CHAPTER 28. Perianesthesia Complications
Lois Schick
OBJECTIVES
At the conclusion of this chapter, the reader will be able to:
1. List three potential airway complications that may occur in the immediate postanesthesia period.
2. Describe the signs and symptoms associated with pulmonary edema.
3. Describe the signs, symptoms, and treatment of a patient with suspected pseudocholinesterase deficiency.
4. Identify two common causes of hypovolemia in the immediate postoperative setting.
5. Identify three risk factors that predispose a patient to postoperative nausea and vomiting (PONV).
I. PERIANESTHESIA SETTING
A. Patient complications can occur at any time
B. Critical communication
1. Safe transfer of care (Table 28-1)
a. Anesthesia provider, either an anesthesiologist or a Certified Registered Nurse Anesthetist
b. Special procedure unit reports to PACU nurse.
c. Surgery nurse conveys report to the PACU nurse.
| PACU, Post anesthesia care unit. | |||||
| Expected communications PACU nurse receives on patient admission | |||||
| COMMUNICATE | ASSESS | ||||
|---|---|---|---|---|---|
| Patient’s name and age | Airway patency | ||||
| Preoperative medical history | Breathing quality | ||||
| Anesthetic technique and duration | Cardiovascular stability | ||||
| INTRAOPERATIVE MEDICATIONS, TIMES, DOSES | DETERMINE AND MANAGE | ||||
| Sedatives, narcotics, relaxants | Consciousness | ||||
| Reversal medications | Pain | ||||
| Antibiotics, steroids, adjunctives | Muscle strength | ||||
| Fluid balance | Wounds and drains | ||||
| Critical procedural events | |||||
2. Written or computerized record
a. Convey patient’s stable progressive transition from sedation to wakefulness.
b. Inform all caregivers of:
(1) Events
(2) Complications
(3) Consultations
(4) Interventions
c. Complete, accurate, legible
C. PACU nurses
1. Assess continually the patient’s status.
2. Identify potential complications.
3. Treat untoward reactions.
II. CRITICAL POSTANESTHESIA ASSESSMENTS
A. Assessment priorities
1. Simultaneous overview of organ systems and responses during admission
a. Respiratory effort, oxygen saturation: artificial airway, intubated
b. Cardiac rate, rhythm, and vital signs: hypotensive, hypertensive, abnormal rhythm
c. Awareness, level of consciousness, and ability to move: arousable
d. Pain severity and anxiety: agitated or calm, implement pain scale
e. Residual effect of local anesthetic blocks, regional anesthetics
(1) Motor and sensory dermatome levels after spinal or epidural block
(2) Regional block renders extremity numb and difficult to control.
(a) Block effect provides wonderful pain management.
(b) Safety concern: protect from flailing, floppy extremity.
f. Thermoregulation: temperature and comfort
2. Determine need for 1:1 nursing care according to American Society of PeriAnesthesia Nurses (ASPAN) standards.
3. Repeat assessment at regular intervals according to standards and policies.
B. Surgery-specific observations
1. Integrity of dressings or visible suture lines, any drainage
2. Position, patency, and function of every monitoring line and wound drain
3. Abdominal girth, distention, nausea
4. Neurological and neurovascular status
a. Consciousness, respiratory effort, pupil size and equality, seizures, posturing, and movement after intracranial surgeries
(1) Stimulus required to elicit response
(a) Spontaneous?
(b) Touch or voice?
(c) Sternal rub?
(2) Degree and quality of response
(3) Improvement or decline during PACU observation
b. Capillary refill, sensation, motion, strength after spinal, orthopedic, peripheral vascular procedures
(1) Pulses, color, motion, sensation, temperature
(a) Shoulders to fingertips
(b) Hips to toes
(2) Doppler assessment if circulation or pulse quality questionable
(a) Cool or vasoconstricted extremity
(b) May be normally diminished if peripheral vascular disease
(3) Is any deficit new or present preprocedure worse or improved?
c. Impairment related to surgical position or events
(1) Vision impairment reported after hypotensive episodes
(2) Skin damage at pressure points: redness, blisters, breaks
(3) Peroneal nerve compression after legs in stirrups
(a) Numbness or tingling after urological, gynecological procedures
(4) Ulnar nerve stretch while areas extended and muscle relaxed
(a) Numbness
(b) Tingling
(c) Weakness
d. Impairment related to procedure
(1) Circulation distal to line site with:
(a) Intravenous (IV) infiltration
(b) Medication extravasation
(c) Arterial monitoring lines
(2) Edema or bleeding in surgical extremity can impair circulation.
(3) Tight casts, splints, and wraps can restrict venous return.
(4) Compartment syndrome
(a) Increased pressure in extremity’s fascial compartments
(b) Perfusion impaired: muscle and nerve ischemia result.
(c) Prompt pressure released lest tissue necrosis result.
(i) Surgical fasciotomy
(ii) Remove or split cast.
(iii) Monitor for hyperkalemia after muscle destroyed.
(d) Report immediately:
(i) Extreme pain unrelieved by narcotics
(ii) Paresthesia or paralysis
(iii) Pallor
(iv) Pulselessness of limb
5. Genitourinary status
a. Bladder distention: urge to void? Verify time of last void.
b. Catheter patency, urine color, clarity, volume, clots
c. Titrate flow of bladder irrigation systems.
d. Bladder ultrasound to assess bladder volumes
e. Determine necessity of urination before discharge.
(1) Consider increasing IV fluid rate to promote bladder volume.
(2) Instruct to strain urine for particles after lithotripsy.
6. Obtain, report, and review necessary x-rays, laboratory assessments.
a. Chest x-ray to verify placement of new central lines, endotracheal (ET) tube
b. Spinal or extremity x-rays per surgeon orders
c. Arterial blood gases if patient intubated and mechanically ventilated
d. Serum glucose in diabetics
e. Hemoglobin if significant blood loss during procedure
f. Electrolytes if extended surgery with multiple transfusions, extensive muscle destruction
C. Clearly document all assessments and events according to facility style and policy.
1. Observed deficits, physician consultations, orders
2. Outcomes of interventions
3. Times of each assessment, intervention
a. Increase frequency of assessments when deficit or compromise.
b. Every change in clinical status, improvement or decline
c. Airway removal, monitoring line insertion, laboratory and x-ray results
III. AIRWAY INTEGRITY (Box 28-1)
A. Complications heralded by:
1. Hypoxia: oxygen desaturation, decreasing partial pressure of oxygen (Pa o 2)—insufficient delivery
a. Arterial oxygen saturation (Sa o2) of 90% corresponds with partial pressure of oxygen in arterial blood (Pa o2) of 60 mm Hg.
b. Monitored oxyhemoglobin saturation <90%
c. Reduced respiratory rate, depth, effort
d. Oversedation: limited consciousness reduces stimulus to breathe.
e. Restlessness: still anesthetized patient may actually be disoriented, “air hunger.”
(1) May indicate return of narcotic or muscle relaxant effect
(2) Always ensure adequate oxygenation and ventilation before sedating.
(3) Only provide judicious, sparing analgesia until patient alert.
f. Cardiovascular status varies: hypertension to hypotension, dysrhythmias.
g. “High” spinal blockade
2. Hypercarbia: respiratory acidosis, increasing partial pressure of carbon dioxide (Pa co 2)
3. Factors that may increase airway risk
a. Anatomy: limit chest expansion, diaphragm, respiratory muscle movement.
(1) Obesity or pregnancy
(2) Neck: large and/or short neck
(3) Receding chin, “no” jaw
(4) Upper abdominal surgery
(5) History of obstructive sleep apnea
b. Poor muscle tone
(1) Medication effects
(a) Narcotics
(b) Muscle relaxants
(2) Neuromuscular diseases
(a) Myasthenia gravis
(b) Quadriplegia
c. Facial, throat swelling
(1) Anaphylaxis
(2) Surgical manipulation
(3) Edema
B. Obstruction: interrupted patency—an emergency in any PACU
1. Common when patient very sedated: airway reflexes blunted
a. Soft tissue obstruction: oropharynx blocked to air entry
(1) Slippage of tongue
(2) Foreign body (i.e., loose teeth)
b. Partial airway obstruction: snoring signals
(1) Reposition or elevate head.
(2) Turn patient to side-lying position.
