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AP 1 > Test 4: PACU (pt. 2/3) CV, Delirium, Pain > Flashcards

Test 4: PACU (pt. 2/3) CV, Delirium, Pain Flashcards

1
Q

What is the definition of hypotension?

A

Compromise should be indicated by the clinical signs of hypoperfusion, rather than numerical numbers.

Classically, it has been defined as a fall in arterial blood pressure (BP) of more than 20% below baseline, or an absolute value of systolic BP (SBP) below 90 mm Hg, or of mean arterial pressure (MAP) below 60 mm Hg.

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2
Q

What is the MOST COMMON cause of hypotension in the PACU?

A

Hypovolemia !!! secondary to inadequate replacement of intraoperative fluid and blood loss (decreased preload).

May be due to:
-Volume depletion r/t inadequate fluid replacement during surgery
-Blood loss during surgery
-Ongoing postop blood loss

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3
Q

What are the clinical signs of hypoperfusion?

A

-Altered mental status
-Hypotension, tachycardia and tachypnea
-Decreased capillary refill, peripheral cyanosis, cool/clammy skin, and mottling
-Oliguria

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4
Q

What is the treatment for hypotension in PACU?

A

Initial treatment should focus on restoring circulating volume.
-Assess for active bleeding
-300 to 500 mL fluid bolus of saline or LR
-If no response is noted, r/out myocardial dysfunction as the cause

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5
Q

What is the differential diagnosis for Hypotension?

A

-Hypovolemia (most common)
-MI, tamponade, PE
-Dysrhythmias
-Tension PTX
-Anaphylaxis/Histamine release (Anesthetic agents)
-Vasodilators (if overly sensitive response)
-Sepsis

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6
Q

How do you define Hypertension?

A

Hypertension is defined as a rise in arterial BP of more than 20% above baseline or an absolute value of arterial BP above age-corrected limits.

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7
Q

What are some causes of Hypertension?

A

-SNS Stimulation
-Pain
-Respiratory compromise
-Visceral distention
-Inc in plasma catecholamines that produce vasoconstriction

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8
Q

What is the leading cause of hypertension and tachycardia in the PACU?

A

Pain

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9
Q

How does pain cause hypertension?

A

Pain results in stimulation of the somatic afferent nerves, producing a pressor response known as the somatosympathetic reflex.

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10
Q

When should planning for postop pain control start?

A

In the holding room (pre-op) where you must set realistic goals, manage expectations (be honest - it will hurt), and continue current pain medications whenever possible.

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11
Q

What are some agents you can use in a multimodal approach?

A

-Acetaminophen and NSAIDs
-Ketamine
-Alpha agonists
-Gabapentinoids
-Regional anesthesia / local anesthetics
-Corticosteroids (anti-inflammatory and helps with N/V)
-Opioids
-Repositioning and reassurance (Hand holding/it will be ok)

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12
Q

What is the differential diagnosis for hypertension?

A

-Pain
-Hypoxemia/hypercarbia (stimulation of the vasomotor area of the medulla, leading to inc vasomotor tone)
-Distention of the bladder, bowel, or stomach (stimulation of afferent SNS)
-Hypothermia/Shivering (inc catecholamines)
-Pre-existing HTN (30% of patients, continue BB throughout periop period)
-Medications (Vasopressors, Withdrawal from opioids, Narcan administration, Ketamine, and rebound effects of clonidine and/or beta blockers)

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13
Q

T/F: Dysrhythmias seen in the PACU are often transient and most commonly have an identifiable cause that is not an actual myocardial injury.

A

True

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14
Q

What are the major postanesthetic and surgical factors that lead to a relatively high incidence of perioperative dysrhythmias?

A

-Hypokalemia (r/t hyperventilation, respiratory alkalosis, gastric suctioning, diuretic use
-Fluid overload
-Anemia (impaired O2 transport)
-Hypoventilation with hypercarbia (hypoxia leads to myocardial ischemia and cardiac irritability. Hypercarbia stimulates the SNS)
-Altered acid-base balance
-Substance withdrawal
-Circulatory instability (hypotension)

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15
Q

Incomplete reversal of neuromuscular relaxation can lead to postoperative pulmonary complications including ?

A

-compromised cough
-obstruction
-airway patency
-hypoventilation

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16
Q

Why should objective monitoring measures (e.g., train-of-four ratio > 0.90 and double burst stimulation) be performed regularly in the early postanesthesia phase?

