Introduction
Delirium is an important diagnosis, both because it is challenging to manage and because
it portends a poor prognosis in the hospital and beyond.1 Delirium is particularly
prevalent in the intensive care unit (ICU) setting, where it is associated with longer
hospital stays,2 prolonged mechanical ventilation,3 increased hospital costs,4 and
increases in mortality.1 In fact, studies have shown the incidence of delirium in
mechanically ventilated patients to be as high as 85%.5, 6 Furthermore, the negative
ramifications of delirium extend beyond hospitalization, as afflicted patients are
less likely to be discharged home and more likely to have long‐term cognitive impairment.7
Consequently, prevention as well as prompt identification and treatment of delirium
in the ICU is critical.
While ICU delirium has been the subject of intense research and numerous review articles,
little attention has been placed on the unique aspects of delirium related to patients
in the cardiac ICU (CICU). In this article, we review recent understanding of the
etiology, epidemiology, prevention, and treatment of delirium in the CICU, concluding
with suggested future directions.
Definition and Subtypes
Delirium is a syndrome defined by the Diagnostic and Statistical Manual of Mental
Disorders, 5th edition (DSM‐V), as an acute onset of a fluctuating disturbance in
the following cognitive functions: attention; environmental awareness; and cognition
and/or perception.8 Delirium may be most readily identified in patients with sleep/wake
cycle disturbances, emotional lability, hallucinations or delusions; however, none
of these are required for a diagnosis. There are three subtypes based on patients'
motor activity: hypoactive, hyperactive, and mixed (Figure 1).9
Figure 1
Subtypes of delirium and their characteristics.
Etiology of ICU Delirium: General and CICU Specific
The pathogenesis of ICU delirium is complex, with contributions from neurotransmitter
alterations, physiological stressors, metabolic derangements, inflammation, electrolyte
imbalances, and genetic factors. The development of delirium typically depends on
a combination of predisposing, often nonmodifiable, risk factors, which are then subject
to a “second hit” in the form of precipitating, often modifiable, factors (Figure 2).10
Both predisposing and precipitating factors are common in the CICU, as in other ICU
settings. The vulnerability of the patient has significant influence on the development
of delirium. In vulnerable patients, such as those with underlying dementia and multiple
comorbidities, a mild insult, such as an uncomplicated urinary tract infection, may
be enough to precipitate delirium. Conversely, in a young healthy patient, delirium
may only occur after exposure to a series of insults, such as general anesthesia,
sleep deprivation, multiple psychoactive medications, and an ICU stay.
Figure 2
Risk factors and etiologies of delirium in the cardiac intensive care unit. TAVR indicates
transcatheter aortic valve replacement, mechanical support refers to extracorporeal
membrane oxygenation, impella, or other temporary cardiac support.
The CICU has grown considerably more complex from its original inception as a unit
treating sequelae of acute myocardial infarction and has several unique risk factors
for delirium.11, 12 For example, advanced heart failure patients are now commonplace
in the CICU, as are temporary13 and permanent14 mechanical ventricular support devices.