(3) Jaw support
(4) Insert oral or nasal airway.
c. Total obstruction: rocking, asynchronous chest movements indicates:
(1) No chest expansion, no air entry audible with auscultation
(2) Flaring nostrils, tracheal tug, abdominal, accessory muscles
(3) Muscle relaxation or reintubation if jaw support ineffective
2. Risk
a. Hypoventilation or even apnea
b. Vomiting and aspiration
(1) Peptic ulcer
(2) Hiatal hernia
(3) Obesity
3. Nursing responsibility
a. Never leave the bedside of the sedated, inadequately breathing patient.
b. Be prepared.
(1) Sudden, silent vomiting
(2) Airway obstruction
(3) Apnea
(4) Wild disorientation
c. Ask a colleague to contact help or obtain supplies, medications.
d. Open airway.
(1) Turn patient to side.
(2) Mandibular extension or jaw thrust
(3) Insert artificial nasal or oral airway.
(4) Backward tilt of head
(5) Towel roll under shoulders
C. Laryngospasm and airway edema
1. Spasm of laryngeal muscles with partial or complete closure
a. Stridor: high-pitched, crowing respirations indicates partial obstruction.
b. Absent breath sounds indicates total obstruction.
2. Airway spasm precipitated by irritants or allergy
a. Blood, vomitus, mucus on vocal cord
(1) Suction well before extubation.
(2) Reduce stimulation of extubation.
(a) Remove ET tube or laryngeal mask airway (LMA) while deeply anesthetized.
(b) Wait until fully awake.
b. Smoking
c. Chronic obstructive pulmonary disease (COPD)
d. Airway irritability
e. History of asthma (bronchospasm)
f. Airway trauma
(1) Procedure: long or difficult intubation or LMA
(2) Never remove LMA while patient deeply sedated, unresponsive.
(3) Premature extubation or LMA removal predisposes patient to:
(a) Airway spasm plus aspiration
(b) Coughing
(c) Retching
(d) Obstruction
(4) Procedures
(a) Frequent suctioning
(b) Laryngoscopy
(c) Difficult intubation
g. Postintubation croup common among children
h. Coughing, upper respiratory infection
3. May be able to speak, indicating partial closure
a. Auscultate lungs for wheezes, air entry; monitor oximetry.
b. Constant nurse presence and assessment
c. Coach calmness, slow breathing; perhaps hyperextend head.
(1) Elevate head; provide humidified oxygen.
(2) Racemic epinephrine inhalations reduce swelling.
(3) Lidocaine to reduce irritability
(4) Decadron to reduce inflammation
(5) Edema symptoms may recur: observe several hours later.
d. Consult anesthesia provider, immediately if total obstruction.
(1) Provide 100% oxygen by positive pressure ventilation.
(2) Low (subparalytic) dose of succinylcholine to relax laryngeal muscles, then reintubate per anesthesia provider.
(3) Corticosteroids and/or lidocaine may be ordered to reduce airway irritation and swelling.
D. Bronchospasm
1. Event
a. Constriction of bronchial smooth muscle
b. Closure of small pulmonary airways
(1) Edema
(2) Increased secretions
c. Reaction caused by stimulating airway irritants
(1) Allergic response: airway and vascular response
(a) Occurs within 3 minutes after IV injection
(b) Sensitivity to:
(i) Medications
(ii) Chemicals
(iii) Latex
(2) Aspiration
(3) Intubation or endotracheal suctioning
d. Response more likely if preexisting COPD, asthma
2. Symptoms
a. Wheezing, often shallow, “noisy” respiration
b. Decreased oxygen saturation
c. Dyspnea
d. Intercostal retractions
e. Increased respiratory rate
3. Intervention
a. Increase oxygen delivery; consider humidified source.
b. Remove the irritant.
c. Therapy with inhaled aerosol of bronchodilator like albuterol or patient’s personal inhaler
d. Relax airway passages in severe responses.
(1) Muscle relaxants
(2) Lidocaine
(3) Epinephrine
(4) Hydrocortisone
E. Pulmonary edema: pink frothy sputum, dyspnea, wheezing, rales, hypoxia
1. Fluid accumulation in the alveoli causes:
a. Increase in hydrostatic pressure
(1) Fluid overload
(2) Left ventricular failure
(3) Mitral valve dysfunction
(4) Ischemic heart disease
b. Decrease in interstitial pressure
(1) Prolonged airway obstruction
c. Increase in capillary permeability
(1) Sepsis
(2) Aspiration
(3) Transfusion reaction
(4) Trauma
(5) Anaphylaxis
(6) Shock
(7) Disseminated intravascular coagulation
2. Noncardiac origin: sudden onset in young, healthy patients
a. Etiology: upper airway obstruction, rapid naloxone injection
(1) A strong patient’s effort to breathe against closed glottis
(2) Negative pressure increases within chest cavity.
(3) Sharp increase in hydrostatic pressure pulls water to lungs.
b. Symptoms
(1) Decreased lung compliance
(2) Chest x-ray findings
(a) Normal heart size
(b) No congestive heart failure
3. Cardiac origins: maximized cardiac compliance
a. Etiology
(1) Fluid overload
(2) Ischemic heart disease, cardiomyopathy
(3) Ventricular failure and/or cardiac valve dysfunction
(4) Increase in pulmonary capillary permeability
(a) Sepsis
(b) Critical multisystem illness
(c) Debilitation: cancer, liver failure
(5) Anaphylaxis or transfusion reaction
b. Symptoms
(1) Tachycardia
(2) Dyspnea
(3) Tachypnea
(4) Confusion
(5) Wheezing
(a) Rales
(b) Crackles
(6) Decreased blood pressure
(7) Paroxysmal nocturnal dyspnea
4. Intervention: treat cause.
a. Evaluate chest x-ray: pulmonary infiltrates
(1) Reintubation
(2) Mechanical ventilation to maintain oxygen
b. Morphine relaxes patient and pulmonary vasculature.
c. Diuretics if cardiac origin—not deemed useful if noncardiac
d. Monitor hemodynamics.
e. Reduce hypoxemia.
f. Upright sitting position
g. Oxygen administration
F. Pulmonary embolus: blood flow obstruction in pulmonary vessels
1. Likely causative factors in perianesthesia period
a. Thrombus as a result of perioperative venous stasis and immobility
b. Fat embolism after pelvic or long-bone fracture and/or surgery
c. Hypercoagulability conditions, dehydration, or damaged vessels
2. Symptoms and assessment
a. Acute onset of pleuritic chest pain
b. Tachypnea
c. Tachycardia
d. Agitation
e. Apprehension
f. Hemoptysis
g. Hypoxia
h. Hypotension likely
3. Intervention
a. Correct hypoxia, cardiovascular instability.
b. Prompt anticoagulation, initially with heparin
c. Prophylactic prevention
(1) Elastic hose
(2) Sequential compression sleeves/devices
(a) Foot
(b) Calf
G. Aspiration pneumonitis: prevention most prudent therapy
1. Always a potential, albeit rare complication among the sedated or anesthetized
2. Inhalation of gastric contents as a result of:
a. Full stomach: residual gastric volume, especially if particulate
b. Acidic gastric contents
c. Inability to protect airway: inhibited airway reflexes
d. Obesity
e. Pregnancy
f. Hiatal hernia
g. Diabetic: gastroparesis
h. Upper abdominal surgery. Laryngeal mask airway (LMA)
(1) Aspiration: an underreported complication
(2) If malpositioned, coughing, straining on LMA, risk is increased.
(3) Potential greater when placed by the inexperienced provider
i. Trauma patients
3. Inhalation of blood or foreign body
a. Loose teeth
b. Trauma during oropharyngeal manipulation or surgery
4. Assessment
a. Coughing, wheezing, hypoxia, hypercarbia, tachypnea
b. Bronchospasm or atelectasis, particularly if foreign body
c. Heart rate changes, dysrhythmias, hypotension
5. Interventions
a. Prevent by reducing risk.
(1) Ensure nothing by mouth (NPO) status of recommended duration.
