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Review > Chapter 37 Pain Control in the Critically Ill Patient > Flashcards

Chapter 37 Pain Control in the Critically Ill Patient Flashcards

1
Q

patients in critical care settings often

experience pain from

A

prolonged immobility, routine nursing
care (airway suctioning, dressing changes, and patient
mobility) and monitoring and therapeutic devices (catheters,
drains, and endotracheal tubes).

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2
Q

Anxiety may stem from

A

pain, being in an unfamiliar
environment, and lack of control or even a fear of
impending death.

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3
Q

Significant anxiety may lead to

A

agitation
and delirium, complicating diagnosis and interfering with
treatment leading to increased morbidity and mortality.

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4
Q

Behavioral physiologic

scales use pain-related behaviors such as

A

posturing and facial expressions along with physiologic indicators
such as heart rate, blood pressure, and respiratory rate to assess pain intensity in patients who are unable to participate in unidirectional pain assessment scales.

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5
Q

Undersedation may result in

A

ventilator dysynchrony, increased
oxygen requirements, self-removal of devices and
possibly post-traumatic stress disorder from a stay in the critical care unit.

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6
Q

oversedation may result

in

A

prolonged tracheal intubation and mechanical ventilation,
increasing the chance of pneumonia and respiratory
deconditioning.

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7
Q

Richmond Agitation Sedation Scale

A

sedation scale with scores ranging from 14, a violent dangerous patient, to –5, an
unarousable patient. A sedation score of 0 is most often
therapeutically targeted as it correlates with an alert and calm patient

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8
Q

Ramsay Sedation Scale

A

the most
simplistic and allows for a numeric score from 1 to 6 based
on responsiveness of the patient

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9
Q

Riker Sedation Agitation Scale

A

scores a patient’s level of sedation from 1 to 7 and is especially
adapted to warn the clinician of extremes of sedation and
agitation

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10
Q

Adaptation to the Intensive Care

Environment (ATICE

A

a complex scoring system consisting
of two domains, consciousness and tolerance.9 The
consciousness domain evaluates wakefulness and comprehension
while the tolerance domain monitors agitation,
ventilator dysynchrony, and facial expressions.

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11
Q

Few objective measures are available to assess sedation.

A

Vital signs such as heart rate, blood pressure, and respiratory rate are not specific or sensitive to sedation in the
critically ill.

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12
Q

bispectral index (BIS)

A

aims to provide an objective measure of a patient’s sedation by
assigning a numerical value to a patient’s electroencephalogram
activity

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13
Q

Patient comfort in the critical care setting is obtained with
the use of

A

both hypnotic and analgesic agents. Focusing first on providing analgesia and then on hypnosis may provide more effective sedation.

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14
Q

recommended first-line therapy for the

treatment of pain.

A

Acetaminophen and nonsteroidal anti-inflammatory drugs

NSAIDs

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15
Q

NSAIDs

A

nonselectively inhibit cyclooxygenase,
blocking the production of inflammatory
mediators

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16
Q

limit

the use of NSAIDs in the intensive care unit.

A

clinical concerns of renal insufficiency and bleeding from

platelet dysfunction and gastrointestinal tract mucosa

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17
Q

Renal insufficiency due to Keterolac

results from

A

from the decreased of production of prostacyclins

that increase renal blood flow.

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18
Q

Migraine without Aura

A 
At least five headache attacks
Headaches last 4–72 hr if untreated
Has at least two of the following, but not weakness: Unilateral pain, Pulsating, Intensity is moderate to severe, Aggravated by routine physical activity, Has at least one of the following:
Phonophobia, Photophobia
Nausea, Emesis
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19
Q

Migraine with Aura

A

At least two headache attacks that also fulfill the characteristics of migraine without aura.
Headaches usually follow the aura but may begin with it and last 4–72 hr if untreated. Has at least one of the following reversible symptoms (lasting 4 min to 60 min), but no weakness.
Positive or negative visual symptoms such as scintillating scotomas, blind spot (scotoma), blurred vision, zig-zag lines, homonymous hemianopsia.
Positive or negative sensory symptoms such as tingling or numbness.

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20
Q

Basilar Migraine

A

At least two attacks of migraine with an aura whose symptoms are reversible and localize to the brainstem or are bihemispheric, but without weakness.
Symptoms can include: Dysarthria
Dizziness or vertigo
Bilateral visual symptoms, including temporary blindness
Diplopia, Nystagmus
Ataxia, Decreased level of consciousness
Bilateral paresthesiae
Tinnitus with or without decreased hearing

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21
Q

Aura without Headache

A

At least two attacks of symptoms typical of auras, but not weakness, such as visual, sensory or speech disturbances that resolve within 1 hr and are
not followed by a headache

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22
Q

Hemiplegic Migraine

A

At least two attacks of migraine with a reversible aura of motor weakness that can last 1 hr to days
Also includes one of the following:
Positive or negative visual symptoms,
Positive or negative sensory symptoms,
Dysphasia or dysarthria.
Frequently accompanied by symptoms typical of basilar migraine.
If at least one first- or second-degree relative has a migrainous aura that includes motor weakness, it is familial hemiplegic migraine and is associated with a mutation in the neuronal calcium channel. If no first- or second-degree relative has a migrainous aura that includes motor weakness, it is sporadic hemiplegic migraine

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23
Q

Opioids produce

analgesia mainly by stimulating

A

g- and k-receptors
located both centrally and peripherally; however, interaction
with other opioid receptors may lead to adverse
effects.

