• cardiac = most important!
• respiratory and airway
• CNS
• endocrine (esp DM, thyroid)

• facial anatomy 
• thyromental distance
• neck length and thickness
• neck ROM
• mouth opening 
• dentition
• Mallampati classification
• intraoral structures

• I - uvula, tonsils, hard and soft palates all visualized completely
• II - can visualize hard and soft palates, and upper portions of tonsils and uvula
• III - can visualize hard and soft palates and base of uvula
• IV - can only visualize hard palate
• III and IV = more difficult to intubate

• ASA classification grades pt's severity of illlness and physiologic reserve as means of predicting perioperative M&M
• ASA class is assigned as part of pre-sedation assessment

• I - healthy patient
• II - patient with mild systemic disease
• III - patient with severe systemic disease that limits activity, but is not incapacitating
• IV - patient with incapacitating disease that is a constant threat to life. (Anesthesiologist should be present).
• V - moribund patient, not expected to survive 24 hours with or without surgical procedure
• VI - brain dead patient (organ donor)

• clear liquids - 2 hours fasting (min)
• breast milk/formula - 6 hours fasting (min)
• all other foods - 6-8 hours fasting (min)

• inadequate NPO
• pregnancy
• obesity
• GI obstruction
• gastroesophageal dysfunction
• DM (gastroparesis)
• emergency surgery

• 55% of body weight in males
• 45% of body weight in females
• 80% of body weight in infants
• amount of body water is decreased in obese pts, because fat contains little water.

• Intracellular water: 2/3 TBW 
• Extracellular water: 1/3 TBW
• extravascular: 3/4 of extracellular water
• intravascular: 1/4 of extracellular water

• How long has pt been NPO?
• Have they been receiving IV fluids?
• Urinary output 
• vital signs (HR, BP)
• sx of peripheral vasoconstriction (cold distal extremities, pallor, cap refill)
• serum electrolytes and osmolarity
• meds and comorbidities that alter fluid homeostasis

• First HR increases, then BP decreases
• Body is trying to keep brain and heart perfused. 
• BP decreases because: afterload increases, preload decreases

• Heart rate
• Preload (= endi diastolic volume/venous return)
• Afterload (=systemic vascular resistance)
• Contractility
• AV synchrony (maintenance of sinus rhythm)

BP = CO X systemic vascular resistance

CO = HR X SV

SV is affected by preload, afterload, contractility, and AV synchrony

• It is a systolic bp decrease >20 mmHg from supine to standing
• Indicates fluid deficit of 6-8% of body weight
• HR should increase as compensatory measure (no increase = autonomic dysfxn or beta blocker tx)

• evaporation of water from
• respiratory tract
• sweat
• feces
• urine

• It covers insensible fluid losses.
• Calculate using 4-2-1 rule:
• 4 ml/kg/hr for first 10 kg of body weight
• 2 ml/kg/hr for second 10 kg body weight
• 1 mk/kg/hr for each subsequent kg of body weight
• Ex. 70 kg guy: (4x10)+(2x10)+50 = 110
• Ex. 4 kg baby: 4x4 = 16
• Ex. 12 kg child: (4x10)+(2x2) = 44

• NG suctioning
• vomiting
• ostomy output (99% water)
• diarrhea
• fever
• denuded surfaces
• bowel prep (usually causes about 1 L fluid loss)

• Isotonic transfer of extracellular fluid from functional fluid compartments (i.e. intravascular & intracellular) and to non-functional fluid compartments (interstitial fluid/edema).
• This always occurs to some extent because organs swell as a result of surgical manipulation.

• Site of procedure (larger area → more fluid loss)
• Duration of procedure
• Amount of tissue trauma
• Temperature
• Comorbidities

• replacement with crystalloids - 3 ml for each ml of blood loss (because crystalloid doesn't stay intravascular as long)
• replacement with blood products or colloids - 1 ml for each ml of blood loss

• combination of water and electrolytes
• it can be simple salt solution = composed of a single salt ex. normal saline (note: normal saline: 0.9%, is not hypertonic)
• or it can be a balanced salt solution = composed of >1 salt ex. lactated Ringer's, plasmalyte, normosol
• Can be iso, hypo, or hyper-tonic (only iso used in OR)
• Can have other additives (ex. dextrose)

