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.