Category Archives: Acute Med

Acute care of the medically sick adult

CHEST study to evaluate starch

No results to report here, just a heads up that the CHEST study is underway: a randomised controlled trial of 7000 patients comparing of 6% hydroxyethyl starch (130/0.4) with 0.9% sodium chloride for all fluid resuscitation needs whilst in the intensive care unit (ICU).  This is how the authors explain the rationale for the study:

Much of the evidence currently available to inform clinicians on the efficacy and safety of starch solutions for fluid resuscitation involves studies conducted using older, high molecular weight and high molar substitution starches. Meta-analyses of these studies suggest that when comparing starches to other fluids, the relative risk of mortality ranges from 1.00 (95% CI 0.80–1.25) to 1.35 (95% CI 0.94–1.95) and for kidney failure 1.50 (95% CI 1.20–1.87). There are insufficient data, however, on the newer low molecular weight, low molar substitution starches. To date, most published studies on these newer generation starches have been conducted in perioperative settings with small sample sizes and limited follow-up. They have been designed to examine surrogate outcomes and not important patient outcomes such as mortality or renal failure.

It is possible to overdo the starch

 
These are some of the same people who brought us the SAFE study on albumin and the NICE-SUGAR study on glycaemic control, so this will be one to watch. It is anticipated that recruitment will be completed by December 2011.

PURPOSE: The intravenous fluid 6% hydroxyethyl starch (130/0.4) (6% HES 130/0.4) is used widely for resuscitation but there is limited information on its efficacy and safety. A large-scale multi-centre randomised controlled trial (CHEST) in critically ill patients is currently underway comparing fluid resuscitation with 6% HES 130/0.4 to 0.9% sodium chloride on 90-day mortality and other clinically relevant outcomes including renal injury. This report describes the study protocol.
METHODS: CHEST will recruit 7,000 patients to concealed, random, parallel assignment of either 6% HES 130/0.4 or 0.9% sodium chloride for all fluid resuscitation needs whilst in the intensive care unit (ICU). The primary outcome will be all-cause mortality at 90 days post-randomisation. Secondary outcomes will include incident renal injury, other organ failures, ICU and hospital mortality, length of ICU stay, quality of life at 6 months, health economic analyses and in patients with traumatic brain injury, functional outcome. Subgroup analyses will be conducted in four predefined subgroups. All analyses will be conducted on an intention-to-treat basis.
RESULTS AND CONCLUSIONS: The study run-in phase has been completed and the main trial commenced in April 2010. CHEST should generate results that will inform and influence prescribing of this commonly used resuscitation fluid.

The Crystalloid versus Hydroxyethyl Starch Trial: protocol for a multi-centre randomised controlled trial of fluid resuscitation with 6% hydroxyethyl starch (130/0.4) compared to 0.9% sodium chloride (saline) in intensive care patients on mortality
Intensive Care Med. 2011 May;37(5):816-823

Hyperbaric O2 for the sick and the well with CO poisoning

A French study, large by hyperbaric oxygen trial standards, did not confirm that hyperbaric oxygen therapy improves recovery from pure CO poisoning. In addition, in comatose patients, repeating hyperbaric oxygen therapy resulted in worse outcomes compared to one session.

I don't care if it doesn't work - something looking like a retro-sci-fi time machine is COOL.

INTRODUCTION: Although hyperbaric oxygen therapy (HBO) is broadly used for carbon monoxide (CO) poisoning, its efficacy and practical modalities remain controversial.
OBJECTIVES: To assess HBO in patients poisoned with CO.
DESIGN: Two prospective randomized trial on two parallel groups.
SETTING: Critical Care Unit, Raymond Poincaré Hospital, Garches, France.
SUBJECTS: Three hundred eighty-five patients with acute domestic CO poisoning.
INTERVENTION: Patients with transient loss of consciousness (trial A, n = 179) were randomized to either 6 h of normobaric oxygen therapy (NBO; arm A0, n = 86) or 4 h of NBO plus one HBO session (arm A1, n = 93). Patients with initial coma (trial B, n = 206) were randomized to either 4 h of NBO plus one HBO session (arm B1, n = 101) or 4 h of NBO plus two 2 HBO sessions (arm B2, n = 105). PRIMARY ENDPOINT: Proportion of patients with complete recovery at 1 month.
RESULTS: In trial A, there was no evidence for a difference in 1-month complete recovery rates with and without HBO [58% compared to 61%; unadjusted odds ratio, 0.90 (95% CI, 0.47-1.71)]. In trial B, complete recovery rates were significantly lower with two than with one HBO session [47% compared to 68%; unadjusted odds ratio, 0.42 (CI, 0.23-0.79)].
CONCLUSION: In patients with transient loss of consciousness, there was no evidence of superiority of HBO over NBO. In comatose patients, two HBO sessions were associated with worse outcomes than one HBO session.