1. maintenance fluids (x duration of procedure)
2. fluid deficit
• NPO deficit (maintenance X # hrs NPO)
• other fluid deficit (ex. bowel prep, 1000 ml)
3. third space losses - according to procedure type and duration
4. blood loss - if replacing with crystalloids, multiply by 3

• fluids containing molecules sufficiently large enough to prevent transfer across capillary membranes
• solutions stay in the space into which they are infused
• ex. albumin (MC), hetastarch, dextran

• urine output - at least 1.0 ml/kg/hr; marker of perfusion & end-organ fxn as well as volume status
• vital signs
• physical exam
• invasive monitoring (CVP, PCWP)
• labs: HgB, acid-base status (markers of perfusion)

• Oxygen delivery (DO2) = CO X O2 content
• CO = HR X SV
• O2 content (CaO2) = (Hgb X 1.34)O2 saturation + PaO2 (0.003)

• Must have adequate fxn of at least 2 out of 3:
• Hgb
• O2 saturation
• CO
• 3-legged stool analogy

What is the "transfusion trigger"? (definition, cutoffs)

• Hgb level at which transfusion is recommended; varies with patients and procedures
• For most healthy patients: Hgb level of 7 g/dL
• For compromised patients (i.e. pts with CV problems), require HgB > 10.

• maintenance of intravascular volume
• ability to increase CO output
• increases in 2,3-DPG

• amount of blood a patient can safely lose before initation of transfusion
• ABL = [TBV x (Hgbstarting - Hgbtrigger)]/Hgbstarting
  
• TBV = total blood volume
  

• 70 ml/kg in adults
• 75 ml/kg in children
• 80 ml/kg in neonates, up to 100 ml/kg in preemies

• Hct = 70-80%
• 1U raises Hgb by ~1g/dL in an adult
• Administered w/ normal saline
• B/c calcium in Ringer's lactate may cause clot formation if mixed with PRBCs

• Tx of thrombocytopenia or if pt is @ perioperative platelet transfusion trigger (Plt of 50K to 100K)
• 1U increases platelet count by 5000-10,000 cells/mm³

• plasma frozen within 6 hours of collection
• contains coagulation factors (except platelets)
• Tx of isolated factor deficiencies
• Must be replaced in massive transfusion along with PRBCs and platelets
• Rapid transfusion can cause life-threatening hypocalcemia

• Febrile (MC) - controlled by slowing infusion and antipyretics
• Allergic - give antihistamines, stop infusion
• Hemolytic - occurs with administration of wrong blood type; can result in DIC
• Viral transmission - Hep B&C, HIV, CMV (MC)
• Hypocalcemia - calcium binding by citrate
• Hypothermia

• O2 delivery and oxygenation
• inspiratory gas analysis
• continuous pulse oxymetry - O2 saturation (SpO2)
• Circulation
• ECG
  
• arterial bp - at least q 5 min
• Ventilation - tidal volume, capnography (etCO2) = gold standard for confirming endotracheal tube placement
  
• Body temp
  

• Detects: dysrhythmias, myocardial ischemia, electrolyte abnormalities (K, Mg)
• Reflects electrical activity, but does not measure CO

• lead  II - best look at P-wave → facilitates detection of arrhythmias/presence of sinus rhythm and inferior wall ischemia
• lead eV - detects anterior and lateral wall ischemia

• Indications: wide swings in bp likely, need for tight control of bp, need for frequent blood draws, monitor during cardiopulmonary bypass
• Arteries commonly used: radial/ulnar, femoral, posterior tibial (or dorsalis pedis), axillary, (brachial)

• Monitor right atrial pressure
• Normal: 3-13
• Elevated CVP may indicate volume overload or RV dysfxn.
• Sites for cannulation: internal jugular v (R>L), subclavian v, femoral v
• Indications: anticipate need of vasoactive meds, TPN (=hyperalimentation), need transvenous pacing, potential of air emboli

• hypoventilation
• rebreathing
• exhausted CO2 absorbent
• increased metabolic rate (ex. malignant hyperthermia)
• exogenous CO2 (laparoscopy)

• unreliable during states of decreased peripheral perfusion (hypotension, high SVR, hypothermia)
• abnormal Hgb variants (carboxyHgb, metHgb)
• IV dyes