A

-Patients who received a reversal agent often exhibit signs of residual neuromuscular blockade in the PACU, particularly the elderly.
-Should be performed to determine depth of residual blockade and prevent pulmonary complications

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17
Q

What are the objective monitoring measures used to assess NMB?

A

-TOF > 0.90
-Double burst stimulation

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18
Q

How can you decrease the incidence of residual paralysis?

A

-Use of short-acting relaxants
-Reversal agents

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19
Q

What is the main advantage of Sugammadex?

A

The main advantage of sugammadex is reversal of neuromuscular blockade without relying on inhibition of acetylcholinesterase and earlier spontaneous postoperative ventilation.
-Specifically designed to reverse rocuronium.

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20
Q

Which is more dangerous: Marginal reversal or near-total paralysis?

A

Marginal Reversal is more dangerous

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21
Q

Why is Marginal reversal more dangerous than near-total paralysis?

A

-an agitated patient exhibiting uncoordinated movements and airway obstruction is more easily identified.
-A somnolent patient exhibiting mild stridor and shallow ventilation from marginal neuromuscular function might be overlooked.
-Insidious hypoventilation leading to respiratory acidemia or regurgitation with aspiration can occur later into recovery.

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22
Q

What medications potentiate NMB?

A

-Aminoglycosides
-Lasix
-Inderal
-Dilantin

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23
Q

What underlying neuromuscular diseases exhibit exaggerated or prolonged responses to muscle relaxants?

A

-Myasthenia gravis
-Eaton-Lambert syndrome
-muscular dystrophies

Such patients can exhibit postoperative respiratory insufficiency from inadequate neuromuscular reserves.

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24
Q

Periodic mental and behavioral status assessments are recommended during what times?

A

Postoperative mental status changes may be associated with poor anesthetic outcomes; therefore, periodic mental and behavioral status assessments are recommended from the time of emergence and throughout the early postanesthesia recovery period.

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25
Q

What is Delirium?

A

A condition characterized by extreme disturbances of arousal, attention, orientation, perception, intellectual function, and affect.
-It is most commonly accompanied by fear and agitation.

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26
Q

Which procedure has the highest incidence of postop delirium?

A

62% after operative hip procedures (geriatric).

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27
Q

What are the causes of postoperative delirium?

A

-Withdrawal psychosis
-Toxic psychosis (exposure to toxins)
-Circulatory and respiratory origin (hypoxemia, hypercarbia, and hypotension)
-Functional psychosis (brief rxn of paranoia and other changes not caused by an organic abnormality)

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28
Q

How can withdrawal psychosis cause emergence delirium?

A

Withdrawal of various substances such as alcohol and illicit drugs.

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29
Q

What drugs contribute to Postop Delirium?

A

Premedications, including anticholinergics, benzodiazepines, and opioids, may induce untoward reactions.
-Anticholinergics, specifically atropine and scopolamine, have been noted to cause central anticholinergic syndrome. These drugs cross the blood-brain barrier, altering the neurotransmitter balance and causing agitation, combativeness, and lack of cooperation.
-Benzodiazepines may contribute to postoperative delirium, especially in the elderly.

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30
Q

What are the most frequently occurring neurologic phenomena in older adults?

A

Postoperative Delirium (POD) and postoperative cognitive dysfunction (POCD)

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31
Q

How do you define POD?

A

A disruption of perception, thinking, memory, psychomotor behavior, sleep-wake cycle, consciousness, and attention.

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32
Q

POD is associated with an increased risk for what negative things?

A

-Periop mortality
-Institutionalization
-Dementia

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33
Q

What are the risk factors for POD?

A

-Age > 65 (same as POCD)
-renal insufficiency and metabolic derangements
-Poorly controlled pain: multimodal management
-Polypharmacy (pyschoactive drugs)
-Functional impairment (frailty)
-Urinary retention and presence of a urinary catheter

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34
Q

What drugs are associated with the development of delirium and should be avoided during the perioperative period, especially in geriatric population?

A

benzodiazepines, anticholinergics, and antihistamines

35
Q

What is the treatment for POD?

A

1) R/out Hypoxemia first!!!
2) Treat potential causes (anxiety, pain, residual anesthesia, etc)

Goal is to maintain patient safety!!

36
Q

How do you define delayed awakening?

A

A clinician’s expectation in a specific circumstance that the patient “should be awake by now” but is not.

37
Q

What is the MOST COMMON cause of delayed awakening?

A

Prolonged action of anesthetic medications.

38
Q

What are other causes of delayed awakening?

