PACU - Exam 3 Flashcards
What is the immediate priority in the PACU once pt has arrived?
assess respiratory + circulatory adequacy
CRNA job in PACU once pt is delivered
-get O2 on pt
-check airway, ventilation, VS ( pt is our responsibility until monitors on AND status is ok)
-give report (allow RN to ask Qs)
-give suggested endpoints
-stay with pt until PACU RN “accepts” pt
Info to give during report (SHOULD BE VERBAL)
-pt name/age; cultural info/ contact person
-procedure done, surgeon name, anesthesia team
-Hx (acute + chronic, allergies, OSA, cognitive/sensory deficits)
-airway technique (ETT/LMA/current O2 or vent settings, etc)
-anesthesia technique (IA/TIVA/regional or local/GA/etc)
-drugs given (doses, last given, reversals, abx, fluids, pressors)
-EBL, UO, PONV
-labs + other events during case (low BP/HR, etc)
-DC criteria (physician will DC pt); anticipated issues; PACU plan (pain mgmt)
Things that can compromise the quality of your PACU handoff report
-multiple providers
-different communication styles
-loud environment/ distractions
-poor pt transfer prep
-production pressure from workplace
-lack of standardization
-not letting RN ask Qs
Things to check before and enroute to PACU
-upper airway patency
-hand over mouth
-chest rise
-precordial steth
-O2? (GA pts usually need some)
PACU RN/pt ratios
1:2 if pt stable
1:1 if pt in unarousable and has ETT or child < 8yr
How often are pt and VS checked upon admission to PACU?
-on admission
-Q 5 min x 3
-Q15 min after that
4 main causes of hypoxemia in PACU
-hypoventilation
-diffusion limitation
-shunt
-V/Q changes
Hypoxia
-respiratory s/s
-shallow, rapid respirations or infrequent respirations
-tachypnea / dyspnea
-O2 sat <90%
Hypoxia
-neuro s/s
-anxiety, restless, inattentive
-AMS/ confusion
-dim periph vision
-seizures
-combative (LATE)
-unresponsive (LATE)
Hypoxia
-skin s/s
diaphoresis
cyanosis
Hypoxia
-cardiac
Early:
-tachycardia
-increased CO
-increased SV
-HTN
Late:
-bradycardia, HoTN
-dysrhythmias
Key assessment points before DC from PACU :
-pain
-conscious state
-BP
-N/V
Most widely used scoring system in PACUs is
Aldrete Postanesthetic Scoring System
Aldrete Postanesthetic Recovery Score has 5 main components scored 0-2:
Activity:
0-can’t lift head or move extremities voluntarily/on command
1- moves 2 extremities voluntarily or on command and can lift head
2 -4 extremities on command lifts head w controlled movement (exception for pt with Bupivicaine block who can’t move extremity for 18hr, or previously immobile pts)
Respiration:
0-apneic, needs vent or help respiration
1- labored or limited respirations, may have OPA
2- deep breath and good cough, normal RR and depth
Circulation:
0-high or low BP ~50mmHg of preop BP
1- BP within 20-50mmhg of pre anesthetic level
2- stable BP, HR. BP within 20mmHg of preop level or 90SBP (pt can be released from anesthesia after drug therapy)
Neuro status
0-no response or only painful stim
1-responds to verbal command but drifts quickly
2- awake, alert, oriented
O2 sat:
0-sat<90% with o2 supp
1- needs supp o2 to keep sat>90%
2- can keep O2 sat >92% on RA
Which 2 systems of the body are assessed FIRST in PACU?
Respiratory and Cardiac
-THEN Neuro (not a head to toe!)
