Page 1743 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

1212 PART 11: Special Problems in Critical Care

a transient response to the initial calcium infusion. Calcium gluco- Failure to diagnose CO poisoning can have disastrous consequences for
nate (0.6 mL/kg of a 10% solution every 15-20 minutes) has also been the patient and other members of an affected household.
recommended if central venous access is not immediately available. Laboratory confirmation of elevated HbCO is available by cooximetry.
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Glucagon, given as a bolus of 5 to 10 mg IV over 3 to 5 minutes followed by Pulse oximetry is unreliable in detecting HbCO because it cannot
an infusion of 3 to 5 mg/h, may decrease vasopressor requirements. 2,176,188 distinguish carboxyhemoglobin from oxyhemoglobin. Pulse oximetry
As described in the section on β-blocker toxicity, high-dose insulin overestimates oxyhemoglobin by the amount of HbCO present, and may
is also an effective therapy in severe CCB toxicity. Also as described in be normal despite high concentrations of HbCO. Arterial blood gases
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the section on β-blocker toxicity, use of ILE therapy has been described typically demonstrate a normal P O 2 , contrasting with low oxyhemoglo-
in the literature for patients with refractory hemodynamic collapse and bin saturation by cooximeter, and metabolic acidosis. Of note, venous
cardiac arrest associated with CCB overdose. blood can be used for screening because venous HbCO levels accurately
■ CARBON MONOXIDE predict arterial levels. 197
Treatment of CO poisoning consists of immediate removal of the
Carbon monoxide (CO) is a nonirritating, colorless, tasteless, and odor- patient from the exposure and administration of 100% supplemental
less gas formed by incomplete combustion of carbon-containing mate- oxygen. Breathing 100% oxygen reduces the half-life of HbCO from 5
rials (complete oxidation produces carbon dioxide). Poisoning occurs to 6 hours on room air to 40 to 90 minutes. Breathing oxygen that con-
in the setting of smoke inhalation, attempted suicide from automobile tains 4.5% to 4.8% carbon dioxide allows for greater minute ventilation
exhaust, and poorly ventilated charcoal and gas stoves. Rarely, CO is while maintaining normocapnia and further accelerates CO clearance.
generated during hepatic metabolism of dichloromethane, a component In one study of seven healthy volunteers, this method decreased the
of paint and varnish removers. half-life of CO from 78 ± 24 minutes to 31 ± 6 minutes compared to
Carbon monoxide binds to hemoglobin with an affinity that is 240 times 100% O 2 at resting minute ventilation. It is generally recommended
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greater than oxygen. Fetal hemoglobin binds carbon monoxide to an that patients with mild CO poisoning receive normobaric 100% oxygen
even greater degree, placing the fetus at particularly high risk during CO via nonrebreather mask for no less than 6 hours. Hyperbaric oxygen
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exposure. Carboxyhemoglobin (HbCO) decreases oxyhemoglobin satu- (HBO) (2.8 atmospheres) further decreases the half-life of HbCO to 15
ration and blood oxygen-carrying capacity in a way that is analogous to to 30 minutes.
anemia (an HbCO concentration of 50% effectively lowers hemoglobin The role of HBO, which can increase arterial oxygen tensions to
concentration by half). However, CO poisoning causes significantly greater than 2000 mmHg and oxygen tensions in tissues to 400 mmHg,
more toxicity than similar degrees of anemia because in CO poisoning is debated. 200,201 In a Cochrane review, of six randomized controlled trials
(1) HbCO shifts the oxyhemoglobin dissociation curve to the left, inter- evaluated, four found no benefit of HBO over normobaric oxygen (NBO)
fering with off-loading of oxygen in tissue beds; (2) CO reacts with myo- therapy with pooled analysis showing no benefit. Although earlier
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globin to form carboxymyoglobin; (3) CO blocks myoglobin-facilitated studies had shown benefit of HBO in patients with loss of consciousness,
diffusion of oxygen (particularly in tissues rich in myoglobin), as well as in a recent randomized clinical trial, there was no evidence of superiority
myoglobin-mediated oxidative phosphorylation, resulting in impaired in 1-month neurologic recovery among patients with history of loss of
cardiac contractility; (4) CO inhibits enzymes of the mitochondrial consciousness who received HBO versus NBO. 202,203 In addition, a nega-
