2008)
ACLS PROTOCOLS & ARRHYTHMIAS
V. Fib/Pulseless V. tach
Synchronized Cardioversion
50 J A flutter, SVT
100 J A. fibrillation
Direct current (DC) cardioversion is NOT useful and NOT indicated in an
unstable patient with Multifocal atrial tachycardia
Narcan
Atropine
Vasopressin
Epinephrine
Lidocaine
Neonatal Resuscitation
Epinephrine, 0.1 ml/kg of 1:10,000 soln for asystole or spontaneous HR < 60
Naloxone, 0.01 mg/kg IV or 0.2 mg/kg IM if opioids given to mother within last 4
hours of labor
Sodium bicarbonate, 2 mEq/kg, only for severe metabolic acidosis
Calcium gluconate 60 mg/kg only with documented neonatal hypocalcemia or
Calcium chloride 20 mg/kg
Atropine 0.02 mg/kg
Glucose only for hypoglycemia, 2 ml/kg 20% glucose
Dopamine at 5 mcg/kg/min to support BP
Surfactant via ETT to premature neonates with respiratory depression syndrome
Sign
Appearance (Color)
0
Blue or pale
Pulse
Grimace (reflex
irritability in response
to catheter in nose)
Activity (muscle tone)
Absent
No
response
Flaccid
1
Body pink,
extremities blue
< 100
Grimace
2
All pink
Some flexion
Active motion
> 100
Crying
Respirations
Absent
Slow, irregular
Good, crying
Atrial Fibrillation
Acute therapy = identify and treat associated factors i.e. hypotension, hypovolemia,
or anemia:
o D/C countershock with synchronous mode: 50-100 Joules o DO
NOT shock in setting of digitalis toxicity
o Digitalis loading dose = 1 mg and daily dose 0.125-0.375 mg day o
Verapamil, propranolol
o Pacing is effective for atrial flutter
Maintenance
o Rate control with digitalis, verapamil, propranolol o Maintain SR
with quinidine or disopyramide
o AVOID lidocaine increases A-V conductance accelerated
ventricular response
Digitalis o Inhibits Na+-K+ ATPase prolonged A-V conductance, (+) inotropy,
automaticity o T = 2 days
o Concern for CPB due to hypokalemia causing toxicity
o
o Withdrawal of propranolol acute MI and death o Toxicity = N/V,
AV block, ventricular arrhythmias, VF Treat arrhythmias with
lidocaine, phenytoin, K+
DO NOT SHOCK! o
Predisposition to toxicity:
Hypokalemia
Hypothyroid
Hypomagnesemia
Hypercalcemia
WPW Syndrome
Impulses conduct through accessory pathway resulting in EKG: short P-R interval,
wide QRS complex, delta wave
Anesthetic goals:
o AVOID sympathetic stimulation, i.e. pain, hypovolemia, ketamine,
pancuronium o AVOID Digoxin!! enhances cardiac conduction via
accessory pathways o Atropine is OKAY!
Glossopharyngeal (IX)
Innervation hypopharynx & pharynx (tonsils, base of tongue, epiglottis,
vallecula), omohyoid
Controls gag reflex
Taste & sensation posterior 1/3 tongue
BLOCK: posterior to angle of mandible, used for pain of malignant tongue base
growths
Complications of block: o Ipsilateral VC paralysis, tachycardia from vagus (X)
block. CN X exits w/CN IX o Ipsilateral tongue paralysis. CN XI exits with CN IX.
Vagus (X) - sensation of airway inferior to epiglottis
Superior Laryngeal Nerve - sensation & motor of larynx
External br = motor to cricothyroid muscle VC tensor (closes VC), sensory
anterior subglottic mucosa
Internal br = sensory above the VC (+ false VC, laryngeal & buccal surfaces of
epiglottis), pierces thyrohyoid membrane
BLOCK: inferior to greater cornu of hyoid bone will block laryngospasm
(caused by external br due to cricothyroid muscle tensing VC)
Recurrent (Inferior) Laryngeal Nerve - sensation below VC & motor of all intrinsic
laryngeal muscles, except cricothyroid (external br of superior laryngeal n.)
Runs in groove b/t trachea & esophagus
Bilateral injury ADDuction of VC to midline position (due to unopposed
cricothyroid tension), severe respiratory obstruction
BLOCK: transtracheal approach through cricothyroid membrane
Hypoglossal (XII)
Innervation hypopharynx & motor to tongue
Not necessary to block for oral or nasal intubation!
Awake Nasal Intubation Blocks: (1) RLN, (2) CN V, (3) Superior laryngeal nerve
Awake Oral Intubation Blocks: (1) glossopharyngeal (CN IX), (2) RLN, (3) Superior
laryngeal nerve
Blood supply
Superior laryngeal artery branch of superior thyroid artery off of external
carotid
Inferior laryngeal artery br of inferior thyroid artery off of thyrocervical trunk
of subclavian **Injuries**
Unilateral paralysis of superior laryngeal nerve subtle clinical findings, b/c
external branch only innervates cricothyroid muscle
Bilateral paralysis of superior laryngeal nerve hoarse voice, risk aspiration
Unilateral paralysis of recurrent laryngeal nerve paralysis of ipsilateral vocal
cord, paramedian position loss of voice quality
Acute bilateral recurrent laryngeal nerve injury midline, nearly closed vocal
cords, stridor with inspiration, risk aspiration
Bilateral vagus nerve injury flaccid, mid positioned vocal cords
Alveoli
Type I pneumocytes: flat, form tight junctions, prevent albumin passage
Type II pneumocytes: round, contain lamellar bodies which contain surfactant;
resistant to O2 toxicity; produce type I pneumocytes
Blood-Gas Interface
Ficks law of diffusion: amount of gas that moves across a sheet of tissue is
proportional to the area of the sheet, but inversely proportional to its thickness
Path of alveolar gas = layer of surfactant alveolar epithelium interstitium
pulmonary capillary basement membrane endothelium plasma RBC
membrane
Combitube Avoid in patients with intact gag reflex, esophageal pathology or h/o
substance ingestion
Orotracheal intubation
If multiple units of Group O WHOLE blood (contains anti-A & anti-B) have been
transfused to Group A or B blood one should NOT switch back to the patients
blood type
FFP and blood need to be ABO compatible
Platelets (just preferred) & cryoprecipitate DO NOT need ABO compatibility
Hetastarch
T 1.5 days
Max amount 20 ml/kg (1.5 liters)
DOES NOT interfere with crossmatching of blood or affect coagulation at 20 ml/kg
dose
Complications:
o Transient elevation serum amylase o Anaphylactoid rections o
Coagulopathy dose-related due to procoagulants, quality and
number of platelets
Dextran
Degraded to glucose
Delays systemic absorption of local anesthetics
Complicatons:
o Can interfere with cross-matching of blood (rouleaux formation) o
Decreases platelet adhesiveness
o Allergic rxns histamine release Promit (Dextran-1) decreases life
threatening anaphylactoid reactions by 100 fold. Blocks receptors and
decreases histamine release
o Interfere with coagulation
o Pulmonary edema by direct toxic effect on capillaries
Albumin
T = 20 days
Made from fractionated pooled human plasma HEATED kills VIRUSES
STOP transfusion!
Treat hypotension - IV fluids, Dopamine, other blood
Establish diagnosis repeat clerical check, Direct Coombs, repeat type &
cross, serum haptoglobin
Treat renal vascular ischemia IV fluids, mannitol, UOP > 1 ml/kg/hr, if no
response give furosemide, low-dose dopamine
Evaluate and treat DIC plt count, PTT, fibrinogen
(2) Allergic-Urticarial-Pruritic
2nd most common
If hives are the only sign, DO NOT stop transfusion
(3) Febrile NON-hemolytic
One of the most common
Temperature rise (> 1 degree C)
Give antipyretics & diphenhydramine, stop infusion to r/o hemolytic rxn
Effectively treated with leukocyte-poor saline washing blood
(4) DELAYED Hemolytic Reaction = Extravascular
Occurs in those who have compatible cross-matched, but over 4-21 days the
transfused RBCs are destroyed via phagocytosis by macrophages in the
reticuloendothelial system
Involves antigens and antibodies that do not bind
complement
(5) Non-cardiogenic pulmonary edema = TRALI
Due to transfusion of anti-leukocytic or anti-HLA antibodies that interact with
patients WBCs aggregate in pulmonary circulation damage to alveolar/capillary
membrane triggers
Rx is similar to ARDS
Resolves 12-48 hrs with supportive care
(6) Anaphylactic Reactions
Typically is IgA-deficient patients with anti-IgA antibodies who receive IgA
containing blood
IgA deficient patients need thoroughly washed pRBCs, deglycerolized frozen red cells,
or IgA free blood units
Massive Transfusion = 10 units/ 24 hrs
Most common problem is dilutional thrombocytopenia
o Hyperkalemia
o ARDS
Other problems:
vWF Disease
Most common hereditary bleeding disorder, 1% of population
Autosomal dominant
Hallmark: prolonged BT, vWF levels & factor VIII activity, NORMAL PT, PTT
platelet #
Treatment vWF:
o
DDAVP 1st line for type 1 and 2A, Avoid in 2B
thrombocytopenia o Cryoprecipitate contains vWF and factor VIII,
given for urgent correction o
Factor VIII concentrate also
contains vWF
Some patients are not responsive to DDAVP, emergent rx requires cryoprecipitate
Hemophilia A
Hemophilia B
X-linked recessive, low factor IX
Vitamin K Deficiency
Vit K required for hepatic synthesis of factors II, VII, IX, X, protein C & S
Factor VII depleted first elevation in PT, with prolonged deficiency, the PTT will
also increase. Normal platelet count
Can de seen in those on TPN without vitamin K supplementation & newborns with
a sterile gut at birth
Treatment:
o
No bleeding: urgent rx is best accomplished by IM or IV Vitamin K
(1-5 mg) improvement within 8 hours. Give slowly, can cause
hypotension o
Bleeding: vitamin K 10 mg IV + FFP
Sickle Cell Anemia
0.2% black population, inherited d/o of -chain, valine substituted for glutamic acid
Predominant Hgb in 2-mo infant is Hgb F, protects infant from sickle cell
anemia
Always concern for excessive blood transfusions hemochromatosis
Blood
Therapy Triva
Factor IV (Ca2+) and VIII are not synthesized by the liver
Most sensitive test is PT (PeT = extrinsic pathway) b/c Factor VII t = 4-6 hrs
PTT (PiTT = intrinsic pathway) tests factors VIII, IX
3 leading causes of transfusion-related death (1) ABO incompatibility, (2) TRALI, (3)
sepsis
5% of patient who receive heparin for 5 days will develop HIT clinical si/sx due to
thrombosis and thromboembolism, than to thrombocytopenia
Cryoprecipitate = source of factor VIII, XIII, vWF, fibrinogen, no need for ABO
compatibility
Hyponatremia
Decreases MAC
Treatment: hypertonic saline (3%), d/c once Na+ rises to 120 mEq/l and give NS
CARDIOVASCULAR PHYSIOLOGY & ANESTHESIA
Fick Equation to calculate cardiac output (Q)
SvO2 = SaO2%
CO
mL/min
Q =
VO2
CaO2 CvO2 x 10
VO2__________
x Hgb/dL x 1.34 ml O2/g Hgb
Pacemaker Codes
Anti-bradycardia functions
I
Chamber(s)
paced
A = atrium
V = ventricle
II
Chamber(s)
sensed
A = atrium
V = ventricle
III
Response to
sensing
T = triggered
I = inhibited
Programmability
IV
Programmability
Antitachycardia
V
Antitachycardia
fx
P = pacing
S = shock
P = simple pro
M = multiple
modes
D = dual A & V
D = dual A & V