Most common cause of airway obstruction in immediate PACU phase is:
loss of pharyngeal muscle tone in sedated/obtunded pt
-not tongue, that is in PACU pts in general
In PACU pts in general, most upper airway obstructions are caused by:
the tongue
-falls back, occludes pharynx, blocks flow in AND out of lungs
Upper airway obstruction
-s/s
-snoring
-activation of accessory muscles of ventilation
-intercostal/ suprasternal retractions
-somnolent/ difficult to arouse
Upper airway obstruction
-risk factors
-obesity
-large neck/ short neck
-poor musc tone (residual sedation, opioids, NMBD, or NM disease)
-swelling (surg manipulation, edema, anaphylaxis)
Upper Airway Obstruction
-tongue obstruction releif
-stim pt to make them take deep breaths
-reposition airway w jaw thrust/ chin lift (CPAP if necessary 10-15cmH2O)
-OPA/nasal airway (nasal tolerated BETTER, less likely to gag/vomit)
-reintubate if needed
T/F Laryngospasms occur when one set of muscles contract and force the glottis closed
false,
-this could be partial or complete and from the intrinsic and extrinsic muscles acting
-glottic closure is typically partial obstruction and laryngeal closure elicits a complete obstruction
During a laryngospasm, a glottic closure results from the _ muscles and the laryngeal closure results from the _ muscles.
glottic- intrinsic - intermittent obstruction
laryngeal - extrinsic- complete obstruction
What can cause a laryngospasm?
-airway irritation
-laryngoscopy
-vomiting
-blood/secretions
-artificial airway placement
-coughing
-bronchospasm (double spasm?? no thanks!!)
-frequent suctioning
Laryngospasm
-s/s
-agitation
-O2 sat decrease
-crowing sound/stridor (partial) or lack of BS (complete)
-acute resp distress
Laryngospasm
-Tx
-move quickly but carefully
-jaw thrust with CPAP ~40cmH2O
-subparalytic dose of IV sux 0.1-1mg/kg or 4mg/kg IM (MUST ASSIST W VENTILATION FOR 5-10 MIN AFTER THIS THO AND SHOULD PROLLY GIVE VERSED-TRAUMATIZING!! :()
-reintubate ONLY if spasm persists or if there is severe airway edema
Laryngospasm
-prevention
-steroids
-topical or IV Lido
-ensure hemostasis
-suction well before extubation
-extubate deep or awake (NOT IN 2nd plane!)
OSA is associated with:
-increased complications
-difficult intubation
-longer LOS(length of stay) in PACU
-unplanned admissions
-resp/cardiac complications
Screening tool for OSA with the highest validity and ease of use is
STOP-BANG
ASPAN’s Practice Recommendations-10 OSA (box 55.6)
- Assess/ screen pt for risks/comorbidities associated w OSA
2.Assess/ screen undiagnosed pts for s/s of OSA - Use standardized screening tool to identify pt at risk of OSA
-STOPBANG
-ASA OSA Checklist - Consider preop interventions
- Initiate postanesthesia management of pts with diagnosed or suspected OSA
- Plan for pt discharge in phase 1 or 2 with diagnosed or suspected OSA
- Provide discharge education for pts with suspected/diagnosed OSA
OSA
-pre op management
-well planned anesthesia method (regional, minimal sedation when able)
-if pt has known OSA and a CPAP, bring that in for immediate use in PACU
OSA
-postop management
-analgesia
-positioning
-oxygenation
-monitoring
-CPAP if they brought it in
Hypoxemia is defined as:
low ARTERIAL O2 pressure
-PaO2 <60 mmHg
Hypoxemia
s/s
-not specific s/s
-agitation/somnolence
-HTN/HoTN
-Tachy/Bradycardia
-pulse ox MAY confirm ( SpO2<90%)
-ABG MAY confirm (PaO2 < 60mmHg)
Hypoxemia
-causes
-delivered airway obstruction
-low O2 concentration
-hypoventilation
-V/Q mismatch
-increased intrapulmonary shunting
MOST COMMON IN PACU
-atelectasis
-pulm edema
-PE
-aspiration
-brochospasm
-hypoventilation
T/F The relationship between % Hgb saturated with O2 (SaO2) and partial pressure of oxygen in alveoli (PAO2) describes the oxyhemoglobin dissociation curve
FALSE
-not alveoli (PAO2), partial pressure of O2 in the BLOOD(arterial- PaO2)
-sorry that was mean but so are Linda’s Qs …
Shifts in O2-Hgb dissociation curve could be caused by:
-abnormal pH
-temp changes
-partial pressure of CO2
-2,3 DPG levels
-Hgb level too (think anemia)
Most common cause of postop arterial hypoxemia
Atelectasis
Atelectasis causes an increase of _ - _shunt
Right to Left
Atelectasis
-causes
-bronchial obstruction (secretions, decreased lung volumes, spasm?)