These devices may contribute to delirium given prolonged immobility and increased
need for sedative medications. Other advances such as transcatheter aortic valve replacement
(TAVR) have enriched the CICU population with frail older patients.15 There is considerable
use of targeted temperature management in CICU patients who have survived cardiac
arrest, with high rates of delirium.16 In addition to the changing landscape of CICU
technology and cardiology case‐mix, there have also been concomitant increases in
patient complexity.12
The following are considerations of particular relevance for the practicing CICU cardiologist:
Patients with heart failure may be especially predisposed to delirium with an incidence
rate as high as 1 in 3 patients.17 B‐type natriuretic peptide concentrations are often
higher in patients with delirium, the link possibly being cerebral hypoperfusion in
the setting of a low cardiac output.17 Plasma clearance of deliriogenic medications
is also reduced in heart failure, which can result in toxicity at standard doses.18
Hardware‐related immobility is a significant risk factor for CICU delirium. In addition
to use of urinary catheters, vascular access devices, and endotracheal intubation,
both temporary mechanical circulatory support and temporary cardiac pacing function
as restraints in the CICU. A prospective study of 200 patients in the CICU reported
that those with restraints or devices that precluded mobilization were more likely
to develop delirium (odds ratio: 2.9, P<0.01).19
Patients undergoing TAVR are also at high‐risk for delirium. The incidence of delirium
appears to be higher in patients undergoing nontransfemoral TAVR compared with transfemoral
(50% versus 10%; P<0.001).15 This association may reflect the presence of advanced
vascular disease seen in the nontransfemoral cohort rather than a causal effect of
access site.15 Ischemic brain injury is hypothesized as an additional risk factor
for delirium in this cohort, triggered by cerebral embolization of aortic plaque or
valve particles dislodged during prosthesis positioning and deployment.20 Cerebral
protection devices may reduce stroke in TAVR patients.21 A recent randomized trial
of cerebral embolic protection in surgical aortic valve replacement patients suggested
a reduction in delirium, a finding that warrants future study in the TAVR cohort.22
The CICU also commonly admits patients after cardiac arrest. One recent study demonstrated
that 100% of 107 noncomatose survivors of cardiac arrest who received targeted temperature
management in the ICU had at least 1 day of delirium during their ICU stay, with a
median delirium duration of 4 days (interquartile range, 2.0–7.5).16 However as there
was no matched comparison group in this study, it is unclear whether the development
of delirium was a consequence of targeted temperature management or if it was instigated
by impaired cerebral perfusion from the initial insult of the cardiac arrest, and
this warrants further investigation.
Several cardiovascular agents have been shown to be associated with delirium including:
procainamide,23 metoprolol,24 lidocaine,25 amiodarone,26 and digoxin.27 However, these
reported associations are limited by the fact they are based on case reports. Lidocaine
deserves a particular mention as it has been associated with a range of psychiatric
reactions, it's often administered by cardiologists as a continuous intravenous infusion
over many hours, and has drug levels that can be measured to assist with evaluation
of toxicity.
Epidemiology
The reported burden of delirium in the CICU has varied greatly, likely reflecting
the screening tool and methodology used for assessment (Table 1). In one cross‐sectional
study of 590 CICU patients, rate of delirium was 20% and had higher ICU mortality
(27% versus 3%; P<0.001).28 Whether delirium causes death or is a marker of people
at high risk of death, or both, in not fully known. A recent prospective study of
726 European CICU patients reported that 15% of these patients were diagnosed with
delirium during their hospital stay, a rate which was 50% in patients over the age
of 85 years.29 Another prospective study of 309 patients admitted to the CICU, found
a 19% prevalence of delirium, with a 2‐month incidence rate of 9% among those who
were free of delirium at baseline.30 Similarly, in the largest prospective study to
date by Naksuk et al, the incidence rate of delirium among 11 079 patients was 8%
while in the CICU.31
Table 1
Cardiac ICU Specific Delirium Studies
Article
Study Enrollment Years
Study Design
Number of Patients
Prevalence/Incidence (Combined) of Delirium
In‐Hospital Mortality
Limitations
Pauley et al28
2012 to 2014
Prospective observational study
590
NR/NR (20.3%)
33%
Single center, retrospective, observational
Falsini et al29
2014 to 2015
Prospective observational study
726
6.3%/8.9% (15.3%)
17.1%
Only two centers, observational
Lahariya et al30
2010
Prospective observational study
309
18.77%/9.27% (28.8%)
27%
Single center, observational
Naksuk et al31
2004 to 2013
Prospective observational study
11 079
NR/8.3% (NR)
17.3%
Single center, observational
NR indicates not reported.