Hyperbaric oxygen therapy for acute domestic carbon monoxide poisoning: two randomized controlled trials
Intensive Care Med. 2011 Mar;37(3):486-92

Salt or sugar on the brain

A meta-analysis suggests hypertonic saline may be more effective at lowering intracranial pressure than mannitol. An accompanying editorial cleverly entitled ‘Salt or sugar on the brain: Does it matter except for taste?’ suggests one reason hypertonic saline (HTS) has not replaced mannitol in clinical practice is that too many different regimens of HTS, in terms of concentration, dose, bolus vs. continuous infusions, and plus or minus supplementation of colloids, have been utilised. Because only 112 patients with 184 episodes of increased ICP were treated with each medication in this meta-analysis, the editorialist agrees with the authors in suggesting a larger randomised study is needed.

OBJECTIVES: Randomized trials have suggested that hypertonic saline solutions may be superior to mannitol for the treatment of elevated intracranial pressure, but their impact on clinical practice has been limited, partly by their small size. We therefore combined their findings in a meta-analysis.
DATA SOURCES: We searched for relevant studies in MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials (CENTRAL), Scopus, and ISI Web of Knowledge.
STUDY SELECTION: Randomized trials were included if they directly compared equiosmolar doses of hypertonic sodium solutions to mannitol for the treatment of elevated intracranial pressure in human subjects undergoing quantitative intracranial pressure measurement.
DATA EXTRACTION: Two investigators independently reviewed potentially eligible trials and extracted data using a preformed data collection sheet. Disagreements were resolved by consensus or by a third investigator if needed. We collected data on patient demographics, type of intracranial pathology, baseline intracranial pressure, osms per treatment dose, quantitative change in intracranial pressure, and prespecified adverse events. Our primary outcome was the proportion of successfully treated episodes of elevated intracranial pressure.
DATA SYNTHESIS: Five trials comprising 112 patients with 184 episodes of elevated intracranial pressure met our inclusion criteria. In random-effects models, the relative risk of intracranial pressure control was 1.16 (95% confidence interval, 1.00-1.33), and the difference in mean intracranial pressure reduction was 2.0 mm Hg (95% confidence interval, -1.6 to 5.7), with both favoring hypertonic saline over mannitol. A mild degree of heterogeneity was present among the included trials. There were no significant adverse events reported.
CONCLUSIONS: We found that hypertonic saline is more effective than mannitol for the treatment of elevated intracranial pressure. Our meta-analysis is limited by the small number and size of eligible trials, but our findings suggest that hypertonic saline may be superior to the current standard of care and argue for a large, multicenter, randomized trial to definitively establish the first-line medical therapy for intracranial hypertension.

Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: A meta-analysis of randomized clinical trials
Crit Care Med. 2011 Mar;39(3):554-9

Cardiac arrest drugs and pupils

Although not predictive immediately post-cardiac arrest in the emergency department, dilated unreactive pupils two or three days later on the ICU may indicate a hopeless prognosis. We know from our experience with adrenaline (epinephrine) infusions that this drug does not prevent pupils from reacting to light, but what about atropine?

A letter by Dr Sophie MacDougall-Davis in Resuscitation describes a 66 year old male patient admitted to the ICU after an intraoperative PEA arrest during which he received 3 mg intravenous atropine. Post arrest and post anaesthesia he was awake with no neurological deficit, but eight hours after the cardiac arrest his pupils remained fixed and dilated, and were dilated with only a very slight reaction the next morning and remained sluggish at forty-eight hours, normalising at seventy-two hours. A possible reason for its prolonged action may be uptake of atropine from the plasma into the aqueous humor of the eye, followed by its slow release.
Dr MacDougall-Davis cautions:

When assessing pupils in comatose cardiac arrest survivors, the potential for atropine to have a prolonged effect on pupil size and reactivity should be considered.