D = Dual T & I
C =
D= P&S
communication
O = none
O = none
O = none
R = rate adaptive
O = none
O = none
*if patients HR is above the rate at which the pacer is set, then edrophonium or a
Valsalva maneuver slows the HR and tests the normal pacemaker function. Use of
a magnet tests only the ability of pacemaker to convert into a fixed rate, asynchronous
mode
Pacemaker Indications:
3rd degree (complete) heart block
Asymptomatic Mobitz type II (dropped QRS, 2:1, 3:1, 4:1)
Symptomatic bradycardia
Symptomatic bifascicular block
Orthotopic heart transplantation
Hypertrophic and dilated cardiomyopathy
Long QT syndrome
10
Frank-Starling Curve
Relates LV filling pressure to LV work o LV
filling pressure (x-axis) = LVEDV, LVEDP,
LA pressure, PAOP, CVP o LV work (Y-axis) =
LV stroke volume or stroke index, CO, CI, arterial
blood pressure
11
Basic Circuit
(2) Oxygenator
2 types o (1) Bubble oxygenator cheaper, easier to use, lower priming volume o
(2) Membrane oxygenator less RBC damage, best for long cases
12
Potassium Cardioplegia
extracellular K+ reduces transmembrane potential (less negative inside)
interferences with Na+ current during depolarization Na+ channels eventually
become inactivated and heart is arrested in diastole **
Contents:
o K+ = 15-40 mEq/L (keep < 50 mEq/L b/c risk paradoxic energy & high K
load) o
Na+ = 100-120 mEq/L o
Cl2- = 110-120 mEq/L o
Mg2+
= 15 mEq/L
o Glucose = 28 mmol/L (can use glutamate, aspartate)
o Bicarbonate = 27 mmol/L
May not reach areas distal to high-grade stenosis give retrograde via coronary
sinus
Reperfusion of myocardium can be associated with extensive cell injury, rapid
accumulation of intracellular calcium and irreversible cellular necrosis o
Oxygen-derived free radicals may play a role o Free radical scavengers,
mannitol therapy, may help
13
14
High dose (0.03 0.15 mcg/kg/min) = 1 SVR ( SV) , reduce splanchnic &
renal blood flow
15
Adenosine
Used to treat WPW & supraventricular tachycardia narrow complex
Raidly metabolized such that it is not influenced by liver or renal function
Effects enhanced by Dipyridamole asystole occurs if given standard dose
Methylxanthines Caffeine, Theophylline and Amrinone are antagonists of
adenosine increase drug dose
Side effects bronchospasm, dyspnea, HA, flushing, neck or throat discomfort
Contraindictions 2nd or 3rd degree AV block & SA nodal dysfunction risk asystole
Amiodarone
Chemical structure similar to thyroxine casues hypo- or hyperthyroidism
Action - prolongs duration of action potential of both atrial & ventricular muscle
without altering resting membrane potential depresses SA and AV node function
Treatment of choice for:
Recurrent supraventricular & ventricular tachydysrhythmias
WPW increases refractory period of accessory pathway
Side effect Atropine-resistant bradycadia & hypotension during general
anesthesia due to anti-adrenergic effect Rx with isoproterenol or temporary pacing
Aprotnin
Mech inhibits serine proteases plasmin, kallikrein, trypsin
Most common side effect = anaphylactic reactions in redo cardiac surgery 100%
renally excreted!
Beta Blocker Side Effects
Beta Agonist Effects
HyperK+
Bronchodilation hypoglycemia
Renin secretion
Excessive myocardial depression, AV block
Lipolysis
Rebound tachycardia with abrupt Glycogenolysis discontinuation insulin
secretion = hyperglycemia
Pulmonary edema
Heparin
Mucopolysaccharide produced by mast cells, activates anti-thrombin III
inactivates factors II (thrombin), IX, X, XII
16
100 U = 1 mg
T heparin = 1-3 hours, re-dose with 100 U/kg q 2 hrs, t is temperature & dose
dependent
Inactivated by liver & kidneys, t prolonged in hepatorenal syndrome
T is dose and temperature dependent
Side effects: hemorrhage, alopecia, osteoporosis, thrombocytopenia
Neutralized by protamine 1mg /1 mg heparin inactive complex without
anticoagulant activity
If hx anaphylactic protamine rxn, reverse heparin with hexadimethrine or omit
reversal & wait
Protamine
Highly positive charged base that binds and effectively inactivates heparin (highly
negative charged acid) heparin complexes are removed by reticuloendothelial
system
Dose protamine based on the amount of heparin initially required to produce that
desired ACT given in a ratio of 1-1.3 mg of protamine/100 U of heparin
Protamine given in excess has anti-coagulant activity (1/100th that of heparin)
Adverse effects:
o Myocardial depression
o Histamine release vasodilatation, flushing, severe pulmonary HTN from
systemic hypotension, pulmonary vasoconstriction, edema, bronchospasm
o Anaphylactic or anaphylactoid reactions o Patients allergic to fish may be at
higher risk
o Most severe, type II reaction mediated by elevated complement &
thromboxane A2 severe hypotension from R heart failure requiring reinitiation of CPB.
Intra-Aortic Balloon Pump
Indications
Acute cardiac failure refractory to pharmacologic intervention
Low-output states after CPB
Hypotension and low CI (<1.8) with high wedge pressure (>25 mmHg) despite
pressors
Cardiogenic shock 2/2 myocardial ischemia
Bridge to cardiac transplant
Equipment
Percutaneous insertion into common femoral artery high in descending thoracic
aorta
Inflation is triggered from the R wave on the EKG and occurs during diastole,
immediately following closure of the aortic valve just after dicrotic notch
Balloon deflation occurs during isovolemic contraction (late diastole) just
prior to opening of the aortic valve.
Hemodynamic effects
afterload, MVO2 and myocardial work SV & C.O.
intra-aortic diastolic pressure by 70% with balloon inflation coronary
blood flow
R shift of Starling curve
Complications
17
RA
RV
85% incidence
forms PDA
inferior wall LV
SA/AV nodes
Bundle of His
PDA
Inferior
ventricular
septum
Posterior LV
Inferior LV
Posterior
papillary
muscle of MV
Circumflex
Lateral wall
15% incidence
forms PDA
inferior wall LV
LAD
**at risk of
injury during
MV replacement
Leads V5, V6, aVL
LA
Anterior wall LV
Anterior/mid
ventricular
septum
Apex
Anterior papillary
muscles MV
Leads V1 V4
18
Bleeding Post-CPB
Vocabulary to Know
Pulsus paradoxus = defined as inspiratory fall in SBP > 10 mmHg cardiac
tamponade
Pulsus parvus = diminished pulse wave aortic stenosis
Pulsus tardus = delayed upstroke aortic stenosis
Pulsus alternans = alternating smaller and larger pulse waves severe LV
dysfunction
Bisferiens pulse = 2 systolic peaks aortic regurgiation
Adrenergic Reception Up & Down Regulation
# receptors is inversely proportional to the ambient concentration of
catecholamines
Increased adrenergic activity myocardial post-synaptic 1 receptors
down regulate
Calcium-induced inotropism is not impaired because 2 receptor numbers remain
relatively intact, can account for 40% of inotropism of the failing heart
Tachyphylaxis to infused catecholamines is from acute down-regulation of receptor
numbers Seen with chronic use of -agonists (terbutaline or isoproterenol).
Reversible with termination.
Reduction in number or sensitivity of -receptors in HTN patients w/elevated
catecholamines
Down regulation is the explanation for the lack of correlation b/t catecholamine levels
and BP elevation in those with pheochromocytoma
Chronic treatment with non-selective -blockade causes 100% increase in # of receptors propranolol withdrawal syndrome tachycardia, sweating,
tremor and general malaise
19
AVOID:
Ketamine b/c increase in sympathetic tone, even though a direct myocardial
depressant
Ca2+ channel blockers b/c decrease afterload
Digitalis or isoproterenol b/c of increase outflow obstruction Isoflurane
Treat A. fibrillation with cardioversion, not digitalis
Aortic Stenosis
If occurs with rheumatic fever, mitral valve is also affected
Si/Sx: SAD Syncope, Angina (without CAD), Dyspnea life expectancy < 5 years
Compensatory concentric increase in thickness of LV wall (minimal change in LV
size). As becomes more severe, LV becomes dilated and myocardial contractility
diminishes
HD significant disease = valvular pressure gradient > 50 mmHg
LV filling if very dependent on atrial contraction maintain sinus rhythm
Mitral Regurgitation/Aortic Regurgitation
Large V wave = mitral regurgitation
PDA occlusion posterior papillary muscle rupture acute MR
Achieve small increase in HR and decreases in SVR o Digitalis decrease size of LV
and lessens regurgitation, helps control A. fib o Nitroprusside decreases afterload
reduces pulmonary edema o Atropine beneficial o Isoflurane decrease in SVR and
increase in HR o Isoproterenol decrease in SVR and increase in HR
Mitral Stenosis
Exclusively in rheumatic fever pathophysiologic changes proximal & distal to
abnormal valve
Women > men, latency period 20-40 years
LV is protected, thus rarely see LV dysfunction
PCWP transudation of fluid into pulmonary interstitial space lower pulmonary
compliance & increases WOB
Patients are more susceptible to ventilatory depressant effects of sedative drugs
Increases in central blood volume ie. Trendelenburg position can precipitate R
heart failure
Wide Complex Tachycardia
Could be paroxysmal supraventricular tachycardia with aberrant accessory pathway
= WPW
If HD unatble cardioversion
If HD stable consider amiodarone (150 mg IV) or procainamide
20
TEG
1 = normal
= factor deficiency
3 = hypofibrinogenemia
4 = fibrinolysis
5 = hypercoagulable
2
21
o
o
o
o
o
o
o
o
Of these, only of the patients are responsive to calcium channel blockers in the long
term o
Ca channel blockers used: nifedipine 30-240 mg/day or diltiazem 120-900
mg/day Increases in PVR
Decreases in PVR
Metabolic acidosis
o
Metabolic alkalosis o Hypoxia
o
Hypocarbia
Hypercarbia
o
SNP
Sympathetic stimulation o
Nitroglycerin *best b/c least systemic effects o
Atelectasis o HCT
Low lung volumes due to compressed vessel from extra-alveolar vessels
High lung volumes b/c alveolar capillaries are compressed
Hypothermia
N 2O
High airway pressures/PEEP
ELECTROLYTES
Hypophosphatemia
Due to: (1) magnesium-containing antacids, (2) severe burns, (3) DKA, (4) EtOH
withdrawal, (5) prolonged respiratory alkalosis, (6) TPN
Often a serious and unrecognized complication of TPN that can contribute
to post-op muscle weakness and respiratory failure
Low PO4 reduces ATP reduce 2,3 DPG Left shift oxy-Hgb curve
unloading O2
Hyponatremia = Na+ < 135 mEq/L
Na+ < 120 = cerebral edema confusion, restlessness, drowsiness, seizure, coma
Na+ < 100 = V. tach, V. fib
Treatment: water restriction, loop diuretics, 3% NS if severe
Dose Na+ needed: i.e. 100 kg patient, Na+ 105 mEq/L, How much Na+ to
bring up to 120?