• Shivering
• Impaired drug metabolism
• Coagulopathy
• Wound infxns
• Dysrhythmias

Temperature monitoring sites

• Esophagus - reflect core (blood & brain) temp
• Bladder/rectal - responds slowly to core temp and altered by urine/stool temp
• Skin - reflect temp of skin that probe is in contact with but gives little info about core temp
• Nasopharynx
• Pulmonary artery
• Tympanic membrane

• If the curve is shifted to the right, then less O2 is bound to Hgb at a given arterial partial pressure of O2 → increased O2 delivery to tissues
• RIGHT mnemonic. Right shift occurs with Increased 2,3-DPG, H+, and Temp. (and CO2)

• Base excess is deviation from normal bicarbonate level (=24) under normal respiration (i.e. PaCO2=40)
• It's a quick way of determining whether or not there's a metabolic derangement in addition to a possible respiratory derangement.

• AG = Na - (Cl + bicarb)
• Normal range: 8 - 12
• (low albumin can falsely lower AG by 2.5 mEq for every 1 g/dL of albumin.)

• M - methanol
• U - uremia (kidney failure)
• D - DKA
• P - poisons, paraldehyde
• I - INH, iron
• L - lactic acidosis
• E - ethylene glycol
• S  - salicylates

• GI - bicarb loss or acid gain
• GU - renal bicarb loss (renal tubular acidosis)

• Ischemia → lactic acidosis (hypovolemia, low CO)
• Renal failure
• Diabetes
• Sepsis
• Hyperchloremic acidosis (too much normal saline)

• Cardiac: catecholamine resistance, decreased contractility, arteriolar vasodilation, ventricular irritability
• CNS: cerebral vasodilation, mental status changes
• Pulmonary: hyperventilation, pulmonary vasoconstriction
• Metabolic: elevated K+, insulin resistance, right shift of Hgb dissociation curve

• Treat underlying cause
• Hyperventilation
• Do NOT give bicarb!! (leads to increased CO2 and worsening of acidosis, esp intracellular acidosis)

• antacid therapy
• nasogastric suctioning
• bicarbonate therapy
• massive transfusions (citrate)
• diuresis
• volume contraction
• post-hypercapnic ventilation

• CNS/cardiac: arteriolar vasoconstriction, decreased cardiac perfusion, ventricular dysrhythmias
•  pulmonary: hypoventilation → hypoxemia
• Metabolic: decreased levels of ionized K, Ca, Mg phosphorus

• Treat underlying disorder
• Hypoventilation
• Replenish volume with normal saline

• ΔpCO2 = 1.3 X ΔHCO3-
• (Normal pCO2 = 40)

• acute: ↑ pCO2 of 10 = ↑ HCO3- of 1
• chronic: ↑ pCO2 of 10 = ↑ HCO3- of 4

• acute: ↓ pCO2 of 10 = ↓ HCO3- of 2
• chronic: ↓ pCO2 of 10 = ↓ HCO3- of 5

• every ↑AG (normal cutoff = 12) =  ↓ in HCO3- by 1 mEq

• morphine
• hydromorphone
• fentanyl
• *meperidine (demerol) not used any more b/c of CNS side effects (seizures) caused by toxic metabolite: normeperidine.

• sites of action: mesencephalic periaqueductal grey in the brain and substantia gelatinosa in the spine
• mechanism: membrane hyperpolarization through K channel and inhibition of Ca channel

• morphine: PO, IV, intrathecal (IT)
• hydromorphone: PO, IV, IT
• oxycodone: PO
• methadone: PO, IV
• Hydrocodone: PO
• fentanyl: PO, IV, IT, transdermal

1. Presence of an initiating noxious event or a cause for immobilization
2. Continuing pain, allodynia, or hyperalgesia, with which pain is disproportionate to any inciting event.
3. Evidence at some time of edema, changes in cutaneous blood flow, or abnormal sudomotor activity in the region of pain.
4. Dx of exclusion

1. Presence of continuing pain, allodynia, or hyperalgesia after a nerve injury, not necessarily limited to the distribution of the injured nerve.
2. Evidence at some time of edema, changes in cutaneous blood flow, or abnormal sudomotor activity in the region of the pain.
3. Dx of exclusion.

