SRNA Exam III — High-Yield Study Guide

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How to prioritize this exam

Spend your time according to the blueprint, not according to which lecture feels longest.

Highest return

Coagulation/TEG + PACU = 20 of 40 questions. These sections contain many clean classification questions: abnormal finding → physiologic defect → treatment.

Most likely safety vignettes

Anaphylaxis, oculocardiac reflex, intraocular gas + nitrous oxide, airway obstruction, laryngospasm, aspiration, and delayed emergence.

Likely SATA construction

Expect 4–6 options mixing true mechanisms, correct treatments, plausible but wrong drug classes, and one unsafe “continue/observe” choice.

Recommended review order

TEG + pathways→ PACU airway/respiratory→ OCR + IOP + eye drugs→ Anaphylaxis→ PONV numbers

Lecture-specificMemorize the numbers as they appear in the slides when the test is based on the lecture. Several values—especially Apfel percentages and some treatment doses—are presented in a lecture-specific way.

Hypersensitivity & Anaphylaxis

Approx. 7 questions • Classification + recognition + perioperative triggers + immediate treatment.

Absolute must knowPerioperative anaphylaxis may present without obvious skin findings. Under anesthesia, the earliest visible clues may be unexplained hypotension, difficult ventilation/bronchospasm, tachycardia or bradycardia, falling ETCO₂, and cardiovascular collapse.

Types I–V: separate them by mediator, timing, and example

Type	Core mechanism	Timing	Classic examples / test hooks
I — immediate	Th2 → B-cell production of antigen-specific IgE; IgE binds mast cells/basophils; re-exposure cross-links receptors → Ca²⁺ influx and degranulation. Histamine is the major mediator.	15–30 min	Anaphylaxis, drug allergy, hay fever, asthma. Bronchoconstriction, vasodilation, ↑ vascular permeability, mucus, urticaria/pruritus.
II — cytotoxic	IgG or IgM against cell surface/tissue antigen + complement; macrophage activation.	Minutes to hours	Drug-induced hemolytic anemia, transfusion reaction, thrombocytopenia, myasthenia gravis, type 1 DM.
III — immune complex	Soluble antigen–antibody complexes (IgG/IgM) deposit in tissue; complement-mediated inflammation; not tissue-specific.	Hours to weeks	SLE, rheumatoid arthritis, serum sickness.
IV — delayed / cell mediated	T lymphocytes, monocytes, macrophages; no antibody involvement.	24 h–14 d	Poison ivy/contact dermatitis, TB/leprosy granulomatous response; PPD/Mantoux is a diagnostic type IV reaction.
V — stimulatory	IgG autoantibody stimulates a receptor, mimicking normal ligand activity.	Variable	Graves disease: antibody stimulates the TSH receptor.

Easy separator

I = IgE + immediate.
II = antibody attacks a cell.
III = immune complexes deposit.
IV = T cells, delayed, no antibody.
V = antibody stimulates a receptor.

Prior exposure trap

Classic IgE-mediated type I requires sensitization. However, non-IgE mast-cell activation can occur on first exposure, and many NMBA reactions occur during the patient’s first documented anesthetic exposure because of prior environmental sensitization to quaternary ammonium structures.

Perioperative anaphylaxis: triggers and distinctions

Agent / category	High-yield point
Neuromuscular blockers	Lecture: responsible for about 60–70% of allergic reactions under anesthesia. The chapter identifies NMBAs as the most frequently implicated anesthetic drugs. Succinylcholine and rocuronium are prominent culprits; quaternary ammonium is the suspected antigenic structure.
Atracurium	Can cause histamine release that is not necessarily IgE anaphylaxis. A flushing/hypotension response is not automatically proof of allergy.
Sugammadex	Has been proposed to encapsulate rocuronium during rocuronium-associated anaphylaxis, but sugammadex itself can cause anaphylaxis. Do not treat it as a guaranteed antidote.
Antibiotics	Close second—or first depending on the study. Lecture emphasizes penicillin and possible cephalosporin cross-reactivity. Avoid a cephalosporin when the history is true penicillin anaphylaxis unless the plan is specifically evaluated.
Vancomycin	Infuse slowly to reduce the non-IgE infusion reaction commonly called “red man syndrome.”
Latex / chlorhexidine / iodine prep / dyes / contrast	Topical and surgical-field agents matter. Latex incidence has decreased with prevention policies, but chlorhexidine, dyes, and antiseptics remain possible hidden triggers.
Propofol	The lecture states that patients with egg or soy allergy are not more susceptible to propofol anaphylaxis.
Blood / colloids	Can trigger reactions. Stop the product, maintain the line with appropriate fluid, verify the product/patient, and treat the physiologic reaction.
Local anesthetic	True allergy is uncommon; many cardiovascular events are caused by intravascular injection or toxicity, not hypersensitivity.