-HoTN and low CO
-poor perfusion
Atelectasis
-Tx
-humidified O2
-coughing
-deep breathing
-postural drainage
-increased mobility
-incentive spirometry
-intermittent PPV
Atelectasis
-prevention
-stop smoking 6-8 wks prior to case
-pain control
-caution in use of NG tube
Pulm edema is fluid accumulation in the alveoli and patho consists of 3 potential causes:
-increase in hydrostatic pressure (HEART)
-decrease in interstitial pressure (airway obstruction)
-increase in capillary permeability (ARDS)
Pulm Edema
-Increased hydrostatic pressure causes:
-fluid overload
-LV failure (esp with Systolic HTN)
-Mitral valve dysfunction
-Ischemic heart disease
HEART
Pulm Edema
-Decreased interstitial pressure causes
-prolonged airway obstruction (laryngospasm, postobstructive/ neg pressure pulm edema)
Pulm Edema
-Increased capillary permeability causes
-sepsis
-aspiration
-transfusion reaction
-trauma
-anaphylaxis
-shock
-DIC
ARDS!!!
3 names for acute pulm edema after severe upper airway obstruction:
-postobstructive pulm edema
-neg pressure pulm edema
-noncardiogenic pulm edema
Explain patho of neg pressure/postobstructive pulm edema:
- Obstruction caused a lot of negative intrapleural pressure
- This increased pulm transvascular hydrostatic pressure gradient
- Rapid movement of fluid from pulm vessels to interstitium faster than lymph system’s clearing capacity
- Alveoli become flooded
Negative pressure/ Postobstructive/ NonCard Pulm Edema
-causes
-very muscular pts (typically have high NIF)
-bolus dosing with narcan
-incomplete reversal of NM blockade
-significant period of hypoxia
Pulm Edema
-s/s
-hypoxemia
-cough
-frothy sputum
-rales on auscultation
-poor lung compliance
-CXR showing infiltrates
Pulm Edema
-Tx
Goal is to treat cause and reduce hydrostatic pressure
-O2 mask
-CPAP w mask or intubate w PEEP
-Diuresis (lasix) or fluid restriction (FR)
-Dialysis (if from renal failure)
-Preload and Afterload reduction (NTG or Nipride to decrease myocardial work)
NonCard/Neg pressure/ Post Obst Pulm edema usually clears up in 12-48hr if treated promptly
Leading cause of morbidity and mortality in US
PE
_ _ is the first symptom of PE in 25% of people
Sudden Death
-yikes
3 main risk factors for PE (Virchow’s Triad)
-venous stasis
-hypercoag state
-abnormalities in blood vessel wall
PE
-risk factors beyond Virchow’s Triad
-Virchow’s Triad (venous stasis, hypercoag state, vessel wall abnormalities)
-obesity
-varicose veins
-immobility
-malignancy
-CHF
-old age
-pelvic/ long bone injury/trauma (most come from DVT in legs but postop from freeing tissue factors causing thrombin)
PE
-s/s
-acute onset tachypnea
-dyspnea + pleuritic CP at rest (classic sign)
-tachycardia
-HoTN
-hemoptysis
-dysrhythmias
-CHF
-esp if pt is already on supp O2
Gold standard for PE dx:
CT
Well’s Clinical Prediction Rule for Likelihood of PE
-table 55.1
Predisposing Factors:
-Previous VTE - 1.5 pt
-Recent Surg or immobilization - 1.5pt
-Cancer - 1pt
Symptoms:
-Hemoptysis - 1 pt
Signs:
-HR >100 - 1.5pt
-Clinical signs of DVT - 3pt
Clinical Judgement:
-Alt Dx less likely than PE - 3 pt
Clinical Probability:
-Low = <2pt
-Moderate = 2-6pt
-High = >6pt
PE
-prevention
-antiembolic stockings
-SCD
-Subcut Heparin (not for tx!)