(2) Side-lying position for sedated or obtunded patients
(3) Rapid sequence induction for at-risk patients
b. Chest x-ray to document infiltrates
c. Ensure airway patency; turn sedated patient to side.
d. Provide humidified oxygen; intubate if necessary.
e. Constant observation: never step away from bedside.
f. Count minute respiratory rate; observe depth.
g. Stimulate patient toward consciousness, deep breathing.
h. Frequently assess vital signs and act to maintain stability.
i. Continuously monitor oxygen saturation, even after PACU discharge.
j. Bronchoscopy if foreign body, large particles
k. Steroids controversial; antibiotic use only if indicated
l. Histamine antagonists
(1) Antacids
(2) Antiemetic therapy
(3) H 2 receptor blockers
(a) Cimetidine
(b) Ranitidine
(c) Famotidine
H. Hypoventilation: ineffective respiratory effort
1. Results in:
a. Decreased oxygen saturation (P o 2), which may be first sign
b. Subdued respiratory rate, depth, effort
c. Obliterated airway protective gag and cough reflexes
d. Increased risk of pulmonary aspiration
e. Decreased level of consciousness: minimal responsiveness
f. Hypercarbia: increasing P co 2
(1) Compounds unresponsiveness
(2) Respiratory acidosis; if unresolved:
(a) Less responsiveness
(b) Cardiac dysrhythmia
(c) Unstable blood pressure
2. Contributing origins
a. Associated conditions
(1) Obesity
(2) Pregnancy
(3) Lengthy or upper abdominal surgeries/procedures
(4) Prolonged exposure to:
(a) Muscle relaxants
(b) Narcotic doses
b. Hemoglobin loss
(1) Reduces hemoglobin available to transport oxygen
(2) Consider low hemoglobin.
(a) Patient pale
(b) Oxygen saturation low
(c) Tachycardia
c. Renarcotization: residual narcotic or sedative effect
(1) Recurrence of extreme somnolence, poor ventilation
(2) Caused by gradual migration of narcotics and sedatives from tissues back into bloodstream
(3) Consider titrating a narcotic or benzodiazepine antagonist.
(a) Dramatically reverses narcotic effect
(b) Expect quick wakefulness, pain, agitation, tachycardia.
(c) Extend observation period at least 30 minutes.
(d) Opioid half-life is longer than single dose of antagonist.
d. Reparalysis or recurarization: protracted muscle weakness
(1) Neuromuscular blockade recreated
(2) Residual nondepolarizing muscle relaxants in tissue “outlive” effects of anticholinesterase (reversal) medications.
(3) Migrate into bloodstream and recreate weakness
(4) Muscles uncoordinated, weak, “floppy”
(5) Respirations shallow, gaspy; chest expansion minimal
(6) Awake patients panicked, anxious, restless
(7) Often pain despite weakness: no analgesia in muscle relaxants
(8) May need additional reversal doses, respiratory support, even temporary intubation
e. Pseudocholinesterase deficiency: genetic absence or lack
(1) Insufficient amount of the intrinsic enzyme needed to hydrolyze succinylcholine, the depolarizing muscle relaxant
(a) Normally breaks down within 3 to 5 minutes
(b) Affects 1 in 2500 to 1 in 2800 individuals
(c) Patient may be unaware of genetic predisposition until after receiving succinylcholine.
(2) Prolonged duration of succinylcholine effect in patients with abnormal or low levels of plasma cholinesterase
(a) Liver disease
(b) Malnutrition
(c) Severe anemia
(d) Pregnancy
(e) End-stage renal disease
(f) Acidosis
(3) Irreversible muscle weakness (“floppy”) and apnea
(4) Requires mechanical ventilation to support respiration
(a) Necessary until muscle strength gradually returns
(b) Psychological support, information, sedation
(5) Constant vigilance: patient alert, fearful, feels pain
(6) Educate patient and family to reveal before next anesthetic.
(7) Physician may recommend laboratory measure of dibucaine levels.
f. Pneumothorax: air entry into pleural space
(1) Acute chest pain, dyspnea, reduced or absent breath sounds in affected area from deflation of lung, lobe, or pleural bleb
(2) Caused by:
(a) Alveolar rupture from mechanical ventilation
(b) Surgical chest procedures that invade pleura
(c) Central line placement
(d) Complication of nerve blocks
(i) Interscalene
(ii) Intercostals
(iii) Brachial plexus
(3) Tension pneumothorax: after air entry into chest, intrapleural pressure increases and lung deflates; heart and great vessels pulled toward the intact lung.
(a) Hypoxia and inability to ventilate
(b) Decreased venous return
(c) Hypotension
(d) Tachycardia
(4) Monitor oxygenation.
(5) Elevate head of bed.
(6) Serial chest x-rays
(a) If <20% deflation, observe.
(b) If >20% or patient symptomatic, insert chest tube.
3. Care of intubated, perhaps ventilated patient
a. Verify effective placement of ET tube.
(1) Auscultate breath sounds.
(a) Bilateral air entry all lobes
(b) Clear sounds without rhonchi
(c) Chest x-ray as indicated
(2) Continuous monitoring of oxygen saturation with pulse oximetry
(3) Sample arterial blood gases.
(a) Basis to assess adequacy of ventilator settings
(b) Determine acidosis.
b. Periodically suction via ET tube to clear secretions using sterile technique.
c. Sedate, relax to minimize stress of awareness while intubated.
(1) Propofol infusion: sedation, quick consciousness within minutes
(2) Precedex infusion: short-term sedation without respiratory depression. Use sanctioned for up to 24 hours only
(3) Paralytics: muscle relaxants used to prevent activity, gagging on ET tube
(4) Narcotics, analgesics must be given.
(a) Sedatives, muscle relaxants offer no pain reduction.
(b) Torture for patient to be responsive with light sedative but in pain and unable to indicate by movement or communication
d. Be aware of sedation goals.
(1) Deep sedation if intubated for days
(2) Light sedation allows for regular, brief wake-up intervals to assess neurological status.
e. Stir up regimen
(1) Every 10 to 15 minutes
(a) Deep breathe.
(b) Cough.
(c) Move extremities.
(d) Turn from side to side.
f. Extubation criteria
(1) Return of muscle strength after muscle relaxants
(a) Equal hand grasps
(b) Able to initiate head lift from bed and sustain at least 5 seconds
(2) Respiratory parameters
(a) Tidal volume at least 5 mL/kg
(b) Vital capacity at least 15 to 20 mL/kg
(c) Negative inspiratory force of 20 to 25 cm water pressure
(3) Patient should respond appropriately to questions.
(a) “Yes” or “no” head movements
(b) Other forms of communication
(i) Sign or picture board
(ii) Writing
(c) Protrude the tongue.
(d) Open eyes widely.
(4) Swallow and cough reflexes present.
(5) Regular respiratory pattern >10 breaths per minute
(6) After extubation, close observation for hypoventilation
(a) Presence of ET tube may have stimulated patient to remain awake and breathing adequately.
BOX 28-1
RESPIRATORY ASSESSMENT
Assessments and Perianesthesia Nurse Competencies Related to Respiratory Evaluation
Critical Nursing Behaviors
Never leaves patient unattended
Lists signs and symptoms of respiratory depression
Stimulates wakefulness, movement, and deep breathing
Assesses ventilation
▪ Monitors oxygen saturation
▪ Auscultates lungs and observes chest movement
▪ Provides supplemental oxygen as appropriate
Positions patient for effective respiratory effort and chest expansion
▪ Slight head and chest elevation, particularly if patient is obese
▪ Ensures adequate blood pressure and patent airway
Plans interventions for airway obstruction
▪ Demonstrates mandibular lift (jaw support) for airway patency
▪ Suctions airway with proper technique before extubation and as needed
▪ Inserts oral or nasal airway when appropriate
▪ States indications for endotracheal reintubation
▪ Secures endotracheal tube and demonstrates use of bag-valve-mask device
▪ Describes criteria for extubation readiness
Describes physiology and interventions for renarcotization, recurarization, pseudocholinesterase deficiency, and pulmonary edema
▪ Monitors and provides oxygen
▪ Obtains and prepares appropriate medications and emergency equipment
▪ Remains within sight near the patient’s head
▪ Uses touch and soft, reassuring words
Prepares equipment for positive pressure airway support or mechanical ventilation
Consults anesthesiologist and communicates airway status
Documents events and interventions
IV. CARDIOVASCULAR STABILITY (Box 28-2)
A. Hypotension: consider an array of possible causes to plan interventions.
1. Evidence: clinical signs of hypoperfusion
a. Measured blood pressure 20% to 30% below baseline
b. Mean arterial pressure (MAP) <65 mm Hg
c. Initially, compensates with peripheral vasoconstriction unless sepsis
(1) Pale, cool, clammy skin (“cold” shock)
(2) Warm extremities and hypotension suggest sepsis (“warm” shock).