• Pharmacological mangement: antiepileptic drugs, antidepressants, NSAIDs
• Interventional mangement: sympathetic nerve blocks, neuromodulation
• PT - desensitization, ROM, mobilization (PT may be considered the most important tx modality!)
• Psychological therapy

• Developed to guide treatment of cancer pain
• Level 1: non-opioids (NSAIDs, acetaminophen), +/- adjuvants (ex. TCAs, gabapentin).
• Level 2: weaker opioid (codeine, tramadol, vicodin), +/- non-opiods, +/- adjuvants
• Level 3: stronger opioids (morphine, fentanyl, oxycodone), +/- non-opioids, +/- adjuvants
• Level 4: Interventional - spinal injections or stimulation, pumps, nerve blocks, neurolytic injections, etc.

• Diagnosis is made when injection of an anesthetic at the specific facet joint results in pain relief. (Should use a control).
• Tx: PT facilitated by intrarticular steroid injection, medical branch radiofrequency ablation, cryo (block sensory input to joint).

• Depressed level of consciousness but patient retains ability to maintain the airway independently and continuously and to respond appropriately to physical stimulation and verbal command.
• spectrum includes: minimal, moderate, and deep sedation (after deep sedation is general anethesia).

• Drug induced anxiolysis during which patient responds normally to verbal commands (may have mild slowing of baseline mental status)
• Airway, spontaneous ventilation, and CV system are all unaffected.

• a.k.a. "conscious sedation"
• drug-induced depression of consciousness during which patient responds purposefully to verbal commands (i.e. when spoken to in normal voice or touched lightly) - somnolent/sleepy, but easily arousable.
• airway unaffected
• spontaneous ventilation remains adequate
• CV system usually maintained

• Drug-induced depression of consciousness during which patients cannot be easily aroused, but respond purposefully to repeated or painful stimulation. (arousable, but not easily arousable)
• Airway may be impaired, spontaneous ventilation may be inadequate (frequently need supplemental oxygen), CV usually maintained. 

• drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation.
• Airway and ventilation are impaired and CV system may be impaired. 

• Naloxone = competitive antagonist @ opioid receptors. Abrupt reversal can result in sympathetic stimulation and acute withdrawal syndrome (if pt is opioid dependent), and vomiting.
• Flumazenil = competitive antagonist of BDZ and BDZ receptor. Abrupt reversal can result in anxiety rxn, increased ICP in pts with head injury, and seizure activity in pts with seizure d/o.

• uses: inexpensive anesthetic/analgesic
• concerns: diffuse hypoxia (high concentrations required to achieve effect), B12 suppression (inhibition of B12-dept enzymes, i.e. those involved in DNA synthesis), NV, bone marrow supression with prolonged exposure, expansion of air-containing cavities.
• systemic effects: CV system is mostly unaffected; decreases hypoxic respiratory drive; increased cerebral blood flow and blood volume, mild increase in ICP.

• uses: analgesia, sedation
• concerns: dose-dependent respiratory depression
• mechanism: binding to receptors inhibits presynaptic release & postsynaptic response to excitatory NTs from nociceptive neurons.
• systemic effects: no mjaor CV impairment; does cause respiratory depression, decreased hypoxic drive, and chest wall rigidity. Decreases cerebral blood flow, ICP, cerebral O2 demand. Increased NV.

• uses: IV sedation, induction, and maintenance of general anesthesia (no analgesic effect)
• concerns: must use smaller dose in elderly patients b/c of hypotension, patients with metabolic d/o, pain @ injection site
• systemic effects: CV effects include hypotension, decresed CO. Dose dependent respiratory depression, airway obstruction, apnea. Decreased NV.

• uses: induction in patients with bronchospasm trauma, hypovolemia (burns). indirectly stimulates sympathetic drive
• concerns: CV stimulation, increased oral secretions, hallucinations
• mechanism: stimulates NMDA receptors in cortical areas and opioid receptors in spinal cord
• systemic effects: CV - stimulates sympathetic outflow causing increased HR, BP, O2 demand. Minimal central respirtaroy depression, ↑ bronchodilation. CNS - sedation, hypnosis, analgesia, increased ICP, IOP, and cerebral O2 demand. (Combining with bdz can help offset CV and CNS effects).

