Anesthesia Clerkship Study Guide
This section is a compilation of the study guide provided to students on the anesthesia rotation in 2008 and an older version. Several "old" questions that have been removed from the new study guide have been so labeled with answers provided where possible. You're recommended to read the textbook during the hours of spare time that you will have on this rotation. Please note that the chapters are ordered according to the anesthesia study guide. Reference text is Basics of Anesthesia – Fifth Edition, Eds. Stoelting RK and Miller RD, Churchill Livingstone 2007. It is available to check out through the library.
Please note, this is not a complete study guide. You should refer to the packet
- 1 History and of Anesthesia
- 2 Basic Pharmacologic Principles
- 3 Clinical Cardiac and Pulmonary Physiology
- 4 Autonomic Nervous System
- 5 Anesthetics
- 6 Preoperative Evaluation and Medication
- 7 Spinal and Epidural Anesthesia
- 8 Anesthetic Monitoring
- 9 Fluid Management
- 10 Cardiovascular Disease
- 11 Chronic Pulmonary Disease
- 12 Obstetrics
- 13 Pediatrics
- 14 Outpatient Surgery
History and of Anesthesia
List the characteristics of an ideal volatile anesthetic. (pg 8)
- 1) absence of airway irritant effects 2) absence of cerebral vasodilatation; 3) absence of hepatic/renal toxicity; 4) absence of flammability; 5) easily vaporized at ambient temperatures; 6) low blood solubility to ensure rapid induction and recovery; 7) minimal metabolism; 8) compatible with epinephrine; 9) skeletal muscle relaxation; 10) suppression of excess SNS activity; 11) bronchodilatation; 12) absence of excessive myocardial depression
2. List 2 defects of inhaled anesthetics prior to the mid 20th century? (pg 8)
- Explosive and flammable. Ether - explosive in oxygen. Cyclopropane - toxic, flammable
3. For what are the following remembered:
- William Morton (pg 4) – dentist who used diethyl ether vapor instead of nitrous oxide in front of an audience
- Crawford Long (pg 5) – used ether in 1842 but didn’t publish until 1849
- Carl Koller (pg 6) – used cocaine for local anesthesia of cornea , 1884
- James Simpson (pg 5)- obstetrician who proposed chloroform as alternative to ether, used in labor 1847
- John Snow (pg 5)- the first anesthesiologist; popularized chloroform
4. Curare is a compound derived from what and used for what? (pg 7)
- Derived from lianas (vines) growing in South America and is used as neuromuscular junction blocker for hunting. Related compounds are used in modern anesthesia for the same effect.
Scope of Anesthesia Practice
1. What is the mortality rate for anesthesia? Compare this with the rate from motor vehicle accidents?
- Anesthesia mortality rate = 1 in 250,000
- MVA mortality rate = 41 in 250,000
2. What are the ten most important patient safety issues as identified as anesthesiologists? (pg 16)
- 1)difficult airway management; 2) production pressures; 3) anesthesia delivery outside the OR at remote sites in hospital; 4) anesthesia delivery in physician offices; 5) neurologic deficit attributed to the anesthetic technique; 6) presence of coronary artery disease in pts; 7) occupational stress; 8) fatigue; 9) medication errors; 10) time available for pre-op evaluation
3. How did ether differ from chloroform and how did this influence the development of anesthesia as a medical specialty in the U.S. and Great Britain? (pg 12)
- Chloroform in G.B.; potent ventilatory depressant; only MD’s considered competent to administer
- Ether in US; stimulates ventilation and maintains BP; was used by inexperienced MD or nurse; thought to have ‘built-in’ protection for pt
- It took >60 years after ether demonstration by Morton to develop anesthesia into full-time medical practice
Approach to Learning Anesthesia
1. List 4 major questions in the preoperative interview and explain why they are important. (pg 22)
A) What is the indication for proposed surgery? Is it elective or emergency?
- May modify anesthesia plan, choice (local, block, general) and may preclude additional testing.
B) What are the inherent risks of this surgery?
- Type of surgery carries different risks (e.g. cataracts vs. CABG)
C) Coexisting medical problems? Does surgery or care plan need to be modified because of them?
- A pt with poorly controlled HTN may have increased response to larygnoscopy and the anesthesia can change the plan to increase induction dose and give a beta-blocker.
D) Has pt had anesthesia before? Complications? Risk factors for difficult airway management?
- Most important is ease of airway management, OR hemodynamic and respiratory instability. Remember the ABCs!
2. List the steps of a basic operating room setup for a general anesthetic?
- Suction, Oxygen, Circuit, Airway, IV Access, Monitors, Drugs, Stethoscope.
Basic Pharmacologic Principles
1. Describe the Characteristics of ionized vs. non-ionized drug molecules (pg 38)
- Ionized=inactive, water soluble, does not cross lipid barriers, renal excretion, no hepatic metabolism
- Non-ionized-=active, lipid soluble, crosses lipid barriers, no renal excretion, hepatic metabolism
2. What factors determine drug absorption? (pg 38)
- Lipid or water solubility; molecular weight; concentration of drug; drug form.
- Liquids/crystalloids > solids/colloids
- Increased area of absorption
- Increased blood supply
- Heat/vasodilatation > shock/vasoconstriction
- Degree of ionization of drug in environmental pH
3. What is first pass hepatic effect? (pg 38)
- Drugs absorbed from GI tract enter portal circulation and pass through liver before entering systemic circulation for delivery to receptor. The first-pass effect decreases a drug’s potency because some of the drug is metabolized before it reaches the target receptor.
4. What factors determine drug distribution? (pg 39)
- pH of drug’s environment; degree of ionization; pKa of drug (dissociation constant); protein binding; molecular weight of drug; lipid solubility
5. What is drug redistribution? Describe how redistribution is important when comparing the duration of action following single administration of a drug vs. multiple doses? (pg 39)
- Redistribution is transfer of drugs to inactive tissue sites. If given repeated doses, the receptor will be saturated at inactive tissue sites leading to longer duration of action until metabolism can decrease plasma concentration. Ex: Thiopental has a long half-life(3-11hours), but only produces sedation for 5-30 mintues because this highly lipophilic drug quickly redistributes out of the central nervous system and collects in adipose tissue. Given repeated doses of thiopental, the amount of drug that initially redistributes from the brain (active site) to adipose tissue (inactive site) can once again redistribute from the adipose tissue to the brain (albeit at a slower rate), and can lead to a greatly prolonged effect of thiopental.
6. Draw and label parts of a curve depicting plasma concentration after intravenous injection. What is elimination half-time? (pg 39)
- Elimination half-time (t1/2) is time necessary for plasma drug concentration to decrease 50% during the elimination phase.
7. What is effect of site equilibration and why is this important for logical drug administration? (pg 42)
- Site equilibration is the time between IV administration of drug and onset of its clinical effects or time for equilibration between drug concentration in plasma and drug effect. It is important when determining dosage intervals.
- Pharmacodynamics (pg 43) - the responsiveness of receptors to drugs and to the mechanism by which these effects occur (i.e. what the drug does to the body)
- Pharmacokinetics (pg 47) - absorption, distribution, metabolism, and excretion of inhaled or ingested drugs (i.e. what the body does to the drug)
- Therapeutic index (pg 46) – LD50/ED50; the higher the therapeutic index, the safer the drug
- Competitive antagonism (pg 47) - competes for same receptor site as agonist; is displaced by increasing the concentration of agonist; is reversible; shifts dose response curve to the right
- Noncompetitive antagonism (pg 47) – produces a conformational change of receptor that results in diminished receptor response to the agonist even at high doses of agonist; slope decreased, max pharm response diminishes and curve shifts downwards; reversible or irreversible.
- Stereospecificity (pg 47) – drugs interact with receptor in a geometrically specific way; two isomers of opposite shape have different pharmacokinetrics/dynamics, side effects, etc.