PE
-Tx
Goal= correct hypoxemia, support hemodynamics
-IV heparin (want APTT 1.5-2 x normal value) (also is drug of choice for renal pts -DOC)
-subcut LMW Heparin or Fondaparinux (Arixtra) or PO Rivaroxaban (Xarelto) for low risk PE, don’t need coag monitoring
Aspiration of Foreign matter
-s/s
-cough
-airway obst
-atelectasis
-bronchospasm
-pneumonia
-HoTN from profound SNS response
Aspiration of Foreign matter
-Tx
-if not complete obstruction, supportive care after matter is expelled or removed via bronch
Aspiration of Blood
-causes
-trauma
-surg manipulation
What could happen if a pt aspirates blood?
Small amount:
-minor airway obst that is quickly cleared with couhg, resorption and phagocytosis
Large amount:
-mech blockage of airway impairing gas exchange
-causes chronic fibrinous air space changes and pulm hemochromatosis from accumulation of phagocytes
-also infection if extra tissue is aspirated
Aspiration of Gastric Contents
-s/s
-chemical pneumonitis
-diffuse bronchospasm (reflex airway closure)
-hypoxemia (compromised alveolar capillary membrane)
-atelectasis (loss of surfactant)
-interstitial edema (loss of capillary integrity)
-hemorrhage
-ARDS
-laryngospasm
-infection
-pulm edema
Aspiration
-risk factors
-pregnant
-obese
-full stomach
-hiatal hernia
-PUD
-trauma
Aspiration
-prevention
-H2 blocker
-gastrokinetic agent
-nonparticulate antacid (Bicitra)
-anticholinergics
-RSI
-NG tube intraop and remove to decompress stomach
-leave pt intubated postop until airway reflexes return!!
-don’t give prophylactic agents for pt not at risk, antiemetics are ok
When to apply supp O2, CPAP, PEEP, or reintubate after aspiration:
-hypoxemia
-increased airway resistance
-atelectasis
-pulm edema
T/F After aspiration, give abx, steroid, and lasix to prevent infection, reduce inflammation, and assist with pulm edema
FALSE
-abx ONLY after culture
-no steroids
-diuresis is not indicated for pulm edema caused by increased capillary permeability
-reread that diuretic bit, that seems like a Linda-ism bc diuretics are appropriate for OTHER causes of pulm edema
Patho of bronchospasm:
-increase in bronchial smooth musc tone
-causes closure of small airways
-NIF against narrowed airways causes edema and increased secretions
Bronchospasm
-causes/ risks
-aspiration
-pharyngeal or tracheal suctioning
-intubation
-histamine release 2/2 medications/allergy
-asthma
-COPD
Bronchospasm
-s/s
-wheezing
-dyspnea
-accessory musc use
-tachypnea
-increased airway resistance
-increased PIP
Bronchospasm
-Tx
Goal - confirm and remove cause, decrease airway irritability, promote bronchodilation
-IA (SEVO is great for refractory)
-beta 2 agonists(Albuterol-SABA, Salmeterol-LABA)
-Atropine, Glyco, or Ipratropium Nebs (decrease secretions)
-IV Epi (if critical)
-IV Lido (actually better than intratracheal!)
-steroids (if cause was inflammatory disease-asthma)
Hypoventilation causes:
(residual meds, srug in upper abd, NM disease, lytes/acid/base)
-decrease in central resp drive
-poor resp muscle function
-both
Hypoventilation
-signs
-RR low
-increased PaCO2
Potential problem with giving opioid for pain before heading to PACU:
-pt resp drive will decrease
-may not peak until pt is in PACU, esp if given IM
Central resp depression is most profound in
PACU on admission
What is the secondary stage of respiratory depression seen in PACU?