• uses: tx of anxiety, conscious sedation
• concerns: when combined with other CNS depressants may cause severe respiratory depression & hypotension; elderly are extra sensitive. H2 blockers & liver cirrhosis decrease clearance.
• mechanism: potentiates effect of GABA-mediated neuro-inhibition.
• Systemic effects: decreased systemic vascular resistance and CO; depression of central respiratory drive; anxiolysis, sedation, amnesia, anticonvulsant.

• Esters - ester linkage
• cocaine, procaine, prilocaine, chlorprocaine
• broken down rapidly by plasma cholinesterases (exception-cocaine, different enzyme)
• more allergenic - broken down to PABA
• Amides (amide linkage, i.e. nitrogens)
• I's in their names:lidocaine, bupivicaine
• metabolized by liver (slower)
• true allergy is very rare
• Both esters and amides have a hydrophobic end and a hydrophilic end (the amide/ester linkage connects the 2 ends).

• LA: ringing in ears, numb lips, metallic taste
• Epi: palpitations, feeling of doom/anxiety
• vasovagal rxn to fear of procedure: fainting

• First, must be applied to outside of nerve membrane.
• Then the drug must penetrate the membrane - hydrophobic part
• And activate intracellular receptor - hydrophilic part (within Na channel)
• When LA binds receptor→ 1) prevents conformational change necessary for activation & 2) physically occludes the channel.
• This blocks Na conductance → no changes in membrane potential → pain signal does not get propagated.

• Lipid soluble drugs pass through the membrane more easily and are, therefore, more potent than less lipid soluble drugs (less amount needed to achieve same effect).
• ex.: Bupivicaine is more lipid soluble & more potent than lidocaine.

• The % refers to the "weight percent"
• To interpret: shift decimal over one place to right and that is the concentration in mg/ml. 
• ex. 0.5% = 5 mg/ml; 2% = 20 mg/ml
• If a fraction, change fraction to decimal. Ex. 1/8%
• 1/8=0.125→0.125%→ 1.25 mg/ml
• lower concentrations →  less anesthetic effect, but also less toxicity.

• LAs that have greater protein binding have longer duration of action because they stay bound to the receptor longer.
• Also have longer duration because drugs that are bound to plasma proteins are broken down less.
• At the same time, remember protein bound drug cannot cross membrane (less drug available). This is good sometimes: ex. bupivicaine is highly protein bound and thus good for use in OB because small amnt crosses from mom to baby.

• LAs are weak bases (pKa>7.4) - always have some in base (B) form and some in acid (BH+) form.
• Uncharged (B) form can penetrate the lipid membrane more easily/quickly.
• Therefore, more uncharged form (B) = faster onset time

• pKa  tells you the pH where 50% is B and 50% is BH+.
• If pH is below the pKa value, more will be in the BH+ form (think: more H+ in environment) → slower onset.
• ex. pKa of bupivicaine = 8.1. time of onset = 20 min; pKa of lidocaine = 7.7. time of onset =12 min
• BL: pKa closer to physiologic pH (7.4) = faster time of onset
• [HH eq: pH = pKa + log(B/BH+)
• Note: the effect of pKa on time of onset can be overcome by giving greater dose (can give ↑ dose of ester b/c quick breakdown)

2 effects of adding bicarb to LA solution;

how much is added?

1. Can produce faster time of onset (increases local pH → more drug in B form)
• ex: lido by itself: onset of 12 min; lido with bicarb: 8 min
2. Injection hurts less
3. Dose: 1 ml/10 ml LA

• Infected/ischemic area - lower pH
• This means more LA is in charged form/ion trapping → poor onset/poor block.
• Solution = block nerve proximal to ischemic area

• Local vasoconstriction → ↓ reabsorption
• increases block duration
• decreases toxicity
• Do NOT give epi in areas with no collateral blood supply!
• 1:1000 means 1 g/1000 ml (=1000 mg/1000 ml = 1 mg/ml). 
• 1:200K works out to be 5 mcg/ml (1 mg=1000 mcg)

• Mix of lidocaine and prilocaine with lower melting point than either one alone.
• Used as topical anesthetic - weight based dose (8mg/kg)
• Can overdose - methemoglobinemia (d/t prilocaine)

• Sx: ringing ears, numb lips, metallic taste, sedation, mental status change, seizure
• Mech: inhibition of inhibitory neurons, excitation of excitatory neurons (glutamate), higher doses depress both excitatory and inhibitory 

• sx: dysrhythmias, hypotension, cardiac arrest
• mechanisms: all LAs slow conduction - eventually sinus node slows enough to produce asystole/sinus arrest. (esp bupivicaine?)