- Tachyphylaxis (pg 47) – acute tolerance to effects of drugs when administered at short intervals; occurs with ephedrine and amphetamine and reflects depletion of NE stores or altered dissociation of drug from its receptor site
- Drug dependence (pg 47) – psychologic or physical states characterized by behavioral responses including compulsion to take drug on continuous or periodic basis to experience its effect or avoid the discomfort of its absence.
Clinical Cardiac and Pulmonary Physiology
1. How is blood pressure (MAP) related to systemic resistance (SVR) and cardiac output (CO)? (pg 49)
- MAP = SVR x CO
2. Describe the effects of anesthetic medications on BP, SVR, CO, and preload. (pg 50-1)
- BP – decreased except with N2O, ketamine.
- SVR – decreased
- CO – decreased with halothane and enflurane; increased with N2O; no change with desflurane and isoflurane
- Preload – decreased due to venodilatation occurring with general anesthesia
- HR – no change with halothane and N2O, increased with desflurane at high doses; increased with enflurane
3. What is afterload? Contractility? Preload? What are common causes of low preload? (pg 51)
- Afterload – resistance to ejection of blood from LV after each contraction; determined by SVR
- Contractility – measure of force of contraction independent of preload and afterload
- Preload – amount of cardiac muscle that is stretched before contraction or the EDV of the heart.
- Low preload caused by hypovolemia and venodilatation; tension pneumothorax and pericardial tamponade (prevent ventricular filling); pulmonary embolism and pulmonary HTN
4. Draw an oxyhemoglobin dissociation curve. What events cause it to shift? What is/are the clinical significance of this shift? (pg 55)
- Left shift (P50 < 26.8 mmHg): ↓ H+, ↓ temperature, ↓ 2, 3 – DPG
- Right shift (P50 >26.8 mmHg): ↑ H+, ↑ temperature, ↑ 2, 3 – DPG
- Left shift – fetal Hgb; O2 bound more tightly to Hgb, less O2 delivery to tissue
- Right shift – exercise; allows greater amount of O2 to dissociate from Hgb to tissue
5. How is alveolar ventilation (V’) related to arterial CO2 tensions (PaCO2)? (pg 59)
- PaCO2 = k x (V’CO2/V’A), where PaCO2 is arterial partial pressure of CO2, V’CO2 is carbon dioxide production, and VA is alveolar ventilation.
6. What is expected to happen to arterial pCO2 under anesthesia? Why? (pg 61-2)
- Most anesthesia drugs are respiratory depressants. Sedative-hypnotics act on GABAA receptors that provide inhibitory input to neurons of the respiratory system. Volatile anesthetics decrease excitatory neuronal transmission. PaCO2 is lowered during anesthesia because of assisted ventilation which may result in cessation of voluntary ventilation.
Autonomic Nervous System
1. What is the most practical preoperative test for autonomic nervous system (ANS) dysfunction? (pg 64)
- Orthostatic hypotension: Dysfunction when decrease in SBP > 30mmHg and absence of an increased HR on assuming upright position.
2. At what cord level does peripheral sympathetic nervous system arise (SNS)? Parasympathetic (PSNS)? (pg 64-65)
- SNS – thoracolumbar region (T1 to L3) ; PSNS – craniosacral region (CN III, VII, IX, X and S1-3)
3. What are the clinical uses of dopamine, epinephrine, and isoproterenol? (pg 68-9)
- Dopamine – used for CHF, cardiogenic shock and septic shock
- Epinephrine – used as continuous infusion to treat decreased myocardial contractility; decreases systemic absorption of local anesthetics and local hemostasis when used subcutaneously; DOC in life-threatening allergic/hypersensitivity reactions; restores cardiac rhythm in pts with cardiac arrest; treats refractory bradycardiaIsoproterenol – used as continuous infusion to increase HR after heart transplant; chemical pacemaker in complete heart block; pts with valvular heart disease to decrease pulmonary resistance of vasculature
4. Ephedrine and phenylephrine are what class of drugs and how do they differ? (pg 71)
- Sympathomimetics. Ephedrine is indirect because it stimulates release of NE with α- and β- adrenergic activity. Ephedrine produces reduced effects with repeat administration secondary to depletion of NE from nerve terminals (tachyphylaxis). Phenylephrine is direct and selective for α-1 receptors that increase venous constriction > arterial. Phenylephrine is longer-acting than ephedrine and primarily affects BP. Administration can cause reflex bradycardia since phenylephrine exerts minimal effects on heart rate.
5. What drug class is clonidine and how is it used clinically? (pg 72)
- Clonidine is an α-2 adrenergic receptor agonist in CNS that decreases SNS activity in the periphery. Used to differentiate essential HTN from pheochromocytoma (pts with essential HTN have ↓↓ NE); ameliorates signs/symptoms of opioid withdrawal and tobacco craving; decreases the MAC of injected and inhaled drugs; attenuates SNS response evoked from larygnoscopy; antihypertensive; injection into epidural/subarachnoid space produces analgesia without causing hypoventilation/pruritis/nausea/vomiting.
6. When are beta-blocker drugs used for preoperative administration and who would likely benefit? (pg 74)
- Recommended for pts at risk for myocardial ischemia (e.g., CAD, + stress test, DM II, LVH) and during high risk surgery (vascular, thoracic, intra-abdominal, large blood loss).
1. Inhaled anesthetics, with the exception of halothane, are derivatives of what chemical compound? (pg 78)
- Methyl ethyl ether. Halothane derives from an alkane.
2. What were the main drawbacks of inhaled anesthetics between 1920 and 1940? (pg 79)
- Flammable (diethyl ether, divinyl ether, ethylene, cyclopropane) and toxic (halogenated with chlorine – chloroform, ethyl chloride, trichloroethylene).
3. What major scientific advance led to the development of modern inhaled anesthetics? (pg 80)
- Fluorination increases stability and lessens toxicity. Developed from efforts to produce atomic weapons.
4. What is the major advantage of sevoflurane and desfluarne compared to older inhaled anesthetics? (pg 80)
- Sevoflurane and desflurane are halogenated exclusively with fluorine and are less soluble in blood, therefore allowing faster awakening.
5. What is MAC? (pg 82)
- Minimum alveolar concentration (partial pressure) of an inhaled anesthetic dose required to suppress movement in 50% of pts in response to surgical incision. 95% of pts should not move at dose of 1.2 x MAC and 99% at 1.3 x MAC. Allows for potency of drugs to be compared.
6. What factors decrease or increase MAC? (pg 83)
- Decreased MAC– preop meds, hypothermia, IV anesthesia, neonates, elderly, pregnancy, α-2 agonists, acute EtOH ingestion, lithium, CV bypass, opiates, PaO2< 38 mmHg (hypoxia), anemia, hyponatremia
- Increased MAC – hyperthermia, increased CNS catecholamines (MAOIs, TCAs, acute use of amphetamines/cocaine), infants, chronic EtOH, red hair, hypernatremia
7. How does solubility of an inhaled anesthetic influence anesthetic induction and emergence? (pg 86)
- The more soluble a gas in blood, the longer it is for both induction and emergence.
8. What are the main circulatory effects caused by inhaled anesthetics? (pg 88-90)
- MAP – decreased by desflurane, sevoflurane, isoflurane, halothane, and enflurane; dose-related
- Halothane decreases MAP by decreasing CO
- The rest decrease MAP by decreasing SVR (can be countered by substitution of N2O for some of inhaled anesthetic because it increases MAP)
- HR – increased with high-dose desflurane, increased with enflurane; no change with halothane and N2O
- CO – no change with desflurane, sevoflurane, isoflurane
9. What do the inhaled anesthetics do to evoked potentials? (pg 94)
- All volatile anesthetics and N2O depress amplitude and increase the latency of evoked potentials in a dose-dependent manner.