Atropine, fixed dilated pupils and prognostication following cardiac arrest
Resuscitation. 2011 Feb;82(2):232

Emergency tracheal intubations outside the OR

Most data regarding RSI complication rates traditionally come from the operating room setting. I and my colleagues made a small attempt address this in the UK with a publication in 2004. The latest, much larger, study on the subject from Michigan shows a 10% rate of difficult intubations and a 4.2% rate of airway complications.

BACKGROUND: There are limited outcome data regarding emergent nonoperative intubation. The current study was undertaken with a large observational dataset to evaluate the incidence of difficult intubation and complication rates and to determine predictors of complications in this setting.
METHODS: Adult nonoperating room emergent intubations at our tertiary care institution from December 5, 2001 to July 6, 2009 were reviewed. Prospectively defined data points included time of day, location, attending physician presence, number of attempts, direct laryngoscopy view, adjuvant use, medications, and complications. At our institution, a senior resident with at least 24 months of anesthesia training is the first responder for all emergent airway requests. The primary outcome was a composite airway complication variable that included aspiration, esophageal intubation, dental injury, or pneumothorax.
RESULTS: A total of 3,423 emergent nonoperating room airway management cases were identified. The incidence of difficult intubation was 10.3%. Complications occurred in 4.2%: aspiration, 2.8%; esophageal intubation, 1.3%; dental injury, 0.2%; and pneumothorax, 0.1%. A bougie introducer was used in 12.4% of cases. Among 2,284 intubations performed by residents, independent predictors of the composite complication outcome were as follows: three or more intubation attempts (odds ratio, 6.7; 95% CI, 3.2-14.2), grade III or IV view (odds ratio, 1.9; 95% CI, 1.1-3.5), general care floor location (odds ratio, 1.9; 95% CI, 1.2-3.0), and emergency department location (odds ratio, 4.7; 95% CI, 1.1-20.4).
CONCLUSIONS: During emergent nonoperative intubation, specific clinical situations are associated with an increased risk of airway complication and may provide a starting point for allocation of experienced first responders.

3,423 emergency tracheal intubations at a university hospital: airway outcomes and complications.
Anesthesiology. 2011 Jan;114(1):42-8

CVT guideline

Thanks to neuro-icu.com for highlighting this one: The American Heart Association and American Stroke Association have produced guidelines for the diagnosis and management of cerebral venous thrombosis. Here is a summary of their recommendations. The full text of the guidelines is available via the link at the bottom.
Routine Blood Work

  • In patients with suspected CVT, routine blood studies consisting of a complete blood count, chemistry panel, prothrombin time, and activated partial thromboplastin time should be performed (Class I; Level of Evidence C).
  • Screening for potential prothrombotic conditions that may predispose a person to CVT (eg, use of contraceptives, underlying inflammatory disease, infectious process) is recommended in the initial clinical assessment (specific recommendations for testing for thrombophilia are found in the long-term management section of this document) (Class I; Level of Evidence C).
  • A normal D-dimer level according to a sensitive immunoassay or rapid enzyme-linked immunosorbent assay (ELISA) may be considered to help identify patients with low probability of CVT (Class IIb; Level of Evidence B). If there is a strong clinical suspicion of CVT, a normal D-dimer level should not preclude further evaluation.

Common Pitfalls in the Diagnosis of CVT

  • In patients with lobar ICH of otherwise unclear origin or with cerebral infarction that crosses typical arterial boundaries, imaging of the cerebral venous system should be performed (Class I; Level of Evidence C).
  • In patients with the clinical features of idiopathic intracranial hypertension, imaging of the cerebral venous system is recommended to exclude CVT (Class I; Level of Evidence C).
  • In patients with headache associated with atypical features, imaging of the cerebral venous system is reasonable to exclude CVT (Class IIa; Level of Evidence C).