Dose Na+ = (wt in kg)(0.6) x (desired Na+ level current Na+)
(100 kg)(0.6) x (120 105) = 900 mEq
Give 3% NS (no faster than 100 ml/hr, once Na+ reaches 120, further treatment is
water restriction and diuretics
Metabolic Alkalosis
22
Chloride sensitive:
o Vomiting hypokalemic,
hypochloremic metabolic
alkalosis. K+ is lost in
emesis & urine in exchange
for trying to retain H+.
Alkalosis due to H+ loss in
emesis and volume
contraction.
o Volume contraction o
Diuretics
Chloride resistant:
o Cushings o
Hyperaldosteronism
(Addisons)
Respiratory compensation: PCO2 PCO2 equals the last two digits of the pH
Hyperventilation compensation is never complete b/c the ability to
hyperventilate is limited
Anion gap = Na+ (Cl + HCO3-); normal 4-12 mEq
Correct for low albumin add 3 to anion gap for every 1 g/dL of albumin; i.e.
albumin = 1.5, must add 4.5 to anion gap
Anion Gap
Methanol
Uremia
Diabetic ketoacidosis, alcoholic ketosis, starvation
ketosis
Paraldehyde (anti-convulsant)
INH/Iron
Lactic acidosis/Lactate (rhabdomyolysis)
Ethylene glycol/Ethanol
Salicylates
23
ENDOCRINOLOGY
Diabetes Mellitus
Diagnosis: fasting glucose > 140 mg/dL or random glucose > 126 mg/dL
DKA = diabetic ketoacidosis o insulin activity promotes amino acid buildup and
lipolysis with the release of free fatty acids free fatty acids converted into
ketone bodies in the liver acetoacetate & hydroxybutyrate anion-gap
metabolic acidosis
o Profoundly depleted of K+, yet serum levels are not often low b/c of the
acidosis o Treatment: treat hypovolemia from osmotic diuresis,
hypokalemia, start NS gtt
10 U/hr regular insulin or 0.1 U/kg/hr
As glucose moves intracellularly, so does K+
Monitor K+, glucose, serum ketones, UOP hourly
Avoid LR since liver converts lactate to bicarbonate, use NS
Once glucose reaches 250 mg/dL, start D5W
Give bicarbonate if pH is < 7.1 or base excess is > -7 caution b/c
bicarbonate can cause alkalosis with intracellular shift of K+
Lactic acidosis = lactate > 6 mmol/L, absence of urine & plasma ketones
Alcoholic ketoacidosis = recent EtOH history, +/- glucose, -hydroxybutyrate
>> acetoacetate
Hyperosmolar hyperglycemia non-ketotic coma (HHNKC) o Three
components are involved:
(1) Insulin deficiency: liver insulin levels are high enough to permit the
metabolism of free fatty acids, generally dont develop ketosis
(2) Renal deficiency-insufficiency: impairs the ability to excrete glucose and
leads
to hyperosmolarity
(3) Thirst deficiency: either b/c of a stroke or CNS depressant
o
24
25
Maternal Diabetes o
Hyperglycemia in the mothers leads
to hyperglycemia in the fetus!
o Causes a state of chronic hyperinsulinemia and increased glycogen
synthesis, lipogenesis, protein synthesis macrosomia
o At birth, can see neonatal hypoglycemia from chronic hyperinsulinemia o
Other associated problems:
Respiratory distress syndrome 2/2 to inhibitory effects of
hyperinsulinemia upon surfactant production
Cardiomegaly
Congenital abnormalities
Anesthetic Considerations
Those with HTN have 50% chance of co-existing diabetic autonomic
neuropathy:
o Orthostatic hypotension: > 30 mmHg SBP with upright position o
Painless MI: most frequent cause of death in long term diabetic o
Lack of HR variability
o Reduced HR response to atropine and propranolol
o Neurogenic bladder o
Lack of sweating o Impotence o Gastroparesis
Renal dysfunction manifested first by proteinuria, then elevated serum creatinine
Chronic hyperglycemia can lead to glycosylation of tissue protein and limitedmobility joint syndrome check TMJ, cervical spine mobility
Peri-operative:
o give dose of total morning insulin as NPH o start D5W gtt at 1.5
ml/kg/hr
o Insulin units/hr = plasma glucose
150
o 1 unit insulin lowers plasma glucose 30 mg/dL
Those requiring NPH or protamine zinc insulin have higher risk of protamine
sulfate allergic reaction
Large volumes of LR given can rise glucose levels for 24-48 hrs post-op
Regular
NPH
Protamine
Z
1 hour
onset
2 hour
onset
4 hour
onset
3 hour peak
6 hour duration
6 hour peak
24 hour
duration
24 hour
duration
12 hour
peak
THE THYROID
Thyroid gland secretes: triiodothyronine (T3), thyroxine (T4), calcitonin
Dietary iodine is absorbed by the GI tract thyroid gland oxidized back into
iodine bound to tyrosine triiodothyronine (T3) & thyroxine (T4)
HYPERTHYROIDISM
Causes: Graves disease, toxic multinodular goiter, thyroiditis, TSH secreting
pituitary tumor, functioning thyroid adenomas, overdosage of thyroid
replacement hormone
Medical treatment:
26
Propylthiouracil or methimazole to inhibit hormone synthesis, takes 68 weeks o Propranolol rx adrenergic overactivity & peripheral
conversion of T4 to T3 o Sodium iodide + propranolol lead to
euthyroidism within 10 days
Elective surgical procedures should be postponed until euthyroid
Emergency surgery, use esmolol gtt to control hyperdynamic circulation
Thiopental is best b/c is possesses some antithyroid activity at high doses
Patients can be chronically hypovolemic and vasodilated prone to hypotension
Display accelerated drug biotransformation & may be more prone to halothane
hepatitis and kidney toxicity from enflurane
NMB agents should be given cautiously; thyrotoxicosis is associated with
myopathies & myasthenia gravis
Hyperthyroidism DOES NOT increase MAC
o
27
HYPERPARATHYROIDISM
Hallmark: serum Ca2+ > 5.5 meq/L (normal 4.5-5.5 meq/L)
Primary hyperparathyroidism: parathyroid adenoma, carcinoma, hyperplasia
Secondary hyperparathyroidism: adaptive response to hypocalcemia 2/2 to
renal failure or intestinal malabsorption syndromes
Parathyroid hormone-related peptide secreted by a carcinoma (hepatoma,
bronchogenic) is the most common cause of humoral hypercalcemia of
malignancy
Effects of Hyperparathyroidism:
o short QT & prolonged PR intervals
o Hyperchloremic metabolic acidosis, polyuria, dehydration, polydipsia,
renal stones, renal failure
o Ileus, N/V, PUD, pancreatitis o Skeletal muscle weakness,
osteoporosis
o MS changes
Treatment: maintain UOP, hydrate, give Mithramycin in severe cases
HYPOPARATHYROIDISM
Due to hypocalcemia (< 4.5 meq/L) NM irritability (+) Chvosteks sign
(painful twitch of facial muscles after tapping facial nerve) or Trousseaus sign
(carpopedal spasm after inflation of TQ above SBP x 3 mins)
Hallmark: neuromuscular irritability (tetany) and laryngospasm,
prolonged QT interval
Treatment Calcium chloride
Avoid using 5% albumin solutions which might bind and lower ionized calcium
*HYPERCALCEMIA* = Level > 12 mg/dL
Si/Sx: HTN, dysrhythmias, shortened QT interval, kidney stones, seizure, N/V,
weakness, depression, personality changes, psychosis
Caution with administration of digitalis b/c some may exhibit extreme digitalis
sensitivity
Rx: 1st line Furosemide & fluid hydration with NS o
Other options
calcitonin, mithramycin, corticosteroid
ADRENAL GLAND
Adrenal cortex secretes 2 classes of steroids, (1) corticosteroids (glucocorticoids
& mineralocorticoids) and the androgens
Glucocorticoid = cortisol = use hydrocortisone for replacement o
Used
for anti-inflammatory and immunosuppressive effects, but also have
mineralocorticoid activity (Na+ retention)
Mineralocorticoid = aldosterone = use fludrocortisone for replacement
50 mg prednisone = 7.5 mg dexamethasone = 200 mg hydrocortisone
Hypothalamus
CRH
ACTH
28
Aldosterone
Aldosterone enhances Na+-K+ ATPase activity; also enhances H+ secretion
via K+-H+ ATPase HTN, hypokalemic ametabolic alkalosis
A mineralocorticoid steroid, produced in the zona glomerulosa
Acts on the distal tubules and collecting ducts to conserve Na+, secrete K+,
water retention
Its activity is reduced in Addison's disease and increased
in Conn syndrome
Aldosterone is stimulated by several factors:
o plasma concentration of Angiotensin III, a metabolite of Angiotensin II
29
o
o
o
o
30
31
Risk for aspiration pneumonia from GERD, HH, delayed gastric emptying o
Hyperacidic gastric fluid (pH < 2..5) o High gastric volume (> 25
ml)
THE PITUITARY
32
ADH = Vasopressin o
Hormones formed in the supraoptic (ADH) neuron o
Most important stimulus are osmoreceptors in the hypothalamus (i.e. 295
mOsm/L) o
Also stimulated by peripheral vascular stretch receptors, reduced
intravascular volume, painful stimulation, and PEEP
Oxytocin o Hormones formed in the paraventricular (oxytocin) neurons o Acts on
areolar myoepithelial cells, part of milk letdown reflex, enhances uterine activity
Hallmark: high UOP, poorly concentrated urine (s.g. < 1.005) , low UrineOsm < 150
mOsm/kg hypovolemia & hyperNa+
Central DI
Mechanism: absence of ADH due to posterior pituitary destruction
33
Dx: h/o polydipsia, polyuria (> 6L/day), absence of hyperglycemia, urine osmolality
< plasma osmolality o
Confirmed by increase in urine osmolality following
administration of exogenous ADH (desmopressin)
Treatment:
o Desmopressin hormone replacement intranasal or oral o Vasopressin (5U
SC q4 h)
o Chlorpropamide- an oral hypoglycemia agent, promotes renal response to
ADH or to desmopressin
o Carbamazepine enhances response to ADH o
Clofibrate increases
ADH release
Nephrogenic DI
Mechanism: failure of renal tubules to respond to ADH o Can be congenital or 2nd
to drugs: amphotericin B, lithium, demeclocycline, mannitol
Dx: failure to produce a hypertonic urine following exogenous ADH
Treatment: correct underlying disorder o Low salt, low protein diet o NSAIDS
o Thiazide diuretic (HCTZ) results in hypovolemia induced Na-H2O
reabsorption, thus less H2O delivery to ADH sites
o Amiloride for induced DI
SIADH
Diagnosis: HypoNa+ < 130 mEq/L, PlasmaOsm < 270 mOsm/kg, Urine [Na+] >
20 mEqlL
Hallmark: inappropriate natriuresis
Main clinical difference between cerebral salt wasting & SIADH CSWS leads to a
relative or overt hypovolemia, whereas SIADH is consistent with a normal to
hypervolemic patient
Treatment:
o Restrict fluid intake
o Demeclocycline to antagonizes effects of ADH on renal tubules o Normal
saline gtt 100-400 mEq/day o If acute symptoms (coma, confusion) can give
3% hypertonic NS
o Do not exceed > 8 mEq/ 24hr central pontine myelinolysis = sudden
para or quadraparesis, dysphagia, dysarthria, double vision and LOC. Lockedin syndrome where cognitive function is intact, but all muscles are paralyzed,
except eye blinking.