10. How might this influence anesthetic management of a patient for spine surgery?
- Decrease reliability of motor evoked potential monitoring.
11. What do inhaled anesthetics to do patients with malignant hyperthermia? (pg 94)
- Volatile anesthetics can induce malignant hyperthermia in people susceptible to this adverse reaction.
1. Why do intravenous anesthetics act so rapidly? (pg 97)
- They are lipophilic and bind preferentially into highly-perfused lipophilic tissues like brain and spinal cord resulting in fast onset.
2. Why do all anesthetic induction drugs have similar duration of action for a single dose despite different pharmacokinetic profiles? (pg 97)
- Redistribution of drug into less-perfused and inactive tissues like muscle and fat due to their highly lipophilic property is the primary determinant of duration of action for a single dose of anesthetic induction drugs.
3. What is the most common drug used for induction of anesthesia? (pg 97)
4. What food allergy influences the choice of propofol? (pg 98)
- Egg yolk.
5. Why is propofol not associated with a “hangover” effect and utilized effectively as a continuous infusion? (pg 98)
- The “hangover effect” refers to the greatly increased duration of action of thiopental with repeated administration of the drug. The effect is primarily due to redistribution from the brain to other body tissues and subsequent slow release from these tissues. This slow release can lead to an increase in thiopental’s effects from a few minutes to several hours.
- With propofol, the “hangover effect” does not occur due to the rapid metabolism resulting in efficient plasma clearance in conjunction with slow redistribution. As a result, it can be used in a continuous infusion rather than a one-time dose.
6. What does propofol do to blood pressure and ventilation? (pg 99-100)
- BP - Causes arterial and venous vasodilatation causing profound decrease in BP, inhibits baroreceptor reflex , and very small increase in heart rate.
- Ventilation – Potent respiratory depressant and produces apnea after induction dose. Maintenance infusions reduce minute ventilation by decreasing tidal volume and respiratory rate. Decreases response to hypoxia and hypercapnia, decreases upper airway reflexes, and decreases wheezing.
7. What drugs were commonly used prior to the introduction of propofol? (pg 100)
- Barbiturates like thiopental and methohexital.
8. What do barbiturates do to blood pressure and ventilation? (pg 103)
- Barbiturates cause a modest decrease in BP (less than propofol) by peripheral vasodilatation and increased heart rate. Barbiturates depress the medullary respiratory center. Barbiturates decrease cerebral blood flow by decreasing cerebral blood volume and intracranial pressure. Barbiturates decrease cerebral requirements for O2.
9. What benzodiazepines are commonly used in the perioperative period? (pg 104)
- Diazepam, midazolam, and lorazepam.
10. What do benzodiazepines do to blood pressure and ventilation? (pg 106)
- BP - Midazolam decreases BP > diazepam due to peripheral vasodilatation. Midazolam greater effect in decreasing BP in hypovolemic pts.
- Ventilation – Decrease minimally. May have apnea with rapid administration of midazolam. Decreases ventilation response to CO2. Effects more severe if given with opioids.
11. What are the main clinical uses of benzodiazepines? (pg 106)
- Preop meds, IV sedation, IV induction of anesthesia, and suppression of seizure activity.
12. What is ketamine and how does it differ from most other intravenous sedative hypnotics? (pg 106)
- Ketamine is a PCP derivative and is different from other IV sedative hypnotics because it produces significant analgesia. Dissociates limbic system from the thalamus.
13. What does ketamine do to the circulatory system? In what patients might this be beneficial? (pg 107)
- Produces central SNS stimulation to increase BP, HR, and myocardial contractility (only induction drug to stimulate CV system). May be beneficial in pts with reactive airways and in the management of pts experiencing bronchoconstriction.
14. What is unique about etomodate? (pg 108)
- Hypnotic but not analgesic properties and with minimal hemodynamic effects. Has endocrine side effects (adrenocortical suppression). Pts wake up faster than those given barbs.
15. What is dexmedetomidine? How is it used (pg 109-110)
- Highly selective α-2 adrenergic agonist. Used for short-term sedation of intubated and ventilated pts in ICU. In OR, used as adjunct to general or provide sedation during awake fiberoptic tracheal intubation or during regional anesthesia. Sedation of dexmedetomidine resembles physiologic sleep state without respiratory depression.
1. What advantages does etomidate have compared to other IV induction drugs?
- Patients wake up faster than those who are given barbiturates, no alteration in cardiovascular status.
1. List the relative potency of opioid drugs? (pg 113)
- Morphine – 1.
- Meperdine – 0.1
- Alfentanil 10-25
- Fentanyl – 75 – 125
- Ramifentanil - 250
- Sufentanil - 500-1000
2. What are the receptors principally responsible for opioid-induced analgesia? (pg 113)
- Mu (morphine preferring) receptor responsible for supraspinal and spinal analgesia. Mu-1 = analgesia and Mu- 2 = hypoventilation, bradycardia, and physical dependence.
3. How do neuraxial opioids work? (pg 113)
- Spinal/epidural opioid analgesia binds to receptor on substansia gelatinosa of spinal cord. Not associated with SNS denervation, skeletal muscle weakness, or loss of proprioception. Is specific for visceral rather than somatic pain
4. What are the side effects of neuraxial opioids? (pg 114)
- Pruritus, N/V, urinary retention, depression of ventilation, sedation, CNS excitation, activation of latent viral infections, sexual dysfunction, and water retention.
5. Describe the classic ventilatory depression induced by opioids? (pg 115)
- Depressed level of consciousness caused by hypercarbia…slow breathing rate, slightly increased tidal volume.
6. What are the common side effects of opioids? (pg 116-117)
- CV – orthostatic hypotension and syncope due to SNS impairment; decreased BP due to histamine release; bradycardia from increased PSNS.
- Respiratory – depression at brain stem
- CNS – cerebral vasoconstrictor, miosis, skeletal muscle rigidity, unreliable unconsciousness
- Sedation – sedation before analgesia
- Biliary/GI – spasm, decreased peristalsis, increased sphincter tone, can worsen biliary colic
- N/V – stimulates dopamine receptors
- Tolerance and dependence
- Immunosuppression – alters cellular components
7. How is meperdine unique compared to morphine and other opioids? (pg 117)
- Produces mild atropine-like antispasmodic effects, is well absorbed from GI tract, and suppresses post-op shivering, mydriasis, decreases myocardial contractility.
8. In what patients in meperidine contraindicated (pg 118)
- Pts receiving antidepressants (SSRIs, MAOIs) that may evoke serotonin syndrome.
9. How is fentanyl used clinically? (pg 119)
- Low doses for analgesia; adjuvant to inhaled anesthetics to blunt circulatory responses to laryngoscopy or surgical stimulation; decreased intraop tachycardia but not effective after stimulation has caused HTN.
- High doses as sole anesthetic (good hemodynamics but pt awareness intact because not complete anesthetic)
10. How is naloxone used? Why must it be carefully titrated? (pg 121)
- Reverses opioid induced analgesia and respiratory depression quickly. Must be titrated carefully because of danger of increased SNS activity (tachycardia, HTN, pulmonary edema, dysrhythmias like V-fib).
1. How do local anesthetics work? (pg 124)
- Block transmission of the action potential by inhibition of voltage-gated Na+ channels.
2. List the ester and the amide local anesthetics. (pg 127) Which ones have a higher potential for allergy? (pg 131)
- Esters – Procaine, cholorprocaine, tetracaine; more likely allergic rxn due to PABA-like metabolites
- Amides (two i’s in name) – Lidocaine, mepivacaine, prilocaine, bupivacaine, levobupivacaine, ropivacaine
3. How are local anesthetics metabolized? (pg 129)
- Esters metabolized by hydrolysis (plasma esterases) and amides by hepatic metabolism.