Screening
Despite the common occurrence of delirium in the CICU, cardiologists are often ill‐prepared
to diagnose, prevent and treat this condition. While this may not differ from physicians
working in other ICU settings, further education of cardiologists is needed. For example,
without routine use of assessment tools, delirium often goes undiagnosed; with ICU
physicians recognizing as little as one‐third of delirious critically ill patients.32
Several screening tests for delirium have been developed,33 however, only 2 are recommended
by the Society of Critical Care Medicine34: the Confusion Assessment Method for the
Intensive Care Unit (CAM‐ICU) (Figure 3) and the Intensive Care Delirium Screening
Checklist (ICDSC).
Figure 3
Confusion assessment method for the intensive care unit tool. This tool should be
used daily for each patient. Steps for completion; (1) Assess for mental status—if
patient has had a change in mental status from baseline or fluctuating mental status
in the past 24 hours proceed to second step; (2) Assess for inattention—have the patient
squeeze your hand when you say the letter “A” then read 10 letters in a row, 3 seconds
apart. A suggested series is SAVEAHAART. Errors are counted when the patient fails
to squeeze on the letter “A” or squeezes for letters other than “A”. If greater than
2 errors then proceed to third step; (3) Assess level of consciousness—if RASS is
anything other than zero then the patient is CAM‐ICU positive. RASS of zero equates
to being alert and calm. If RASS is zero then proceed to final step; (4) Assess for
disorganized thinking—ask the following set of yes/no questions, (a) Will a stone
float on water?, (b) Are there fish in the sea? (c) Does one pound weigh more than
2 pounds?, and (d) Can you use a hammer to pound a nail? Then proceed with the following
commands: Say to patient: “Hold up this many fingers” (Hold 2 fingers in front of
the patient) and “Now do the same thing with the other hand” (Do not repeat number
of fingers) *if patient is unable to move both arms, for 2nd part of command ask patient
to add one more finger. An error is counted if patient is unable to complete the entire
command if >1 error then the patient is CAM‐ICU positive. Reprinted from Ely et al1
with permission. Copyright @ 2002, E. Wesley Ely and Vanderbilt University, all rights
reserved. CAM‐ICU indicates Confusion Assessment Method for the Intensive Care Unit;
and RASS, the Richmond Agitation and Sedation Scale.
A meta‐analysis of 5 ICU delirium screening tools found that the CAM‐ICU and ICDSC
screening tests were the most sensitive and specific tools for identifying delirium.35
In another systematic review and meta‐analysis of nine studies evaluating CAM‐ICU
(including 969 patients) and four evaluating the ICDSC (including 361 patients), the
pooled sensitivity of CAM‐ICU was 80% (95% confidence interval (CI): 77–83%), with
a specificity of 96% (95% CI: 95–97%) and an AUC of 0.97. The pooled sensitivity of
ICDSC was 74% (95% CI: 65–82%), with a specificity of 82% (95% CI: 77–86%) and an
AUC of 0.89.36 While not developed specifically for ICU, the 3D‐CAM is also a useful
tool with a median assessment time of just 3 minutes.37 Implementation of screening
tools has been shown to be feasible on daily rounds and requires minimal training
of nurses to implement. Therefore every attempt should be made to incorporate it as
a daily report on rounds.38
Prevention
Central to the management of delirium is effective prevention (Figure 4), as treatment
options are more limited. Nonpharmacological methods of prevention focus on minimizing
the disorienting aspects of hospital care and are proven to reduce delirium in the
non‐ICU setting.39 Several studies have demonstrated that implementing a multicomponent
structured approach to reorientation including: the use of clocks and calendars; daily
reminders to the patient on date, time, place, and reason for hospitalization; sleep
preservation by avoiding late night medication administration; early mobilization
from bed; early urinary catheter removal; and use of home hearing aids and glasses
may reduce the incidence and duration of delirium compared with usual care.40, 41
Unfortunately, to our knowledge, no data have reported on how often such reorientation
strategies are performed in the CICU setting.