Mapleson Circuits
A Dog Can Bite type A is best for spontaneous ventilation o
ml/kg/min FGF to maintain normocarbia
Requires 200
34
35
y descent = when tricuspid opens early in diastole, blood in RA flows passively into
RV, RA pressure falls again, making a 2nd trough o abolished in cardiac tamponade o
exaggerated in constrictive pericarditis
v wave = filling of RA during systole o Large v wave = mitral regurgitation or
tricuspid regurgitation
36
Surgical Diathermy
Malfunction of the grounding pad may result from disconnection from the
electrosurgical unit, inadequate patient contact, or insufficient conductive
gel. In these situations, the current will find another place to exit (eg, EKG
pads or metal parts of the OR table), and result in a burn
To avoid pacemaker malfunction, place the grounding pad as close to the surgical
field and as far away from the heart as practical
Fires and Explosions
Probability of ignition depends on:
o PVC OETT tubes >> red rubber OETT
o Wattage of the laser beam o
Duration of
exposure o
Gas mixture in the ETT
Prevention: ETT can be wrapped with copper, aluminium or use a specialty tube;
run lowest flow O2 and substitute air for nitrous oxide
Thermal Injury &
Response:
o Thermal injury from direct exposure to the flame
o Inhalation of smoke causes chemical burn acute respiratory failure:
bronchospasm, intra-alveolar hemorrhage, edema, loss of surfactant
o PVC ETT release HCl when burned severe pneumonitis o Red
rubber ETT releases carbon monoxide
37
1. Disconnect O2 source at the Y-piece and remove burning objects from the
airway
2. Irrigate the site with water if fire is still smoldering
3. Ventilate the patient by mask or reintubate the trachea and ventilate with low
FiO2
Secondary
4. Evaluate the extent of injury by (rigid) bronchoscopy & laryngoscopy
5. Reintubate or perform a tracheostomy
6. Monitor with oximetry, ABG, CXR x 24 hours
7. Use ventilatory support, steroids, antibiotics as needed
Sources of Medical Gases
Wall outlets supply oxygen, nitrous oxide, air at a pressure of 50-55 psi
Outlets and supply hoses to the machine are diameter indexed
Critical temperature is the temperature above which a substance cannot be liquified
regardless of the pressure that is placed on it.
Oxygen
Critical temperature = - 119C (gaseous state at room temp)
E-cylinder, green = 2000 psi = 660L
i.e. Pt is being transported on nasal cannula at 4 L/min from an E-cylinder with gauge
pressure 1200 psi. How many hours will O2 last?
o
P1/V1 = P2/V2 o 2000 psi/660 L =
1200 psi/ X X = 400L 100 mins
Nitrous Oxide
Critical temperature = 36.5C kept liquified without refrigeration
E-cylinder, Blue = 750 psi = 1500L
NIOSH: < 25 ppm N2O alone or < 0.5 ppm with other agents
Energy is consumed in the conversion of a liquid to a gas (latent heat of
vaporization), the liquid N2O cools drop in temperature lower vapor pressure and
lower cylinder pressure
The only reliable way to determine residual volume of N 2O is to weigh the
cylinder
When all liquid N2O has evaporated, pressure in the cylinder falls rapidly
starting at 400 L
Gas
Color (U.S.)
Oxygen
Carbon Dioxide
Green
Gray
70 F Service
Pressure
(psi)
2000
840
State in
Cylinder
E Cylinder
Capacity (L)
Gas
*Liquid
660
1500
Nitrous Oxide
Blue
750
*Liquid
1500
Air
Yellow
1800
Gas
625
Humidity - decreases likelihood of static discharges, a relative humidity of at least 50% is
recommended
38
39
tidal volume,
pulmonary compliance
pulmonary edema
Trendelenburg
pleural effusion
ascites
abdominal packing
peritoneal gas
insufflation
tension pneumothorax
endobronchial
intubation
VAPORIZERS
Vaporization requires energy (the heat of vaporization), supplied as a loss of heat
from the liquid. As vaporization continues, liquid temperature drops and vapor
pressure decreases unless heat is readily available to enter the system
Decreased ambient pressure does not affect the [agent] delivered, but decreases the
partial pressure of the agent. At altitude, must increase the concentration control
dial to attain the desired anesthetic partial pressure
1 mL of liquid anesthetic = 200 mL of anesthetic vapor
Vapor Output (L/min) = CG x VP
vapor output
BP VP
total gas flow
[Anesthetic] =
VP = vapor pressure
BP = barometric pressure
Example: How does the vaporizer deliver the agent? O2 flow rate 2 L/min, if all of it
passes via the vaporizer, what will be the concentration of sevoflurane (VP = 150
mmHg) at the machine outlet?
vapor output = 2 L/min x 150 mmHg = 0.49 L/min
24%
(760 150) mmHg
2L/min
VP
MAC
Hal
o
243
0.75
Enfluran
e
172
1.6
Sev
o
160
1.8
Iso
Des
240
1.1
669
6.6
40
At extremely high flow rates, 15 L/min, the output is less than the dial setting
b/c of incomplete mixing and saturation in the chamber decreased output
concentration.
2. Temperature o Vapor pressure is affected only by temperature and not by
ambient pressure o At 20C VP of isoflurane is 238 mmHg, at 35C is it 450
mmHg (nearly double) o Vaporizers are made with metals having high
specific heat and high thermal conductivity to minimize heat loss.
o
3. Intermittent Back-Pressure o
Intermittent back pressure (pumping
effect) transmitted to the vaporizing chamber, associated with PPV or O 2
flush, could increase vapor output
o Pumping effect is increased by rapid RR, high PIP due to retrograde pressure
transmission from the patient circuit to the vaporizer during the inspiratory
phase of PPV
41
42
Hole in Bellows
Ventilator is named by the direction of the bellows during exhalation
In a time cycled ventilator, a hole in an ascending bellows (like on HMC Narkomeds)
can lead to alveolar hyperventilation and barotraumas as ventilator driving gas is
forced into the circuit for the length of the inspiratory phase (when bellows
collapses).
In a volume cycled ventilator, the driving gas volume will never exceed the tidal
volume even if driving gas leaks through the bellows to the patient, alveolar
hyperventilation will not occur.
If the bellows driving gas is 100% O2, will see increase in O2 analyzer.
Laminar Flow
Occurs when gas flows down parallel sided tubes at a rate less than critical velocity
Resistance to gas flow is directly proportional to viscosity of the gas
Flow = P 4
8L
Flow = P/ R
Turbulent Flow
Occurs when Reynolds number > 2000
(density)
R= 8L
P 4
Orifice flow is a special case of turbulent gas flow where the diameter of the tube is
considerably larger than its length (e.g. larynx)
Flow through a tube increases radius2
Occurs when flow exceeds critical velocity
Resistance to gas flow is directly proportional to density of the gas
substituting helium for nitrogen will decrease the density of the gas mixture and
decrease the resistance!!