- First pass lung and renal clearance <5% of dose.
4. Why is epinephrine commonly added to the local anesthetic solution? (pg 129)
- Epinephrine co-administration decreases systemic absorption and prolongs the duration of action via vasoconstriction without affecting onset of anesthesia.
5. What are the CNS signs of local anesthetic toxicity? (pg 130)
- Circumoral numbness, facial tingling, restlessness, vertigo, tinnitus, slurred speech which culminate in tonic-clonic seizures. Also apnea and death
6. What are the cardiotoxic effects of local anesthetics? Which have the greatest cardiotoxicity? (pg 131)
- More resistant than CNS toxicity. Hypotension, PR prolongation with widened QRS, dysrhythmia. Bupivicaine has highest cardiotoxicity.
7. What is EMLA? (pg 133)
- Eutectic Mixture of Local Anesthetic. Mixture of 2.5% lidocaine and 2.5% prilocaine cream used to achieve anesthesia of intact skin (topical anesthetic cream). Requires 10-20 minutes before effective.
8. Which local anesthetic is associated with the following: (pg 131)
- Transient neurologic symptoms - Lidocaine
- Methemoglobinemia - Prilocaine
- Cardiotoxicity – Bupivacaine
1. What are the primary uses of neuromuscular blocking drugs? (pg 135)
- Neuromuscular blocking drugs produce skeletal muscle relaxation for tracheal intubation, facilitate mechanical ventilation, and produce optimum surgical conditions.
2. What influences the choices of a NMBD? (pg 136)
- Influenced by speed of onset, duration of action, route of elimination, and side effect profile.
3. What are the entrajunctional receptors and when do they occur? (pg 137)
- Present throughout skeletal muscles and are normally suppressed by neural activity. Prolonged inactivity, sepsis, denervation/trauma of skeletal muscles increases EJ receptors. When activated, stay open longer and permit more ions to flow. We see the EJ receptors become clinically relevant with resistance/tolerance to nondepolarizing NMBDs in burn patients.
4. How do they impact succinylcholine and the use of nondepolarizing NMBD’s? (pg 136-137)
- Explains exaggerated hyperkalemic response when SCh is given to burn pts or pts with denervation injury. Explains why there is resistance to nondepol NMBD in burn pts and pts on prolonged mechanical ventilation.
5. What is unique about succinylcholine? (pg 135)
- Only depolarizing NMBD used clinically and has both rapid onset and ultra short duration of action, making it ideal when attempting to intubate as patient can be bag masked until it wears off if intubation is unsuccessful.
6. When is succinylcholine used? (pg 138) What are its side effects? (pg 141) How is it metabolized? (pg 140) Why has it not been replaced by a nondepolarizing NMBD despite these side effects? (pg 138)
- Used for tracheal intubation. Side effects include bradycardia, junctional rhythm, sinus arrest; fasciculations; hyperkalemia; myalgia; myoglobinuria; increased intraocular pressure; increased intragastric pressure; trismus.
- Metabolized by hydrolysis via plasma cholinesterase (psuedocholinesterase) which metabolizes most of dose before it reaches NMJ (no enzyme at junction) so metabolic rate secondary to diffusion away from NMJ. Pt may genetically lack pseudocholinesterase, which can greatly increase the duration of effect of SCh.
7. Why is succinylcholine relatively contraindicated in children? (pg 142)
- In boys with undiagnosed muscular dystrophy has resulted in acute hyperkalemia and cardiac arrest.
8. What drug dose is used to antagonize nondepolarizing-induced neuromuscular block? (pg 150) What other drug must be administered concomitantly and why? (pg 75)
- Antagonist for nondepol NMBD is anticholinesterase (neostigmine, edrophonium, pyridostigmine): ACh acts as a competitive antogonist against the nondepolarizing NMBD.
- Administer anticholinergic (atropine or glycopyrrolate) concomitantly to prevent muscarinic side effects, most importantly bradycardia.
A. What things potentiate neuromuscular blockage?
- Volatile anesthetics, aminoglycosides, Mg, local anesthetics, cardiac antiarrythmics, calcium channel blockers, decreased potassium
- Hypothermia – atracurium, vecuronium
- Decreased pH – atracurium
B. What are the most sensitive clinical signs for recovery from neuromuscular blockade? What percentage of receptors can be occupied and still have normal appearing neuromuscular function on nerve stimulator?
- Most sensitive clinical sign of recovery – patient able to lift head off bed x 5 secs, can continue to monitor twitches as well; 75-80% of receptors can be occupied but still have normal neuromuscular function on nerve stimulator.
Preoperative Evaluation and Medication
1. What are the goals of the preoperative evaluation? (pg 157)
- 1) inform pt of risk for informed consent; 2) educate pt regarding anesthesia and events to take place in periop period; 3) answer questions and reassure the pt and family; 4) notify the pt about prohibition of ingesting food; 5) instruct pt about which meds to take on day surgery or the meds to stop taking; 6) use operative experience to motivate pt to more optimal health and improved health outcomes.
2. What are the most common causes of anesthetic mishap? (pg 161)
- Human error; emergency surgery, vascular surgery are high risk b/c large blood loss or fluid shifts.
3. What preoperative tests should be ordered for a 51-year old man for elective surgery? (pg 162)
- Hgb or Hct and ECG.
4. Which patients should receive preoperative b-blocker therapy? (pg 162) Why? (pg 163)
- Given to pts with at least one cardiac risk factor because it decreases rates of cardiac related mortality and nonfatal MI. Risk factors include age >70 yrs, angina, previous MI (history or Q-waves on ECG), CHF, current tx of ventricular dysrhythmia, current tx of diabetes; limited exercise capacity, dobutamine-inducible ECHO ischemia.
5. Describe the ASA physical status classification of the American Society of Anesthesiologist. (pg 163)
- PS-1: a normal healthy patient
- PS-2: a pt with mild systemic disease that results in no functional limitations (e.g., HTN, DM, chronic bronchitis, morbid obesity, extremes of age)
- PS-3: a pt with sever systemic disease resulting in functional limitations (e.g., poorly controlled HTN, DM with vascular complications, angina, previous MI, pulmonary disease that limits activity)
- PS-4: a pt with severe systemic disease that is a constant threat to life (e.g., CHF, unstable anginal, advanced pulmonary/renal/hepatic dysfunction)
- PS-5: a moribund pt not expected to survive without the operation (e.g., ruptured AA, PE, head injury with increased ICP)
- PS-6: a declared brain dead pt whose organs are being removed for donation.
- Emergency Operation (E): any pt in whom an emergency operation is required.
6. What are the specific predictors of postoperative respiratory failure?
- Postop respiratory failure is inability to extubate pts trachea 48hrs after surgery. Predictors include type of surgery (AAA (#1), thoracic (2), upper abdominal, peripheral vascular, neck); emergency surgery; albumin <30g/L; BUN >30mg/dL; partially or fully dependent status; hx of COPD; age > 70 or 60-69.
Choice of Anesthetic Technique
1. What considerations influence the choice of anesthetic technique? (pg 179)
- Preference of pt/anesthesiologist/surgeon; coexisting disease that may or may not be related to reason for surgery (GERD, diabetes, asthma); site of surgery; body position of pt during surgery; elective or emergency surgery; likelihood of increased amounts of gastric contents at induction time; suspected difficult airway management and tracheal intubation; duration of surgery or procedure; pt age; anticipated recovery time; post anesthesia care unit discharge criteria.
2. When is a regional anesthetic desirable? (pg 181)
- Are desirable to control postoperative pain without excessive opioid requirements and when necessary to maintain the pt’s consciousness.