Figure 4
Preventative strategies for delirium.
Balas et al, implemented the combination of awakening and breathing coordination,
delirium monitoring/management and early exercise/mobility (ABCDE) bundle in intubated
ICU patients. In this pre‐post comparison, a 50% decrease in the odds of delirium
was reported (OR 0.55, P=0.03).42 Note that “awakening and breathing coordination”
refers to frequent use of spontaneous awakening trials and spontaneous breathing trials.
In addition, several trials have demonstrated that physical and occupational therapy
decrease delirium in the ICU. One group demonstrated that when early rehabilitation
interventions were performed during daily interruption of sedation the median duration
of delirium was 2.0 days compared with 4.0 days without rehabilitation (P=0.02).43
Similar results were reported in a study randomizing mechanically ventilated surgical
ICU patients to early mobilization versus standard therapy.44
Occupational therapy may also play an important role. A randomized control study showed
that occupational therapy in nonintubated ICU patients reduced delirium incidence
(3% versus 20%, P<0.001).45 Finally, a quality improvement study implementing early
physical and occupational interventions along with reduced benzodiazepine use for
mechanically ventilated patients in the medical ICU resulted in a reduced incidence
of delirium (21% versus 53%, P=0.003) and a reduction in hospital length of stay by
3.1 days (95% CI; 0.3–5.9 days), compared with historical rates before the interventions
were implemented.46 As described above, early mobilization is an important tool in
preventing delirium, however, this can prove challenging in certain CICU patients,
particularly patients with mechanical support devices and temporary pacemakers. However,
just as medical ICUs have worked successfully to mobilize intubated patients, CICU's
should work to increase mobility, for example by opting for mobile friendly devices
such as subclavian intra‐aortic balloon pumps and active fixation temporary pacemakers
when feasible.
The ICU is known to contribute to poor sleep; such sleeplessness increases the risk
of delirium.47 By enacting a series of nonpharmacologic interventions (closing doors,
decreased alarm volumes, ear plugs, eye masks, and timed “lights off”) to improve
sleep in the ICU, Patel et al were able to reduce the incidence of delirium compared
with the nonintervention arm (33% versus 14%, P<0.001).48 Similarly, in a quality
improvement initiative, Kamder et al found that implementing a 3‐stage strategy to
improve sleep decreased the incidence of delirium/coma (OR: 0.46; 95% CI, 0.23–0.89;
P=0.02).49 In this study, stage 1 focused on reducing sleep disruptions by minimizing
overhead pages, turning off patient televisions, dimming hallway lights, and grouping
care activities.49 Stage 2 used nonpharmacological sleep aids such as earplugs, eye
masks and soothing music for nondelirious patients. For patients unable to sleep despite
the stages 1 and 2 interventions, pharmacological agents were initiated (stage 3).49
Benzodiazepines, opiates, and diphenhydramine were avoided. While these studies all
derived from noncardiac ICU settings, many of these steps are applicable to patients
in the CICU and, thus, every attempt at reorientation and nonpharmacologic prevention
should be made.
In terms of pharmacologic interventions, antipsychotics are frequently used for the
prevention of delirium, however, there is no high‐quality evidence to support their
use. A recent meta‐analysis examined pharmacologic prevention and treatment of delirium
in ICU patients.50 Among 5 studies that examined antipsychotics compared with placebo,
only 1 showed a reduction in the incidence of delirium. Based on the lack of evidence,
the 2013 Society of Critical Care Medicine guidelines on pain, agitation and delirium
provide no recommendation for using antipsychotics for delirium prevention in adult
ICU patients.34 It is also worth mentioning that antipsychotics are known to cause
several cardiovascular side effects, most notably QT prolongation.51
Sedatives are an important modifiable risk factor for delirium. Clegg and Young showed
that delirium was associated with benzodiazepines (OR 3.0, 95% CI 1.3–6.8) in hospital
patients and long‐term care residents.52 Thus, there has been interest in finding
alternative sedatives to reduce the incidence of delirium. One widely used alternative
to benzodiazepines is propofol, which has quick onset/offset and may be useful for
sedation interruption protocols as mentioned above. Several studies have shown that
propofol compared with midazolam reduces length of mechanical ventilation.53, 54,