Imaging in the Diagnosis of CVT

  • Although a plain CT or MRI is useful in the initial evaluation of patients with suspected CVT, a negative plain CT or MRI does not rule out CVT. A venographic study (either CTV or MRV) should be performed in suspected CVT if the plain CT or MRI is negative or to define the extent of CVT if the plain CT or MRI suggests CVT (Class I; Level of Evidence C).
  • An early follow-up CTV or MRV is recommended in CVT patients with persistent or evolving symptoms despite medical treatment or with symptoms suggestive of propagation of thrombus (Class I; Level of Evidence C).
  • In patients with previous CVT who present with recurrent symptoms suggestive of CVT, repeat CTV or MRV is recommended (Class I; Level of Evidence C).
  • Gradient echo T2 susceptibility-weighted images combined with magnetic resonance can be useful to improve the accuracy of CVT diagnosis (Class IIa; Level of Evidence B).
  • Catheter cerebral angiography can be useful in patients with inconclusive CTV or MRV in whom a clinical suspicion for CVT remains high (Class IIa; Level of Evidence C).
  • A follow-up CTV or MRV at 3 to 6 months after diagnosis is reasonable to assess for recanalization of the occluded cortical vein/sinuses in stable patients (Class IIa; Level of Evidence C).

Management and Treatment

  • Patients with CVT and a suspected bacterial infection should receive appropriate antibiotics and surgical drainage of purulent collections of infectious sources associated with CVT when appropriate (Class I; Level of Evidence C).
  • In patients with CVT and increased intracranial pressure, monitoring for progressive visual loss is recommended, and when this is observed, increased intracranial pressure should be treated urgently (Class I; Level of Evidence C).
  • In patients with CVT and a single seizure with parenchymal lesions, early initiation of antiepileptic drugs for a defined duration is recommended to prevent further seizures (Class I; Level of Evidence B).
  • In patients with CVT and a single seizure without parenchymal lesions, early initiation of antiepileptic drugs for a defined duration is probably recommended to prevent further seizures (Class IIa; Level of Evidence C).
  • In the absence of seizures, the routine use of antiepileptic drugs in patients with CVT is not recommended (Class III; Level of Evidence C).
  • For patients with CVT, initial anticoagulation with adjusted-dose UFH or weight-based LMWH in full anticoagulant doses is reasonable, followed by vitamin K antagonists, regardless of the presence of ICH (Class IIa; Level of Evidence B).
  • Admission to a stroke unit is reasonable for treatment and for prevention of clinical complications of patients with CVT (Class IIa; Level of Evidence C).
  • In patients with CVT and increased intracranial pressure, it is reasonable to initiate treatment with acetazolamide. Other therapies (lumbar puncture, optic nerve decompression, or shunts) can be effective if there is progressive visual loss. (Class IIa; Level of Evidence C).
  • Endovascular intervention may be considered if deterioration occurs despite intensive anticoagulation treatment (Class IIb; Level of Evidence C). In patients with neurological deterioration due to severe mass effect or intracranial hemorrhage causing intractable intracranial hypertension, decompressive hemicraniectomy may be considered (Class IIb; Level of Evidence C).
  • For patients with CVT, steroid medications are not recommended, even in the presence of parenchymal brain lesions on CT/MRI, unless needed for another underlying disease (Class III; Level of Evidence B).

Long-Term Management and Recurrence of CVT

  • Testing for prothrombotic conditions, including protein C, protein S, antithrombin deficiency, antiphospholipid syndrome, prothrombin G20210A mutation, and factor V Leiden, can be beneficial for the management of patients with CVT. Testing for protein C, protein S, and antithrombin deficiency is generally indicated 2 to 4 weeks after completion of anticoagulation. There is a very limited value of testing in the acute setting or in patients taking warfarin. (Class IIa; Level of Evidence B).
  • In patients with provoked CVT (associated with a transient risk factor), vitamin K antagonists may be continued for 3 to 6 months, with a target INR of 2.0 to 3.0 (Table 3) (Class IIb; Level of Evidence C).
  • In patients with unprovoked CVT, vitamin K antagonists may be continued for 6 to 12 months, with a target INR of 2.0 to 3.0 (Class IIb; Level of Evidence C).
  • For patients with recurrent CVT, VTE after CVT, or first CVT with severe thrombophilia (ie, homozygous prothrombin G20210A; homozygous factor V Leiden; deficiencies of protein C, protein S, or antithrombin; combined thrombophilia defects; or antiphospholipid syndrome), indefinite anticoagulation may be considered, with a target INR of 2.0 to 3.0 (Class IIb; Level of Evidence C).
  • Consultation with a physician with expertise in thrombosis may be considered to assist in the pro- thrombotic testing and care of patients with CVT (Class IIb; Level of Evidence C).