3. What are the advantages of a spinal anesthetic? Epidural? (pg 182)
- Spinal: less time to perform; produces a more rapid onset of better quality sensory and motor anesthesia; is associated with less pain during surgery
- Epidural: lower risk for post-dural puncture headache; less systemic hypotension if epinephrine is not added to the LA solution; ability to prolong anesthesia through an indwelling catheter; option of using the epidural catheter to provide postop analgesia
4. What are the relative contraindications to a regional anesthesia? (pg 182)
- Only absolute contraindication is pt refusal. Conditions that increase risk are hypovolemia,
- Increased intracranial pressure, coagulopathy/thrombocytopenia, sepsis, infection at cutaneous
- Puncture site, pre-existing neurological disease.
1. Describe the components of the airway examination and the presence of signs that indicate a possible difficult intubation. (pg 211)
|Airway Exam Component||Non-Reassuring Finding|
|Length of upper incisors||Relatively long|
|Relationship of maxillary and mandibular incisors during voluntary protrusion of mandible||Pt cannot bring mandible out to/past maxillary incisors|
|Relationship of maxillary and mandibular incisors during normal jaw closure||Prominent overbite (maxillary incisors anterior to mandible|
|Interincisor distance||< 3 cm|
|Visibility of the uvula||Not visible when tongue protruded with pt sitting|
|Shape of palate||Highly arched or very narrow|
|Compliance of mandibular space||Stiff, indurated, occupied by mass or nonresilient|
|Thyromental distance||< 3 finger breadths|
|Thickness of neck||Thick|
|Range of motion of head and neck||Pt cannot touch tip of chin to chest or cannot extend the neck (limits ability to get into “sniffing position”|
2. Describe the Mallampati classification. (pg 213)
- Correlates oropharengeal space with the ease of direct laryngoscopy and tracheal intubation.
- Class I – soft palate, fauces, uvula, and tonsillar pillars are visible
- Class II - soft palate, fauces, and uvula are visible
- Class III - soft palate and base of uvula are visible
- Class IV – soft palate not visible
3. What is the sniffing position and why is it important to intubation? (pg 214)
- Flexion of the neck by elevating the head approximately 10 cm. Aligns the laryngeal and pharyngeal axes combined with extension of the head on the atlanto-occipital joint. It allows for alignment of oral/pharyngeal/laryngeal axes for line of vision during direct laryngoscopy.
4. Does placing a shoulder roll and extending the head assist tracheal intubation? (pg 214)
5. What are the predictors of difficult ventilation by face mask? (pg 215)
- Age older than 55 years, BMI > 26 kg/m2, and history of snoring.
6. What are the indications for tracheal intubation? (pg 216)
- Provide a patent airway; prevent inhalation/aspiration of gastric contents; need for frequent suctioning; facilitate positive-pressure ventilation of lungs; operative position other than supine; operative site near or involving upper airway; airway maintenance by mask difficult.
7. How does use of the curved blade differ from straight? (pg 217)
- Straight blade (Miller) directly lifts the epiglottis. Curved blade (Macintosh) is placed between the base of tongue and the pharyngeal space.
8. What does the cuff on the endotracheal tube do? (pg 218)
- Inflated to create a seal against the tracheal mucosa which facilitates positive pressure ventilation of the lungs and decreases aspiration risk.
9. How does the infant airway differ from the adult? (pg 232)
- Larynx higher in neck; tongue larger relative to mouth size; epiglottis larger, stiffer, and angled more posteriorly; head and occiput larger relative to body size; short neck; narrow nares; cricoid ring is narrowest region (in adults narrowest region is glottic opening.
10. Why is croup more common in children than adults? (pg 238)
- Croup caused by too large tube or when cuff inflated too much. This results in edema that very significantly results in a narrowed airway. Children already have a smaller airway than adults.
A. How is infant airway different from adult? Why do we insist on small air leak around the ET tube with children?
- Difference - newborn head and tongue are large with short neck, larynx more cephalad than in adult, epiglottis "U"-shaped and floppy in child, glottic opening and cricoid are narrowest point thus resist passage of tube prevent edema postoperatively. We insist on a small air leak to ensure that there is not too high a pressure on the mucosa of the airway because too much pressure can result in damage, inflammation, and development of edema and croup.
Spinal and Epidural Anesthesia
1. How does spinal anesthesia differ from epidural? (pg 241)
- Epidural space is a potential space that has no CSF, epidural position is not as important, epidural inject over 1-3 minutes (NOT seconds). Epidural anesthesia has slow onset of hypotension from sympathetic nervous system blockade. Can have sudden hypotension from spinal anesthesia
2. What tissues does an epidural needle pass through for an epidural anesthetic from a mid-line approach? (pg 245)
- Epidural: Skin → Subcutaneous tissue → Supraspinous ligament → Interspinous ligament → Ligmentum flavum epidural space
- Spinal: Skin → Subcutaneous tissue → Supraspinous ligament → Interspinous ligament → Ligmentum flavum → Dura mater/arachnoid mater → Subarachnoid space
3. Describe the steps in performing a spinal anesthetic. (pg 253)
- Local anesthetic at site of entry → insert needle at top margin of lower spinous process → advance cephalad
- Note: The fibers of the dura mater run rostrally to caudally, so the bevel of a Quincke needle should be aligned laterally so that it “splits” the fibers rather than “cuts” them. This practice is thought to decrease the probability of a post-dural puncture headache.
4. Why do patients become hypotensive with the spinal anesthesia? (pg 259) How is this treated (pg 260)
- Hypotension results from SNS block that decreases venous return to heart and decreases CO and/or SVR. Treat by restoration of venous return to increase CO via a modest head-down position (5 to 10 degrees) and adequate hydration before spinal. The next step is pharmacologic treatment via sympathomimetics (ephedrine and phenylephrine). If all else fails, give epinephrine.
5. What is the mechanism of a post-dural puncture headache? Describe its appearances. Who are more at risk? How is this treated? (pg 260)
- It is a direct consequence of puncture hole in dura resulting in CSF loss causing downward displacement of brain and stretch of supporting structures. Pain is also from distension of blood vessels that compensate for loss of CSF. Headache begins 12-48 hours after dura puncture (can occur immediately or up to several months later). Intensifies with sitting/standing and relieved by recumbency. Symptoms include occipital or frontal, dull/throbbing, N/V, anorexia, malaise, diplopia, blurred vision, photophobia, “spots”, auditory tests reveal dysfunction. Risk factors are age (increased at puberty then slowly declines), pregnant women, past history of dural headache. Treat with bed rest, fluids, analgesics, IV caffeine, or blood patch.
A. What are some common objections by patients to spinal anesthesia? What are the borders of the spinal canal?
- Objections: needle sticks, being awake during surgery, paralysis, permanent sequelae
- Borders: spinal cord, pia mater, arachnoid, dura mater, anterior longitudinal ligament, posterior longitudinal ligament.
B. What level of anesthesia is required for Cesarean section? perineal surgery? Foot? Lower abdominal? Upper abdominal? What landmarks do these levels correlate with?
- Cesarean section: T4 (nipple)
- Perineal surgery: T10 (umbilicus)
- Foot surgery: L2-3 (knee)
- Lower abdominal surgery: T6 (xiphoid)
- Upper abdominal surgery: T4 (nipple)
C. How does the baricity of solution affect level of spinal block? What else influences level of blockade?
- Hyperbaric - settles to most dependent area of subarachnoid space
- Hypobaric - rise up to nondependent area
- Isobaric - stays in one place
- Influences: position of patient, contour of spinal canal (most importantly – lumbar lordosis and thoracic kyphosis), volume of anesthetic administered
1. What are the ASA standards for monitoring? (pg 674)
- Standard I: Qualified anesthesia personnel shall be present in the room throughout the conduct of all general anesthesia, regional anesthesia, and monitored anesthesia care.