A

-Metabolic causes: hypoglycemia, hyperglycemia, electrolyte disturbances, and hypothyroidism
-Neurologic injury: rare cause of delayed awakening of the nonneurosurgical patient. Potential causes include: CVA, intracranial hemorrhage, increased ICP, uncontrolled extreme hypertension or hypotension, and emboli.

Prolonged action of anesthetic drugs is the most common cause of delayed awakening!!!

39
Q

What causes Serotonin Syndrome?

A

The concurrent administration of two or more serotonergic medications (Antidepressants and chronic pain).

40
Q

What are the S/Sx of Serotonin Syndrome?

A

Mild: mydriasis, diaphoresis, myoclonus, tachycardia, anxiety, restlessness
Severe: fever, mental status changes, muscle rigidity, multiple organ failure

41
Q

What is the most important measure of Pain?

A

Patient self-report !!

42
Q

What are ways to assess pain?

A

-Verbal rating or visual analog scale
-patient’s exposure to painful procedure
-behavioral signs, such as crying or agitation
-a proxy pain rating by someone who knows the patient well
-physiologic indicators, such as elevated vital signs, and genetic factors can interfere with pain perception and the effectiveness of medications used to treat pain.
-Genetic factors interfere with pain perception and medication effectiveness.

43
Q

What is the definition of Pain?

A

Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

44
Q

What are the four processes of Nociceptive Pain?

A

Transduction
Transmission
Perception
Modulation

45
Q

What is Transduction?

A

The transformation of a noxious stimulus into an action potential.

46
Q

What is Transmission?

A

The process by which an action potential is conducted from the periphery to the CNS.

47
Q

What is Perception?

A

Occurs once the signal is recognized by various areas of the brain.
-Amygdala, somatosensory areas of the cortex, the hypothalamus, and the anterior cingulate cortex

48
Q

What is Modulation?

A

Altering neural afferent activity along the pain pathway; it can suppress or enhance pain signals.

49
Q

What are Nociceptors?

A

Pain receptors. Free nerve endings.
-Conduct noxious stimuli to the dorsal horn of the spinal cord
-Categorized according to morphology (diameter, myelination, and conduction velocity).
Generally, the larger the diameter, the faster the conduction velocity

50
Q

Which fibers have the fastest conduction velocity?

A

A Alpha Fibers (Largest Diameters)

51
Q

Which fibers have the slowest conduction velocity?

A

C Fibers (Smallest Diameter)

52
Q

What do the myelinated, A-Delta neurons do?

A

-Conduct APs at velocities between 6 and 30 m/s
-Elicit fast-sharp pain
-They are responsible for the initial mechanical or thermal pain that is felt and alert an individual of tissue damage, thereby resulting in the reflex withdraw mechanism.

53
Q

What do the unmyelinated C Fibers do?

A

-Slower velocities, between 0.5 and 2 m/s
-Known as Polymodal fibers (respond to mechanical, thermal, and chemical injuries)
-Delayed, slow, second pain
-“dull,” “burning,” “throbbing,” and “aching.”

54
Q

What do the A Beta Fibers do?

A

-Large, myelinated
-Touch, pressure, and proprioception

55
Q

What occurs when peripheral tissues (skin, bone, and viscera) receive chemical, thermal, or mechanical stimuli or are traumatized by either surgery or injury?

A

-Release of chemical mediators from the inflammatory response
-Release of NTs from nociceptive nerve endings

56
Q

What is Transmission?

A

The process by which an action potential is conducted from the periphery to the CNS.
-There are multiple pathways that carry noxious stimuli to the brain. Spinothalamic tract is the most important.

57
Q

Describe how action potentials are generated.

A

Chemical mediators and neurotransmitters stimulate the peripheral nociceptors, causing an influx of sodium ions to enter the nerve fiber membranes (depolarization), and a subsequent efflux of potassium ions (repolarization). An action potential results, and a pain impulse is generated.

58
Q

Which pathway is the most important that carries noxious stimuli to the brain?

A

Spinothalamic.
-Nociceptive fibers traveling from the spinal cord to the thalamus.

59
Q

What makes up the Spinothalamic (Anterolateral) System?

A

-Carries signals from the periphery (trunk and lower extremities)
-Uses A Delta and C Fibers
-Cell bodies are located in the dorsal root ganglia of the spinal cord
-Ascend/Descend using Tract of Lissauer
-Synapse with 2nd order neurons in the gray matter of the dorsal horn (A Delta with Laminae I and V, C with Laminae II)
-2nd order neurons cross the midline, and ascend via the anterolateral pathway to the thalamus
-In the Lateral Thalamus, 2nd order neurons synapse with 3rd order neurons, which then project to the Cerebral Cortex

60
Q

Where does the Spinothalamic System carry signals from?