55 However, high quality evidence evaluating delirium outcomes is still evolving.
Sleep deprivation has been shown to be a risk factor for the development of ICU delirium,
and critically ill patients have been shown to have low levels of melatonin.56 There
have been several trials examining the use of melatonin in ICU patients with delirium
and some have shown promise but overall these studies are limited by small sample
sizes and varied methodologies, and larger randomized trials are needed.57
Opiate use should be minimized at every opportunity but not at the expense of uncontrolled
pain. The acronym eCASH has been developed which stands for early Comfort using Analgesia,
minimal Sedatives and maximal Humane care. The concept is designed to achieve early
pain control and maintain comfort with minimal use of sedation in order to promote
natural sleep and early mobilization, all of which may reduce the likelihood of developing
delirium.58
An alternative to the traditional sedatives of benzodiazepines and propofol is dexmedetomidine,
which is an α2‐agonist and has been the subject of intense delirium research because
it has analgesic properties and results in a sedate but arousable state with little
effect on respiratory drive.59 These properties may decrease delirium, both by avoiding
deliriogenic opiates and sedatives but also by more direct neuroprotective mechanisms.60
This has led to several clinical studies involving dexmedetomidine in the ICU. The
SEDCOM (Safety and Efficacy of Dexmedetomidine Compared with Midazolam) trial was
a multicenter trial, randomizing 375 intubated ICU patients to dexmedetomidine or
midazolam and showed that patients in the dexmedetomidine group had less time on the
ventilator and less delirium (54% versus 76.6%, P<0.001). Of note, several common
cardiac conditions were exclusion criteria for this trial including: unstable angina
or acute myocardial infarction, ejection fraction less than 30%, heart rate less than
50/min, second or third‐degree heart block, and a systolic blood pressure less than
90 mm Hg despite continuous infusions of 2 vasopressors, which could limit the generalizability
of this trial to CCU patients.61
In a randomized placebo‐controlled trial, Su et al demonstrated that patients over
65 years who received prophylactic dexmedetomidine (administered from ICU admission
to postoperative day 1) significantly decreased the incidence of ICU delirium during
the first 7 days after surgery (9% versus 23%, P<0.0001).62
Three studies, of special relevance to the CICU, involved post‐cardiac surgery patients
in the ICU. The DEXCOM (Dexmedetomidine Compared to Morphine) study randomized such
patients to dexmedetomidine or morphine and showed that dexmedetomidine reduced the
duration but not incidence of delirium.63 Djaiani et al randomized patients to dexmedetomidine
versus propofol and found that dexmedetomidine reduced the incidence of delirium (17.5%
versus 31.5%, OR 0.46; P=0.028) and reduced duration (2 days versus 3 days, P=0.04).64
However, a randomized placebo controlled trial undertaken by Li et al failed to demonstrate
any reduction in the incidence of delirium when dexmedetomidine was administered during
anaesthesia and during the early postoperative period (4.9% in the dexmedetomidine
group versus 7.7% in the control group, P=0.345).65 However, the incidence of delirium
was low in this trial and thus the trial may have been underpowered.
In the PRODEX (Propofol Compared to Dexmedetomidine) and MIDEX (Midazolam Compared
to Dexmedetomidine) trials66 patients who were already sedated were randomized to
continue their current regimen (midazolam or propofol) or switch to dexmedetomidine,
demonstrating that the combined endpoints of anxiety, agitation, and delirium were
lower in the dexmedetomidine group. Important cardiac exclusion criteria included:
heart rate less than 50/min, second or third‐degree heart block, mean arterial blood
pressure less than 55 mm Hg despite appropriate vasopressor use, and use of α agonists
or antagonist within 24 hours of randomization.