electron-transfer chain, further interfering with cellular function; and tive dose response was noticed for patients with CO-induced coma. 203
(5) CO binds and inhibits various intracellular enzymes including cyto- As the use of HBO remains controversial, decision to initiate HBO
chrome P-450 and NADPH reductase. 189,190 Tissues with high oxygen therapy among patients with CO poisoning should be discussed with
consumption (namely, heart and brain) are particularly vulnerable to a medical toxicologist. Particularly controversial is whether a patient
toxic effects. with severe CO poisoning should be transferred solely for the purpose
The severity of CO poisoning depends on its concentration, the dura- of HBO. Also controversial is the relative efficacy of single versus mul-
tion of exposure, and minute ventilation. Carboxyhemoglobin levels do tiple HBO treatments. Since CO poisoning may occur with other life-
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not correlate well with clinical severity of CO poisoning. However, mild threatening injuries (eg, burns or other trauma), the judgment to utilize
exposures (HbCO 5%-10%) generally cause headache and mild dyspnea. HBO must take into consideration the patient’s stability and the ability to
These concentrations may be seen in heavy smokers and commuters monitor and treat the patient during HBO therapy.
of documented coronary artery disease and ventricular ectopy. ■ COCAINE
on busy highways and are generally well tolerated, even in the presence
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Carboxyhemoglobin concentrations between 10% and 30% cause Cocaine may be snorted nasally, inhaled orally, or injected subcutane-
headache, dizziness, weakness, dyspnea, and irritability. These concen- ously or intravenously. Freebase cocaine is prepared for smoking by
trations may cause angina and myocardial infarction even in young and dissolving cocaine salt in an aqueous alkaline salt solution and then
otherwise healthy patients. Exposures to >50% HbCO result in coma, extracting the freebase form with a solvent such as ether. Heat is often
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seizures, cardiovascular collapse, and death. used to speed this process, creating a fire hazard. One freebase prepara-
Ten to thirty percent of survivors of CO poisoning develop delayed tion for smoking is crack cocaine, which is a potent, rapidly absorbed,
neurologic sequelae (DNS) of hypoxic brain injury. 193,194 Clinical water-soluble alkaloid form of the drug.
manifestations of DNS are variable, including persistent vegetative Cocaine is often mixed with other substances of abuse including
state, parkinsonism, memory deficits, behavioral changes, and hearing heroin (“speedball”), phencyclidine, and amphetamines. In the presence
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loss. Neurologic sequelae cannot be predicted by severity of carboxy- of ethanol, cocaine is transesterified in the liver to cocaethylene, which
hemoglobin exposure, age, method of exposure (accidental or inten- has similar properties to cocaine but a longer half-life. Cocaethylene is a
tional), or results of early neuroimaging (which may be normal or show myocardial depressant capable of reducing stroke volume and blood pres-
low-density lesions in the globus pallidus or deep white matter changes). 195 sure while increasing pulmonary artery wedge pressure. Cocaethylene
The diagnosis of CO poisoning is often made on clinical grounds in also prolongs QRS and QTc intervals. Individuals combine cocaine and
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the setting of smoke inhalation or attempted suicide. However, the diag- ethanol to achieve a more pronounced and prolonged euphoria, but this
nosis can be missed if the history is incomplete and the clinical presenta- combination is more toxic than either drug alone. 207
tion is nondescript. A high index of suspicion is warranted, particularly Toxic effects of cocaine stem from excessive central nervous system
during cold weather in patients with acute coronary syndrome, arrhyth- stimulation and inhibition of neuronal uptake of catecholamines. The
mias, mental status changes, headache, and unexplained weakness. result is generalized sympathetic overstimulation similar to that of
Rarely, cherry-red skin discoloration reflecting high venous oxygen amphetamine intoxication. Onset and duration of symptoms depend
saturation (arteriolization of venous blood) provides an important clue. on route of administration, dose, and patient tolerance. Smoking and

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