Korogoda emphasisPrevention starts with a deliberate allergy history and cross-reactivity review. Routine pretreatment is not recommended because it usually does not prevent anaphylaxis.

Intraoperative anaphylaxis: action sequence

Stop the suspected triggering agent and announce the emergency.
100% oxygen; secure/assist the airway and ventilation.
Epinephrine is definitive first-line treatment. It treats vasodilation, capillary leak, bronchospasm, and myocardial depression.
Rapid IV fluid resuscitation. Lecture: approximately 20 mL/kg or more; the chapter’s treatment box gives a broad 10–30 mL/kg crystalloid range.
Treat persistent bronchospasm with inhaled β₂ agonist; use vasopressors/vasopressin for refractory shock as directed by severity.
Antihistamines and corticosteroids are secondary. They do not replace epinephrine.
After stabilization: obtain serum tryptase within 120 minutes, document the timeline and every exposure, notify the patient/family, and refer for allergy evaluation.

Lecture dose framing

The slide lists epinephrine 5–10 mcg boluses for slight hypotension and 500–1000 mcg for grade 3–4 reactions, plus 100% O₂, fluids, albuterol, antihistamines, and hydrocortisone.

Book severity framing

The chapter grades reactions from cutaneous signs to arrest and escalates epinephrine with severity. Route, concentration, and grade matter. For testing, prioritize “epinephrine early” and do not choose antihistamine or steroid as the first lifesaving drug.

Biphasic and refractory reactions

Biphasic anaphylaxis can recur after an asymptomatic period without re-exposure; most second episodes occur within 8 hours but may be delayed.
Risk rises with a severe initial event, multiple epinephrine doses, or delayed epinephrine.
Antihistamines and glucocorticoids do not reliably prevent a biphasic event.
For a patient taking a β-blocker with refractory hypotension/bronchospasm, the chapter lists glucagon as a rescue consideration.

Primary source locations: Hypersensitivity lecture pp. 2–22; Immune System chapter pp. 13–16 (PDF pagination).

Coagulation, Hematologic Disorders & TEG

Approx. 10 questions • Largest concentration of predictable matching and “what product fixes this?” items.

Core sequence

Vasoconstriction→ Platelet plug→ Coagulation / fibrin→ Clot stabilization→ Fibrinolysis

Primary hemostasis: platelet adhesion vs aggregation

Step	Molecule / receptor	What it does
Adhesion	Subendothelial collagen + vWF + platelet GPIb	vWF forms the bridge that makes platelets adhere to the injured vessel wall.
Activation	Collagen, thrombin, ADP, TXA₂	Platelet becomes irregular, releases granules, recruits more platelets, and provides a phospholipid surface.
Aggregation	GPIIb/IIIa receptors linked by fibrinogen	Connects activated platelets to one another to form the primary plug.
Stabilization	Fibrin + factor XIII	Cross-linked fibrin strengthens the platelet plug into a stable secondary clot.

Platelet granules: alpha granules contain proteins such as vWF, fibrinogen and platelet factor 4; dense granules contain nonproteins such as ADP, ATP, serotonin, histamine and epinephrine.

Pathways: memorize the clean map

Extrinsic

III + VII → X

Triggered by tissue factor outside the vessel. Faster pathway. Assessed by PT/INR. Warfarin prominently affects this test because factor VII falls early.

Intrinsic

XII → XI → IX + VIII → X

Contact activation / collagen within the vascular system. Assessed by aPTT. Unfractionated heparin is monitored here.

Common

X + V → II → I; XIII stabilizes

Xa + Va converts prothrombin (II) to thrombin (IIa); thrombin converts fibrinogen (I) to fibrin (Ia); XIII cross-links fibrin.

Slide wording trapThe coagulation slide on platelet plug formation contains shorthand that can read as though prothrombin becomes fibrin. Use the later lecture summary and textbook sequence: prothrombin → thrombin → fibrinogen → fibrin.

Vitamin K dependent

II, VII, IX, X + proteins C and S

Mnemonic: “1972” or “2, 7, 9, 10.”

Notable synthesis exceptions

Most factors are made in the liver. III is tissue factor, IV is calcium from the diet, and vWF is produced by endothelial cells.