High flows through a rotameter will be influenced by increasing altitude (low
barometric pressure) b/c density (not viscosity) is decreased at high altitudes and
high gas flows, rotameter will be greater than expect, but accurate at low flows
(laminar flow not affected by altitude due to dependence on viscosity)
Pulse Oximetry
Depend on pulsatile waveform poor reading during cardiac arrest,
hypovolemia, hypothermia, vasoconstriction or bypass, hypotension < MAP
50
More sensitive to movement artifact during low-pulse-amplitude state
Earlobe is the LEAST sensitive area to pulse signal loss
Carboxyhemoglobin at high levels of CO, SpO2 overestimates true SaO2 b/c it is
reading a mixture of O2HB and Hb
Methemoglobin at MetHb increases, SpO2 = 85%, regardless of the ture level of
O2Hb
Indigo carmine produces the smallest changes compared to methylene blue or
indocyanine green
Pulse oximetry is NOT possible in deeply pigmented patient b/c of a failure
of LED light transmission
43
Succinylcholine IOP o
Mechanism drug induced cycloplegia can still
see IOP when intraocular muscles are cut
o Occurs if given by single bolus, infusion, or IM injection
o Pre-treatment w/non-depolarizing drugs reduces, but doesnt reliably
eliminate the
IOP o
Peaks 2-4 mins after
administration
o Causes sustained contraction, rather than paralysis may affect the forced
duction test used to estimate any restriction in movement of the extraocular
muscles
Causes IOP o
Coughing & vomiting cause greatest increase IOP, up
to 35-50 mmHg o
Respiratory acidosis/ hypercarbia by inducing choroidal
vasodilation o
Hypoxia by inducing choroidal vasodilation
o CVP
o Ketamine IOP changes are controversial, does cause blepharospasm and
nystagmus o
N2O in presence of intraocular air will IOP
Strabismus
44
o
o
45
Facial nerve (CN VII) supplies motor to orbicularis oculi in eyelid allows
squinting need to block to place lid speculum.
Complications:
o
Hemorrhage (most common), globe perforation, optic
nerve atrophy o
Block oculocardiac reflex o Acute
neurogenic pulmonary edema o
Seizures from injection in
ophthalmic artery
Post-retrobulbar apnea syndrome due to injection of LA into the optic nerve sheath with
spread into the
CSF unconsciousness without seizure, apnea within 7-20 mins, resolves with in an
hour
GENERAL ANESTHESIA
o
EQUATIONS
PaO2 = 102-Age i.e. 72 yo estimated PaO2 = 102-72/3 = 78 mmHg
LaPlaces Law: T =
P r / 2h
3
MAP = CO x SVR
1 mmHg = 1.36 cm H2O
SVR = MAP-CVP x 80
CO
Na deficit = wt in Kg x 0.6 x (140- desired Na+)
46
PACU
First half is delivered in the first 8 hours, and the remaining half is delivered in the
remaining 16 hours.
The "Rule of 9's" is as follows: Head and each arm = 9%
Back and chest each = 18%
Each leg = 18%
Perineum = 1%
Relative resistance to nondepolarizing relaxants b/c of (1) altered protein binding, (2)
proliferation of NMJ and (3) extrajunctional ACh receptors
Decreased serum albumin after injury
alpha1-acid glycoprotein (AAG) free fraction of NMB is reduced due binding
with AAG
Increased vascular permeability due to decreased capillary integrity, however Vd of
NMB agents is unchanged
Discharge Criteria
Orientation to person, place, and time
Stable vital signs for 30-60 mins
Ability to ambulate unassisted
Absence of significant pain or bleeding
Ability to tolerate oral fluids may not be mandatory in all patients
Ability to void - may not be mandatory in all patients
47
TURP Syndrome
Hypoosmolality is the main culprit contributing to CNS serum [Na+] & Osmolality
Can present intra-op or post-op (15 mins to 24 hours post-op)
Si/Sx: HA, restlessness, confusion, cyanosis, dyspnea, arrhythmias, hypotension,
seizures from fluid overload, water intoxication, irrigating solute toxicity, HTN or with
reflex bradycardia
Hypotonic non-electrolyte irrigating solutions:
o Glycine 1.5%
o Sorbitol 2.7% & mannitol 0.54% o
Distilled water massive hemolysis
Absorption of irrigation depends on (1) duration AND (2) height (pressure) of fluid (<
40 cm)
Most last < 1 hour, 20 mL/min is absorbed (1.2 liters)
Hypothermia can result from cold irrigation fluid coagulopathy, delayed awakening
Hyponatremia
o CNS: < 120 meq/L confusion, irritability, restlessness due to cerebral
edema (edema stops when [Na+] > 130 meq/L) or acute hypoosmolality b/c
BBB is permeable to free water, impermeable to Na.
Seizure Rx: Magnesium (negative effective on NMDA receptor)
48
PMMA = Polymethymethacrylate
Hypotension due to microembolization
Femoral shaft venting hypotension by intrafemoral pressure = microembolization
of PMMA
Partial hardening strengths PMMA by decreasing porosity and hypotension associated
with it
Fat Embolism Syndrome
Si/Sx: fever, tachycardia, tachypnea
ABG hypoxemia, widened A-a gradient
Blood lipidemia, anemia, platelet aggregation, thrombocytopenia, prolonged PT, PTT
CV tachycardia and hypotension, EKG with right heart strain
CNS cerebral edema = confusion, obtundation, coma
Renal lipuria
Respiratory increased Vd/Vt, widen A-a gradient
Skin petechial hemorrhage on anterior chest, neck, axilla and conjunctiva
Renal
Creatinine clearance (GFR estimation) = [(140-age) x lean body weight]
(72 x Creatinine)
** Multiply by 0.85 in females
UOP
Urine [Na+]
% Fractional excretion
[Na+]
Urine Osm
BUN:Cr
Pre-Renal
< 0.5 ml/kg/hr
< 20 meq/L
< 1%
Renal
< 0.5 ml/kg/hr
> 40 meq/L
> 2%
> 400
mOsm/L
> 20
300 mOsm/L
< 20
49
o
Anemia due to low erythropoietin production & uremic toxins that
marrow function o R shift oxy-Hbg curve due to 2,3 DPG o
Leukocyte
dysfunction sepsis is major cause of death, high incidence of Hep B
Coagulopathy: platelet dysfunction, check PT & PTT
Endocrine o Hyperglycemia resistance to insulin
o Hyperparathyroidism b/c cannot excrete phosphate elevated levels of PTH
Skeletal: osteodystrophy (= dystrophic growth of the bone)
Skin:
hyperpigmentation, ecchymosis, pruritus
Infection: Sepsis is the major
cause of death!
o 20-50% are infected with Hepatitis B
Increased
Glucose levels due to (1) fall in
insulin, (2) rise in Epi-Norepi, (3) rise
in cortisol
Hct & viscosity
H+ ions = acidosis
Left shift hemoglobin
K+ ions
More sensitive to NMB agents
Decreased
Intravascular volume & BP due to (1)
cold suppresses ADH
Low ADH
metabolic O2 consumption
CMRO2 => 6% per 0C
CBF
Flat EEG at 25 0C
platelet count & function due to
sequestration
MAC => 7% per 0C
P aO2 due to more V/Q mismatch
50
Heat Loss
40% radiation = form of electromagnetic energy
30% convection = wind chill
29% evaporation
1% conduction = direct skin contact
Hyperbaric Oxygen Therapy
Pulmonary formation superoxides, hydrogen peroxide, hydroxyl radicals retrosternal
chest pain/burning, coughing, fibrosis. Oxygen toxicity is PaO 2 and duration dependent
CNS - CBF, see at 2 ATM tonic/clonic seizure activity
CV HTN, bradycardia
Liver Physiology
Dual blood supply, 70% portal vein & 30% hepatic artery (supplies most of oxygenated
blood, 55%)
Blood flow determined by perfusion pressure splanchnic vascular resistance
What decreases hepatic blood flow?
o All volatile anesthetics decrease hepatic blood flow by hepatic pressure
pressure, reduce BP and increase hepatic vascular resistance by releasing
catecholamines
o Close surgical site is to liver, greater the reductions in hepatic blood flow o
PEEP
o Hypoxia & hypocarbia o
Pain
CHILD Classification: bilirubin, albumin, ascites, encephalopathy, prothrombin time
Albumin t = 23 days acute liver dysfunction will not decrease albumin level.
Pseudocholinesterase t = 14 days
All factors, except Factor VIII, are produced in the liver
Increase in unconjugated bilirubin results from liver parenchymal disease vs. increases in
conjugated bilirubin is due to biliary tract obstruction
Immediate post-op concerns should address hypoglycemia. Can occur b/c of insufficient
insulin degradation by the liver, impaired glucose formation, or glycogen depletion
What is malignant hyperthermia?
Earliest signs masseter spasm, tachycardia, hypercarbia & concomitant
respiratory acidosis
(most sensitive) myoglinemia, myoglobinuria, arrhythmias, elevated CK, hyperK+,
hyperNa+
Muscle rigidity is not consistently present
51
Ventricular fibrillation can follow onset within minutes and is most common cause of
death
< 50% of patients with trismus (masseter spasm) & sux develop malignant
hyperthermia. Best to cancel an elective case, if not able to cancel, then administer nontriggering agent
52
53
Single twitch
Tetanic stimulation
Post-tetanic
facilitation
Train of four
Phase I
depolarizing
Decreased
Decreased height, no
fade
None
Phase II
depolarizing
Decreased
Fade
Decreased
Fade
Yes
Yes
tidal volume
twitch height
TOF
Sustained tetanus at 50
Hz
Sustained tetanus at 100
Hz
Head lift and hand grip
Non-depolarizing
Marked fade
<0.7
Antagonizes
period of time after,
% receptors
occupied when
response returns
to normal
80%
75-80%
70-75%
70%
50%
50%
54
Vecuronium
Hepatic metabolism & biliary excretion
T is prolonged in patients with renal failure decreased clearance of the drug
The only NMB without CV effects
Atracurium (intubate: 0.5 mg/kg, intra-op: 0.1 mg/kg)
Hoffman elimination & ester hydrolysis inactive metabolite LAUDANOSINE
excitation CNS, caution in seizure pts
Side effect: transient SVR, HR with 3 x ED95
Avoid in asthmatics 2nd bronchospasm from histamine release at high doses
Cisatracurium
55
56
The specific enzyme deficit in each type of porphyria results in a partial block in
heme biosynthesis and lower intramitochondrial heme levels negative feedback
from low levels of heme elevated baseline ALA synthetase activity
Si/sx are due to (1) high ALA synthetase activity, (2) increased porphyrin
accumulation in tissues, or (3) decreased heme production
Elevated heme precursors that are colorless and non-fluorescent porphyrinogens
Porphyrins are highly reactive oxidants
Accumulation of porphyrins in the epidermal skin layers cutaneous
photosensitivity Acute porphyria causes severe neuropathy
Unsafe drugs:
o Barbiturates thiopental, etc
o Etomidate
Nitrazepam/flunitrazepa
mo
Enflurane o
Alpha-methyl dopa o
Hydralazine o
Griseofluvin
o Oral contraceptive pills
Only the inducible forms (acute intermittent porphyria, variegate porphyria,
hereditary coproporphyria) show acute symptoms (e.g. neurologic) from drug
exposure
Porphyria cutanea tarda is non-inducible form (not affect by drugs) and most
often appears as photosensitivity in males older than 35 yrs avoid excessive
pressure or irritation of the skin (.e.g during mask ventilation, taping OETT, etc)
Acute intermittent porphyria is the most serious form! Affects central &
peripheral nervous system pain, change mental status, paralysis (respiratory
distress) o
Triggers: starvation, dehydration, stress, sepsis, drugs (ketorolac,
pentazocine, BZDs, barbiturates, etomidate)
Naltrexone
Pure opioid antagonist pt. will have opioid requirments if taking at time of
surgery
T = 24 hrs, stop the day before surgery
N-cyclopropylmethyl derivative of oxymorphone
Blocks the euphoric effects of injected heroin in addicts who have been detoxified
Buprenorphine
Mixed agonist-antagonist strong affinity for -receptor (50 x MSO4)