(3) Tachycardia: may precede blood pressure decrease
d. Perfusion deficits as cardiac output continues to fall: act quickly to restore.
(1) Nausea, sometimes vomiting
(2) Dizziness
(3) Confusion or even loss of consciousness if extreme
(4) Chest pain, dysrhythmias if susceptible or preexisting cardiac disease
(5) Oliguria and metabolic acidosis if hypotension uncorrected
e. Consider causes.
(1) Hypoxia
(2) Hypoglycemia
(3) Electrolyte imbalances alter contractile strength of cardiac muscle.
(a) Hypomagnesemia
(b) Hypocalcemia
(c) Acidosis exacerbates electrolyte disturbance (Table 28-2).
| ABG, Arterial blood gas; NaHCO3, sodium bicarbonate. | ||||||||
| *Total Carbon Dioxide (CO 2) = Bicarbonate (HCO 3−) +Dissolved CO 2+ Carbonic Acid (H 2CO 3). Total CO 2 should nearly equal HCO 3−. |
||||||||
| †Anion gap is a guide to acidosis severity. It is calculated by subtracting primary anions from primary cations: (Na +) – (Cl − + HCO 3−). |
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| Quickly intervene when hypotension and hypoxia occur in critically ill patients; inadequately treated hypoperfusion and hypoxia contribute to worsening metabolic acidosis. | ||||||||
| Normal Values | Severe Acidosis | |||||||
|---|---|---|---|---|---|---|---|---|
| pH | 7.35-7.45 | <7.20 | ||||||
| HCO 3 | 22-26 mEq/L (ABG) | <22 mEq/L | ||||||
| Total CO 2 | 24-32 mEq/L (chemistry panel) * | |||||||
| Anion gap | 8-12 mEq/L† | >13 mEq/L as HCO 3− ions are depleted when used to buffer acids | ||||||
| Acidotic Conditions | Clinical Signs | Interventions | ||||||
|
Lactic acidosis
Ketoacidosis
Diabetic
Uremic
Starvation
Aspirin intoxication
|
Hyperkalemia
Cardiac contractility decreases
Pulmonary resistance increases (edema)
Poor catecholamine response
Ventricular fibrillation more likely
Hyperventilation
Decreased muscle energy
Weakens respiratory strength
|
Correct cause
Perfusion
Oxygenation
Monitor ABG
Titrate NaHCO 3
Controversial in therapy; few studies report improved outcomes, though usually ordered
|
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f. Consider allergic response: accompanied by angioedema, urticaria.
g. Prompt, aggressive fluid resuscitation: multiple methods to calculate need
(1) Improve cardiac output and therefore contractility first.
(2) Calculate overall fluid replacement by “3 in 1” rule (Table 28-3).
(a) Replace 300 mL isotonic fluid rapidly for every 100 mL shed blood.
| BP, Blood pressure. | |||||||
| *Fluid replacement examples. |
|||||||
| †Calculation: Diastolic BP + ⅓(systolic BP − diastolic BP). |
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| Guide to approximate fluid replacement requirements | |||||||
| Goal | Action | Outcome | |||||
|---|---|---|---|---|---|---|---|
| Increase preload | Volume replacement: Rapidly! | First priority | |||||
| Also increases contractile force | Rate guide: 300 mL for each 100 mL of fluid loss* |
Mean arterial pressure >65 mm Hg†
Lower heart rate
|
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| Restore hemoglobin | Laboratory measure if persistent hypotension | ||||||
| Clinical shock if 20% loss of circulating volume* |
Transfuse according to physician orders.
Review patient history and clinical status.
Increase oxygen-carrying capacity.
|
Improve O 2 delivery.
Less hypoxia
Less acidosis
pH toward 7.4
|
|||||
| Initiate vasopressors. | Only after fluid volume replaced! | ||||||
| Deliver oxygen | Find most effective method. | Raise oxygen saturation. | |||||
| If | Then Replace | ||||||
|
1. Blood loss ~800 mL
Heart rate <100 beats/min
BP normal
|
Up to 2400 mL
Isotonic crystalloid
|
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|
2. Blood loss ~1500 mL
Heart rate >100 beats/min
BP normal
|
About 4500 mL
Isotonic crystalloid
|
||||||
|
3. Blood loss >2000 mL
Heart rate >140 beats/min
Hypotensive
Tachypneic, oliguric
|
About 6000 mL
Crystalloid + transfuse
|
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(3) Infusion of 500 mL saline bolus; then assess, repeat.
(4) Vasopressin infusion may augment response to vasopressor medications; improves survival outcomes in critically ill.
2. Colloid versus crystalloid controversy
a. No studies clearly indicate improved outcomes with either therapy.
b. To restore circulating volume and improve blood pressure, most perianesthesia patients need only boluses of isotonic fluid.
c. Measure hemoglobin: does patient need blood transfusion?
d. Critically or chronically ill may respond to colloid to increase osmotic effect in vascular system (extracellular fluid).
(1) Albumin
(2) Hetastarch
(3) Needed blood components
3. Often transient, mild, but must plan response to profound low blood pressure
a. Orthostatic (postural) hypotension
(1) In ambulatory surgery or procedural areas, may not be evident until patient sits or stands
(2) Peripheral vessels incompetent: remain vasodilated from effect of anesthetic medications
(3) Monitor blood pressure as patient changes position, walks.
b. Continued effect of spinal or epidural (regional) anesthetic
(1) Remaining vasodilation from sympathetic block
(a) Increases relative size of vascular compartment
(b) Peripheral pooling of blood
(2) Most likely after high residual motor and sensory block
(a) Respiratory compromise above level T4
(b) Symptoms persist until blockade recedes.
(i) Hypotension
(ii) Heat loss
(3) Nursing intervention: remain at stretcher side.
(a) Generous fluid volumes to fill expanded vascular space
(b) Reclining, foot-elevated position
(c) Consult anesthesia provider.
(d) Explain situation.
(e) Support emotionally.
(f) Observe constantly.
(4) Give vasopressors.
(a) Epinephrine
(b) Neosynephrine
(5) Monitor oxygen saturations; observe respiratory quality.
(a) Recognize hypoventilation.
(b) Intubate, mechanically ventilate if hypoventilation persists.
c. Hypothermia: rewarm slowly, cautiously.
(1) Initially, vasoconstrictive responses caused by cold temperature
(a) Masks inadequate circulating fluid volumes
(2) Peripheral vessels dilate as temperature normalizes.
(a) Relative vascular space increases.
(b) Blood pressure plummets.
d. Sepsis
(1) Consider rewarming if hypotension does not resolve after fluid.
(2) More likely after:
(a) Urological procedure
(b) Preexisting infection
(c) Intra-abdominal leaks
(d) Gastrointestinal necrosis
(e) Trauma
(3) Massive peripheral vasodilation
(a) Low vascular resistance
(b) Maintains large vascular space
(4) Provide copious fluid volumes, antibiotics, vasopressors.
(5) Act quickly to normalize blood pressure, electrolytes.
(6) Close, even 1:1 observation in PACU, then consider intensive care unit admission
e. Cardiogenic causes
(1) New-onset periprocedural myocardial infarction
(2) Cardiac tamponade
(3) Embolism
(4) Inability to respond with tachycardia, vasoconstriction
(a) Medication effects: negative inotropics and chronotropics
4. Hypovolemia: intravascular volume deficit
a. Most common cause of hypotension, particularly in perianesthesia areas
(1) Procedure-related bleeding
(2) Insufficient replacement of fluid volume, considering:
(a) Intraoperative blood loss
(b) NPO duration
(c) Insensible losses
b. Assessment indicators
(1) Hypotension: always ask, “Is patient hypovolemic?”