-stimulation is gone and they relax too much
-could happen from extubation(tube not irritating them)
-monitor SpO2 and EtCO2!
-verbal or tactile stim, tell pt to breathe
Factors that can prolong NM blockade:
-aminoglycoside abx (mycins)
-mag
-lithium
-hypermag, hypokalemia
-resp acidosis, hypothermia
Factors impairing resp muscle function
-obesity (increased intraabdominal pressure)
-upper abd surg (reduced VC 2/2 poor diaphragmatic function)
-NM diseases (best to leave these pts intubated in PACU until total return of function)
-drugs not reversed
A reduction in VC of up to _% is noted on first postop day
60%
HoTN definition
20% drop from baseline
-SBP <90
-MAP<60
-focus on clinical signs instead tho
HoTN in PACU is most commonly caused by:
-hypovolemia 2/2 blood loss and inadequate fluid admin
HoTN
-can cause:
-CVA
-MI
-renal ischemia
-bowel ischemia
-spinal cord damage
If pt is not bleeding and low BP is not responding to 300-500mL bolus, what is the problem likely?
Cardiac dysfunction
Cardiogenic HoTN can occur with:
-what is patho?
-MI
-tamponade
-PE
-acute fall in ventricular emptying and CO; pump failure
Secondary cardiac dysfunction can occur from
-negative inotropic/chronotropic meds
-surgical case
How can certain drugs impact/cause HoTN
-histamine release causing vasodilation (morphine, atracurium, or allergy - contrast, latex,propofol, abx)
-relaxing arterial smooth musc causing vasodilation (IA, LA)
-sensitivity to vasodilator meds (NTG, nipride, hydralazine)
Latex impact on HoTN
-allergic reaction occurring ~40 min after exposure
-hypotension and vascular collapse
How Methyl Methacrylate causes HoTN
-can cause hypotension 30-60 sec after cement is placed
-tissue damage 2/2 exothermic reaction of cement
-release of vasoactive substances when cement is hydrolyzed to methacrylate acid
-embolization as bone is reamed
-vasodilation from absorption of volatile monomer
How Opioids cause HoTN
-decreased sympathetic tone causing bradycardia
Most common meds to cause allergic reactions:
NM blockers and abx(mostly abx)
Concerns around pt taking ACEi
-refractory HoTN
Hypnotics impact on HoTN
-vasodilation
Propofol impact on profound HoTN
-allergic reaction possible from eggs/soybean component
-also just causes HoTN normally
-didn’t Nagelhout dispute this? whatev
How do IA cause HoTN
decrease SVR, dose dependent
How do LA cause HoTN
LAST
-this is a late sign
How NMBD cause HoTN
-rapid injection
-Suggamadex injected rapidly is a new cause of anaphylaxis
How regional anesthesia causes HoTN
-vasodilation
-occurs BELOW level of block 2/2 block of SYMPATHETIC conduction fibers
HoTN
-Tx
-ALWAYS give O2
-elevate legs
-check volume status-give fluids if needed
-ensure BP cuff is right size or no artifcact
T/F If pt is hypotensive from myocardial dysfunction they will benefit from coronary vasodilators, inotropic therapy, and afterload reduction like NTG or Dobutamine or both.
-true!