• Acidosis increases toxicity
• cerebral vasodilation - ↑ levels of LA in brain.
• less protein binding = more free drug
• ion trapping
• Tx of toxicity: resuscitation/ventilation.
• If standard resuscitation measures are ineffective: lipid infusion - speeds removal of bupivicaine from cardiac muscle

• Spinals have a definite end point (CSF comes back).
• Epidurals do not have a definite end point ("potential space"), if CSF comes back, you've gone too far.

• Spinal is like filling a tube of liquid - whole tube fills at once
• mixes well & easily catches all nerves 
• cord "transection" at highest level (no innervation from that level downward)
• can slosh up too high (c-spine, bad)
• Epidural: filling tube of gogurt/filling a "potential tube"
• starts at 1 spot, spreads up and down
• catches each nerve individually, takes time to spread, more "patchy" block
• has top and bottom

• Spinal: very small amount (2 ml) - drug only needs to get to the top of the area that needs to be numbed.
• Epidural: large amount (20 ml) - need to fill entire column completely & "push" the drug where you want it to go (gogurt)
• Spinal: time limited - depends on drug and dose, "one shot deal"
• Epidural: almost always use catheter - can keep adding drug

• The initial pattern of numbness is different
• spinal: numbness from top level down
• epidural: band of numbness formed
• Pattern of eventual numbness can be the same.

• Complications of spinal and epidural are basically the same
• infxn
• bleeding
• nerve damage
• HA
• failure of block
• low bp d/t sympathetic block

• Can occur if the dura is punctured.
• in spinal, dura is punctured everytime, but hole is tiny
• in epidural, dura may be punctured accidentally = big hole
• As CSF leaks out of IT space → tug on neural structures
• Onset is 1-7 days after puncture
• HA goes away when you lie down
• Tx: conservative vs. blood patch

• Useful because it related cardiac output to size of individual
• Cardiac index = CO/Body Surface Area
• Normal CI = 2.5-4.2 L/min/meter²

• Venous return - blood volume, posture, pericardial pressure, venous tone [note almost all anesthetics cause vasodilation]
• Rhythm - in normal sinus rhythm, the atrial kick contributes 20-30% of LV filling. Pts with cardiac disease are more dependent on atrial kick to fill the LV (30-50%)
• HR - faster HR means less filling time in diastole

• basal metabolic rate 
• heart rate
• when HR is fast, there's less time in diastole → decreased coronary perfusion
• wall tension (i.e. hypertension)
• contractility

• HR (↑ HR → ↓ coronary blood flow)
• arterial O2 content: CaO2 = 1.34(Hgb concentration)(% O2 saturation) + 0.003 (PaO2)
• coronary perfusion pressure (CPP)
• coronary vessel diameter

• Should have access with 2 large bore IVs
• ECG
• intra-arterial blood pressure catheter
• CVP
• pulmonary artery catheter (Swan-Glanz)
• TEE (transesophageal echocardiography)
• coagulation monitoring

CPP = ADP - LVEDP

• ADP = aortic diastolic presure
• LVEDP = left ventricular end-diastolic pressure (preload)

• increased HR
• increases myocardial O2 demand
• decreases supply
• Excessive preload
• increased demand d/t increased wall stress
• decreased supply d/t too much diastolic pressure

• LV dysfunction/LV wall motion abnormalities
• elevated LVEDP at rest (>18 mmHg)
• Recent MI or unstable angina
• Post MI complications
• Reoperations
• Emergency surgery

• insertion risks - neck hematoma, pneumothorax
• arrhythmias
• perforation of right heart
• valve damage
• Pulm artery rupture (up to 90% mortality)

• Vasopressors/dilators
• inotropes
• beta blockers & CCBs
• antiarrhythmic tx
• antifibrinolytics
• diuretics
• anesthetics

• hypothermia
• lower LVEDP @ rest (prevent distension)
• asystolic arrest
• cardioplegia (high K solutions that stop heart temporarily during surgery without causing ischemia)
• ice around the heart

• oxygenation and CO2 elimination
• circulation of blood
• systemic cooling (hypothermia for cardioprotection) and rewarming when procedure is done
• diversion of blood from the heart
• protect the myocardium

• Venous blood drained by gravity
• Blood passes through oxygenator and heat exchanger
• Blood passes through arterial filter
• Blood returns to patient via aortic line.