Prolonged duration )8 hrs) due to affinity for -receptor & resistant to naloxone
reversal
Delirium tremens
Occurs 2-4 days after abstinence from EtOH
Treat with fluid replacement, electrolyte replacement, Thiamine
Beta-blockers to suppress overactivity of SNS
Lidocaine for cardiac dysrhythmias
Aggressive use of BZDs to prevent seizures
Smoking Cessation
Restoration of P50 to normal value of 26 mmHg within days
57
Post-Op Shivering Treatment meperideine (via K), butorphanol (via K), clonidine,
serotonin antagonists, propofol, physostigmine
NEUROANESTHESIA
ECT
No change
Methohexital
Ketamine
Remifentanil
Alfentanil
Decreased
duration
Thiopental
Thiamylal
Lorazepam
Midazolam
Propofol
58
59
Verbal
1
Not
opening
None
Motor
None
Eyes
2
Open to pain
Incomprehensib
le sounds
Extension to
pain
3
Open to
speech
Inappropriat
e words
Abnormal
flexion to
pain
4
Spontaneous
Confused
conversation
Flexsion/withdra
w to pain
Oriented
Localizes
to pain
Obeys
Monitoring
1. TEE most sensitive!
2. Precordial Doppler U/S - able to detect 0.25 ml
60
3.
4.
5.
6.
Pathophysiology
1. Pulmonary microvascular occlusion results in increased dead space
2. PA pressure rises C.O. due to high RV afterload
3. M & M is directly related to the volume & rate of air entry
4. Presence of patient foramen ovale (10-25% incidence) paradoxical air embolism
Clinical signs:
1. Drop in ETCO2 or arterial PaO2
2. ABG may show slight PaCO2 from pulmonary dead space
3. Reappearance (or increase) of nitrogen in expired gases
4. Mean PA pressure increases in direct proportion to the amount of air entrained
5. Hemodynamics: sudden hypotension, circulatory arrest by obstructing RV outflow,
changes in BP and heart sounds (mill wheel murmur) are late manifestations
Treatment:
1. Notify surgeon flood field with saline or packs and bone wax applied
2. D/C nitrous oxide, 100% oxygen
3. Head down (Trendelburg) so operative site is below the heart
4. Aspirate multi-orifice central line located at SVC-RA junction
5. Give volume to increase CVP
6. d/c PEEP as it may increase risk of paradoxical embolism or decrease venous effluent
from calvarium increased CBV, ICP
7. Bilateral jugular vein compression slow entrainment, back bleeding to see source
8. If able, place in L lateral decubitus position
Arterial
hypoxemia
Metabolic acidosis
- Central
causes: high ICP,
anxiety, fear,
cirrhosis
Drugs: doxapram
Down ( response)
Aminophylline
- Opioids
Salicylates
- volatile anesthetics:
Catecholamines
enflurane >>
Opioids
halothane >
Metabolic alkalosis isoflurane Denervation of
IV
peripheral
anesthetics
chemoreceptors Normal sleep
Hypothermia
Down and to
Right (
sensitivity &
response to
CO2)
- High dose
opioids neuromuscular
blockade
No
response
- Ketamine
- droperidol
- N 2O
61
During apnea, CO2 rises 6 mmHg 1st minute, 3 mmHg every minute thereafter
Apneic threshold is 5 mmHg below the resting PaCO 2 Hyperventilation to PaCO2 > 20
mmHg x 2 hrs causes transport of HCO3 out of CNS threshold to spontaneously breath seen
at a lower PaCO2 (more likely to breath)
62
Frequency
Hyperoxia
Hypercarbia
Seizure
Diazepam
N20 30-70%
Volatile < 1 MAC
Ketamine
frequency,
amplitude
Hypocarbia
Hypothermia
Etomidate
Narcotics
Volatile > 1 MAC
frequency &
amplitude
Severe hypoxia
Severe hypercarbia
Hypothermia
Hypotension
Large dose
barbiturates
Electrical silence
Brain death
Severe hypoxia
Profound
hypothermia
Coma dose
barbiturates
Isoflurane 2 MAC
Anesthetic Implications:
o More sensitive to the respiratory depressant effects of narcotics and anxiolytics
b/c have reduced respiratory reserve
o Resistant to depolarizing agents, requires 2-3 x SCh dose o Sensitive to
non-depolarizing agents, avoid if possible o
Profound muscle relaxation
63
Autonomic Hyperreflexia
Appears after spinal shock in association with the return of spinal cord reflexes
Most common 6 months to 2 years from time of injury
64
65
Points
Sign
Appearance (Color)
0
Blue or pale
Pulse
Grimace (reflex
irritability in response
to catheter in nose)
Activity (muscle tone)
Respirations
Absent
No
response
Flaccid
Absent
1
Body pink,
extremities blue
< 100
Grimace
2
All pink
Some flexion
Slow, irregular
Active motion
Good, crying
> 100
Crying
Meconium-Stained Neonates
66
Thick or particulate meconium obstructs small airways and causes severe respiratory distress
If neonatal condition does not improve with ventilation & tactile stimulation cannulation of
umbilical artery with 3.5F (<1500g) or 5F (>1500g) umbilical catheter. If catheter does not
advance, leave in place and attempt at 2nd artery as this often relaxes 1 or 2 vessels.
If place catheter in umbilical vein can result in infusion of hypertonic solutions directly into
liver
Volume Resuscitation
10 ml/kg of LR, NS, or type O-negative blood (5 ml/kg) crossmatched with maternal blood
Causes of neonatal hypotension:
o Hypocalcemia o
Hypoglycemia o
Hypermagnesemia
o Polycythemia (Hct >65%) PVR, LV filling pressure R L shunt via ductus
arteriosus & foramen ovale. Can see with delayed cord clamping or stripping blood
from cord.
67
Drug Therapy
Spinal Cord
Epidural space: extends from foramen magnum to sacral hiatus covered by the
sacrococcygeal ligament
Spinal cord ends L2 in adults, L3 in children
Dural sac extends to S2 in adults, S3 in children
Extension of pia mater, the filum terminale, penetrates the dura and attaches conus
medullaris (terminal spinal cord) to coccyx
CSF
Total volume = 150 mL; of which 25-35 mL is in the spinal subarachnoid space
Pressure = 60-80 cm H20
Acid-Base status o
pH 7.32 (slightly lower than serum)
o PCO2 48 mmHg,
o HCO3- 23 mEq/L
Specific gravity = 1.006
Blood Supply
Vertebral artery single anterior spinal artery anterior 2/3 of the cord, found in the
midline of the cord. Gives off numerous circumferential vessels o
Injury = motor lesion,
including anterior horn cells
Posterior inferior cerebellar arteries (PICA) 2 posterior spinal arteries posterior
1/3 of the cord; fed by 25-40 radicular arteries.
Artery of Adamkiewicz (radicularis magna) unilateral, arising from the aorta anterior,
lower 2/3 of the cord, supplies the anterior spinal artery o
T9-T12 (60%), T4 region is
the most tenuously supplied
o
68
Heart rate o
Bradycardia due to blocked pre-ganglinonic T1-T4 & significant RA
pressure (BezoldHarisch reflex )place patient in head down position
Pre-ganglionic nerve
69
Anesthetic Toxicity
CNS manifestations are FIRST!
CNS tinnitus, perioral paresthesias, dizziness, lightheadedness grand mal seizure
Cardiac o < 5 mcg/ml - no symptoms are seen
o 5-10 mcg/ml - prolonged PR interval and wide QRS, low C.O. and peripheral
vasodilation
o > 10 mcg/ml - asystole
o Treatment 100% O2, hyperventilation:
o Prevents ypoxia
o Induced hypoK+ hyperpolarizes neurve membrane to seizure threshold o
pH lidocaine non-ionized increases & get cerebral vasoconstriction causing
less drug delievery to brain
Prilocaine 600 mg
Mepivicaine 500
mg
Bupivacaine 225
mg
Tetracaine 200
mg
EPIDURAL ANESTHESIA
Systemic toxicity is much greater with epidural blockade than spinal b/c higher doses given
Onset of spread is faster cephalad (head) than caudad
Areas first blocked are the last to return to normal
Tetracaine is not used b/c it spreads poorly. Chloroprocaine is not used often b/c of the risk of
adhesive arachnoiditis, likely related to a preservative, sodium bisulfite
Addition of Epi
increases duration of sensory block, NOT motor block
*Factors Affecting Epidural Spread
Major: Age & Site
Minor: weight, height, position
Epidural Opioids
70
o
o
CAUDAL ANESTHEISA
Sacral hiatus, covered by the sacrococcygeal ligament.
Dural sac extends S2 in adults, S3 in infants (spinal cord ends at L3 in infants)
Most common complications - intravascular or subarachnoid injection
Dose: 0.5-1.0 mL/kg of 0.125% to 0.25% bupivacaine with or without Epi.
71
Adhesive Arachnoiditis
Proliferative overgrowth of the pia-arachnoid that can obliterate the subarachnoid space
Typically chronic progressive, chronic, sensory loss and paresis of the lower extremities
Subarachnoid steroid injection is not recommended!
Probably due to the preservative ethylene glycol
Epidural Abscess (EA)
4 classic stages of EA
1. Back or vertebral pain, intensified by percussion over the spine
2. Radicular pain develops
3. Motor and/or sensory deficits or sphincter dysfunction
4. Paraplegia or paralysis
Staphylococcus aureus and Staphylococcus epidermidis
Rx: ABX, decompression (laminectomy)
Prevention: (1) minimize catheter manipulations, (2) micropore bacterial filter, (3) remove
epidural catheter after 96 hours ( 4 days)
Spinal or Epidural Hematoma
Sx/Si are more sudden than epidural abscess
Rx: surgical decompression within 8-12 hours
Anticoagulants & Antiplatelet Agents
Subcutaneous heparin (BID) is not a contraindication
Those requiring intraoperative heparin gtt, blocks may be performed 1 hour or more before
heparin administration. Removal should occur 1 hour prior to, or 4 hours after subsequent
heparin dosing.