(2) Compensatory tachycardia
(3) Significant bleeding: check
(a) Wound drains
(b) On or under dressings, splints, casts
(c) Increasing abdominal girth after abdominal procedures
(d) Hematuria or blood in emesis
(e) Vascular integrity after orthopedic surgery
(4) Cumulative losses from sampling for laboratory measures
(5) Coagulopathy
(a) Preprocedural condition
(b) Aspirin, anticoagulants, and herbals not stopped preoperatively
(c) After multiple transfusions
(d) May require treatment with:
(i) Vitamin K
(ii) Platelets
(iii) Cryoprecipitate
(iv) Fresh frozen plasma
(v) Desmopressin (DDAVP)
(vi) Amicar
c. Intervention: treat underlying cause.
(1) Assess fluid volume status in all perianesthesia phases.
(a) Transfuse with packed red cells if hemoglobin <7 to 9 g/dL.
(b) Individual patient with cardiac disease may need transfusion at higher hemoglobin level.
(c) Autologous: predonated by patient
(d) Donated to patient by another of same blood type
(e) Banked blood: donated by unknown
(2) Always provide oxygen if patient hypotensive and/or bleeding.
(3) Fluid, blood product replacement according to calculated need
(4) Early treatment of acidosis particularly if large blood loss
(5) Return to operating room for reexploration of surgical site.
(6) Elevate legs to increase venous return (preload).
B. Hypertension
1. At least 20% increase above baseline or greater than 140/90 mm Hg can cause:
a. Surgical bleeding
b. Cardiac ischemia or failure
2. Causes in perianesthesia units
a. Preexisting high blood pressure: most common postprocedural cause
(1) Encourage patient to take antihypertensive medications before procedure.
b. Inadequately treated pain, anxiety, or delirium
c. Full, distended bladder
d. After vascular surgeries: carotid endarterectomy, cardiac surgery
e. Fluid overload
f. Preeclampsia among pregnant patients
g. Hypothermia and shivering
3. Treat by alleviating cause.
a. Antihypertensives
(1) Beta-blockers
(a) Peripheral vasodilation
(b) Heart rate reduction
(2) Nitroprusside
(a) Peripheral vasodilation
(b) Reduces afterload
(3) Hydralazine: relaxes arterioles
b. Diuresis, bladder emptying
c. Rewarming: promotes vasodilation
d. Manage pain, anxiety.
4. Autonomic dysreflexia: sudden, dramatic blood pressure elevations
a. Unimpeded discharge of sympathetic neurons
b. Paraplegic or quadriplegic patients
c. Prompted by stimulation
(1) “Oscopy” procedures
(2) Surgical manipulation
(3) Full bladder: verify catheter patency.
(4) Distended colon
(5) Increased muscle spasm
d. Symptoms
(1) Severe, vessel-rupturing hypertension to 250/150 mm Hg
(a) Seizures or stroke
(b) Cardiac arrest
(c) Surgical bleeding
(2) Above level of spinal cord injury
(a) Profuse sweating, flushed skin
(b) Throbbing headache
(3) Below spinal cord injury level
(a) Pale skin
(b) Gooseflesh
e. Quick interventions
(1) Empty bladder.
(a) Void or catheterize.
(b) Straighten tubing kinks.
(2) Treat pain.
(a) Markedly relaxes patient
(b) Dilates peripheral vasculature
(3) Vasodilating medications: nitroprusside, labetalol
(4) Elevate head of bed.
C. Cardiac dysrhythmias (see Chapter 32)
1. Sinus bradycardia: common, usually benign
a. Heart rate less than 60 beats/min
(1) Especially among young, healthy athletes
(2) Sleepy, understimulated patients
(3) Expected response when using beta-blocking medications
(4) Response to anesthetic medications: sinus and junctional
b. No treatment unless:
(1) Dangerously low blood pressure
(2) Progressive heart block
(a) New or chronic cardiac disease
(b) Atropine increases sinus firing and atrioventricular conduction.
(c) Pacemaker for persistent, symptomatic blocks
c. Vagal nerve stimulation: profound bradycardia, even asystole
(1) Normally sustains heart rate balance; opposes acceleration tendencies
(2) Undeterred stimulation as a result of:
(a) Valsalva: straining at stool or urination
(b) Vomiting and retching
(3) Likely results in:
(a) Nausea
(b) Profound hypotension
(c) Dizziness
(d) Lethargy
(e) Unconsciousness
(4) Intervene with:
(a) Recumbent flat position
(b) Close monitoring of vital signs, cardiac rhythm, alertness
(c) Medications as indicated per anesthesia provider or protocols
(d) Defer transfer from PACU.
(i) May occur when moving about in phase II; consider return to phase I care.
2. Atrial fibrillation or flutter
a. Often a chronic condition, especially among elderly surgical patients
b. Report to physician.
(1) New onset could reflect:
(a) Fluid overload in cardiac-sensitive patient
(b) Perianesthesia cardiac concern
(2) Rapid, uncontrolled ventricular response
(3) Physical decompensation
(a) Associated with significant hypotension or hypertension
(b) Chest pain
(c) Respiratory changes: dyspnea, pulmonary congestion
3. Premature ventricular contractions may:
a. Be benign, normally occurring
b. Reflect hypokalemia, acidosis, hypercapnia: assess labs
c. Indicate hypoxia: supplement oxygen, stimulate groggy patient
d. Suggest cardiac ischemia
4. Supraventricular tachycardia: common, usually self-limiting
a. Heart rate 100 to 140 beats/min often a normal compensatory response to:
(1) Surgical stress response
(2) Pain and/or anxiety
(3) Bladder distention
(4) Hypovolemia or low hemoglobin (anemia)
(5) Fever
(6) Reflexive response to medications
(a) Muscle relaxant reversal: glycopyrrolate
(b) Vasoactive medications: nitroprusside, dopamine
b. Malignant hyperthermia
(1) Unexplained, ultrarapid tachycardia
(2) Every PACU staff must be prepared with a protocol, supplies, personnel education to respond promptly to this anesthesia crisis.
D. Chest pain: presume cardiac cause until excluded!
1. At-risk patients
a. Preexisting cardiac disease
b. Obesity
c. Diabetes
d. Debilitation
2. Assess subjective description.
a. Pleural versus angina
b. Sharp versus pressure
c. Location
(1) Jaw
(2) Chest
(3) Left arm
(4) Radiation to neck
(5) Back
(6) Indigestion
d. Notice accompanying diaphoresis, nausea, dyspnea.
e. Associated cardiac arrhythmias or blood pressure instability
3. Differentiate
a. Gas, especially after laparoscopy, colon surgery
b. Referred surgical pain
c. Pleural causes: pneumothorax, pleural effusion, pneumonia
d. Gastrointestinal (GI) causes
(1) Reflux esophagitis
(2) Ulcer, pancreatitis
4. Interventions
a. Monitor rate and rhythm.
(1) Obtain 12-lead electrocardiogram (ECG).
(2) Compare with preoperative ECG.
b. Decrease myocardial work and manage complications.
(1) Relieve pain and consider morphine for vasodilating benefits.
(2) Antianginal (nitroglycerin)
(3) Dysrhythmia treatment
(4) Blood pressure therapies
(5) Adequate oxygenation
(6) Hydration
c. Laboratory tests
(1) Serial troponins
(2) Cardiac enzymes
d. Peripheral vascular integrity
e. Reposition patient
f. Offer antacids, which may relieve noncardiac pain
BOX 28-2
CARDIOVASCULAR ASSESSMENT
Assessments and Perianesthesia Nurse Competencies Related to Cardiovascular Evaluation
Critical Nursing Behaviors
Assesses cardiac and breath sounds and documents peripheral pulses
Discusses causes, physiological responses, and interventions for hypotension
▪ Increases frequency of blood pressure monitoring
▪ Identifies factors that alter vasoconstrictive reflexes and heart rate
▪ Infuses a small bolus (up to 250 mL) of crystalloid
▪ Observes for significant or ongoing blood loss
▪ Consults with anesthesiologist and surgeon
Describes causes, physiological responses, and interventions for hypertension
▪ Increases frequency of blood pressure monitoring
▪ Identifies patients at risk and procedural or anesthesia-related causes
▪ States actions and effects of pharmacological interventions (nifedipine, labetalol, esmolol, hydralazine, nitroprusside, nitroglycerin)
Identifies causes and interventions for common cardiac rhythms
V. GASTROINTESTINAL (GI) ISSUES
A. Nausea and vomiting
1. All too common, miserable, resistant anesthesia outcome
a. Alters patient reports of satisfaction with procedure
b. Sedation increases aspiration risk.