An important caveat to the above trial results relates to a Cochrane meta‐analysis
reporting that there is insufficient high‐quality evidence that dexmedetomidine lowers
the risk of delirium.67 These investigators found that only a small proportion of
dexmedetomidine studies investigated its effect on delirium, reflecting a potentially
lower quality of evidence influenced by risk of bias, imprecision, and significant
publication bias. However, further trials favoring dexmedetomidine were published
since this meta‐analysis62 and a recent meta‐analysis comparing dexmedetomidine to
propofol in post‐cardiac surgery patients that included 8 randomized trials demonstrated
that dexmedetomidine was associated with a lower risk of delirium (risk ratio, 0.4;
95% CI, 0.24–0.64; P=0.0002) as well as shorter length of intubation, but more bradycardia.68
Dexmedetomidine has a similar mechanism of action as clonidine, and, as such, leads
to a reduced sympathetic outflow and augmented vagal activity and can lead to reduced
levels of catecholamines, bradycardia, reduced cardiac output, and hypotension.69
These hemodynamic consequences should be anticipated by treating cardiologists and
influence patient selection.
Finally, there is conflicting data on the impact of statin use on incidence of delirium
in the ICU. Several retrospective and prospective cohort studies have found that statin
use in ICU patients is associated with a reduced risk of delirium70, 71; however,
2 recent randomized control trials showed no benefit to statins in preventing ICU
delirium.72, 73
Treatment
Initial management of delirium should involve treating any identifiable precipitating
factors. Further management goals are aimed at reducing its severity and duration.
Unfortunately, there are few data to guide the treatment of CICU patients with delirium
once it has occurred. Nonpharmacological strategies to reorientate the patient should
be employed; including the use of home hearing aids and glasses. There are conflicting
and limited data to suggest that antipsychotics reduce the duration of delirium (Table 2).
For example, 1 small trial randomizing 36 ICU patients with delirium to quetiapine
or placebo demonstrated that patients who received quetiapine had a shorter duration
of delirium (1 day versus 4.5 days, P=0.001).74 However, another study that randomized
103 patients to either haloperidol, ziprasidone, or placebo showed no difference in
duration of delirium.75 Based on the above evidence, the Society for Critical Care
Medicine guideline on delirium provides no recommendation for the use of haloperidol
in the treatment of ICU delirium, while stating that atypical antipsychotics may reduce
the duration of delirium; noting that these should not be used in patients at significant
risk for torsades de pointes.
Table 2
Pharmacological Agents Investigated for the Treatment of Delirium in the ICU, With
Special Consideration to CICU Patients
Medication
Recommended Dosage
Side Effects
Contraindications
Costs
FDA Approved for Delirium
Evidence
Reference
Quetiapine
100 to 200 mg orally per d in 2 divided doses
QTC prolongation, less extrapyramidal effects than haloperidol
Prolonged QTC
Cheap
No
Quetiapine shortened the duration of delirium compared with placebo (1 d vs 4.5 d,
P=0.001)
74
Dexmedetomidine
0.2 to 0.7 μg/kg per h maintenance dose
Bradycardia, hypotension
Bradycardia, high degree AV block, caution in hypotension
Expensive
No (but approved as an alternative sedative)
Dexmedetomidine shortened the duration of delirium compared with placebo in intubated
patients (23.3 h vs 40.0 h, P=0.01)
76
Haloperidol
Oral: 0.5 to 5 mg every 6 to 8 h IV (haloperidol lactate only): 0.5 to 10 mg q15 to
30 min until response achieved, then give 25% of last bolus dose Q6H
QTC prolongation, large potential for extrapyramidal effects
Prolonged QTC, Parkinson's disease
Cheap
No
Mixed data and is not currently recommended by guidelines for the treatment of delirium
75
Ziprasidone
10 mg Q2H or 20 mg Q4H IM (max 40 mg/daily) for acute agitation
QTC prolongation, less extrapyramidal effects than haloperidol
Prolonged QTC, heart failure, recent myocardial infarction
Cheap
No
Ziprasidone has not been shown to reduce delirium free days compared with placebo
(median 15.0 d vs 12.5 d) (P=0.66)
75
CICU indicates cardiac intensive care unit; FDA, US Food and Drug Administration;
IM, intramuscular; ICU, intensive care unit; IV, intravenous; and QTC, corrected QT.
