Chapter 8: Anesthesia Flashcards
Type of Agents that:
- Blunt hypoxic drive
- Caused unconsciousness, amnesia, some analgesia
- Most have myocardial depression, increase CBF, decrease RBF
Inhalational agent
Smallest concentration of inhalation agent at which 50% of patients will not move with incision
MAC (minimum alveolar concentration)
Inhalational agent that is Fast, minimal myocardial depression; tremors at induction
Nitrous oxide (NO2)
Inhalational agent that is-
Slow onset / offset, highest degree of cardiac depression and arrhythmias
- Least pungent, which is good for children for induction
Halothane
Manifestations of halothane hepatitis
Fever, eosinophilia, jaundice, increased LFTs
Inhalational Agent that is -
Fast, less laryngospasm and less pungent; good for mask induction
Sevoflurane
Inhalational agent
-Good for neurosurgery (lowers brain oxygen consumption; no increase in ICP) (recent studies show no clear difference between all these agents regarding ICP)
Isoflurane
Inhalational agent thatCan cause seizures
Enflurane
IV anesthetic that is:
- (Barbiturate) fast acting
- Side effects: decrease CBF and metabolic rate, decrease blood pressure
Sodium thiopental
IV anesthetic
- Very rapid distribution and on/off; amnesia; sedative
- Not an analgesic
- Metabolized in liver and by plasma cholinesterase’s
- Side effects: hypotension, cardiac and respiratory depression
Propofol
IV anesthetic
Dissociation of thalamic / limbic systems; places patient in a cataleptic state (amnesia, analgesia).
- No respiratory depression
- Contraindicated in patients with head injury
-known for causing hypersecretions
- Good for children
Ketamine
IV anesthetic
Side effects: hallucinations, cathetcholamine release (increase CO2, tachycardia), increased airway secretions and increased cerebral blood flow
Ketamine
IV anesthetic
- Fewer hemodynamic changes; fast acting
- Continuous infusions can lead to adrenocortical suppression (this is why its no longer used as a drip in ICU)
Etomidate
When is RSI (rapid sequence intubation) indicated?
- Recent oral intake
- GERD
- Delayed gastric emptying
- Pregnancy
- Bowel obstruction
Last muscle to go down and first muscle to recover from paralytics
Diaphragm
First to go down and last to recover from paralytics
Neck muscles and face
Only one is succinylcholine; depolarizes neuromuscular junction
Depolarizing agents
- Caused by a defect in calcium metabolism
- Calcium released from sarcoplasmic reticulum causes muscle excitation: contraction syndrome
Malignant hyperthermia
First sign of malignant hyperthermia
Increased end-tidal CO2
Side effects: first sign is increased end-tidal CO2, then fever, tachycardia, rigidity, acidosis, hyperkalemia
Malignant hyperthermia
Malignant hyperthermia; tx dosing
Tx: dantrolene (10mg/kg) inhibits calcium release and decouples excitation; cooling blankets, HCO3, glucose, supportive care
give 2.5mg/kg repeatedly until symptoms go away for maximum of 10-20mg; if does not resolve by then then diagnosis is unlikely
When do you NOT use succinylcholine?
Severe burns. Neurologic injury. Neuromuscular disorders. Spinal cord injury. Massive trauma. Acute renal failure.
Complications of succinylcholine
- Malignant hyperthermia
- Hyperkalemia
- Open-angle glaucoma
- Atypical pseudocholinesterases
Type of agents that
- Inhibits neuromuscular junction by competing with acetylcholine
- Can get prolongation of these agents with myasthenia gravis
Nondepolarizing agents
Non-depolarizer neuromuscular blocker
- Undergoes Hoffman degradation
- Can be used in liver and renal failure
- Histamine release
Cis-atracurium
Non-depolarizer neuromuscular blocker: Fast, intermediate duration; hepatic metabolism
Rocuronium
Non-depolarizer neuromuscular blocker:
- Slow acting, long-lasting; renal metabolism
- Most common side effect: tachycardia
Pancuronium
Blocks acetylcholinesterase, increasing acetylcholine
Neostigmine
Edrophonium
Should be with neostigmine or edrophonium to counteract effects of generalized acetylcholine overdose
Atropine or glycopyrrolate
Work by increasing action potential threshold, preventing Na influx.
Local anesthestics
Why are infected tissues difficult to anesthetize with local anesthetics?