c. Persistent retching
d. Recurrent emesis increases pain.
e. Dehydration
f. May result in unplanned hospital admission after procedures, ambulatory surgery
2. Physiology: narcotics, sedatives can trigger brain’s emetic center.
a. Retching controlled by vomiting center in medulla
b. Vomiting center receives input from:
(1) Cerebral cortex: olfactory, visual, emotional stimuli
(2) GI tract
(3) Vestibular system
(4) Chemoreceptor trigger zone
3. Risk factors for developing PONV (see Chapter 25)
a. Predisposing factors
(1) Patient specific
(a) Female gender
(b) Nonsmoking status
(c) History of PONV
(d) History of motion sickness or vestibular problems
(e) Delayed gastric emptying or pressure
(i) Morbid obesity
(ii) Pregnancy (early stage)
(iii) Gastroparesis
[a] Neurological diseases
[b] Diabetes
(f) Increased gastric volume
(i) Full stomach, insufficient duration of the nothing by mouth (NPO) status
(ii) Anxiety
(g) Hypotension, bradycardia: sudden unexpected emesis
(h) Severe pain
(i) Dehydration including NPO duration in fluid replacement calculations
(2) Anesthetic related
(a) Use of volatile anesthetics
(b) Nitrous oxide
(c) IV medications: ketamine, etomidate
(d) Postoperative use of opioids
(i) Meperidine
(ii) Morphine
(e) Duration of anesthesia
(3) Surgery related
(a) Duration of surgery
(b) Type of surgery
(i) Laparoscopic procedures particularly gynecologic
(ii) Strabismus surgery primarily in children
(iii) Middle ear procedures
b. Intervention: no panacea, “wonder” therapy
(1) Prevention most effective treatment
(a) Assess risk indicators.
(b) Hydration: generous IV fluid replacement
(c) Avoid brisk head movement, restlessness.
(d) Provide adequate analgesia; position for comfort.
(e) Encourage deep breathing, relaxation.
(2) Avoid gastric distention.
(a) Restrict oral fluids until nausea passes.
(b) Oral hygiene: many complain of anesthetic “taste.”
(c) Ensure patent nasogastric tube.
(3) Medicate: preemptive combinations, particularly if high risk or history of PONV
(a) Anticholinergics: scopolamine patch behind ear
(b) Serotonins: ondansetron (Zofran) or cousin dolasetron (Anzemet)
(c) Butyrophenones: droperidol (Inapsine). Consider the black box warning.
(i) Only limited use; recommended for outpatients because of unpleasant extrapyramidal effects, also drowsiness
(d) Corticosteroids: dexamethasone (Decadron)
(e) Sedatives: propofol (Diprivan) has antiemetic properties.
(f) Phenothiazines
(i) Prochlorperazine (Compazine): per rectal suppository, particularly if outpatient with resistant nausea
(ii) Chlorpromazine (Thorazine)
(g) Antihistamines
(i) Hydroxyzine (Vistaril, Atarax)
(ii) Diphenhydramine (Benadryl)
(h) Benzamide
(i) Metoclopramide (Reglan)
(4) Adjunctive complementary modalities to reduce dizziness, nausea
(a) Acupressure antiemetic wrist bands
(b) Power of suggestion
(c) Hydration: up to 2000 mL for even minor procedures
(d) Aromatherapy
(e) Music
(5) May vomit after discharge despite interventions
(a) Persist up to 48 hours after discharge from phase I PACU
(b) Oral fluids and food too soon actually increase likelihood.
(c) For patients discharged home, advise:
(i) Rest
(ii) Nonnarcotic medications if possible
(iii) Gradual increases in fluid intake: “treat yourself as though you had the flu.”
(iv) Contact physician for unrelenting vomiting.
B. GI perfusion: remember the gut!
1. Potential for GI ischemia an overlooked consideration for critically ill patients
a. Mesentery not directly visible for assessment
(1) Absent bowel sounds may mean dead or poorly perfused gut.
(2) Involve gastroenterology assessment quickly in sepsis.
b. Crucial concern when evaluating sepsis, especially if:
(1) Unresolving hypotension, progressive acidosis
(2) Trauma, pancreatitis, burns: potential for GI dysfunction high
c. No specific, convenient measure to assess viability of GI tissue
(1) GI symptoms often not treated until symptomatic—perhaps too late
(a) Outcome worse the longer patient with sepsis is hypotensive with low MAP
(b) Alcoholism history increases risk of GI ischemia.
(i) Poorly functioning liver
(ii) Immunosuppressed
(2) Kupffer cells: critical to protecting “gut”
(a) Immune (phagocytic) cells in liver kill bacteria released from “gut.”
(b) If unhealthy gut, more endotoxins circulate through liver, then seed other organs.
(c) Impaired Kupffer cells predispose to sepsis, pulmonary failure (acute respiratory distress syndrome)
(d) Liver function tests only reflect injury, not systemic function: enzyme levels rise only if cell death.
(3) Tonometry studies cumbersome at bedside but recommend:
(a) Improve oxygen delivery, cardiac output before acidosis
(b) Survival from sepsis increased if maintain oxygenation
2. Prevent multisystem organ failure (MSOF) or dysfunction(MSOD).
a. Per tonometry studies, prevent MSOF if perfuse gut.
b. Recommend postpyloric tube feedings to maintain viability and structural integrity of microvilli in small bowel cell walls.
(1) If not stimulated, microvilli flatten.
(2) Can occur even if NPO for 4 days
(3) Bypass stomach when inserting feeding tube.
(4) Infuse high glutamine solution, even in small amount.
VI. NEUROLOGICAL CONCERNS AND ANESTHESIA
A. Delayed emergence: slow to arouse, failure to return to preanesthetic baseline
1. Consider multiple possible reasons and treat the cause (Box 28-3).
a. Understimulated patient: actively stimulate at regular intervals.
(1) Touch, shake, and call to patient.
(2) Remain at stretcher side; do not leave unresponsive patient unattended.
(3) Know patient’s neurological baseline, medical history, laboratory results.
b. Assess adequate ventilation and oxygenation.
(1) Poor ventilation will only extend arousal period.
(2) Hyperventilation
(a) May be normal response: effort to exhale volatile (gas) anesthetics—observe, may rouse soon.
(b) If diabetic, consider superelevated hyperglycemia and acidosis.
(3) Hypercarbia (increased P co 2) impairs consciousness, extends sedation.
(4) Hypoxia (decreased P o 2) deprives tissues of oxygen, produces acidosis.
(5) Monitor oxygen saturation, deliver oxygen.
(6) Consult anesthesiologist.
(7) Extended unresponsiveness: draw arterial blood gases.
c. Hypothermia
(1) Cold body temperatures delay metabolism of medications.
(2) Gradually rewarm while monitoring vital signs: prevent hypotension.
d. Prolonged action of anesthesia medications: most likely cause
(1) Ongoing neuromuscular blockade: is patient awake but unable to move?
(2) Observe pupils: pinpoint constriction suggests continued narcotic effect.
(3) Has sufficient time elapsed for medication metabolism and elimination?
(4) Consider reversing narcotics, benzodiazepines, muscle relaxants.
e. Metabolic causes: correct imbalances.
(1) Hypoglycemia or hyperglycemia: measure blood glucose.
(2) Electrolyte imbalance
(3) Preexisting reasons: hepatic, renal, Cushing’s disease, hypothyroidism
f. Organic dysfunction
(1) Perioperative myocardial infarction. Assess 12-lead ECG.
