Article Type : Case Report
Authors : Bergeski A, Pavlichko MS, Wyatt KD, Whittle JS
Keywords : Left ventricular assist device; Cardiogenic shock; High velocity therapy; High flow oxygen; Cardiac workload
Patients with indwelling left ventricular assist devices represent a growing population presenting numerous novel diagnostic and treatment challenges. This case describes the complexities of managing a patient with a left ventricular assist device brought to the emergency department unresponsive following a motor vehicle collision. The arrival as a "trauma" patient complicated the diagnostic process, which ultimately revealed the patient had experienced ventricular tachycardia cardiac arrest but maintained minimal perfusion via the left ventricular assist device. The patient was evaluated for trauma and managed supportively with medications, fluid replacement, and high flow nasal oxygen therapy. The patient was successfully defibrillated. Balancing cardiac preload and afterload to maximize perfusion and stabilize the patient was particularly challenging and further complicated by the lack of availability of a left ventricular assist device specialty and the limited available patient history. This case highlights the cognitive challenges accompanying these patients and the need for further research and education to allow emergency department personnel to care for these patients optimally.
Emergency Medicine (EM) physicians care for patients
with complicated medical conditions, such as those with a left ventricular
assist device (LVAD). Limited interaction with LVAD patients can lead to
framing bias, wherein providers fixate on the LVAD, thus neglecting the
non-LVAD-related chief complaints [1]. Additionally, trauma evaluation in these
patients remains undescribed [2]. Here, we present a case of a 40-year-old male
with an LVAD who presented to the ED as a "trauma alert" following a
single-driver, unrestrained motor vehicle crash. Vital signs were difficult to
obtain due to electrical activity generated from the LVAD, which did not
correlate with the physical exam.
A 40-year-old male presented to the ED following a
single-driver motor vehicle collision. The patient was unresponsive and
unrestrained, with no evidence of airbag deployment or obvious bleeding at the
scene. The patient was minimally responsive and declared a "trauma
alert" with his mental status attributed to a head injury.
Initial examination revealed the patient was reactive
to painful stimuli, could protect his airway, and the carotid pulse was faint
but palpable. Repeated attempts to obtain a blood pressure (BP) measurement
were unsuccessful, but capillary refill time remained 2-3 seconds. The
providers questioned what an expected cardiac assessment should yield regarding
peripheral pulses and BP due to the presence of the LVAD. Without the LVAD, lack
of peripheral pulse would indicate no BP; thus, cardiac compressions would have
been indicated. However, compressions are contraindicated when an LVAD is
present [3]. The patient had decreased perfusion and monomorphic ventricular
tachycardia (VT), coinciding with a heart rate of 222 bpm. A bedside ECHO
confirmed the arrhythmia while the LVAD coordinator was contacted. There were
no remarkable electrolyte imbalances; initial arterial blood gas displayed a
severe, partially compensated metabolic acidosis confirmed with an anion gap
(21 mmol/L) (Table 1). An increased creatinine level of 2.6 mg/dL and BUN of 24
mg/dl suggested decreased renal perfusion. These results indicated
dehydration-induced hypovolemic shock or conflicting congestive heart failure.
A severely dehydrated patient could have had a high BUN due to insufficient
fluid volume to excrete waste products. HCT was notably high at 50% PCV,
leading the physician to treat the patient's dehydration issues. Coagulation
studies were therapeutic with anticoagulation therapy. Radiologic images were
unremarkable, and the LVAD showed no obvious misplacement or breakage.
The team concluded the VT was valid and the patient
would benefit from cardioversion. Calcium gluconate (2 g), magnesium sulphate
(2 g), lidocaine (100 mg), and a 500 ml bolus of normal saline were
administered intravenously to optimize cardiac workload in preparation for
defibrillation. Oxygen was applied via a non-rebreathing mask at 15 L/min,
which produced an oxygen saturation of only 89%. Typically, intubation and
mechanical ventilation would be utilized for managing the patient in a
minimally responsive state; however, the physician was concerned that increased
intrathoracic pressure (ITP) would impair cardiac preload and impede survival
in this patient. Therefore, the decision was made to utilize high velocity
oxygen therapy (HVT) to support and reduce breathing effort without increasing
ITP to optimize preload and decrease the cardiac workload. Fourteen minutes
after arrival, the patient was successfully defibrillated (200J x 1), leading
to sinus tachycardia. Mean arterial BP was recorded at 70 mmHg, but the
automated sphygmomanometer had difficulty registering separate systolic and
diastolic pressures. HVT (40 L/min, 55% FiO2) continued as adjunctive therapy
with an additional 500 ml lactated ringer and 500 ml of normal saline
intravenously to reduce cardiac workload consumed by respiratory distress
secondary to cardiogenic shock. Intravenous haloperidol (2.5 mg) was
administered to reduce agitation as the patient became more responsive.