LMWH Neuraxial guidelines
Produce a more predictable anticoagulant response than unfractionated heparin, have a
better bioavailability, longer t , and dose independent clearance
Low dose LWMH
o Placement: 12 hrs after last dose, avoid placement if given within 2 hrs o
Postop: resume dosing 8 hrs after block placement, then q 24 hr
o Removal: remove catheter 12 hours after the last dose, resume dosing 2 hours
after catheter removal
High treatment dose LWMH (enoxaparin 1 mg/kg q12, enoxaparin 1.5 mg/kg daily,
dalteparin 120 U/kg every 12 hours, dalteparin 200 U/kg daily, or tinzaparin 175 U/kg daily) o
Placement: 24 hrs after last dose o
Post-op: 24 hrs after placement o
Removal: 12 hours after the last dose, subsequent dosing 2 hours after catheter
removal.
o Do not maintain continuous catheters while on twice daily dosing
72
Respiratory Effects
MV (50%): progesterone VT, little change in RR
O2 consumption (20-40%): FRC 20% + O2 consumption hastens hypoxemia
airway resistance: progesterone effect
FRC 20% due to RV; closing capacity > FRC
NO CHANGE Vital capacity = ERV + IRV
PaO2 PaCO2: PaO2 103 mmHg, PaCO2 32 mmHg respiratory alkalosis
compensatory
HCO3- 22 mmHg
o 2,3-DPG offsets the effect of hyperventilation (R-shift Hgb curve) o P50
30 mmHg (vs. 27 mmHg)
Elevation of the diaphragm is compensated by anteroposterior diameter of the chest
Flow-volume loops are unaffected
dead space (pulmonary vasodilation)
shunting
Fast rate of induction due to FRC and MV
Cardiovascular Effects
Increase in plasma volume in excess of an increase in red cell mass (blood volume increased
by 1000-1500ml) dilutional anemia and lower viscosity
Hemoglobin remains > 11 g/dL, Hct > 33%
C.O. by 40% ( HR & SV ) & R- shift of Hgb curve (P50 = 30 mmHg) SVR, diastolic >
systemic
Greatest increase in C.O. is seen during labor and immediately after delivery.
Returning to normal within 2 weeks post-delivery
Cardiac chambers enlarge and myocardial hypertrophy is often noted on Echo o
PA, CVP,
PA wedge pressures remain unchanged
Renal Effects
Renal vasodilation RBF & GFR 50% in 1st trimester, decline to normal during 3rd
trimester serum Cr & BUN a normal Cr during pregnancy is highly abnormal!
renin & aldosterone levels Na+ retention
renal tubular threshold for glucose and amino acids mild glyucosuria or proteinuria
**Gastrointestinal Effects**
Lower LES sphincter tone from elevated progesterone levels & upward/anterior
displacement of the stomach
Hypersecretion of gastric acid (pH < 2.5) from production of gastrin by placenta
Higher gastric volumes b/c of hormonal & mechanical obstruction high intragastric
pressure
Narcotics and anticholinergics reduce LES sphincter pressure
Hepatic Effects
Hepatic function and blood flow are unchanged
30% decrease in serum pseudocholinesterase activity rarely significant prolongation of
succinylcholine. Takes up to 6 weeks post-partum to return levels to normal
Elevated tests: SGOT, LDH, cholesterol, alkaline phosphatase (due to placental secretion)
Breakdown of mivacurium and ester-type anesthetics is not noticeably altered
73
Hematologic Effects
Hypercoagulable state
Fibrinogen and factors VII, VIII, IX, X, and XII all increase
Only factor XI levels may decrease
Leukocytosis (up to 21,000) and platelets can be seen
Cell-mediated immunity is markedly depressed increase risk of viral infections
Metabolic Effects
Diabetogenic state insulin levels rise; secretion of human placental lactogen by the
placenta is likely responsible for relative insulin resistance o
Maternal glucose crosses
placenta, insulin does not severe neonatal hypoglycemia following delivery
o Fetal hyperglycemia & hyperinsulinemia may delay fetal lung
maturation and surfactant synthesis
Pancreatic cell hyperplasia occurs in response to increased demand for insulin secretion
Hypertrophy of the thyroid gland and thyroid-binding globulin
T4 & T3 levels, but free T4 & T3 and TSH remain normal
Uterine Blood Flow = 500-700 ml/min
50% decrease is required before see fetal distress (scalp pH normal = 7.25)
Autoregulation is absent, but remains sensitive to -adrenergic agents
uterine blood flow IF severe hypocapnia (PaCO2 < 20 mmHg) fetal hypoxemia, acidosis
Decrease flow after phenylephrine, dopamine & dobutamine
Increase in blood flow after ephedrine
Placental Physiology & Anatomy
Placenta is composed of projections of fetal tissue (villi) that lie in maternal vascular spaces
(intervillous space)
Fetal blood within villi is derived from 2 umbilical arteries (deoxygenated) and returns to
the fetus via 1 umbilical vein (oxygenated)
Respiratory Gas Exchange/Cord Blood Gases
Oxygenated umbilical vein: PaO2 = 30 mmHg, PaCO2 40 mmHg, pH 7.35, SpO2 70%
Deoxygenated 2 umbilical arteries, PaO2 = 20 mmHg, PaCO2 50 mmHg, pH 7.28,
SpO2 40%
Transfer of oxygen across the placenta is dependent on ratio of maternal uterine blood flow to
fetal umbilical blood flow
To aid oxygen transfer, fetal hemoglobin curve is L-shifted (high affinity)
Fetal hemoglobin = 15 g/dL = Hct 45% (maternal = 12 mg/dL)
Maternal hyperventilation (PaCO2 32 mmHg) increases gradient for the transfer of CO2
from fetus into the maternal circulation
Fetal hemoglobin has less affinity for CO2 than maternal hemoglobin
Umbilical
Vein (Birth)
pH
7.35
Umbilical
arteries
(Birth)
7.28
pCO2
pO2
40
30
50
20
60
mins
7.307.35
30
60
24
hrs
Adult
7.4
30
70
40
100
74
Frank Breech (remember Frank Butt) feet against the face and butt presenting
Complete breech butt and feet present together
Incomplete breech one or both feet together
Dx by manual exam
Associated increase risk of maternal mortality with hemorrhage, infection, retained placenta
Fetal risk of cord compression and intracranial hemorrhage (trama)
If uterine relaxation is needed for extraction, a volatile anesthetic with OETT is
preferred
40% incidence of fetal bradycardia & acidosis because high fetal blood levels cause
direct cardiotoxicity
Effective during 1st stage of labor
Injection submucosally at 3 oclock & 9 oclock positions on either side of the cervix
Visceral sensory fibers of the Frankenhuser ganglion from the uterus, cervix, and upper
vagina are blocked as they pass through the paracervical plexus Does not cause
uterine atony, may increase uterine activity
Does NOT cause motor blockade!
Performed prior to 8 cm cervical dilation to prevent fetal injury
75
Late decelerations:
o Begin after onset of uterine contraction and persist after its conclusion
o Uteroplacental insufficiency 2nd maternal hypotension, HTN, or uterine
hyperactivity o Immediate delivery is NOT mandatory check fetal scalp pH
Placental Exchange
Placental exchange from other to fetus primarily occurs by diffusion, which depends on:
o Concentration gradient
o Protein binding of drug in maternal circulation
50% lidocaine bound compared to 95% of bupivacaine o
Molecular weight, lipid
solubility, and degree of ionization of the drug
Non-depolarizing NMB are TOO large (MW to big) to cross placental barrier
Sux is too ionized and has low lipid solubility to cross placenta o
Fetal pH fetal
acidosis can cause ion trapping of local anesthetics and narcotics (weak bases)
Almost all drugs cross the placenta, except He Is Going Nowhere Soon
Heparin
Insulin
Glycopyrrolate
Non-depolarizing NMB
Succinylcholine
76
Mild Pre-eclampsia:
o BP 140/90 or SBP > 30 mmHg and DBP > 15 mmHg over pre-pregnant levels o
Proteinuria > 300 mg/day o
Generalized edema
Most patients have low-normal cardiac filling pressures with high SVR, but C.O. may be low,
normal, or high
77
Modality served
Motor efferents &
afferents
Diameter
(mm)
myelinated
*fastest*
Touch, Pressure
Proprioception
myelinated
myelinated
78
A
Pain somatic
B
C
Dorsal root
C
Sympathetic
myelinated
Temperature
Touch
Pre-ganglionic
sympathetic
-Pain visceral via
postganglionic
sympathetic
-Temperature
-Touch
Post-ganglionic
sympathetic
myelinated
unmyelinat
ed
unmyelinat
ed
Differential Blockade
Sympathetic B & C fibers (temp) > pain & touch (A) > proprioception (A) > motor (A)
Pain Terminology
Nociceptive pain is due to activation or sensitization of peripheral nociceptors
Neuropathic pain is the result of injury or acquired abnormalities of peripheral or central
neural structures
Allodynia - perception of an ordinarily non-noxious stimulus as pain
Analgesia - absence of pain perception
Anesthesia dolorosa - pain in an area that lacks sensation
Dysesthesia - unpleasant or abnormal sensation with or without a stimulus
Hypoalgesia - diminished response to noxious stimulation
Hyperalgesia - increased response to noxious stimulation
Hyperesthesia - increased response to mild stimulation
Hypoesthesia - reduced cutaneous sensation (eg, light touch, pressure, temp)
Hyperpathia - presence of hyperesthesia, allodynia and hyperalgesia usually associated
w/overreaction, persistence of the sensation after the stimulus
Paresthesia - abnormal sensation perceived without an apparent stimulus
Radiculopathy - functional abnormality of one or more nerve roots
Input
Name
A, C
Marginal layer
Substantia gelatinosa
* major role in processing & modulating nociceptive
input from cutaneous nociceptors and major site
79
of opioids
III
IV
V
VI
VII
VIII
IX
X
A, A
A, A, C
A
(sympathet
ic)
A
Nucleus proprius
Visceral & somatic pain
WDR neurons
Nucleus proprius
Intermediolateral column; pre-ganglionic
sympathetic neurons
Ventral (motor) horn
Central canal
Opioids
Receptor
- mu
- kappa
- delta
sigma
Physiologic Effect
Supraspinal analgesia
(1)
Prolactin secretion (1)
Sedation
Respiratory depression
(2)
Spinal analgesia (2)
Tolerance & dependence
Muscle rigidity
Dysphoria
Sedation
Spinal analgesia
Supra- & Spinal Analgesia
Behavioral
Epileptogenic (myoclonus)
Psychotomimetic
Depersonalization reactions
Endogenous agonist
Endorphins
Dynorphin
Enkephalins
- epsilon
*all side effects diminish with time, EXCEPT constipation & myoclonus
Methadone
L-isomer is agonist at receptor, D-isomer is antagonist at NMDA blocks hypersensitivity
& central sensitization in neuropathic pain & tolerance to opioids
Tramadol
Meperidine
80
Synthetic opioid, NOT ideal for chronic pain due to short duration and high abuse potential
Normeperidine, secreted via kidneys myoclonus, tremulous, hallucinations, seizures
Anti-cholinergic (looks like atropine) mydriasis (dilation), orthostatic hypotension,
HR
Rarely causes puritis when given neuraxially, has local anesthetic effects!