- Standard II: During all anesthesia, the pts oxygenation (pulse oximetry), ventilation (capnography, stethoscope), circulation (capnography, blood pressurer), and temperature (esophageal thermometer) shall be continually evaluated.
2. What are the common EKG leads used for monitoring? (pg 306)
- Bipolar – limb leads I, II, and III
- Unipolar augmented – aVR, aVL, aVF
3. What are the primary indications of myocardial ischemia? (pg 307)
- T-wave affected initially followed by ST-segment changes as ischemia worsens. Myocardial necrosis evident by Q-waves.
4. What is the effect of cuff size on blood pressure? (pg 307)
- Too small a cuff causes reading to be high. Too large a cuff causes reading to be low.
5. What are the indications for direct arterial pressure monitoring? (pg 308)
- During cardiopulmonary bypass; when wide swings in BP expected; when rigorous control of BP necessary; when need of analysis of multiple blood gas samples.
6. What are the indications for central venous pressure monitoring? (pg 309)
- Assess intravascular volume status; assessing atrial cardiac dysrhythmias; R-sided cardiac valvular defects; cardiac tamponade; myocardial ischemia (AF, tricuspid surgery, tamponade).
7. What are the indications for pulmonary artery pressure monitoring? (pg 310)
- Poor LV function (EF < 0.4); assessment of intravascular fluid volume; evaluation of response to fluid administration or administration of drugs (vasopressors/vasodilators, inotropes); valvular heart disease; ARDS; massive trauma (shock, hemorrhage); major vascular surgery (cross-clamping aorta, large fluid shifts).
8. What does mixed venous oxygen describe? (pg 311)
- Corresponds to total-body O2 supply and demand.
9. What are the most common measurement errors with pulse oximetry? (pg 312)
- Substances absorb at same wavelength → methemoglobin, carboxyhemoglobin, dyes (methylene blue, indigo carmine, indocyanine green); low blood flow (blood pressure cuff on same arm as pulse ox); pt movement; ambient light; shift in Hgb curve.
10. What does capnography tell you? (pg 314)
|Increase of monitored CO2||Decrease of monitored CO2|
|Sepsis||Decreased cardiac output|
|HCO3administration||Disconnected or extubated|
|Insufflation of CO2during laparoscopy||Cardiac arrest|
Positioning and Associated Risks
1. What are the cardiorespiratory effects of general anesthesia in the supine position? (pg 291-292)
- The supine position produces the least hemodynamic and ventilatory changes. General anesthesia causes sympathectomy – BP is labile immediately following induction, decreased SNS response to postural changes, and diminished venous return to heart. Respiratory effects include decreased tidal volume, decreased functional residual capacity, increased closing volume if breathing spontaneously. Positive ventilation blunts V/Q mismatches induced by general anesthesia.
2. How can the risk of ulnar nerve injury be minimized in a patient under general anesthesia?
- Limit shoulder abduction < 90o with hand and forearm either supinated or kept in a neutral position to decrease external pressure from supporting surface on nerve.
3. What are the possible complications of the lithotomy position? (pg 294)
- Increased preload (↑ CO and ICP transiently); diaphragm displaced cephalad due to abdominal viscera (↓ TV); increased intrabdominal pressure (obstructs venous return) if mass present; loss of normal lordotic curvature of lumbar spine (aggravate previous back pain); finger crush injury while raising foot of bed.
4. What is the purpose of the axillary roll in the lateral position? (pg 294)
- The axillary roll helps to avoid compression injuries to the brachial plexus by ensuring that the weight of the thorax is borne by the chest wall rather than the axilla.
5. What are the possible complications of the prone position? (pg 294)
- External compression of dependent eye; carotid or vertebral arterial blood flow compromise; impairment of jugular venous drainage; abdominal compression may push up diaphragm (↓ pulmonary compliance, ↑ peak airway pressure, ↑ abdominal pressure); may compress IVC and aorta (↑ surgical bleeding during spine surgery via engorgement of epidural veins); pressure injury to breasts/iliac crest/genitalia/femoral vasculature; obese pts have ↑↑ respiratory compromise; pooling of blood to lower extremities; stretching of brachial plexus.
6. What are the possible eye injuries under anesthesia and how do they occur? (pg 301)
- Corneal abrasion – most common; due to direct trauma from facemasks, surgical drapes, or other foreign objects. Also decreased basal tear production or welling of dependent eye in prone position.
- Blindness – ischemic optic neuropathy via prolonged hypotension, long duration of surgery (especially prone), excessive blood loss, excessive crystalloid use, anemia/hemodilution, and increased intraocular pressure from prone position. Blindness is multifactorial with no consistent underlying mechanism.
1. What is meant by redistribution of intravascular fluid volume and when does it occur? (pg 347)
- Redistribution of intravascular fluid volume is typically due to increased capillary permeability and loss of intravascular fluid volume to interstitial and fluid compartments. It can lead to hypovolemia despite lack of external loss of fluid. It occurs in pts with sepsis, ARDS, ascites, pleural effusions, and bowel abnormalities. Other causes include bowel preparations, vomiting, diarrhea, diaphoresis, hemorrhage, burns, and inadequate intake.
2. How does one evaluate fluid volume from noninvasive methods to invasive testing or monitoring? (pg 348)
- Noninvasive – BP, HR, urine output, pt history
- Invasive – Hct, BUN, electrolytes
- Monitoring – pulmonary artery catheters, arterial O2 sats, ABG’s and pH, central venous pressure
3. What do anesthetic drugs do to intravascular volume (pg 348)
- Thiopental ↓ venous return;
- Propofol ↓ SVR, cardiac contractility, preload;
- Ketamine ↑ BP, HR, CO via SNS stimulation and blocked NE reuptake; direct myocardial depression results in paradoxical ↓ in BP when given to pts with exhaustion of catecholamine stores
- Atracurium causes histamine release
- All cause ↓ SVR and venous pooling because of absent muscle tone
- Iso, Des, Sevo ↓ SVR and depress myocardial contractility;
- All cause ↓ preload and ↓ BP due to positive pressure on lungs if pt is hypovolemic
- Neuraxial blocks SNS tone leading to vasodilatation, pooling of blood, ↓ venous return to heart
4. Estimate the fluid requirements for a 60 kg man for a colon resection who has been NPO after midnight. (pg 349)
4 mL x 10 kg → 40
2 mL x 20 kg → 40
+ 1 mL x 30 kg → 30
Total: 110 mL/hr
5. How can one replace the volume loss from blood loss? (pg 349)
- Replace blood loss with isotonic crystalloid solution at 3:1 ratio of crystalloid administration to blood loss or mL per mL of colloid or blood.
6. What is third spacing? (pg 351)
- Third spacing is internal redistribution of fluids. Can cause large fluid shirts and severe IV fluid volume depletion especially during major abdominal or thoracic procedures. Traumatized, inflamed, or infected tissue can sequester fluid in interstitial space.
7. Why are glucose-containing fluids generally avoided for intraoperative fluid management? (pg 351)
- They are avoided because hyperglycemic-induced hyperosmolality, osmotic diuresis, and cerebral acidosis are known complications. Hypoglycemia is a risk with abrupt discontinuation of glucose-containing solution during intraoperative period.
8. What are colloid solutions?
- Homogeneous noncrystalline substances consisting of large molecules dissolved in a solute, most commonly isotonic saline. Have greater capacity than crystalloids to remain in IV space and are more efficient volume expanders. Examples are albumin, hydroxyl ethyl starch and dextran.
9. What is the crystalloids-colloid controversy? (pg 352)
- The controversy is over surgical resuscitations. No distinct advantages for either but colloids more expensive and don’t share same safety profile as crystalloids due to bleeding problems and are therefore not used outside situations of rapid IV fluid expansion.
1. How much of the adult population undergoing surgery will have or be at risk for coronary artery disease? (pg 365)
- 40% of adult surgery pts will have or be at risk for CAD.