Approximately 90 minutes after arrival, the patient was alert and stable. The
patient's spouse arrived and revealed that the patient had been working in a
hot environment during a heat wave. This history and elevated BUN and HCT led
the physician to believe the patient had become dehydrated to the point of
shock. LVAD patients are extremely fluid sensitive and therefore required to
restrict fluids due to heart failure, and the patient had underlying renal
insufficiency.
Repeated venous blood work revealed marked improvement
in blood gas measurements and lactate levels (Table 1). The patient was
transferred in stable condition to an LVAD center.
This case report describes the diagnostic challenges
for caring for an unresponsive patient with an LVAD. Patients presenting to the
ED with activated "trauma alert" systems and those with LVADs pose a
similar risk for anchoring bias, which can cause clinicians to focus on
extraneous ideas, potentially leading to incorrect conclusions. In this case, a
multidisciplinary and analytical approach ultimately led to this patient's
proper diagnosis and treatment.
Patients with newer-generation LVAD systems providing
continuous flow may have no palpable pulse, and ventricular arrhythmias have
been reported to occur in 22-59% of all LVAD recipients [4]. Chest compressions
are contraindicated, except when an LVAD team is present to replace any
dislodged parts [3]. These patients are intravascular volume sensitive,
balancing between heart failure from preload reduction or increased afterload
and volume overload. Typically, it is reasonable to begin resuscitation with
250 – 500mL crystalloid when intravascular volume depletion is suspected [5].
LVAD patients may require intubation and mechanical ventilation when hypoxia,
hypercarbia, or acidosis worsens or when the airway cannot be protected.
However, high levels of positive ITP should be avoided to prevent worsening of right
ventricular dysfunction in an already preload-dependent patient [6]. While
acute heart failure (AHF) is typically managed with pressure-based respiratory
support there is a small amount of evidence that high flow nasal oxygen therapy
(HFNO) may be an acceptable alternative for selected patients [7,8].
While HFNO generates a small amount of positive
end-expiratory pressure, patients with sensitivity to cardiac preload may
exhibit greater benefit from HFNO. Positive pressure within the nasopharyngeal
space can be generated by overcoming the resistance against expiratory flow,
secondary to rapid flush. This mild positive ITP has shown to be auto-titrated
by the patient, dependent on inspiratory flow, minute ventilation and
resistance, with peak effect occurring during expiration only [9]. This mild
CPAP effect tends to promote recruitment of collapsed alveoli while enhancing
lung aeration to further decrease the patient's breathing effort and perhaps
impact alveolar ventilation [10,11]. HFNO can be an effective treatment for AHF
patients, despite its relatively low and variable pressure generation compared
to other more invasive and closed systems [10-12]. Overall, HVT reduces
metabolic demand while decreasing myocardial workload, further fighting the sympathetic
surge, as previously measured by inferior vena cava dynamics using ultrasound
[13]. Therefore, usage of HVT warrants further study in this patient
population. Another interesting observation was the rapid clearance of the
lactate, which fell from 10.7 mmol/L to 4.76mmol/L in approximately 60 minutes.
However, the dynamics of lactate clearance and the development of guidelines
for respiratory failure prognosis warrant further research [14,15]. This case
study demonstrated the collaborative effort of all medical and pharmaceutical
interventions that led to a positive outcome for this patient. Decreased
cardiac workload using HVT seemed evident in the rapid reduction in lactate and
breathing effort, which suggests this concept may also warrant further exploration.
Utilizing a comprehensive approach could prove beneficial in the acute
management of respiratory failure in LVAD and other preload-dependent patients.
No funding was received or used for this study.
AB is Manager of Clinical Research for Vapotherm, Inc.
MSP is Director of Professional Development and Education for Vapotherm, Inc.
KDW has been employed within the past 12 months as a scientific consultant. JSW
is VP of Clinical Research for Vapotherm, Inc – a manufacturer of high flow
oxygen systems.
AB, MSJ, and JW participated in this manuscript's
conception, development, and writing. KDW assisted in the writing of this
manuscript. All authors agree to be accountable for the content of the work.