(2) Cerebrovascular issues: stroke, seizure, intracerebral hemorrhage
(3) Air embolism related to surgical procedure
(a) Cardiopulmonary bypass during heart surgery
(b) Sitting position during cervical (neck) surgery
(4) Craniotomy: new hematoma
BOX 28-3
SAFE EMERGENCE: DELIRIUM AND DELAYED RESPONSE
Assessments and Perianesthesia Nurse Competencies Related to Emergence Delirium and Delayed Arousal After Anesthesia
Critical Nursing Behaviors
Discern hidden causes of agitation, especially hypoxia, undetected internal hemorrhage, or acidosis
Identify physiological possibilities for delayed emergence from anesthesia and appropriate nursing and medical interventions
Explain physiological influence of medications used to calm the restless patient or to stir the slow-to-respond patient
▪ Medicate only when oxygenation is adequate
▪ Phyostigmine, an anticholinesterase medication, penetrates the blood-brain barrier to increase neuromuscular acetylcholine: quickly transforms agitation to calm
▪ Titrate midazolam, lorazepam, narcotics prn
▪ Narcotic or benzodiazepine antagonists to reverse sedation
▪ Medications to correct physiologic imbalance
▪ Quickly transforms agitation to calm
Describe rationale to ensure the agitated patient’s safety while restless
▪ Remain with the patient and frequently assesses oxygenation
▪ Loosely apply limb restraints; aware that limiting movement may increase fear, disorientation, and agitation
▪ Protect sensitive corneas from abrasion by flailing hands that rub eyes
▪ Involve family members
▪ Parents calm a wild child.
▪ A familiar voice might help reorient a patient with visual, hearing, intellectual, or emotional impairment.
Describe rationale to ensure safety of a patient with delayed arousal
▪ Always remain with the patient
▪ Closely monitor oxygenation, airway patency, and respiratory quality
▪ Frequently attempt to arouse patient
▪ Consult physician as appropriate when sedation persists
▪ Rewarm a hypothermic patient; consider other medical possibilities
B. Emergence delirium: “Waking up wild!” (see Box 28-3)
1. Suspect hypoxia first!
a. Ensure adequate ventilation, oxygenation before giving any sedation.
b. Patient may move but remain anesthetized, disoriented, air hungry.
(1) Residual muscle relaxants: unable to “get enough air”
(2) Narcotics, sedatives: hypercarbia from ineffective respiratory effort
(3) Electrolyte or acid-base imbalance, hemoglobin deficiency
c. Agitation may signal cerebral hypoxia.
d. Consider severe anemia: is patient bleeding actively?
(1) Consider procedural blood loss according to preanesthetic hemoglobin.
(2) Measure hemoglobin: adequate to transport oxygen to tissues?
2. Transient restless, agitated, confused, or dysphoric arousal
a. Squirmy, crying, strongly pushing away caregiver common in children, teens
b. Normal response to pain, urgent call of a full bladder when not fully awake!
c. Untoward response: fewer than 10% of all surgical patients
(1) History may indicate prior occurrence with anesthetic exposure.
(2) Confluence of multiple medications
(a) Dreams, hallucinations when adults receive ketamine
(b) Extrapyramidal effects caused by droperidol
(c) Anesthetics and medications to treat organic brain syndrome
(3) Continuation of preprocedural anxiety about life or procedure
d. Signals chronic alcoholism: consult physician.
(1) Drinkers often underestimate consumption.
(2) When was the last drink? Is patient also tachycardic?
(3) Consider delirium tremens.
(a) Arrange for close observation after PACU discharge.
(b) Initiate sedation protocol, often with lorazepam (Ativan), per physician order.
e. Signals substance abuse, either legal or illicit
3. Consider systemic causes.
a. Acute dilutional hyponatremia: measure serum sodium.
(1) May absorb intraoperative irrigant after transurethral resection of prostate (TURP), also known as “TURP syndrome”
(2) Women after hysteroscopy
b. Hypotension: inadequate oxygen delivery
c. Sepsis
d. Hypothermia: unable to express feeling cold and slows medication elimination
4. Safety: irrational, agitated, thrashing patient is usually extremely strong.
a. Constant presence of nurse required to ensure safe passage through this stage
b. Multiple personnel needed at bedside to:
(1) Restrain patient.
(2) Keep patient on stretcher.
(3) Avoid bodily injury to patient and nurse.
c. Remain calm, speak softly to connect with and reorient patient.
(1) Encourage, guide patient toward stillness.
(2) When you can interact with patient, ask questions to assess.
(a) Breathing: “getting enough air?”
(b) Pain: presence and severity
(c) Awareness of situation
(i) Does patient recall having procedure?
(ii) Know who he or she is?
(iii) Where he or she is?
(d) Feeling cold?
(3) Although tempting, overwhelming patient with forceful restraint and loud commands serves only to further agitate.
(4) Carefully apply limb restraints according to facility protocol.
(5) Maintain quiet environment.
(6) Prevent injury.
(a) Fall from stretcher
(b) Scratched corneas with random movements
d. Protracted delirium may resolve with physostigmine; consult anesthesia provider.
e. Judiciously treat pain: chemical restraint
(1) Prevent sudden somnolence.
(2) Pain may be severe in patients who chronically use oral narcotics.
(a) Did patient take scheduled narcotics preprocedure?
(b) If not, likely reacting incoherently to severe pain
C. Recall of intraoperative or procedural events
1. Rare and haunting occurrence for patient and anesthesia provider
a. Alert, oriented patient, perhaps ready for discharge, relates details of intraoperative events.
(1) Specifics of conversations, comments, or an occurrence
(a) Pain and being “unable to tell anyone”
(b) Interprets conversations he or she overheard to be about self, even if they were not
(2) Most associated with “light” general anesthetic for:
(a) Cesarean section
(b) Bypass cardiac surgery
b. Allow to talk.
(1) May feel scared, angry, sad, confused
(2) Listen closely; document all communication.
(3) Acknowledge that awareness does occur.
(4) Consult and inform anesthesia provider, who should visit patient.
D. Local anesthetic toxicity
1. Central nervous system effects: cross blood-brain barrier
a. Tinnitus
b. Light-headedness and/or confusion
c. Circumoral numbness
d. Unresponsiveness
e. Seizures
2. Cardiovascular and respiratory effects
a. Peripheral vasodilatation: relaxation of vascular smooth muscle
b. Hypotension, circulatory collapse at extremely high doses
c. Dysrhythmias
(1) Bradycardia
(2) Atrioventricular block
(3) Intraventricular conduction delay
d. Respiratory arrest
3. Cause: large intravascular bolus of local anesthetic
a. Sudden release or failure of tourniquet during Bier Block
b. Inadvertent injection when placing regional blocks
c. Improperly set infusion rate of IV lidocaine
4. Intervention: largely supportive to resuscitate
a. Oxygenation, airway maintenance
b. Generous IV fluid volume
c. Symptomatic treatment of:
(1) Seizures
(2) Hypotension
(3) Apnea
VII. THERMOREGULATION (see Chapter 24)
A. Hypothermia: iatrogenic complication
1. Perianesthesia origins
a. Vasodilating anesthetic medications and techniques
(1) General anesthetics: alter thermoregulation at the hypothalamus
(a) Patient cools to temperature of room (poikilothermia).
(2) Spinal blockade: lose heat through dilated peripheral vessels
(a) Heat loss continues until spinal resolved, even in PACU.
b. Open body cavities, room temperature tissue irrigants during procedure
c. Cold room temperatures in procedure rooms
2. Heat loss physics
a. Radiation: heat transfer between two surfaces of different temperatures
b. Convection: surface loss of heat when fluid flows across at a lower temperature
c. Conduction: heat transfer between two touching objects of different temperatures as when warm human body in direct contact with cooler surgical table
d. Evaporation: heat loss through insensible water loss from skin, the respiratory tract, open incisions, and wet drapes
3. Potential consequences: vary with significance of heat loss
a. Increased oxygen consumption as a result of shivering
(1) Normal autonomic response to generate heat
(2) Heat production by muscular contractions
(3) Potential cardiac or pulmonary failure for compromised patient
(a) Oxygen consumption increases 400% to 500%.
(b) Tachycardia and hypertension
(c) Pain and thermal discomfort: feels cold
(i) Temperature may actually meet discharge criteria.
(ii) Patients describe as “thought I’d freeze to death.”
b. Wound infection: studies indicate hypothermia delays wound healing.
c. Cardiac disturbance: marked increase in cardiac output, breathing
d. Delayed emergence from anesthesia: prolonged medication effect and delayed elimination, especially if temperature below 95° F (35° C)
e. Coagulopathy
f. Assessment interference
(1) Vasoconstriction and shivering movements impede measurement of oxygen saturation.