Lab test → pathway → interpretation

Test	What it assesses	High-yield interpretation
Platelet count	Number, not function	Normal count does not guarantee normal function. Chapter thresholds: >100,000 generally sufficient; ~50,000 raises surgical bleeding concern; <20,000 risks spontaneous bleeding.
Bleeding time	Microvascular contraction + platelet function	Altered by aspirin/NSAIDs, but a modest isolated prolongation is a poor predictor of operative bleeding.
PT / INR	Extrinsic + common	Factor VII and common pathway defects; monitor warfarin.
aPTT	Intrinsic + common	Factors XII, XI, IX, VIII and common pathway; monitor unfractionated heparin.
Thrombin time	Final fibrinogen-to-fibrin reaction	Ending phase of coagulation; less emphasized when fibrinogen is measured directly.
ACT	Rapid whole-blood clotting test	Used intraoperatively for high-dose heparin; lecture/book normal range roughly 80–150 or 90–150 seconds depending on source.
Fibrinogen	Substrate for fibrin	Low fibrinogen = weak clot kinetics; think cryoprecipitate.
D-dimer / FDP	Products of clot breakdown	Reflect fibrinolysis; elevated in DIC and many thrombotic/inflammatory conditions, so sensitive but not specific.

Blood products and targeted replacement

Product / drug	Contains or does	Think of it for…
PRBC	Red cells; no meaningful factor replacement	Improve oxygen-carrying capacity / symptomatic anemia.
Platelets	Platelets and some plasma factors	Thrombocytopenia or platelet dysfunction; low TEG MA.
FFP	All coagulation factors; especially useful for multiple factor deficiency	Prolonged R time / factor deficiency, warfarin reversal when PCC unavailable, DIC with bleeding.
Cryoprecipitate	Fibrinogen (I), VIII, XIII, vWF	Hypofibrinogenemia; prolonged K / low alpha angle; selected vWD treatment when preferred products are unavailable.
DDAVP	Stimulates endothelial release of vWF	Type 1 / selected type 2A vWD, uremic platelet dysfunction; lecture lists 0.3 mcg/kg.
Protamine	Heparin antagonist	Reversal of unfractionated heparin; partial reversal of LMWH.
Vitamin K / 4-factor PCC	Vitamin K restores synthesis; PCC supplies II, VII, IX, X	Warfarin reversal. Serious bleeding requires rapid factor replacement plus vitamin K.
TXA / aminocaproic acid	Antifibrinolytic; inhibits plasmin-mediated fibrin breakdown	Excess fibrinolysis / elevated LY30.

Disorders that are built for MCQ/SATA

von Willebrand disease

Most common inherited bleeding disorder.
Defective platelet adhesion + reduced factor VIII protection.
Prolonged bleeding time; decreased vWF activity measured by ristocetin cofactor assay.
Treatment may include DDAVP, vWF/FVIII concentrate, TXA; cryo if preferred therapies unavailable.

Hemophilia

A = factor VIII.
B = factor IX / Christmas disease.
X-linked recessive; predominantly affects males.
Intrinsic pathway defect → prolonged aPTT; platelet function is not the primary problem.

DIC

Secondary to an underlying process: sepsis, HELLP/obstetric catastrophe, transfusion reaction, malignancy or major trauma.
Can produce thrombosis, bleeding, or both.
Typical pattern: falling platelets and fibrinogen, prolonged PT/aPTT, elevated D-dimer/FDP.
Treat the cause; replace FFP, platelets and/or cryo when clinically bleeding.

HIT type II

Immune IgG response to heparin–platelet factor 4 complex.
Think HIT when platelets fall >50% after heparin/LMWH.
It is a prothrombotic emergency, not merely a bleeding disorder.
Stop all heparin and use a non-heparin anticoagulant; future heparin is contraindicated unless specialist-guided.

Sickle cell disease

Prevent sickling: maintain oxygenation, hydration, normothermia, analgesia, and perfusion.
Avoid acidosis, hypoxemia, hypothermia, dehydration and prolonged vascular compression.

Warfarin early effect

Factor VII and protein C have short half-lives.
Early protein C depletion may transiently create a prothrombotic state.
Warfarin takes days to achieve full effect because existing factors must clear.