-sounds weird to give vasodilator and afterload reducer but it will help
Vasodilation causing low SVR and symptomatic hypoperfusion can be treated with:
vasoactive agents via bolus or infusion
-Ephedrine (5-50mg)
-Epi (10-100mcg)
-Phenylephrine (50-200mcg)
-Vasopressin(1-4 units)
-dopamine or epi infusion
HTN definintion
-rise in arterial BP 20% above baseline or absolute value above AGE-CORRECTED LIMIT
HTN causes in PACU
-SNS stim
-pain
-resp compromise
-increases in plasma catecholamines
-preop HTN
-hypervolemia
-shiver
-emergence excitement
-increased ICP
-Hypercapnia
-Bowel or urinary distention
Leading cause of HTN and tachycardia in PACU
PAIN
-causes stim of somatic AFFerent nerves causing pressor response known as SOMATOSYMPATHETIC REFLEX
-analgesics help pain and fix BP
Patho of HTN from hypoxemia and hypercarbia
-DIRECT stim of vasomotor area of MEDULLA causing increased vasomotor tone, arteriolar constriction, and increased BP
-fixing hypoxemia/hypercarbia should fix BP
T/F Continue all BP meds preop
false, not ACEi or angiotensin II antagonists
Agent of choice for vasodilation
NTG and nipride
PONV
-Which is more common, N or V?
N
T/F Prepubescent females are 2-3x more likely to experience PONV than males
false!
-POST pubescent
How is Apfel and Koivuranta PONV risk scores different?
-Koivuranta has everything Apfel does but adds in case duration >1hr as a factor
Eberhart PONV Risk Score for children includes which 4 main factors?
-case >30 min
-3yo or older
-strabismus surgery
-hx of POV or fam history of PONV
other factors not in this list include:
-post-pubescent females
-tonsillectomies
-eye surg
-otoplasty
-VA and anticholinergic use
-postop long acting opioids
T/F Multimodal prophylaxis for PONV should be administered if pt has only 1 or more risk factors
true!
T/F Using propofol as main anesthetic is a viable method to prevent PONV
true
-multimodal approach is best tho
Largest anesthetic risk factor contributing to PONV is:
using volatile anesthetics
Adult PONV Rx Management Algorithm
-Fig 55.5
- Risk factors
-female
-younger
-nonsmoker
-surgery type
-hx of PONV/ motionsickness
-opioid analgesia - Risk mitigation
-minimize use of N2O, VA, and high dose Neostigmine
-consider regional
-opioid sparing multimodal analgesia
3.Risk stratification
-1-2 risks = give 2 agents
->2 risks = give 3-4 agents
- Prophylaxis
-5HT3 receptor antagonists
-Antihistamines
-Propofol
-Acupuncture
-Steroids
-Dopamine antagonists
-NK-1 receptor antagonists
-Anticholinergics - Rescue Tx
-use antiemetic from diff class than prophylactic drug given
Distention of the bladder, bowel, or stomach causes stim of _ nerve fibers in SNS leading to increased catecholamine levels and HTN
afferent
How can hypothermia cause HTN?
-increase catecholamine in serum and as body warms, vessels are more sensitive and arteries and veins vasoconstrict
How can cardiac and vascular surgery or endarterectomy cause HTN?
-revascularization
-baroreceptor reflex
Meds to control HTN in PACU:
-hydralazine- relaxes vasc smooth musc- 2-4mg
-labetalol- alpha and beta blockade = vasodilation and slows HR- 5-10mg
-metoprolol-b blocker control SNS response during recovery 1-2mg
-esmolol - slows HR 10-50mg
Torsades is linked to medication that are known to:
-prolong QT interval
-lots of anesthesia drugs do this
Signs of cardiac irritability:
-conduction delays
-heart block
-dysrhythmias
Early signs of hypercarbia:
tachycardia and HTN
EKG changes you will see with hypokalemia
-wide QRS
-U wave and ST segment abnormalities
-PVC, VT, Vfib
Risk factors for dysrhythmias:
-hypokalemia
-excess fluid
-anemia
-hypoventilation and hypercarbia
-acid/base abnormalities
-substance withdrawal
-hypothermia (bradycardia and afib->AV block and Vfib)
-circulation issues (HoTN->ischemia->ekg changes; preexisting heart disease, vagal reflexes)
Meds that can contribute to dysrhythmias in PACU:
-ketamine (increase Bp, HR)
-anticholinergics(increase BP, HR)
-opioids (hypoxemia and hypercarbia-indirect)
-AntiChE (bradycardia and heart blocks)