Secondary to acidosis.
Length of action of local anesthetics: greatest to least
Bupivacaine > lidocaine > procaine
Side effects of local anesthetics
Tremors
Seizures
Tinnitus
Arrhythmias (CNS symptoms occur before cardiac)
What does addition of epinephrine to local anesthetics allow?
Allows higher doses to be used, stays locally
When do you not use epinephrine with local anesthetics?
No epi with:
Arrhythmias, unstable angina, uncontrolled hypertension, poor collaterals (penis and ear), uteroplacental insufficiency
Two different genres of local anesthetics
Amides (all have “i” in first part of their name)
Esters
Allergic reactions: amides vs esters
Esters: increased allergic reactions due to PABA analogue
Metabolism: opioids
Metabolized by the liver and excreted via kidney
What can narcotics cause precipitate in patients on MAOIS?
Hyperpyrexic coma
Analgesia, euphoria, respiratory depression, miosis, constipation, histamine release (causes hypotension), decreased cough
Morphine
Analgesia, euphoria, respiratory depression, miosis, tremors, fasciculations, convulsions
Demerol
Does demerol cause histamine release?
NO.
Why avoid demerol in patients with renal failure?
Can cause seizures (buildup of normeperidine analogues)
simulates morphine, less euphoria
Methadone
Fast acting; 80x strength of morphine (does not cross-react in patients with morphine allergy); no histamine release
Fentanyl
Very fast acting narcotics with short half lives
Sufentanil and remifentanil
Most potent narcotic
Sufentanil
Anticonvulsant.
Amnesic.
Anxiolytic.
Respiratory depression.
Benzodiazepines
Do benzodiazepines have pain relief?
No.
Metabolism: benzos
Liver
Benzo:
- Short acting
- Contraindicated in pregnancy
- Crosses placenta
Versed (midazolam)
Benzo:
- Intermediate acting
Valium (Diazepam)
Benzo:
- Long acting
Ativan (lorazepam)
- Benzo OD
- Competitive inhibitor
- May cause seizures and arrhythmias
- Contraindicated in patients with elevated ICP or status epilepticus
Flumazenil
MC side effect flumazenil
Nausea
Allows analgesia by sympathetic denervation.
Vasodilation.
Epidural anesthesia
Epidural with morphine
Can cause respiratory depression
Lidocaine in epidural
Decreased heart rate and blood pressure
How can motor function be spared with epidural?
Dilute concentrations
Tx: acute hypotension / bradycardia with epidural
Turn epidural flows down.
Fluids.
Phenylephrine.
Atropine
Epidural level: affect cardiac accelerator nerves
T1-5
Contraindications: epidural
Hypertrophic cardiomyopathy.
Cyanotic heart disease.
Why h-cmp and cyanotic heart disease contraindications to epidural anesthesia?
Sympathetic denervation causes decreased after load, which worsens these conditions
Injection into subarachnoid space, spread determined by baricity and patient position
Spinal anesthesia
Contraindications: spinal
Hypertrophic cardiomyopathy.
Cyanotic heart disease.
Caused by CSF leak after spinal / epidural.
Headache gets worse sitting up.
Spinal headache
Tx: Spinal headache
Rest. Fluids. Caffeine. Analgesics. Blood patch to site if it persists > 24 hours.
Associated with most postop hospital mortality
- Pre-op renal failure
2. CHF
May have no pain or EKG changes. Can have hypotension, arrhythmias, increased filling pressures, oliguria, bradycardia.
Postop MI
Patients who need cardiology workup pre-op (x13)
Angina. Previous MI. SOB. CHF. METs 5min. High grade heart block. Age >70. DM. Renal insufficiency. Patients undergoing major vascular surgery.
Considered high risk surgery
Most aortic, major vascular, peripheral vascular surgery
Risk: carotid endarterectomy (CEA)
Considered moderate risk surgery
Biggest risk factors for post MI
Age > 70. DM. Previous MI. CHF. Unstable angina.
Best determinate of esophageal vs tracheal intubation
End-tidal CO2
Intubated patient undergoing surgery with sudden transient rise in ETCO2
Dx? Tx?
Dx: most likely hypoventilation.
Tx: increased tidal volume or increased respiratory rate.