Antiplatelet drugs: identify the target

Class	Examples	Mechanism / testable detail
COX inhibition	Aspirin, NSAIDs	Blocks TXA₂ production. Aspirin is irreversible for platelet lifespan; lecture uses 8–12 days. NSAID effect is reversible and shorter, about 12–48 h in the slide.
ADP/P2Y12 inhibition	Clopidogrel, ticlopidine	Reduces ADP activation of GPIIb/IIIa; effect persists for the platelet’s lifespan.
GPIIb/IIIa blockade	Abciximab, eptifibatide	Prevents fibrinogen cross-bridging and platelet aggregation; bleeding and thrombocytopenia are major adverse effects.

The specific TEG picture: read left to right

The uploaded exam image maps each segment of the tracing to a specific deficiency and product. Use the tracing’s time sequence: initiation → fibrin build-up → final strength → clot breakdown.

TEG variable	What it represents	Normal in uploaded image	Abnormal means	Treatment shown
R time	Time until clot begins forming	5–10 min	Coagulation factor deficiency	FFP
K time	Time until clot reaches a fixed strength	1–3 min	Fibrinogen problem	Cryoprecipitate
Alpha angle	Speed of fibrin accumulation / clot strengthening	53–72°	Fibrinogen problem	Cryoprecipitate
Maximum amplitude (MA)	Highest vertical amplitude / overall clot strength	50–70 mm	Platelet number/function problem	Platelets and/or DDAVP
LY30	% amplitude reduction 30 min after MA	0–8%	Excess fibrinolysis	TXA and/or aminocaproic acid

One-sentence TEG rule: Long R = replace factors; long K/low alpha = replace fibrinogen; low MA = platelets; high LY30 = stop fibrinolysis.

Primary source locations: Coagulation lecture pp. 2–40; Hematology chapter pp. 1–21; uploaded TEG/ROTEM picture.

Ophthalmic Anesthesia

Approx. 9 questions • Cranial nerves, IOP, OCR, systemic eye-drug effects, gas expansion, and block complications.

Clinical frameThe ophthalmic procedure may be relatively low risk, but the patient is often elderly, at an age extreme, and medically complex. The drape and turned table reduce airway access while absolute immobility may still be required.

Cranial nerves and eye movement

Nerve	Function / target	High-yield link
II — optic	Visual afferent input	Outgrowth of the brain, covered by meninges. Local anesthetic in the optic nerve sheath can track centrally in CSF and cause CNS depression or respiratory arrest.
III — oculomotor	Most extraocular muscles; pupillary function	Most motor movement except SO and LR.
IV — trochlear	Superior oblique	SO4; intorts and depresses.
V1 — trigeminal ophthalmic	Ocular sensation; afferent corneal reflex	Afferent limb of OCR.
VI — abducens	Lateral rectus	LR6; abducts.
VII — facial	Orbicularis oculi / blinking / eye closure	May require facial nerve block when complete eyelid akinesia is needed.
X — vagus	Parasympathetic efferent output	Efferent limb of OCR.

Extraocular muscle shorthand: Superior rectus = up; inferior rectus = down; medial rectus = adduct; lateral rectus = abduct; superior oblique = intort/depress; inferior oblique = extort/elevate.

Intraocular pressure (IOP)

Goldmann equation

IOP = (F / C) + P

F = aqueous humor flow/production; C = outflow; P = episcleral venous pressure.

Lecture normal: 12–20 mmHg.

Aqueous pathway

Produced by ciliary epithelium in the posterior chamber → through pupil → anterior chamber → exits mainly through the canal of Schlemm.

Raises IOP	Lowers or does not significantly raise IOP
Direct laryngoscopy/intubation, airway obstruction, hypercarbia, hypoxia, coughing/bucking, squinting, Trendelenburg, increased venous pressure, succinylcholine (transient 5–10 mmHg for 5–10 min in the lecture).	Volatile agents, nitrous oxide in the absence of an intraocular gas bubble, propofol, benzodiazepines, opioids; nondepolarizers have no effect or may decrease IOP.

Open globe nuanceThe lecture states succinylcholine was historically avoided because it raises IOP, but multiple studies have used it safely and it is not presented as an absolute contraindication. The priority is a smooth, controlled RSI/intubation with no coughing or bucking.

Oculocardiac reflex (OCR)

Definition and pathway

Heart rate decrease >20% after extraocular muscle traction or globe compression.

V1 afferent → vagus efferent.

Also called the Aschner phenomenon or five-and-dime reflex.

Manifestations

Bradycardia, nodal rhythm, AV block, PVCs, idioventricular rhythm, asystole, and even VF. It may be sudden, profound, and unexpected.