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24
Q

Unwanted effects of opioids include

A

nausea, constipation,
urinary retention, pruritus, and excessive sedation
with possible respiratory depression. Severe constipation
leading to ileus has been treated with some success
using intravenous and parenteral opioid antagonists

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25
Q

Respiratory depression occurs with opioids because

A

the ventilatory response to hypercapnia is decreased, while the response to hypoxia is obliterated.

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26
Q

Hypotension is occasionally seen in

hypovolemic patients

A

as a decrease in sympathetic tone

occurs after treatment of pain with opioid administration

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27
Q

Fentanyl

A

an opioid which has a rapid onset and
short duration of action often necessitating continuous infusion therapy of 1 to 2 mg/kg/hr with 1 to 2 mg/kg initial loading doses to provide adequate pain control

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28
Q

Sufentanil

A

a potent lipophilic narcotic with greater protein binding
and smaller volume of distribution than fentanyl, resulting
in a shorter duration of action

29
Q

Alfentanil

A

possesses a small volume of distribution secondary to protein binding and low lipid
solubility, allowing for predictable duration of action.

30
Q

Hydromorphone

A

has a longer onset of action than fentanyl
but also a longer duration of action, allowing for
intermittent dosing at ranges of 10 to 20 mg/kg per 1-2 hr.

31
Q

Morphine

A

has a pharmacokinetic profile similar to hydromorphone but has a potent active
metabolite that depends on renal excretion limiting its
use in the critical care setting

32
Q

Morphine may also rarely lead to significant hypotension mediated by

A

vasodilatation

from histamine release.

33
Q

meperidine

A

generally avoided for prolonged therapy
due to accumulation of its neuroexcitatory metabolite,
normeperidine, which can cause seizures.

34
Q

Meperidine side effects

A

has vagolytic and histamine releasing side effects

both of which may result in tachycardia.

35
Q

Remifentanil

A

an ultra-short-acting opioid as it is metabolized by
nonspecific plasma esterases, providing the most predictability
of duration of action of all the opioid agents.

36
Q

Remifentanil-based sedation regimens

A

at doses of 0.01 to
0.2 mg/kg/min, have shown to produce better sedation
and decrease the length of ICU stays

37
Q

Hypnotic Agents

A

providing anxiolysis, sedation, and amnesia, and decrease analgesic requirements.
Benzodiazepines, propofol, and dexmedetomidine are
the most commonly used hypnotic agents in the critical care setting

38
Q

Benzodiazepines

A

interact with the g-amino-butyric acid (GABA) receptor

creating an increase in intracellular chloride concentration and subsequent hyperpolarization of the cellular membrane.

39
Q

most common used benzodiazepines in the critical care setting

A

Midazolam and lorazepam

40
Q

flumazenil

A

a benzodiazepine antagonist, may cause withdrawal symptoms resulting in
increased oxygen consumption and is therefore avoided in
the critical care setting

41
Q

lengthy therapy of diazepam results in

A

a prolonged sedative effect as the hepatic metabolism of diazepam results in the production of an active metabolite known as desmethyldiazepam forcing diazepam to be considered a long-acting agent.

42
Q

Lorazepam is used frequently in the intensive care unit

at doses of

A

1 to 2 mg every 1 to 2 hr.

43
Q

Lorezapam

A

the least lipophilic benzodiazepine and therefore, has a slower onset of action than other benzodiazepines. This drug has a favorable metabolic profile as it relies on hepatic glucuronidation,
producing an inactive metabolite that makes elimination more predictable.

44
Q

Large doses of prolonged intravenous lorazepam should be avoided

A

they have been associated with acute tubular necrosis, lactic acidosis and hyperosmolar states.

45
Q

Midazolam

A

frequently used in the preoperative and intraoperative areas at doses of 1 to 5 mg secondary to its water-soluble characteristics that allow the drug to
become highly lipid soluble at physiologic pH allowing for a rapid onset

46
Q

Midazolam metabolism

A

Midazolam relies on hepatic metabolism and significant accumulation of midazolam may occur
in patients with hepatic dysfunction during prolonged therapy because of its high lipophilicity and large volume
of distribution.