Goal endotracheal tube placement
2cm above the carina
Associated with lower mortality for abdominal aortic aneurysm repair and for pancreatic resection
Higher volume hospitals
MC PACU complication
nausea and vomiting.
Diagnosis:
pt on profofol infusion develops bradycardia, low UOP, incr cr, hyperkalemia and acidosis? Management?
propofol infusion syndrome
ppx with daily screening with lactate and CPK and changing propofol if >48 hrs
protective factor for perioperative nerve injuries
obesity, proper positioning (although many occur even with this)
risk factors for perioperative nerve injuries
low BMI, diabetic neuropathy
EMG results after perioperative nerve injuries
usually normal but should be done early
during arterial line SBP measurement where is the pressure higher: radial or aortic
radial ( higher as it goes more diatal, smaller and more calcified)
why is morphine generally contraindicated in renal failure
morphine is only opioid that has an active metabolite which in regular pts is no problem bc its quickly excreted howver in renal pts there is a build up
types of ventilator modes
- continuous positive airway pressure (CPAP): all breaths are triggered by the patient and no additional support is provided.
- Pressure support ventilation (PSV) allows the patient to determine the rate and volume of breaths but provides additional pressure to support a patient-triggered breath. -SIMV allows the clinician to mandate a certain number of breaths per minute at a set volume or pressure but allows the patient to breath spontaneously in between the machine-triggered breaths. It is frequently combined with PSV to provide additional pressure to support the patient-triggered breaths.
top three likely offenders in a pt who develops acute hypersensitivity reaction during an operation
neuromuscular blocking agents (-oniums) -60%
latex 20%
abx 13%
ASA designations
- healthy, nonsmoking and no or minial etoh use
- mild systemic disease ( HTN, smoking or social alcohol use, pregnancy, obesity)
- Severe systemic disease ( ESRD, COPD, alcohol dependence, MI>3 months
- Severe systemic disease that is a constant threat to life ( MI<3 months, recent CVA, ESRD but not regularly going)
- moribund not expected to survive without the operation
- brain dead ( organ donation)
malignant hyperthermia genetic association
autosomal dominant
malignant hyperthermia can develop as early as _____ and as late as _______
- 30 mins
2. 24 hrs
maximum dosing of 1% lido w/ and w/o epi
4 mg/kg (typically 1% lido has 10 mg/ml)
7 mg/kg
next step if a pt develops trismus (masseter muscle rigidity) after induction
- wait 20-30 seconds and should resolve
- persistent trismus is NOT a sign of inadequate neuromuscular blockade and should raise suspicion for malignant hyperthermia- surgery should be cancelled and pt placed in observation 24 hrs with referal for muscle bx
main concern for pts undergoing anesthesia that have aortic stenosis
avoiding hypotension ( due to concentric hypertrophy they are preload dependent)- imperative to keep them intravascularly full -increase preload, maintain afterload (coronary filling), avoid bradycardia, or any arythmias (loss of atrial kick)
dopamine effect on receptors depending on dose
- effect on α- and β-adrenergic receptors is generally weaker than epinephrine and norepinephrine.
- At lower doses (1 to 2 mcg/kg per minute), its predominant effect is on the dopaminergic receptors causing renal and visceral vasodilation
- 3 to 10 mcg/kg per minute, the β1-adrenergic receptors predominate; this is most similar to the effects of dobutamine or low dose epinephrine.
- greater than 10 mcg/kg per minute, the α1-adrenergic receptors predominate, leading to peripheral vasoconstriction; this is most similar to the effects of phenylephrine.
pt fails to regain twitches after neuromuscular blockade; etiology? dx? tx?
acquired or genetic pseudocholinesterase deficiency (needed to degrade succinylcholine)
acquired -liver disease
genetic (auto recessive)
dx: decrease plasma cholinesterase enzyme activity)
supportive tx ( wait until spontanously regains muscle function)
pseudocholinesterase deficiency affect breakdown of what drugs?
esters local aneshetics
cocaine
pt is given benzocaine and develops cyanosis however O2 sats is 100%. dx and tx?
methhemoglobunemia
IV methiline blue
if a pt is intubated and pretty sure in right place but capnography reads wrong. what to do? when does this happen?
typically in pts that have received multiple doses of epi during ALS, airway obstruction, poor pulm blood flow
confirm with endotracheal US
what is demerol? how does it differ from morphine?
opioid
does not release histamine thus no hypotension