A

The periphery - trunk and lower extremities.

61
Q

What are the primary afferent neurons in the Spinothalamic System? Where are their cell bodies located?

A

A Delta and C Fibers
Cell bodies are located in the dorsal root ganglia of the spinal cord.

62
Q

Upon entering the spinal cord, how do the A Delta/C Fibers ascend/descend?

A

Via the Tract of Lissauer

63
Q

Where do the primary afferent neurons go after leaving the Tract of Lissauer?

A

They enter the gray matter of the dorsal horn, where they synapse with 2nd order neurons and terminate in the Rexed Laminae (I,II, and V)

64
Q

Which Laminae do the A Delta fibers synapse with? The C Fibers?

A

A Delta - Laminae I and V
C Fibers - Laminae II

65
Q

Where do the 2nd order neurons go after synapsing with the 1st order neurons?

A

-Cross the midline of the spinal cord through the anterior commissure
-Ascend in the anterolateral pathway of the spinothalamic tract to the Thalamus

66
Q

What happens when the 2nd order neurons get to the Lateral Thalamus?

A

They synapse with 3rd order neurons, which then project to the cerebral cortex.

67
Q

What is perception of pain?

A

Occurs once the signal is recognized by various areas of the brain, including the amygdala, somatosensory areas of the cortex, the hypothalamus, and the anterior cingulate cortex.

68
Q

What is Modulation of pain?

A

Modulation of pain transmission involves altering neural afferent activity along the pain pathway; it can suppress or enhance pain signals.

69
Q

How does suppression of pain occur?

A

Via local inhibitor interneurons (brainstem) and descending efferent pathways (spinal cord dorsal horn).
-Also have inhibitory receptors and NTs: Endogenous opioids (enkephalin/dynorphin), glycine, GABA, Norepi, Serotonin, Ach.

70
Q

What is the only pre-emptive treatment that improved all patient outcomes (pain intensity scores, supplemental analgesic consumption, and time to first analgesic consumption?

A

Epidural Anesthesia

71
Q

Review Slide 49

A

Yes

72
Q

What is Multimodal Anesthesia?

A

-Agents with different mechanisms of analgesia may have synergistic or additive effects
-Captures the effectiveness of individual agents at optimal dosages to maximize efficacy while minimizing side effects

73
Q

What is Preventative Analgesia?

A

To suppress central sensitization, analgesia should be maintained throughout the perioperative period.
-Formerly known as pre-emptive analgesia

74
Q

What are the preventative and multimodal analgesia medications?

A

-Opioids
-Non-opioid analgesics (NSAIDS, Acetaminophen)
-NMDA antagonists (Ketamine)
-Alpha 2 agonists (Clonidine, Dexmedetomidine)
-Local anesthetics (Infiltration, PNB, Epidural/SAB, infusion)
-Magnesium infusion
-Anticonvulsants / Membrane stabilizers (Gabapentinoids)
-Glucocorticoids

75
Q

What is an excellent resource for evidence-based guidelines in the field of pain management?

A

The procedure-specific guidelines offered via a web-based program called PROSPECT (Procedure-Specific Postoperative Pain Management).

76
Q

What is the definition of Acute Pain?

A

-Noxious stimulation from traumatic injury (chemical, thermal, or mechanical), surgery, or acute illness.
-Usually diminishes over the course of healing
-Effected by social, cultural, and personality factors
-Tx cause
-If poorly controlled, can lead to chronic pain

77
Q

What are the CV consequences of pain?

A

Increased HR/BP/myocardial work

78
Q

What are the pulmonary consequences of pain?

A

Decreased VC/TV/TLC

79
Q

What are the GI consequences of pain?

A

Decreased gastric emptying/intestinal motility

80
Q

What are the GU consequences of pain?

A

Increased urinary sphincter tone

81
Q

What are the coagulation consequences of pain?

A

Increased platelet aggregation, venostasis

82
Q

What are the immunologic consequences of pain?

A

Decreased immune function

83
Q

What are the psychologic consequences of pain?

A

Fear, anxiety, hopelessness, anger

84
Q

What are the other adverse consequences of pain?

A

-Contribute to increased patient morbidity and mortality (Poorly controlled acute pain may lead to chronic pain states)
-Prolonged hospital stay and patient recovery
-Negative impact surgical/hospital experience and reduced patient satisfaction
-Overall increased healthcare costs

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