2. What are important aspects of the H&P in regards to CAD? (pg 365)
- Signs and symptoms of new onset angina, change in angina pattern, unstable angina, recent MI, CHF, or aortic stenosis.
3. What are the most important aspects of the history with regards to CAD? (pg 366)
- Evaluation of cardiac reserve (exercise tolerance); angina pectoris characteristics; previous MI; medical/interventional cardiology and cardiac surgical therapy for these conditions; CAD meds; other associated comorbid disorders.
4. How should elective surgery for a patient who has had an MI be handled? (pg 367)
- Delay for 2 to 6 months after MI.
5. What factors increase the risk for perioperative MI? (pg 367)
- Site of previous MI, history of CABG, intrathoracic or intrabdominal operations > 3 hours; site of operation if duration of surgery < 3 hours, and techniques that produce anesthesia.
6. What is perioperative risk reduction therapy? (pg 368-369)
- Guidelines that all pts who have CAD, PVD, or 2 risk factors for CAD should get perioperative beta-blockers (if contraindicated give clonidine)
7. How does one evaluate LV function? (pg 369)
- Impaired LV function if previous MI, CHF, EF <0.4, LV EDV > 18mmHg, CI < 2L/min/m2, areas of ventricular dyskinesia.
8. What determines myocardial oxygen requirements and delivery? (pg 370)
- Requirements – HR, BP, myocardial contractility, ventricular volume
- Delivery – coronary blood flow, O2 content of arterial blood
9. Describe the considerations for induction, intubation, and maintenance of anesthesia for a patient with coronary artery disease.
- Pre-op – give beta-blocker or clonidine, give routine meds except for oral hypoglycemic agents, oral benzos, ACE inhibitors, supplemental O2.
- Induction – IV etomidate or propofol in reduced dose; fentanyl plus midazolam with combo of phenylephrine and a nondepolarizing NMBD; if desflurane chosen don’t increase dose rapidly to avoid SNS stimulation. Do not give ketamine because of increases in HR and BP
- Intubation – give succinylcholine or nondepolarizing NMBD, minimize time of laryngoscopy to decrease SNS stimulation. If prolonged give laryngotracheal lidocaine or beta-blocker.
- Maintenance – choice based on LV function; volatile anesthetic +/- N2O; N2O –opioid technique with gas to treat acute increase in BP from surgical stimulation; sevoflurane for sudden increase in BP; IV bolus of long-acting beta-blockers perioperatively; short-acting opioids with N2O for pts with impaired LV function; regional anesthetic with beta-blocker; phenylephrine improves coronary perfusion pressure but increases heart O2 requirement.
10. In which pts should a pulmonary artery (PA) catheter be placed? Why? (pg 372)
- Pts with CAD when EF > 0.5 and no evidence of LV dysfunction b/c RA pressure may not reliably reflect left heart filling pressure.
A. What is aortic stenosis? Does angina in a patient with aortic stenosis mean that he had CAD? Characterize the murmur in AS. Why is AS important?
- Aortic stenosis - narrowed aortic valve causing increased LV systolic pressure and increased thickness of LV wall can see angina in a patient with AS even without CAD
- Murmur – systolic crescendo-decrescendo murmur in 2nd right intercostal space
- Incidence of sudden death is increased in patients with AS
- Pts with AS rely heavily on preload for adequate cardiac output, therefore vasodilatation, especially venous, can greatly reduce CO instead of increase it.
B. Contrast the anesthetic management goals in patients with valvular stenotic versus regurgitant lesions.
- Stenotic lesions- anesthesia should cause minimal change in HR and vascular resistance and should not cause decrease in heart contractility
- Regurgitant lesions - anesthesia should not be allowed to decrease HR or increase systemic vascular resistance, can even increase cardiac output by increasing HR and decreasing systemic vascular resistance.
C. Define hypertension. Describe the preoperative evaluation of patient w/ HTN. Why important to anesthesia?
- Hypertension: sustained increased blood pressure > 160/95
- Evaluation - (1) determine adequacy of blood pressure control, (2) review pharmacology of anti-HTN meds, (3) evaluate associated organ dysfxn (cardiac, renal, CNS), (4) look for evidence of PVD, (5) look at EKG for evidence of myocardial ischemia which is more common in hypertensive patients
- Important because HTN patients are more prone to cerebral ischemia and myocardial ischemia and will have exaggerated increases in blood pressure during direct laryngoscopy.
Chronic Pulmonary Disease
1. What is asthma and how does it impact anesthesia? (pgs 406-408)
- Defined by presence of chronic inflammatory changes in submucosa of airways, airway hyperresponsiveness, and reversible expiratory airflow obstruction. Bronchoconstriction occurs in response to mechanical ventilation. Get PFTs (esp. FEV1), arterial blood gases, give inhaled/systemic steroids in addition to scheduled inhaled beta-blockers and continued through perioperative period.
2. How does COPD impact postoperative outcome? (pg 409)
- Grading system of BMI, severity of airflow Obstruction (e.g. COPD), functional Dyspnea, Exercise capacity (BODE). Pts with increased BODE scores at higher risk for death. Preoperative detection of chronic hypoxemia, pulmonary HTN, cor pulmonale with treatment using supplemental O2 is important.
3. How does obstructive sleep apnea impact anesthesia? (pg 411-412)
- High risk for postoperative complications. Relaxation of upper airway reduces pharyngeal space and results in longer periods of hypopnea, arterial hypoxemia and hypercapnia. Difficult airway management necessitates having a fiberoptic scope ready with adequate preoxygenation. Pts are susceptible to respiratory depression and repetitive apnea in postoperative period.
A. What is the significance of elevated PaCO2 in pulmonary disease?
- These patients are triggered to breathe by hypercapnea, not hypoxemia, so excess administration of oxygen to decrease carbon dioxide will cause the patient to quit breathing. Pt’s will also require higher PaCO2 levels before they begin spontaneous ventilation when recovering from anesthesia.
B. What is the differential diagnosis of intraoperative bronchospasm?
- Tracheal tube obstruction with secretions or by bronchial tube placement, pulmonary edema, gastric fluid, aspiration, pneumothorax
C. What specific findings can predict postoperative complications after thoracic surgery? What are some predictive PFT's for post thoracic surgery morbidity?
FEV1 < 2 L,
FEV1: FVC < 0.5,
VC < 15 ml/kg,
max breathing < 50% of predicted
1. What are the physiological changes in the cardiovascular system in pregnancy? (pg 476)
- Increased IV fluid volume – relative anemia b/c plasma volume increased more that RBC volume
- Increased CO – because increased volume
- Decreased peripheral circulation – decreased systolic and diastolic pressures, decreased SVR, decreased pulmonary vascular resistance. No change in central venous pressure. Increased femoral venous pressure.
2. What is supine hypotension syndrome and how is it managed?
- Decreased maternal BP when supine because of aortocaval compression by gravid uterus. Signs and symptoms are N/V, diaphoresis, and decreased mentation. Treat by lying in left lateral decubitus position (lie on left side to keep uterus from compressing IVC on the right side).
3. What are the pulmonary changes with pregnancy? (pg 478)
- Capillary engorgement of upper respiratory tract; minute ventilation increased 50% by end of 1st trimester; lung volumes decreased later in pregnancy as diaphragm pushed up (similar to restrictive lung disease); PaO2 > 100 secondary to hyperventilation; decreased FRC secondary to decreased reserve so desaturations can occur quickly with apnea.
4. Why are pregnant women at risk for aspiration and how is this managed? (pg 479)
- Displacement of pylorus by uterus leads to decreased gastric emptying and increased reflux (think of pregnant women always having a full stomach). Progesterone also has hormonal effects that slow gastric emptying and gut motility. Managed by sodium citrate antacid and H2 receptor antagonist to increase gastric fluid pH. If pt in active labor, give metoclopramide to decrease gastric fluid volume. This may not work if pt given opioids (opioids slow gut motility).