Management of Late Complications (Other Than Recurrent VTE)

  • In patients with a history of CVT who complain of new, persisting, or severe headache, evaluation for CVT recurrence and intracranial hypertension should be considered (Class I; Level of Evidence C)

CVT in pregnancy

  • For women with CVT during pregnancy, LMWH in full anticoagulant doses should be continued throughout pregnancy, and LMWH or vitamin K antagonist with a target INR of 2.0 to 3.0 should be continued for at least 6 weeks postpartum (for a total minimum duration of therapy of 6 months) (Class I; Level of Evidence C).
  • It is reasonable to advise women with a history of CVT that future pregnancy is not contraindicated. Further investigations regarding the underlying cause and a formal consultation with a hematologist and/or maternal fetal medicine specialist are reasonable. (Class IIa; Level of Evidence B).
  • It is reasonable to treat acute CVT during pregnancy with full-dose LMWH rather than UFH (Class IIa; Level of Evidence C).
  • For women with a history of CVT, prophylaxis with LMWH during future pregnancies and the postpartum period is probably recommended (Class IIa; Level of Evidence C).

Children

  • Supportive measures for children with CVT should include appropriate hydration, control of epileptic seizures, and treatment of elevated intracranial pressure (Class I; Level of Evidence C).
  • Given the potential for visual loss owing to severe or long-standing increased intracranial pressure in children with CVT, periodic assessments of the visual fields and visual acuity should be performed, and appropriate measures to control elevated intracranial pressure and its complications should be instituted (Class I; Level of Evidence C).
  • In all pediatric patients, if initial anticoagulation treatment is withheld, repeat neuroimaging including venous imaging in the first week after diagnosis is recommended to monitor for propagation of the initial thrombus or new infarcts or hemorrhage (Class I; Level of Evidence C).
  • In children with acute CVT diagnosed beyond the first 28 days of life, it is reasonable to treat with full-dose LMWH even in the presence of intracra- nial hemorrhage (Class IIa; Level of Evidence C).
  • In children with acute CVT diagnosed beyond the first 28 days of life, it is reasonable to continue LMWH or oral vitamin K antagonists for 3 to 6 months (Class IIa; Level of Evidence C).
  • In all pediatric patients with acute CVT, if initial anticoagulation is started, it is reasonable to perform a head CT or MRI scan in the initial week after treatment to monitor for additional hemor- rhage (Class IIa; Level of Evidence C).
  • Children with CVT may benefit from thrombophilia testing to identify underlying coagulation defects, some of which could affect the risk of subsequent rethromboses and influence therapeutic decisions (Class IIb; Level of Evidence B).
  • Children with CVT may benefit from investigation for underlying infections with blood cultures and sinus radiographs (Class IIb; Level of Evidence B).
  • In neonates with acute CVT, treatment with LMWH or UFH may be considered (Class IIb; Level of Evidence B).
  • Given the frequency of epileptic seizures in children with an acute CVT, continuous electroencephalography monitoring may be considered for individuals who are unconscious or mechanically ventilated (Class IIb; Level of Evidence C).
  • In neonates with acute CVT, continuation of LMWH for 6 weeks to 3 months may be considered (Class IIb; Level of Evidence C).
  • The usefulness and safety of endovascular intervention are uncertain in pediatric patients, and its use may only be considered in carefully selected patients with progressive neurological deterioration despite intensive and therapeutic levels of anticoagulant treatment (Class IIb; Level of Evidence C).

Diagnosis and Management of Cerebral Venous Thrombosis: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association
Stroke. 2011 Feb 3. [Epub ahead of print] Full Text

Which cardiac arrest survivors have a positive angio?

A retrospective study of out-of-hospital cardiac arrest patients attended by a French pre-hospital system was performed to assess the predictive factors for positive coronary angiography.