4. Interventions: preventing unplanned heat loss recommended
a. Rewarming measures: gradual to prevent sudden hypotension
(1) Active methods for warmth and comfort
(a) Forced-air warming system: billowy blankets filled with warmed air
(2) Passive insulation
(a) Warmed cotton blankets
(b) Thermal drapes
(c) Fluid and blood warmers
(d) Heated humidifiers for oxygen delivery
(e) Infrared lights
(3) Increasing the thermostat to warm the procedure area
b. Supplemental oxygen, particularly if shivering
c. Regularly measure temperature, every 30 minutes if hypothermic.
(1) Discharge only after attaining facility’s discharge temperature.
(2) Discharge criteria per ASPAN discharge criteria: 96.8° F (36° C)
(3) ASPAN clinical practice guideline, established at a multispecialty consensus conference on hypothermia
(a) Defines normothermia as 96.8° F to 100.4° F (36° C to 38° C)
d. Meperidine, as little as 10 mg IV, effectively suppresses shivering.
B. Hyperthermia
1. Fever: normal physiological response to infection
a. May arrive for surgery, perhaps for wound debridement or appendectomy: less febrile postoperatively
b. May be indication for surgery cancellation of elective spine, joint replacement involving implanted hardware
(1) Evaluate for pulmonary infection.
(2) Urinary tract infection
c. Prelude to sepsis
(1) Heighten vigilance and assessment.
(2) Anticipate hypotension, hypoxia.
2. Malignant hyperthermia: a true anesthesia crisis
a. Causes
(1) Rare, genetically determined skeletal muscle response
(a) Calcium prevented from reentering cell
(2) Specific triggers
(a) Succinylcholine
(b) Volatile inhalation agents, including desflurane, isoflurane, enflurane, halothane, and sevoflurane
(3) Most likely in the young and healthy
b. Goal: prevention
(1) Identify susceptibility: ask all preoperative patients if there is a personal or family history of:
(a) Anesthetic-related death
(b) Muscle disorder
(c) Developing a fever or dark urine after previous surgery
c. Observations
(1) Sudden unexplained tachycardia may be initial signal.
(2) Unexpected surge of end-tidal CO 2 in anesthetized patient
(3) Profound muscle rigidity: often first noted at masseter muscle
(4) Extreme metabolic acidosis
(5) Respiratory acidosis
(6) Cyanosis
(7) Tachypnea
(8) Hemodynamic instability
(9) Fever a late sign
d. Interventions: aggressive, intensive to ward off terminal acidosis
(1) Immediate cooling: pack in ice, chilled IV fluids
(2) Massive doses of dantrolene sodium (Dantrium), a skeletal muscle relaxant
(3) Find personnel help: a crisis with multiple tasks
(4) Oxygenate: hyperventilate at 100%.
(5) Work to correct severe metabolic acidosis.
(6) Monitor
(a) Hemodynamics
(b) Urine
(c) Laboratory studies
BIBLIOGRAPHY
1. American Society of PeriAnesthesia Nursing, Standards of perianesthesia nursing practice 2008-2010. ( 2008)American Society of PeriAnesthesia Nursing, Cherry Hill, NJ.
2. Anthony, D.; Jasinski, D.M., Postoperative pain management: Morphine versus ketorolac, J Perianesth Nurs 17 (2002) 30–42.
3. Barnes, S.; O’Brien, D., Considering bypass of phase I PACU?J Perianesth Nurs 17 (2002) 193–195.
4. Bennett, J.; Wren, K.R.; Haas, R., Opioid use during the perianesthesia period, J Perianesth Nurs 16 (2001) 255–259.
5. Benumof, J.L., Obstructive sleep apnea in the adult obese patients: Implications for airway management, Anesthesiol Clin N Am 20 (2002) 789–811.
6. Bogetz, M.S., Using the laryngeal mask airway to manage the difficult airway, Anesthesiol Clin N Am 20 (2002) 863–870.
7. Burns, S.M., Revisiting hypothermia: A critical concept, Crit Care Nurse 21 (2001) 83–86.
8. Burns, S.M., Safely caring for patients with a laryngeal mask airway, Crit Care Nurse 21 (2001) 72–74.
9. Burns, S.M., Delirium during emergence from anesthesia: A case study, Crit Care Nurse 23 (2003) 66–69.
10. Calswell, J.E., Rapid sequence intubation: Is rocuronium an alternative?Semin Anesth Periop Med Pain 21 (2002) 99–103.
11. Childs, S.G., Tension pneumothorax: A pulmonary complication secondary to regional anesthesia from brachial plexus interscalene nerve block, J Perianesth Nurs 17 (2002) 404–412.
12. Connor, E.L.; Wren, K.R., Detrimental effects of hypothermia: A systems analysis, J Perianesth Nurs 15 (2000) 151–155.
13. Cowling, G.E.; Haas, R., Hypotension in the PACU: An algorithmic approach, J Perianesth Nurs 17 (2002) 159–163.
14. Drain, C.; Odom-Forren, J., Perianesthesia nursing: A critical care approach. ed 5 ( 2009)Saunders, Philadelphia.
15. Erickson, L.I., Acquired neuromuscular disorders in the critically ill patient, Semin Anesth Periop Med Pain 21 (2002) 135–139.
16. Floyd, P.T., Latex allergy update, J Perianesth Nurs 15 (2000) 26–30.
17. Golembiewski, J.A.; Obrien, D., A systematic approach to the management of postoperative nausea and vomiting, J Perianesth Nurs 17 (2002) 364–376.
18. Gray, J.R., Steering clear of sepsis skid: Interventions in sepsis, organ, and renal failure. ( 2003)North Memorial Center, Robbinsdale, MN; Lecture on April 21.
19. Irvin, S.M., Sensorineural hearing loss after select procedures, J Perianesth Nurs 17 (2002) 89–101.
20. Kervin, M.W., Residual neuromuscular blockade in the immediate postoperative period, J Perianesth Nurs 17 (2002) 152–158.
21. Knoerl, D.V.; McNulty, P.; Estes, C.; et al., Evaluation of orthostatic blood pressure testing as a discharge criterion from PACU after spinal anesthesia, J Perianesth Nurs 16 (2001) 11–18.
22. Learman, J.B., The challenging role of the perianesthesia nurse in the office-based surgical suite, J Perianesth Nurs 15 (2000) 31–52.
23. Moline, B.M., Pain management in the ambulatory surgical population, J Perianesth Nurs 16 (2001) 388–398.
24. Nagelhout, J.; Plaus, K., Nurse anesthesia. ed 4 ( 2010)Saunders, St. Louis.
25. Nunnelee, J.D.; Spaner, D.S., Assessment and nursing management of hypertension in the perioperative period, J Perianesth Nurs 15 (2000) 163–168.
26. O’Brien, D., Acute postoperative delirium: Definition, incidence, recognition and interventions, J Perianesth Nurs 17 (2002) 384–392.
27. Prielipp, R.C.; Young, C.C., Current drugs for sedation of critically ill patients, Semin Anesth Periop Med Pain 20 (2001) 85–94.
28. Redmond, M.C., Malignant hyperthermia: Perianesthesia recognition, treatment, and care, J Perianesth Nurs 16 (2001) 259–269.
29. Rose, J.B.; Watcha, M.F., Postoperative nausea and vomiting, In: (Editors: Benumof, J.L.; Saidman, L.J.) Anesthesia and perioperative complicationsed 2 ( 1999)Mosby, St Louis.
30. Sandlin, D., Transderm scopolamine: A painless, noninvasive option for control of postoperative nausea and vomiting, J Perianesth Nurs 17 (2001) 427–429.
31. Sommers, M.S., The cellular basis of septic shock, Crit Care Nurs Clin North Am 15 (2003) 13–26.
32. Spitellie, P.H.; Holmes, M.A.; Domino, K.B., Awareness during anesthesia, Anesthesiol Clin N Am 20 (2002) 317–332.
33. Watche, M.F., Postoperative nausea and emesis, Anesthesiol Clin N Am 20 (2002) 471–484.
34. Watkins, A.C.; White, P.F., Fast-tracking after ambulatory surgery, J Perianesth Nurs 16 (2001) 379–387.
35. Watson, C.B., Respiratory complications associated with anesthesia, Anesthesiol Clin N Am 20 (2002) 275–299.
36. Williams, E.L., Postoperative blindness, Anesthesiol Clin N Am 20 (2002) 367–384.
37. Wilson, M., Giving postanesthesia care in the critical care unit, Dimens Crit Care Nurs 19 (2000) 38–43.