Triggers: extraocular muscle traction, globe pressure, local infiltration, retrobulbar block, peribulbar block, and stimulation under GA. It is especially common in pediatric strabismus repair.

Lecture treatment sequence: stop the stimulus → verify ventilation, oxygenation, and depth → atropine/glycopyrrolate if HR does not recover → surgeon may infiltrate local anesthetic. Repeated stimulation can eventually fatigue the reflex, but continuing traction is not the first action.

OCR first step: Tell the surgeon to stop stimulation. Then correct hypoxia/hypercarbia or inadequate anesthetic depth; give atropine or glycopyrrolate if the heart rate does not recover.

Systemic implications of ophthalmic medications

Reduce systemic absorption: keep the eye closed for ~60 seconds, avoid rapid blinking, and apply pressure over the medial canthus to block nasolacrimal drainage.

Drug class	Examples	Anesthetic implication
Mydriatics / alpha agonists	Phenylephrine, epinephrine	Pupillary dilation; can cause systemic hypertension.
Cycloplegic	Atropine	Temporary ciliary muscle paralysis and impaired accommodation.
Miotics / cholinergic agonists	Pilocarpine, carbachol	Miosis; can cause bradycardia and bronchospasm.
Alpha-2 agonists	Brimonidine, apraclonidine	Reduce aqueous production; lecture says contraindicated with MAO inhibitors.
Cholinesterase inhibitor	Echothiophate	Improves outflow and causes miosis; can depress plasma cholinesterase for 4–6 weeks, prolong succinylcholine, and prolong ester local anesthetics.
Topical beta-blocker	Timolol, levobunolol, betaxolol	Reduce aqueous production. Caution with asthma/COPD, heart block, heart failure, hypotension and bradycardia.
Carbonic anhydrase inhibitor	Acetazolamide	Reduces aqueous production; alkaline diuresis and possible potassium depletion. Check electrolytes.
Prostaglandin	Latanoprost, bimatoprost, travoprost, tafluprost	Promotes aqueous outflow.

Intraocular gas + nitrous oxide: a classic safety question

Stop N₂O 15–30 minutes before the surgeon places the bubble. Avoid N₂O afterward until the bubble is completely absorbed—even for an unrelated surgery.

Gas	Approximate persistence in lecture
Air	5 days
SF₆	10 days
C₄F₈	15 days
C₃F₈	30 days

Techniques and regional block complications

Technique	High-yield facts
Topical / MAC	Discuss immobility preoperatively. Not appropriate for posterior chamber procedures in the lecture. Tetracaine 0.5% and lidocaine 2–4% are listed. Small doses of sedatives; omit midazolam in elderly patients with cognitive dysfunction.
Retrobulbar	Intraconal; dense anesthesia/akinesia and may abolish OCR. Lecture: 25-gauge dull needle, negative aspiration, 2–4 mL LA. Risks include optic nerve/vessel/globe trauma, intravascular injection, hemorrhage, vision loss and central spread.
Peribulbar	Extraconal; delayed onset, may require more volume and may not produce complete akinesia. Medial approach is best for eyelid akinesia in the lecture.
Sub-Tenon	Blunt curved cannula into subscleral space under Tenon fascia; fewer side effects than retrobulbar/peribulbar in the lecture.
Facial nerve block	Used for eyelid akinesia. Nadbath is not recommended because of proximity to CN IX/X and potential vocal cord paralysis, laryngospasm, dysphagia and respiratory distress.

Retrobulbar hemorrhage

Proptosis + conjunctival hemorrhage + increased orbital pressure. Can compress the optic nerve and retinal vessels, risking vision loss. Lecture treatment: direct pressure and lateral canthotomy.

Optic nerve sheath / central spread

Contralateral amaurosis or pupillary dilation, CNS depression, apnea/respiratory arrest. Prepare to ventilate and resuscitate. Intra-arterial LA can cause a grand mal seizure.

Open globe: anesthetic goals

IOP approaches atmospheric pressure; prevent further increases.
Smooth induction and intubation; deepen and paralyze before laryngoscopy.
Avoid coughing, bucking, hypoxia, hypercarbia and airway obstruction.
Lecture lists lidocaine, opioid and esmolol as tools to blunt the response.

Primary source locations: Ophthalmic lecture pp. 1–30; ophthalmic anesthesia chapter pp. 1–21.

Postoperative Nausea & Vomiting

Approx. 4 questions • Risk scores, prevention, receptor classes, ondansetron safety, and rescue therapy.