OBJECTIVES: Coronary angiography is often performed in survivors of out-of-hospital cardiac arrest, but little is known about the factors predictive of a positive coronary angiography. Our aim was to determine these factors.
METHODS: In this 7-year retrospective study (January 2000-December 2006) conducted by a French out-of-hospital emergency medical unit, data were collected according to Utstein style guidelines on all out-of-hospital cardiac arrest patients with suspected coronary disease who recovered spontaneous cardiac activity and underwent early coronary angiography. Coronary angiography was considered positive if a lesion resulting in more than a 50% reduction in luminal diameter was observed or if there was a thrombus at an occlusion site.
RESULTS: Among the 4621 patients from whom data were collected, 445 were successfully resuscitated and admitted to hospital. Of these, 133 were taken directly to the coronary angiography unit, 95 (71%) had at least one significant lesion, 71 (53%) underwent a percutaneous coronary intervention, and 30 survived [23%, 95% confidence interval (CI): 16-30]. According to multivariate analysis, the factors predictive of a positive coronary angiography were a history of diabetes [odds ratio (OR): 7.1, 95% CI: 1.4-36], ST segment depression on the out-of-hospital ECG (OR: 5.4, 95% CI: 1.1-27.8), a history of coronary disease (OR: 5.3, 95% CI: 1.4-20.1), cardiac arrest in a public place (OR: 3.7, 95% CI: 1.3-10.7), and ventricular fibrillation or ventricular tachycardia as initial rhythm (OR: 3.1, 95% CI: 1.1-8.6).
CONCLUSION: Among the factors identified, diabetes and a history of coronary artery were strong predictors for a positive coronary angiography, whereas ST segment elevation was not as predictive as expected.

Predictive factors for positive coronary angiography in out-of-hospital cardiac arrest patients
Eur J Emerg Med. 2011 Apr;18(2):73-6

Supplemental oxygen decreases LV perfusion in volunteers

Oxygen therapy in normoxic acute coronary syndrome patients is controversial, and a previous systematic review cautioned against it in uncomplicated MI. A volunteer study using cardiac imaging demonstrates the effects of supplemental oxygen on coronary blood flow.
 

OBJECTIVES: Oxygen (O2) is a cornerstone in the treatment of critically ill patients, and the guidelines prescribe 10-15 l of O2/min even to those who are initially normoxic. Studies using indirect or invasive methods suggest, however, that supplemental O2 may have negative cardiovascular effects. The aim of this study was to test the hypothesis, using noninvasive cardiac magnetic resonance imaging, that inhaled supplemental O2 decreases cardiac output (CO) and coronary blood flow in healthy individuals.
METHODS: Sixteen healthy individuals inhaled O2 at 1, 8 and 15 l/min through a standard reservoir bag mask. A 1.5 T magnetic resonance imaging scanner was used to measure stroke volume, CO and coronary sinus blood flow. Left ventricular (LV) perfusion was calculated as coronary sinus blood flow/LV mass.
RESULTS: The O2 response was dose-dependent. At 15 l of O2/min, blood partial pressure of O2 increased from an average 11.7 to 51.0 kPa with no significant changes in blood partial pressure of CO2 or arterial blood pressure. At the same dose, LV perfusion decreased by 23% (P=0.005) and CO decreased by 10% (P=0.003) owing to a decrease in heart rate (by 9%, P<0.002), with no significant changes in stroke volume or LV dimensions. Owing to the decreased CO and LV perfusion, systemic and coronary O2 delivery fell by 4 and 11% at 8 l of O2/min, despite the increased blood oxygen content.
CONCLUSION: Our data indicate that O2 administration decreases CO, LV perfusion and systemic and coronary O2 delivery in healthy individuals. Further research should address the effects of O2 therapy in normoxic patients.

Effects of oxygen inhalation on cardiac output, coronary blood flow and oxygen delivery in healthy individuals, assessed with MRI
European Journal of Emergency Medicine 2011, 18:25–30

Furosemide infusion in acute decompensated heart failure

A randomised controlled trial of 308 patients with acute decompensated heart failure compared continuous furosemide infusion with ‘low’ dose (equal to their total daily oral loop diuretic dose in furosemide equivalents) or high dose furosemide boluses. There was no outcome difference between infusion and bolus, although the high dose (2.5 times previous oral diuretic dose 12 hourly for 48 hours) improved patients’ symptoms while causing transient elevations in serum creatinine. Editorialist Dr G Fonarow states:
‘..these findings should change current practice. Since a high-dose regimen may relieve dyspnea more quickly without adverse effects on renal function, that regimen is preferable to a low-dose regimen. Administration of boluses may be more convenient than continuous infusion and equally effective.’
 