Dexmedetomidine has also been studied for treating ICU patients with established delirium.
The DahLIA (Dexmedetomidine to Lessen ICU Agitation) study randomized 74 patients
deemed too delirious to extubate to dexmedetomidine versus placebo and found that
delirium resolved more rapidly with dexmedetomidine (23.3 hours versus 40.0 hours;
95% CI, 3.0–28.0 hours; P=0.01).76 Two important caveats of this study are that the
incidence of alcohol withdrawal was not reported and that analgesia control and opioid
use were suboptimal. The Society of Critical Care Medicine guideline on delirium suggests
the use of dexmedetomidine may be considered for the treatment of ICU delirium unrelated
to alcohol or benzodiazepine withdrawal for which benzodiazepines would be the treatment
of choice.34
Future Directions and Conclusion
As the landscape of the CICU continues to evolve and the patient population becomes
increasingly more complex, sick, and aged,77, 78 the burden of delirium will only
increase. One notable aspect of this review article is that none of the studies cited
regarding the prevention and treatment of delirium enrolled CICU patients exclusively,
which highlights the significant need for more delirium studies specific to the CICU
given the generalizability of delirium studies from other ICU settings may not overlap
perfectly with cardiac patients. Tools to screen for delirium should be familiar to
cardiologists practicing in the CICU and should be incorporated into the nursing assessment
of at‐risk patients. Despite the difficulties of conducting randomized control trials
in the critical care setting, high quality studies examining the efficacy and safety
of sedation agents, antipsychotics, and other novel therapies for the prevention and
treatment of delirium in patients in the CICU are urgently needed. Specifically, studies
examining the efficacy and cardiovascular safety of dexmedetomidine and antipsychotics
in CCU patients with complex cardiovascular disease are needed. More research is also
needed on medications and hardware unique to the CICU (such as antiarrhythmic drugs
and temporary mechanical support devices); investigating their impact on delirium
and specific treatment options in this patient population. Furthermore, just as other
medical ICUs have developed and championed algorithms and pathways for daily ventilator
weans, interruptions in sedation and early mobilization, the CICU needs to develop
similar strategies for its unique patients (including those requiring mechanical support
and with other hardware‐related causes of immobility). Specific examples of such strategies
would include active fixation temporary pacemakers that can facilitate ambulation,
as well as brachial intra‐aortic balloon pump placement for patients requiring more
prolonged ventricular support. Finally, many of the current mainstays of treatment
for delirium have important cardiac side effects and their use should be further studied
and tailored to the complex cardiac patients in the CICU.
Sources of Funding
Dr Januzzi is supported in part by the Hutter Family Professorship in Cardiology.
Dr Needham is supported, in part, via Network for Investigation of Delirium: Unifying
Scientists (NIDUS), funded by the NIH/NIA Grant #R24AG054259.
Disclosures
Dr Januzzi has received grant support from Roche Diagnostics, Siemens, Cleveland Heart
Labs and Prevencio, consulting income from Roche Diagnostics, Critical Diagnostics,
Philips, and Novartis, and participates in clinical endpoint committees/data safety
monitoring boards for Abbvie, Bayer, Pfizer, Novartis, Amgen, Janssen, and Boehringer
Ingelheim. The remaining authors have nothing to disclose.