in these patients, although the etiology is not clear. Transfusion, holding antithrombotic therapy, and identifying possible sources are included in the standard approach to management.

There is a high risk of both ischemic and hemorrhagic strokes in the first year after LVAD placement (8). Surgical closure of the aortic valve and off-axis positioning of the cannulas have been suggested as altering shear forces, increasing thrombotic risk, and thus risk of stroke.  Post-surgical risks may include pump thrombosis, infections, supratherapeutic INR, and poorly controlled hypertension. Early diagnosis has led to consideration of interventions such as thrombectomy (8).

LVAD thrombosis can occur on either cannula (inflow or outflow) or the pump. Typically patients receive ongoing anticoagulation, commonly with warfarin, and antiplatelet agents, and often aspirin. Heartmate II® may have higher rate of thrombosis than HVAD or Heart Mate 3, although this is under debate (6). Thrombotic complications range in severity from asymptomatic increase in lactate dehydrogenase or plasma-free hemoglobin, to triggering of LVAD alarms, up to development of heart failure. The inflow and outflow cannulas and pump can be the site of thrombosis. Management typically involves revising the antithrombotic management. If there is no improvement or worsening, replacement of LVAD may be indicated. There is limited evidence to suggest that systemic thrombolysis may be of benefit in treating pump thrombosis, particularly in regards to the HVAD, though better data would be useful

Procedural Management

When a patient with an LVAD requires non cardiac surgery, optimal management includes having an on-site VAD technician, and close involvement of VAD cardiology and cardiac surgery in consultation. Anticoagulation will often be transitioned to heparin infusion prior to elective procedures (9). Suction events (LV wall is sucked into the inflow cannula) can occur secondary to under filled left heart, and this can become more apparent perioperatively. This can also decrease right heart contractility by moving the interventricular septum to the left, and thus decrease cardiac output. Management often involves fluid bolus. Suction events can lead to decreased flow, left ventricular damage, and ventricular arrhythmias. Hemodynamic management can be challenging with non-pulsatile flow, and placement of an arterial line can facilitate optimal management. Postoperative care in a monitored setting is beneficial in case of further volume related events and to watch for bleeding.

Emergent Complications

Arrhythmias occur in many patients after LVAD implantation. Atrial arrhythmias are reported in up to half of LVAD patients, and ventricular arrhythmias in 22-59% (10, 11).  Loss of AV synchrony can lead to decreased LV filling and subsequent RV failure. Rhythm or rate control with rapid atrial arrhythmias is necessary to decrease development of heart failure. Ventricular arrhythmias may be hemodynamically tolerated for some time secondary to the LVAD support (6).  If there is concern that the inflow cannula is touching the LV septum, as may occur with severe hypovolemia, echocardiography can help determine if volume resuscitation should be the initial step in treating ventricular arrhythmia.

If cardiac arrest occurs, the first step of cardiopulmonary resuscitation in patients with LVAD is assessment of appropriate perfusion via physical examination (12). If perfusion is poor or absent, assessment of LVAD function should take place. If the LVAD is not functioning appropriately, checking for connections and power is the next step. If unable to confirm function or restart LVAD, chest compressions are indicated by most recent guidelines from the American Heart Association. There is always concern of dislodgement of LVAD cannula or bleeding during these situations.

Conclusion

Currently implanted LVADS are continuous flow, and provide support via a parallel path from the left ventricle to the aorta. As the number of patients with LVADs increase all medical providers should have a basic understanding of the function and common complications associated with these devices. This will enhance the ability to initiate appropriate care.

References

1. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: Special focus on framing the impact of adverse events. J Heart Lung Transplant. 2017 Oct;36(10):1080-6. [CrossRef] [PubMed]
2. Theochari CA, Michalopoulos G, Oikonomou EK, et al. Heart transplantation versus left ventricular assist devices as destination therapy or bridge to transplantation for 1-year mortality: a systematic review and meta-analysis. Annals of Cardiothoracic Surgery. 2017;7(1):3-11. [CrossRef] [PubMed]
3. Lim HS, Howell N, Ranasinghe A. The physiology of continuous-flow left ventricular assist devices. J Card Fail. 2017;23(2):169-80. [CrossRef] [PubMed]
4. Roberts SM, Hovord DG, Kodavatiganti R, Sathishkumar S. Ventricular assist devices and non-cardiac surgery. BMC Anesthesiology. 2015;15(1):185. [CrossRef] [PubMed]
5. Miller LW, Rogers JG. Evolution of left ventricular assist device therapy for advanced heart failure: a review. JAMA Cardiol. 2018 Jul 1;3(7):650-8. [CrossRef] [PubMed]
6. DeVore AD, Patel PA, Patel CB. Medical management of patients with a left ventricular assist device for the non-left ventricular assist device specialist. JACC Heart Fail. 2017 Sep;5(9):621-31. [CrossRef] [PubMed]
7. O'Horo JC, Abu Saleh OM, Stulak JM, Wilhelm MP, Baddour LM, Rizwan Sohail M. Left ventricular assist device infections: a systematic review. ASAIO J. 2018 May/Jun;64(3):287-294. [CrossRef] [PubMed]
8. Goodwin K, Kluis A, Alexy T, John R, Voeller R. Neurological complications associated with left ventricular assist device therapy. pert Rev Cardiovasc Ther. 2018 Dec;16(12):909-17. [CrossRef] [PubMed]
9. Barbara DW, Wetzel DR, Pulido JN, et al. The perioperative management of patients with left ventricular assist devices undergoing noncardiac surgery. Mayo Clinic Proceedings. 2013;88(7):674-82. [CrossRef] [PubMed]
10. Enriquez AD, Calenda B, Gandhi PU, Nair AP, Anyanwu AC, Pinney SP. Clinical impact of atrial fibrillation in patients with the heartmate ii left ventricular assist device. J Am Coll Cardiol. 2014 Nov 4;64(18):1883-90. [CrossRef] [PubMed]
11. Nakahara S, Chien C, Gelow J, et al. Ventricular arrhythmias after left ventricular assist device. Circ Arrhythm Electrophysiol. 2013 Jun;6(3):648-54. [CrossRef] [PubMed]
12. Peberdy MA, Gluck JA, Ornato JP, et al. Cardiopulmonary resuscitation in adults and children with mechanical circulatory support: a scientific statement from the American Heart Association. Circulation. 2017;135(24):e1115-e34.`[CrossRef] [PubMed]

Cite as: Gali B. Left ventricular assist devices: a brief overview. Southwest J Pulm Crit Care. 2019;19(2):68-72. doi: https://doi.org/10.13175/swjpcc039-19 PDF