47
Q

Midazolam active metabolite

A

alpha-hydroxymidazolam, which relies on renal excretion prolonging its duration of action in patients with renal disease

48
Q

PROPOFOL

A

also a GABA receptor agonist. Propofol is commonly used to induce general anesthesia but can be used at lower doses as a hypnotic agent,
producing a degree of amnesia less than benzodiazepines

49
Q

PROPOFOL Cardiovascular Effects

A

Propofol also acts as a vasodilator and a cardiac
depressant, resulting in a dose-dependent decrease in blood
pressure and possibly heart rate, respectively.

50
Q

propofol a commonly used agent intensive care unit at doses

A

between 10 and 50 mg/kg/min.

51
Q

Long-term continuous infusions of propofol Adverse Effects

A

The phospholipid emulsion of
propofol should be counted as a calorie source and may result
in triglyceridemia and eventually pancreatitis. A rare but morbid complication of prolonged high-dose propofol therapy
above 50 mg/kg/min, propofol infusion syndrome

52
Q

propofol infusion syndrome

A

results in mitochondrial injury, lactic acidosis, dysrhythmias, hyperkalemia, and rhabdomyolysis.

53
Q

Dexmedetomidine

A

a2-agonist with an affinity for the a2
receptor 7 times greater than clonidine. Activation of the post-synaptic a2A-receptor results in hypnosis, mild amnesia and significant analgesia that reduces the need for supplemental opioids

54
Q

A hypnotic effect is produced by dexmedetomidine

that resembles induction of

A

normal sleep at doses between 0.2 to 1.0 mcg/kg/min. The hypnotic effect
of dexmedetomidine is unique, in that patients, when left undisturbed, will sleep; but when aroused with gentle stimulation, patients will be cooperative and follow commands. This effect is mediated by activation of the a2A-receptor in the locus ceruleus

55
Q

major advantages of dexmedetomidine

A

produces virtually no respiratory depression while providing sedation and reducing analgesic opioid requirements. It has been shown to facilitate extubation in patients
who have previously failed extubation attempts due to severe agitation

56
Q

adverse effects of dexmedetomidine

A

enhancement of vagal effects by creating a pharmacologic sympathectomy resulting in hypotension and bradycardia. However, if therapy is initiated rapidly at a high dose, a transient hypertension
and tachycardia may occur. This is then followed by hypotension and bradycardia mediated by the a2A-receptor inhibiting sympathetic tone in the peripheral vascular system.

57
Q

Dementia

A

a progressive disease with a decline in memory and cognitive skills and rarely presents acutely

58
Q

Delirium

A

an acute reversible change in mental
status. It is characterized by fluctuating levels of arousal associated with sleep–wake cycle disruption brought on by the reversal of day–night cycles and is associated with worse outcomes and increased long-term mortality

59
Q

Hyperactive delirium

A

easily recognized as patients are agitated and combative interfering with therapeutic measures;

60
Q

Hypoactive delirium

A

characterized by calm appearance, decreased mobility and inattention, is
actually associated with a worse prognosis

61
Q

In a critically ill patient
with an acute change or fluctuating mental status, the
CAM-ICU (Confusion Assessment
Method for the ICU) aims to

A

evaluate inattention, altered level of

consciousness, and disorganized thinking.

62
Q

In order to be

diagnosed with delirium, a patient must

A

not be heavily sedated and demonstrate inattention along with either altered level of consciousness or disorganized thinking

63
Q

associated with the development of delirium

A

disruption of the sleep cycle

64
Q

Haloperidol

A

haloperidol 0.5 to 5 mg every 5 min until agitation is controlled. Haloperidol
antagonizes dopamine-mediated neurotransmission, stabilizing
cerebral function.

65
Q

Haloperidol Adverse Effects

A

extrapyramidal symptoms, neuroleptic malignant syndrome, hypotension, and QT prolongation is recommended
specifically as QT prolongation can lead to torsades de pointes.

66
Q

Olanzapine

A

newer agent for the treatment of delirium, has similar
efficacy to haloperidol but with fewer extrapyramidal side
effects at doses of 2.5 to 5 mg daily

67
Q

One of the most common reasons to utilize neuromuscular

blocking agents in the intensive care is

A

patient–ventilator dyssynchrony. Such dyssynchrony can result in increased
airway pressures which may predispose the patient to ventilator
induced lung injury. neuromuscular
blocking agents are also used to decrease oxygen consumption
in patients with tenuous oxygen supply versus demand

68
Q

The greatest concern to neuromuscular blockade use is

A

prolonged paralysis, particularly in patients receiving steroid
therapy.

69
Q

The most commonly used neuromuscular blocking

agent in the critical care unit is

A

cisatracurium at infusion rates
of 1 to 5 mg/kg/min as it undergoes Hoffman degradation. Only temperature and pH alter the pharmacokinetics; therefore
patients with renal and hepatic dysfunction can be treated with cisatracurium with minimal concern for prolongationof action.

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