• Anticoagulation (VERY important!): heparin is used most often 
• Cannulation of the heart
• Monitoring
• Cardiac protection
• Preparation for bypass

• Perfusionist checks for adequate flow
• Venous blood is drained
• Arterial (oxygenated) blood returned
• CVP and PAP return to near zero
• Systemic arterial flow at desired levels

• adequately rewarm pt before weaning from CPB
• avoid overheating brain
• meausures to keep patient warm after CPB
• fluid warmer, forced air warmer, warm OR

• correct metabolic acidosis
• optimize hematocrit
• normalize K
• consider giving Mg or checking Mg level
• Check Ca level and correct deficiencies

• suction trachea and ET tube
• inflate lungs gently by hand
• ventilate with 100% O2
• treat bronchospasm with bronchodilators
• check for pneumothorax/pleural fluid (place chest tube if necessary)
• consider need for PEEP, ICU ventilator, nitric oxide

• Heparin is reversed with protamine
• approx 100 U of unfractionated heparin is inactivated by 1 mg protamine; protamine heparin complexes are cleared from circulation
• SE of protamine include:
• hypotension d/t systemic vasodilation (benign, time-limited)
• anaphylactic type rxns
• acute pulmonary vasoconstriction - can be very dangerous and lead to right-side heart failure, decreased CO, systemic hypotension, etc.

• patients that received NPH insulin
• previous rxn to protamine
• meno who have undergone vasectomy (protamine comes from fish sperm)
• note: previously receving protamine is not a risk factor

• hemorrhage
• hypotension d/t decreased SVR with bolus dosing
• anaphylaxis (rare)
• altered concentrations of lipid-soluble drugs d/t activation of lipoprotein lipase
• osteoporosis (long-term use) 

• Ao dissection
• massive systemic air embolism
• oxygenator failure
• obstructed venous returns (mechanical problems with cannula)
• distended right/left heart
• erroneous systemic blood flow
• arterial pump failure
• total electrical failure

• inadequate oxygenation
• electrical failure
• gas embolization
• clotting
• line separation
• blood leaks
• mechanical failure

• STOP CPB
• Put pt in steep trendelenberg position (head down - so air in circulation goes away from brain)
• aspirate maximum air from aorta/arterial perfusion line
• deep hypothermic circulatory arrest (DHCA)
• retrograde flow through SVC to "flush out" bubbles
• +/- steroids, dilantin, hyperbaric tx post op

• Older people have 25% increase in SVR as well as stiffened arteries, therefore have increased systolic BP.
• Eldlery rely more heavily on SVR to maintain BP than younger people. Anesthetics decrease SVR so drop in BP in elderly pt is greater than it would be for younger pt.
• Elderly have decreased CO (↓1%/year after 30 yo) → delayed onset of IV induction agents and increased rate of rise of alveolar concentration of volatile agents
• Increased risk of arrhythmias and CHF.

• exercise tolerance (i.e. 3 flights of stairs) - sensitive predictor of postop px in noncardiac surgery
• stress tests: exercise or pharmacological (adenosine, dobutamine)
• baselike EKG
• orthostatic hypotension (hypovolemia vs. autonomic dysfunction)
• echo helps by telling us about LV fxn (be sure to maximize cardiac fxn before surgery)5

• Maintain MAP within 20% of baseline - don't want hypo or hypertension
• Listen for carotid bruits during pre-op physical. (warrants further evaluation with US or angiogaphy if present - 80% of stroke d/t infarction from carotid emboli)
• Good assessment of baseline mental status prior to surgery

• geriatric pts are at greater risk for perioperative hypoxemia (FEV1 and FVC decreases with age after 30, decreased alveolar surgace area & alveolar membrane permeability)
• Smoking → decreased mucociliary function → increased risk of pneumonia postop. Advise pt to quit smoking at least 8 weeks before surgery,
• Surgeries with most pulm. complications are: upper abdominal surgery < thoracic surgery w/o lung resection < thoracic surgery w/ lung resection
• Good preoxygenation is extremely important; elderly have less reserve.