Lecture-specific numberUse of volatile anesthetics is identified as the strongest predictor of PONV in the presentation.

Adult PONV risk: Apfel score

Four factors

Female sex
Nonsmoker
History of PONV or motion sickness
Postoperative opioid use

Percentages shown in lecture

1 factor = 10%
2 = 20%
3 = 60%
4 = 80%

These are the slide’s displayed values—memorize them for a lecture-based exam.

PDNV score

Six factors: female sex, nonsmoker, history of PONV/motion sickness, postoperative opioids, age <50, and PONV in PACU. The lecture lists risk through five factors: 0=10%, 1=20%, 2=30%, 3=50%, 4=60%, 5=80%.

Pediatric risk: Eberhart simplified score

Procedure duration ≥30 minutes
Age ≥3 years
Strabismus surgery
Personal history of postoperative vomiting or PONV in immediate relatives

Multimodal prevention: reduce baseline risk first

SAMBA-style strategies in lecture

Use fewer opioids
Regional anesthesia when possible
Avoid volatile agents; use propofol/TIVA
Adequate hydration
Sugammadex for NMB reversal
Avoid nitrous oxide for procedures >1 hour

Propofol

The lecture describes propofol as an antiemetic and states that using propofol/TIVA can be as effective as ondansetron for reducing PONV risk.

Receptor classes

Target	Examples / high-yield point
5-HT₃	Ondansetron, palonosetron, granisetron, dolasetron. Work at CTZ and vagal afferents; better anti-vomiting than anti-nausea.
D₂ / D₂-D₃	Droperidol, haloperidol, amisulpride, metoclopramide. Higher metoclopramide doses may be more effective but increase extrapyramidal effects.
H₁	Diphenhydramine; sedating.
Muscarinic	Scopolamine; anticholinergic adverse effects.
NK-1	Substance P antagonism; useful in multimodal high-risk prophylaxis.
Corticosteroid	Dexamethasone; prophylactic and sometimes listed as rescue in the lecture.

Ondansetron administration safety

Lecture: typical dose 4 mg IV (0.15 mg/kg; do not exceed 16 mg IV). Give 4 mg over at least 30 seconds and preferably over 2–5 minutes. Rapid injection can cause severe bradycardia, atrial fibrillation, QTc prolongation and ventricular tachycardia.

Palonosetron

No QT prolongation in the lecture; ~40-hour half-life; administer at the beginning of surgery; duration up to 72 hours.

Rescue rule

If PONV occurs despite prophylaxis, identify mechanical causes and hydration status, then use a drug from a different mechanism/class. Do not simply repeat ondansetron after ondansetron prophylaxis has failed.

Primary source: PONV presentation pp. 1–25.

PACU, Emergence & Postoperative Complications

Approx. 10 questions • Triage, scoring systems, delayed emergence, airway/respiratory emergencies, hemodynamics, temperature and discharge.

PACU priorityAirway, ventilation, oxygenation and circulation come before the report. The anesthesia provider remains involved until the receiving nurse accepts responsibility and the patient is stabilized on appropriate monitors.

Disposition and transport

Concept	High-yield point
Level of postoperative care	Based on comorbidities, surgery, anesthetic, and intraoperative events—not insurance, age alone, ASA alone, or OR vs NORA label.
Fast-track / bypass phase I	Typically MAC or regional cases that meet facility criteria. GA usually cannot bypass phase I. Document that bypass criteria are met.
Transport to PACU	Patient should have a stable open airway, adequate ventilation/oxygenation and stable vital signs. If not, use a secured airway and monitoring.
Transport to ICU	Bring bag-mask device, full O₂ tank, airway equipment, emergency medications and required monitors; protect lines, drains, pacers and tubes.
Handoff	Include history/allergies, anesthetic and airway, last opioid, reversal, antiemetics/antibiotics/vasopressors, EBL, fluids/blood, urine output, events, labs and anticipated PACU problems.

Emergence: what controls speed?

Inhaled agents

Faster with increased alveolar ventilation. Slower with higher blood:gas solubility, higher fat:gas solubility, and longer exposure.

IV agents

Metabolism, volume of distribution, redistribution, context-sensitive half-time, dose and duration.

The lecture defines delayed emergence as failure to awaken within an expected period and cites >15 minutes as a Barash threshold. Most patients regain consciousness within 15 minutes of PACU admission.

Scoring systems

Modified Aldrete: activity, respiration, circulation/BP, consciousness, oxygen saturation. Maximum 10; lecture image requires ≥9 for discharge.

