Chapter 37 Pain Control in the Critically Ill Patient Flashcards Preview

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Flashcards in Chapter 37 Pain Control in the Critically Ill Patient Deck (69):
1

patients in critical care settings often
experience pain from

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

2

Anxiety may stem from

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

3

Significant anxiety may lead to

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

4

Behavioral physiologic
scales use pain-related behaviors such as

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.

5

Undersedation may result in

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

6

oversedation may result
in

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

7

Richmond Agitation Sedation Scale

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

8

Ramsay Sedation Scale

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

9

Riker Sedation Agitation Scale

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

10

Adaptation to the Intensive Care
Environment (ATICE

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.

11

Few objective measures are available to assess sedation.

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

12

bispectral index (BIS)

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

13

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

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

14

recommended first-line therapy for the
treatment of pain.

Acetaminophen and nonsteroidal anti-inflammatory drugs
(NSAIDs)

15

NSAIDs

nonselectively inhibit cyclooxygenase,
blocking the production of inflammatory
mediators

16

limit
the use of NSAIDs in the intensive care unit.

clinical concerns of renal insufficiency and bleeding from
platelet dysfunction and gastrointestinal tract mucosa

17

Renal insufficiency due to Keterolac
results from

from the decreased of production of prostacyclins
that increase renal blood flow.

18

Migraine without Aura

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

19

Migraine with Aura

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.

20

Basilar Migraine

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

21

Aura without Headache

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

22

Hemiplegic Migraine

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

23

Opioids produce
analgesia mainly by stimulating

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

24

Unwanted effects of opioids include

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

25

Respiratory depression occurs with opioids because

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

26

Hypotension is occasionally seen in
hypovolemic patients

as a decrease in sympathetic tone
occurs after treatment of pain with opioid administration

27

Fentanyl

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

28

Sufentanil

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

29

Alfentanil

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

30

Hydromorphone

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

Morphine

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

Morphine may also rarely lead to significant hypotension mediated by

vasodilatation
from histamine release.

33

meperidine

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

34

Meperidine side effects

has vagolytic and histamine releasing side effects
both of which may result in tachycardia.

35

Remifentanil

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

Remifentanil-based sedation regimens

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

Hypnotic Agents

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

Benzodiazepines

interact with the g-amino-butyric acid (GABA) receptor
creating an increase in intracellular chloride concentration and subsequent hyperpolarization of the cellular membrane.

39

most common used benzodiazepines in the critical care setting

Midazolam and lorazepam

40

flumazenil

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

41

lengthy therapy of diazepam results in

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

Lorazepam is used frequently in the intensive care unit
at doses of

1 to 2 mg every 1 to 2 hr.

43

Lorezapam

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

Large doses of prolonged intravenous lorazepam should be avoided

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

45

Midazolam

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

Midazolam metabolism

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

Midazolam active metabolite

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

48

PROPOFOL

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

PROPOFOL Cardiovascular Effects

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

propofol a commonly used agent intensive care unit at doses

between 10 and 50 mg/kg/min.

51

Long-term continuous infusions of propofol Adverse Effects

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

propofol infusion syndrome

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

53

Dexmedetomidine

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

A hypnotic effect is produced by dexmedetomidine
that resembles induction of

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

major advantages of dexmedetomidine

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

adverse effects of dexmedetomidine

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

Dementia

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

58

Delirium

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

Hyperactive delirium

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

60

Hypoactive delirium

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

61

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

evaluate inattention, altered level of
consciousness, and disorganized thinking.

62

In order to be
diagnosed with delirium, a patient must

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

63

associated with the development of delirium

disruption of the sleep cycle

64

Haloperidol

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

65

Haloperidol Adverse Effects

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

66

Olanzapine

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

One of the most common reasons to utilize neuromuscular
blocking agents in the intensive care is

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

The greatest concern to neuromuscular blockade use is

prolonged paralysis, particularly in patients receiving steroid
therapy.

69

The most commonly used neuromuscular blocking
agent in the critical care unit is

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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