• Elderly have decreased RBF, renal mass, & renal fxn.
• Check BUN and creatinine before surgery - remember that elderly have decreased muscle mass so minor increase in BUN/creat. can indicate major loss of renal fxn. Also: normal creatinine does not necessarily mean normal kidneys.
• Compromised renal fxn delays clearance and excretion of drugs - pts may take longer to wake up post-anesthesia (esp: morphine - active metabolite)
• Decreased renin secretion can impair ability to respond to hypovolemia/hyponatremia/hyperkalemia (can cause increased incidence of perioperative metabolic acidosis)

• decreased hepatic size → decreased hepatic blood flow
• Phase 1 drug metabolism (redox, hydrolysis) is impaired (phase 2 - conjugation - not so much) this causes ncreased risk of drug toxicity 

• Neuro: elderly more likely to have perioperative behavior changes, memory deficits, confusion
• Metabolic: correct peri & intraoperative hyperglycemia in patients w/ impaired glucose tolerance
• CT: osteoporosis and arthritis can make elderly more susceptible to positional injuries during surgery, can make airway management more difficult, pt may be more susceptible to c-spine injury

• increased body fat → increased volume of distribution and prolonged action of lipophilic drugs
• water soluble drugs have increased volume in plasma and decreased protein binding → increased concentration of free drug
• want drugs that cause least hemodynamic instability and stay in circulation for shorter time
• increased CNS sensitivity to BDZs and opioids
• 4% decrease in MAC of volatile anesthetics for each decade >40 yrs.

1. HTN
2. renal dz
3. CAD
4. COPD

• Advantages include decreased incidence DVT, PE, decreased need for transfusion, and decreased renal failure.
• Also less pulmonary complications assoc with regional anesthetic, but be aware that if a patient has severe COPD he might rely heavily on accessory respiratory muscles so you don't want to block these muscles - i.e. don't give regional blocks at level of spinal cord that is too high (procedure-dependent).
• Regional anesthesia is contraindicated in patients that are on anticoagulants b/c epidural hematoma could cause permanent paralysis.

• postop renal failure has 50% mortality rate & most pts are asymptomatic until uremic
• fractional excretion of sodium (FENa) can help differentiate between prerenal azotemia and ATN
• FENa<1% is likely prerenal azotemia and hydration may lead to improvement
• FENa>1% is likely ATN - needs further investigation.
• Monitoring fluid balance intraoperatively is very important: U/O is a good indicator of end organ perfusion - want to see at less 0.5 cc/kg/hr during surgery.
• UA may unmask asymptomatic UTI.

• Pt must be lying flat for this surgery. This could be problematic for pts with CHF and orthopnea - these pts may need to be intubated and under general anesthesia.
• ocularcardiac reflex: drop in HR caused by pressure on extraocular muscles/eyeball (CN V and CN X)
• Topical anesthesia or retrobulbar blocks frequently used. Also sedation/meds to keep pt comfortable.

• If pt is not on anticoagulants could do regional anesthetic at T10
• If pt cannot do regional, could do general anesthetic with an unprotected airway (LMA, IV sedation, or mask ventilation) since it is a short procedure - but should be able to switch to secured airway later. 

• Maintain normal SVR
• Maintain normal sinus rhythm

• Hoffman elimination - pH dependent & temperature dependent
• Ester hydrolysis
• Cistracurium would be good to use in patient with renal failure (elevated BUN, K+).

• prone position
• cardiopulmonary bypass
• spine surgeries
• hypotension
• anemia
• increased applied pressure or edema
• long surguries

1. class I: <15% blood loss (0.75 L); some increase in  HR, normal bp; minimal tx
2. class II: 15-30% blood loss (0.75-1.5 L); increased HR, some decrease in bp; tx = IV fluids
3. class III: 30-40% blood loss (1.5-2 L); very fast HR, low bp, confusion; tx = fluids & packed RBCs
4. class IV: >40% (2 L); critical bp and HR; tx = aggressive interventions