PADSS: vital signs, activity, nausea/vomiting, pain and surgical bleeding. Lecture image requires ≥9 for discharge.

Delayed emergence: use an ordered differential

Protect airway and assess GCS; review history, drugs, timing and interactions. Check ventilation, oxygenation, BP, ECG and temperature; consider reversal; assess glucose, electrolytes and ABG; then evaluate neurologic causes and obtain imaging if unresolved.

Do not jump straight to CT. First fix oxygenation/ventilation/hemodynamics and identify residual anesthetic, opioid, benzodiazepine, anticholinergic or neuromuscular blockade. Then evaluate metabolic and neurologic causes.

Hemodynamic complications

Hypotension

Lecture definition: >20% below baseline, SBP <90 or MAP <60. Assess perfusion, not the number alone. Hypovolemia is most common in PACU. Consider cardiac and distributive causes.

Hypertension

>20% above baseline. Pain is the most common cause of PACU hypertension/tachycardia. Also think hypoxemia, hypercarbia, bladder distention, shivering, hypothermia, delirium and hypervolemia. Treat the cause.

Postoperative myocardial ischemia may be silent. Hypotension and tachycardia may be the first signs. Absence of ST-T changes does not rule out ischemia.

Airway and respiratory complications

Problem	Recognition	First actions / treatment
Upper airway obstruction	Snoring, accessory muscle use, suprasternal/intercostal retractions; tongue is the most common obstruction.	Reposition, jaw thrust, oral/nasal airway, CPAP or positive pressure; reverse residual drugs/NMB as appropriate.
OSA	Partial/complete obstruction; opioid sensitivity.	Bring/apply home CPAP; use opioid-sparing plan; continue pulse oximetry until SpO₂ >90% on room air while sleeping per lecture.
Laryngospasm	Partial or complete glottic closure, often after deep extubation.	Stop stimulus, jaw thrust, gentle PPV with 100% O₂, deepen with propofol; succinylcholine if persistent. Lecture lists 0.1 mg/kg IV as a small dose and broader source ranges up to 1 mg/kg IV or 4 mg/kg IM.
Bronchospasm	Wheezing, desaturation, dyspnea, tachypnea, accessory muscle use.	Remove cause, O₂, β₂ agonist, deepen anesthesia if in OR, add anticholinergic if needed. Life-threatening bronchospasm: epinephrine infusion in lecture.
Hypoventilation	Most commonly opioid-induced; also residual sedation/NMB, OSA/obstruction, poor muscle function or splinting from pain.	Fix the cause. Oxygen is a bridge, not definitive treatment. Ventilate/intubate for marked hypoxemia and hypercarbia.
Atelectasis	Lecture: most common postoperative cause of hypoxemia.	Humidified O₂, cough/deep breathe, incentive spirometry, secretion clearance, mobilization and CPAP when appropriate.
NPPE	After forceful inspiration against a closed glottis; hypoxemia, crackles, cough and pink frothy sputum. Muscular patients can generate large negative pressure.	Relieve obstruction, O₂/positive pressure/PEEP; intubate if needed. It is noncardiogenic.
Pulmonary embolism	Vague/rapid: tachypnea, tachycardia, hypoxemia; may deteriorate suddenly.	O₂, hemodynamic support, diagnostic imaging when stable, anticoagulation as appropriate.

Lecture phraseSupplemental oxygen does not address the underlying cause. It may normalize the pulse-oximeter reading while hypercarbia, obstruction, hypoventilation or evolving lung disease persists.

Aspiration: distinguish pneumonitis from pneumonia

Aspiration pneumonitis

Usually larger-volume acidic gastric contents → chemical lung injury and possible ARDS.

Aspiration pneumonia

May be unwitnessed and lower volume → bacterial infection and possible ARDS.

Secretions seen in the oropharynx

Immediate lateral positioning and suction.
Consider reintubation.
Suction the trachea before positive-pressure ventilation when feasible.
Do not instill saline routinely.
Monitor for cough, wheezing, hypoxemia and infiltrates; lecture suggests 24–48 h observation.

Temperature, agitation, and other postoperative issues

Hypothermia

Prolongs PACU stay, increases sympathetic activity, dysrhythmia/MI risk, coagulopathy and infection. CMS quality target in lecture: >36°C. Best prevention is maintaining temperature intraoperatively.

Shivering

May increase O₂ consumption by 400–500%. Rewarm with forced-air warming and warmed fluids/blood. Lecture lists meperidine 10–25 mg IV; fentanyl can also work.