5. What levels must be blocked to block the pain from labor? Delivery? (pg 481)
- Visceral pain (uterine contractions, first stage) blocked at T10-L1. Blocks SNS bundle.
- Somatic pain (vaginal and perineal, second stage) blocked at S2-S4. Blocks pudendal nerves.
6. What are the most widely used techniques for labor analgesia? (pg 483)
- Regional anesthesia consisting of epidural, spinal, or combination spinal/epidural/
7. When would a spinal anesthetic be preferred to an epidural? (pg 488)
- Advanced stages of labor.
A. When is fetal depression greatest after intramuscular meperidine? What does diazepam do to fetal heart rate?
- Depression greatest at 2-4 hours after injection of meperidine
- 5-10 mg diazepam IV causes small beat-to-beat variability in fetal heart rate
B. How are the stages of labor divided? How long are they? How does parity influence this?
- First stage of labor - onset of regular contractions with cervical dilation, latent and active phases
- Second stage - complete dilatation of cervix, expulsion of fetus
- Third stage - time between the delivery of baby and delivery of placenta
- Fourth stage - the hour immediately following delivery of placenta, greatest risk of postpartum hemorrhage
C. What determines the choice of epidural/spinal or general anesthesia for C-section?
- Desires of mom; presence or absence of fetal distress; general is quicker and is used in emergent sections and causes less maternal hypotension
D. What are some of the problems associated with breech presentation? Multiple gestations?
- Beech presentation causes increased cervical lacerations, retained placenta, hemorrhage, increased intracranial hemorrhage, prolapse of cord in babies
- Multiple gestations - prematurity and breech presentation
E. What is toxemia of pregnancy? What organ systems are affected? How is it treated? What does magnesium do to muscle relaxants?
- Pre-eclampsia: gestational hypertension, proteinuria and edema occurring after 20 weeks
- Eclampsia - seizures and pre-eclampsia
- All organ systems are affected
- Treated by delivering fetus and placenta
- Mg potentiates effects of depolarizing and nondepolarizing blockers, as it completes with Ca2+ for entry into muscle cells.
F. What is placenta previa? Abruptio placenta?
- Previa - abnormal low implant of placenta in uterus, symptoms of painless vaginal bleeding ~week 32
- Abruptio - separation of normally implanted placenta after 20 weeks gestation, symptoms of painful bleeding often with contractions.
G. What are the anesthetic considerations in obstetric patients for non-obstetrical surgery?
- Avoid teratogenic drugs - N2O only with caution
- Avoid intrauterine fetal hypoxia and acidosis - avoid maternal hypotension, arterial hypoxemia
- Treat decreased blood pressure with ephedrine
- not phenylephrine because it causes vasoconstriction leading to decreased uterine blood flow
1. How does the pediatric airway differ from that of the adult? (pg 506)
- Kids have a large tongue relative to head, larynx higher in neck (C3-4) than adults (C4-5), large epiglottis but narrow and short, vocal cords have posterior comissure more cephalad than anterior comissure predisposing to subglottic area to injury, narrowest point is cricoid cartilage leading to increased risk of edema and subglottic stenosis.
2. How should an upper respiratory infection be handled in a child for elective surgery? (pg 516)
- Assess pt and family, procedure, surgeon, age, medical/anesthesia history, physical exam, postoperative care. Weigh inconvenience of rescheduling against ignoring risks.
- If short surgery with facemask airway support → minimal risk
- If endotracheal tube → 10x risk
- If LMA → risk lies between facemask and endotracheal
- Younger age with URI → increased risk
3. What is the issue with the ex-preterm child and outpatient surgery? (pg 516, 540)
- Variation in gestational age of delivery and complications in NICU. Requires individual assessment of pt, procedure, time when surgery completed. Ex-premies commonly have chronic lung conditions with reactive airways and abnormal pulmonary function for 1st decade of life or longer, developmental delay, hepatic/renal dysfunction.
4. What is the most common preoperative sedative used for children and how is it dosed? (pg 517)
- Midazolam 0.5 – 1.0 mg/kg PO or 0.05-0.1mg/kg IV.
A. What is the APGAR score? What does it mean?
- Determined after birth – guides how much resuscitation is needed. Does not predict long-term outcome!
- Appearance (skin color), Pulse (heart rate), Grimace (reflex irritability), Activity (muscle tone), Respiration
B. Discuss the difference in presentation and management between epiglottitis and croup?
- Epiglottitis - acute onset, can't swallow, high fever, inappropriate stridor, must admit because can obstruct at anytime and will need intubation, medical emergency
- Croup - younger kids with slower onset and lower fever
1. What are the advantages of outpatient surgery? (pg 539)
- Decreased medical costs, increased availability of beds for pts requiring hospitalization, protection of immunocompromised pts form nosocomial infections, and avoidance of disruption of family unit by hospitalization.
2. What factors determine the type of procedures done on an outpatient basis? (pg 540)
- Reimbursement agencies, pt must be reliable and mentally/physically competent to ensure compliance with pre- and post-operative instructions, caretaker competence, and proximity to ER.
3. How long must patients be NPO before surgery for various foods and liquids? (pg 542)
- Clear fluids in reasonable volumes up to 2 hours before induction.
- Breast milk up to 4 hours before induction.
- Infant formula up to 6 hours before induction.
- Light meal (dry toast, milk) up to 6 hours before induction.
4. What are the most common postop problems causing a protracted stay after intended outpatient surgery? (pg 546)
- Postoperative N/V (PONV), pain, drowsiness, and urinary retention.
A. Name 4 hazards of oxygen therapy.
- Retrolental fibroplasia, CO2 retention due to pulmonary oxygen toxicity, bronchodilatation by O2 so air goes to areas of V/Q mismatch (blood goes to areas with little gas exchange), atelectasis
B. What is racemic epinephrine and what is it used for?
- Mixture of D and L isomers of Epi. Theoretically produces decreased systemic effects. Used as inhaler for bronchodilatation (β-stimulation) but mainly for α-antagonistic effects to decrease laryngeal edema (vasoconstriction)
C. What is the net effect of postoperative pain on pulmonary function? Name and describe 4 methods for preventing postoperative atelectasis?
- Shallow breathing leads to decreased lung volumes after surgery (decreased FRC and VC)
- Voluntary deep breathing and early ambulation
- Intermittent positive pressure breathing
- Incentive spirometry
- Exhalation maneuvers ~ no good
D. What are the goals of anesthetic management in the patient with elevated ICP? How can these be achieved?
- Don't increase PaC02 because increased PaCO2 causes increased cerebral blood flow
- Must be paralyzed fully before intubation b/c intubation can increase intracranial pressure
- Ventilate patient to keep PaCO2 between 35 and 30
E. What is required to produce a venous air embolism? How can we monitor for it? How can it be treated?
- Veins in neurosurgery are above chest; therefore, air is sucked when transected
- Doppler of right ventricle to detect air
- Right heart cath to suck out air
F. What are the controversies of deliberate hypotension? In whom should it be avoided? What are the "safe" limits? Name 4 drugs that might be used?
- Risks of myocardial, cerebral and renal ischemia
- Avoid in patients with chronic hypertension
- Decrease MAP at most 50 in prior normotensive patient
- Drugs: nitroprusside, NTG, trimethophan, volatile anesthetics (halothane and isoflurane)
G. Describe some of the concerns with preoperative management of elderly patients?
- Coexisting diseases; polypharmacy; electrolyte abnormalities secondary to medications; loose teeth; arthritis of cervical spine; weakened posterior trachea; weak skin - must position carefully to avoid pressure sores and neuropathies; increased aspiration risk