BACKGROUND: Loop diuretics are an essential component of therapy for patients with acute decompensated heart failure, but there are few prospective data to guide their use.
METHODS: In a prospective, double-blind, randomized trial, we assigned 308 patients with acute decompensated heart failure to receive furosemide administered intravenously by means of either a bolus every 12 hours or continuous infusion and at either a low dose (equivalent to the patient’s previous oral dose) or a high dose (2.5 times the previous oral dose). The protocol allowed specified dose adjustments after 48 hours. The coprimary end points were patients’ global assessment of symptoms, quantified as the area under the curve (AUC) of the score on a visual-analogue scale over the course of 72 hours, and the change in the serum creatinine level from baseline to 72 hours.
RESULTS: In the comparison of bolus with continuous infusion, there was no significant difference in patients’ global assessment of symptoms (mean AUC, 4236±1440 and 4373±1404, respectively; P=0.47) or in the mean change in the creatinine level (0.05±0.3 mg per deciliter [4.4±26.5 μmol per liter] and 0.07±0.3 mg per deciliter [6.2±26.5 μmol per liter], respectively; P=0.45). In the comparison of the high-dose strategy with the low-dose strategy, there was a nonsignificant trend toward greater improvement in patients’ global assessment of symptoms in the high-dose group (mean AUC, 4430±1401 vs. 4171±1436; P=0.06). There was no significant difference between these groups in the mean change in the creatinine level (0.08±0.3 mg per deciliter [7.1±26.5 μmol per liter] with the high-dose strategy and 0.04±0.3 mg per deciliter [3.5±26.5 μmol per liter] with the low-dose strategy, P=0.21). The high-dose strategy was associated with greater diuresis and more favorable outcomes in some secondary measures but also with transient worsening of renal function.
CONCLUSIONS: Among patients with acute decompensated heart failure, there were no significant differences in patients’ global assessment of symptoms or in the change in renal function when diuretic therapy was administered by bolus as compared with continuous infusion or at a high dose as compared with a low dose. (Funded by the National Heart, Lung, and Blood Institute; ClinicalTrials.gov number, NCT00577135.).

Diuretic strategies in patients with acute decompensated heart failure
N Engl J Med. 2011 Mar 3;364(9):797-805

In V.Fib and talking to you!

Some patients with severe refractory heart failure are kept alive thanks to implantable pumps such as the left ventricular assist device (LVAD). Many emergency physicians are likely to be unfamiliar with these but could encounter patients who have them. One particular peculiarity is that latter generation devices maintain non-pulsatile flow and provide or assist cardiac output independent of cardiac rhythm. In extreme situations patients can have life-sustaining cardiac outputs without palpable pulses or even audible heart sounds.

Click on image for Wikipedia article

A great example of how weird this can get is provided by a case of a 66 year male with an LVAD (HeartMate II (Thoratec Corporation)) who presented due to spontaneous discharge of his internal cardioverter-defibrillator (ICD). He was alert but had no pulses, and no detectable blood pressure using both a manual sphygmomanometer and an automated non-invasive blood pressure device. His 12 lead showed ventricular fibrillation. An invasive blood pressure showed a mean arterial pressure (mAP) of 80 mmHg. Several hours later his VF was successfully terminated and his mAP remained 80 mmHg
Some interesting points made by the authors include:

  • CPR was unnecessary in this guy but in cases of severe RV dysfunction it might need to be done to provide flow into the LV.
  • A danger of CPR in patients with an LVAD is the risk of damage to the device or ventricular rupture

LVAD use is significantly increasing so we can expect to encounter more episodes of previously impossible presentations to our emergency departments.

ABSTRACT
Optimal medical treatment, cardiac resynchronization, and the use of an implantable cardioverter defibrillator are established therapies of severe congestive heart failure. In refractory cases, left ventricular assist devices are more and more used not only as bridging to cardiac transplantation but also as destination therapy. Ventricular arrhythmias may represent a life-threatening condition and often result in clinical deterioration in patients with congestive heart failure. We report a case of asymptomatic sustained ventricular fibrillation with preserved hemodynamics caused by a nonpulsatile left ventricular assist device. Consecutive adequate but unsuccessful discharges of the implantable cardioverter defibrillator were the only sign of the usually fatal arrhythmia, prompting the patient to consult emergency services. Electrolyte supplementation and initiation of therapy with amiodarone followed by external defibrillation resulted in successful restoration of a stable cardiac rhythm after 3.5 hours.

Asymptomatic Sustained Ventricular Fibrillation in a Patient With Left Ventricular Assist Device
Ann Emerg Med. 2011 Jan;57(1):25-8.