Emergence delirium / agitation

Common in healthy pediatric patients and young adults. Before sedating, treat pain, hypoxia, hypercarbia, hypotension and bladder distention. Protect the patient, staff, surgical repair, eyes and IVs.

Serotonin syndrome

Combination serotonergic drugs; triad of autonomic hyperactivity, neuromuscular abnormalities and mental-status change. Stop drugs, monitor, give fluids/O₂ and benzodiazepines.

Postoperative evaluation

The lecture states CMS requires a written follow-up by an individual qualified to administer anesthesia no later than 48 hours. Include respiratory function/airway/SpO₂, cardiovascular status, mental status, temperature, pain, nausea/vomiting and hydration. Document findings and address patient complaints.

Primary source locations: PACU/Postop lecture pp. 1–52; Postanesthesia Recovery chapter pp. 1–21.

✓

Last-minute “absolutely know” list

These are the facts most likely to turn an almost-correct answer into the correct answer.

Type I = IgE, mast cell/basophil, immediate.
Type IV = T-cell mediated, delayed, no antibody.
Anaphylaxis under anesthesia may lack skin signs.
Epinephrine is first-line; antihistamines/steroids are secondary.
NMBA and antibiotics are leading perioperative triggers.
Atracurium histamine release is not automatically anaphylaxis.
Tryptase should be obtained within 120 minutes after the event.
Adhesion: vWF–GPIb. Aggregation: fibrinogen–GPIIb/IIIa.
Extrinsic: III + VII; PT/INR.
Intrinsic: XII, XI, IX, VIII; aPTT.
Common: X, V, II, I; XIII stabilizes.
Vitamin K: II, VII, IX, X, C and S.
vWD is the most common inherited bleeding disorder.
Hemophilia A = VIII; B = IX.
HIT type II is immune and prothrombotic; platelet fall >50%.
DIC can cause clotting and bleeding simultaneously.
TEG R = factors/FFP.
TEG K or alpha = fibrinogen/cryo.
TEG MA = platelets/platelets ± DDAVP.
TEG LY30 = fibrinolysis/TXA or aminocaproic acid.
OCR = >20% HR decrease; V afferent, X efferent.
OCR first action = stop surgical stimulation.
SO4, LR6; III moves most other extraocular muscles.
Anything increasing venous pressure tends to increase IOP.
Open globe: smooth RSI, no cough/buck/hypoxia/hypercarbia.
Residual intraocular gas = no nitrous oxide.
Gas durations: air 5, SF₆ 10, C₄F₈ 15, C₃F₈ 30 days.
Echothiophate may prolong succinylcholine and ester LAs.
Timolol eye drops can cause systemic beta blockade.
Apfel: female, nonsmoker, history, postop opioids.
PONV rescue should use a different drug class.
Rapid ondansetron administration can cause serious dysrhythmia/QT effects.
Most PACU hypotension is hypovolemia.
Most PACU hypertension/tachycardia is pain.
Tongue is the most common source of PACU airway obstruction.
Atelectasis is the most common postoperative cause of hypoxemia in the lecture.
Oxygen can hide—not fix—hypoventilation.
Laryngospasm: jaw thrust + 100% O₂ + gentle PPV; deepen, then succinylcholine if persistent.
Aspiration: lateral position and suction; tracheal suction before PPV when possible.
Modified Aldrete ≥9 and PADSS ≥9 in the lecture images.

Source map

This guide intentionally uses the uploaded course materials as the source of truth for lecture-specific content.

Topic	Presentation	Textbook chapter
Hypersensitivity	Hypersensitivity in Anesthesia — Vadim Korogoda	The Immune System and Anesthesia, Ch. 46
Coagulation / TEG	Coagulation — Vadim Korogoda + uploaded TEG/ROTEM image	Hematology and Anesthesia, Ch. 38
Ophthalmic	Anesthesia for Ophthalmic Procedures — Stacey Schlesinger	Anesthesia for Ophthalmic Procedures, Ch. 44
PONV	Postoperative Nausea & Vomiting — Stacey Schlesinger	No separate PONV chapter was included in this upload set.
PACU / Postop	PACU and POSTOP — Vadim Korogoda, updated by Stacey Schlesinger	Postanesthesia Recovery, Ch. 55

This is an exam-focused study aid, not a substitute for facility policy, current drug labeling, or emergency protocols. Where a lecture used a distinctive number or phrasing, it is labeled as lecture-specific.