AVOID with MAO-I (Selegiline) hyperthermia, rigidity, seizures
Myocardial depression with large doses, related to local anesthetic effect
WHO Stepladder
Step 1: manage pain by non-opioid medications with or without adjuvants
Step 2: if pain is persisting or increasing, add weak opioids (codeine, hydrocodone,
tramadol, oxycodone) to existing non-opioid analgesics and adjuvants
Step 3: strong opioids (morphine, hydromorphone, fentanyl) are used with non-opioids
and adjuvants until patient achieves complete analgesia
Step 4: if pain persists, neurolytic and/or interventional procedures should by employed
*adjuvants = steroids, amitriptyline, gabapentin, NMDA antagonists, clonidine, antihistamines
Neuraxial Opioid Infusions
Advantage of producing profound analgesia WITHOUT motor, sensory or ANS blockade!
Oral MSO4: epidural MSO4 = 1:30
Oral MSO4: SAB MSO4 = 1:300
Central Pain
If patient fails to obtain pain relief despite complete sympathetic, sensory, and motor
blockade, a
central mechanism for pain is likely or the lesion is higher in the CNS that level of blockade
Central pain states may include encephalization, psychogenic pain, or malingering
Persistence of pain in the LE after successful spinal blockade suggests a central source or
psychological source
Phantom Limb Pain
Type of Central Pain
Of those who get it, 85% develop it within the first 4 days
Higher incidence w/ more proximal amputation
NO difference of incidence b/t tramatic & non-tramatic
Can reactivate limb pain with
w/ spinal or epdiural technique
Theories:
o Sympathetic chain activation. Although bilateral sympathetic blocks fail to
relieve pain o Central mechanisms. Somatosensory cells begin to fire at will
Treatment Phantom Limb Pain:
o TENS and Tegretol o
Epidural morphine o
Calcitonin
o IV opioids dont work very effectively
o Nerve blocks trigger pt injections, peripheral & central, sympathetic bocks
Fibromyalgia
Classified by the presence of chronic widespread pain and tactile allodynia
Research has demonstrated that FM is associated with polymorphisms of genes in the
serotoninergic, dopaminergic and catecholaminergic systems
Studies have shown that stress is a significant precipitating factor in the development of
fibromyalgia, and that PTSD is linked with fibromyalgia.
Electroencephalography show a lack of slow-wave sleep and circumstances that interfere with
stage 4 sleep (pain, depression, serotonin deficiency, certain medications or anxiety) may
cause or worsen the condition
Women (10:1), ages 20-60 yrs
81
Characteris
tic
Pain
Extremity
Skin
X-ray
Duration
Acute
3 Phases
Dystrophic
Localized, severe,
burning
More diffuse,
throbbing
Warm
Cold, discolored,
clammy,
edematous Muscle
wasting
Sweaty
Osteoporosis
1-3 months
3-6 months
Atrophic
Less severe; often
involves other
extremities
Severe muscle
atrophy,
contractures
Glossy and atrophic
Severe
osteoporosis,
ankylosis of joint
indefinite
82
83
PEDIATRICS
Respiratory Parameters for Boards
NEONATE
O2 consumption
(ml/kg/min)
TV (ml/kg)
RR
MV (liters)
Vd/Vt (dead space)
FRC (ml/kg)
VC (ml/kg)
PaO2 (mmHg)
Adult
6-9
5-7
3545
1
1
30
35
6090
5-7
10-20
6.5
0.3
40
50-70
75-100
Weight Gain
Average newborn = 3.5 kg
1 year-old = 10 kg
2 - 6 year-old gain 2 kg/yr = 12 kg 20 kg
6 - 10 year-old gain 3 kg/yr
Neonate
Infants
Age
0-30 days
1-12 months
Blood Volume
85 ml/kg
80 ml/kg
Children
1-12 yrs
75 ml/kg
SBP
65
7595
7595
HR
120-160
84
In severe cases, will conserve Na+ at the expense of wasting H+ ions in the
urine paradoxic aciduria = vomit and pee H+
Fluid resuscitation with Normal Saline (LR contains NaHCO3 & worsens alkalosis), once UOP
returns, add KCl to infusion
Risk of post-op ventilatory depression from central apena depression due to metabolic
alkalosis that is worsened by intra-op hyperventilation
Na deficit = (140 current Na) x 0.6 x wt in kg 1 liter NS has 154 mEq
o
Foreign body aspiration = ages 6 mos 5 years o Present with stridor if supraglottic
or glottic o Present with wheezing if subglottic o
Inhalational induction with extraction
of supraglottic object by endoscopy o
RSI with OETT if subglottic
Post-extubation Stridor/Croup
Oxygen, cool mist, racemic epi 2.25% 0.5 ml into 3 ml NS, dexamethasone 1.5 mg/kg
if all fails, intubate
Downs Syndrome
Short neck, irregular dentition, mental retardation, hypotonia, large tongue, strabismus,
cataracts Cardiac anomalies (40%): AV canal, PDA, endocardial cushion defects with
VSD (50%) , TOF
GI anomalies: congenital duodenal atresia
Associated with subglottic stenosis, TE fistula, chronic pulmonary infections, seizures
Endocrine: congenital hypothyroidism
Anesthetic concerns:
o Neck flexion may result in atlanto-occipital dislocation due to laxity of
ligaments o Risk of post-op stridor and apnea o Narrow nasopharynx, large
tongue, large T & A chronic obstruction o
Impaired alveolar
development hypoxemia, pulmonary HTN
o Smaller trachea use 2 size smaller OETT o
High risk malignant
hyperthermia Omphalocele and Gastroschisis
Omphaloceles = occur at the base of umbilicus, have a hernia sac lower risk
dehydration, due to failure of gut to return within abdominal wall o
Associated with
Trisomy 21, diaphragmatic hernia, cardiac & bladder malformations o BeckwithWiedemann Syndrome refractory hypoglycemia, hyperviscosity syndrome, associated
with visceromegaly, hemi-hypertrophy
85
Type A (8%)
Type E (4%)
Type D (1%)
Type B (1%)
Part of VACTERL syndrome o Vertebral, VSD or other Vascular problems (ASD, PDA,
coarctation) o Anal stenosis (imperforate anus) o Cardiac defects
o TE Tracheoesophageal fistula o
Renal or radial abnormalities
o Limb anomalies
Management:
o Pre-op, strict NPO and catheter placed in esophagus to drain saliva
o Awake OETT R main stem bronchus placement then pulled slowly back
until BS heard on the L. Ideally tip of OETT lies b/t the fistula & carina. Not
possible if fistula connects to the carina or a main-stem bronchus, requiring
venting via gastrostomy tube.
o L-lateral position, precordial stethoscopy is placed L side in axilla, since
obstruction of the main-stem bronchus during retraction is not uncommon.
o A-line as retraction can compress the great vessels, trachea, heart and vagus
nerve o
Surgeon 1st performs gastrostomy tube placement; chest
opened and fistula ligated
86
87
Alloimmune condition that develops in a fetus, when IgG antibodies that have been produced
by the mother pass through the placenta and attack fetal RBCs reticulocytosis and
anemia.
Fetal disease ranges from mild to very severe, death from heart failure (hydrops fetalis)
Usually does not occur in 1st pregnancy. Contamination of maternal blood with fetal RBCs
occurs at delivery or abortion
Bilirubin crosses the placenta and is cleared by the mother newborn at birth may not be
clinically jaundiced
Ductus arteriosus
Closes primarily due to [PaO2] & requires arterial muscular tissue by 2-3 weeks
Maintenance of patent ductus include: hypoxia, hypercarbia, acidemia all due to smooth
muscle vasodilation and pulmonary HTN
Prostaglandin E1 = Alprostadil maintains patency o
Vasodilation
o Inhibition of platelet aggregation o Stimulation of intestinal & uterine smooth
muscle o
Patient with low initial PO2 values and < 4 days old respond
best! o
Helpful in liver transplantation by increasing blood flow and
making liver cells more resistant to ischemic injury
o Serious effects = apnea, bradycardia, hypotension, fever o Used to
treat R L shunt lesions cyanotic lesions
Pulmonary atresia/stenosis
Tetralogy of fallot
Coarctation of aorta
Transposition great vessels requires patent foramen ovale for
survival
Fetal Hemoglobin
P50 = 19 mmHg (vs. 27 in adults)
[Hgb] neonate = 17 g/dL, then at 3 - 6 mos. 11 g/dL resulting in O2 carrying capacity
Anemia at 1.5 3 mos as HgbF (gamma, subunit) converted to HgbA (beta,
subunit)
Minimal Hbg = 10 g/dL
Fetal hemoglobin has higher oxygen affinity than that of the maternal carrier due fetal hgb
subunit (gamma), instead of the b (beta) subunit.
The subunit has less positive 2,3-DPG is less electrostaticly bound to fetal hemoglobin as
compared to adult hemoglobin less effective in lowering the oxygen affinity of the fetal
hemoglobin allowing adult Hgb to readily transfer its oxygen to the fetus
Spinal
anesthesia in Children
Spinal cord extends to L3
Loss of sympathetic tone rarely presents as hypotension in children
Respiratory depression = apnea & hypoxia are the first signs of a high-spinal in infants
Endotracheal Tubes
Cuffed OETT used for children < 10 yrs old
Size = age /4 + 4
Depth of insertion = age / 2 + 12
88
Rapid
Vocal cords are in a diagonal position in larynx more likely to lodge OETT in anterior
commissure
Larynx is funnel shaped
Inhalational Induction b/c:
Greater % of CO distributed to VRG vs. adults
Greater % of extracellular TBW
Higher alveolar ventilation
Incrased blood solubility of volatile anesthetics
Diminished FRC
89
90
CNS
Liver
Penicillin Allergy
Okay to give cefazolin as long as the allergic reaction is only a mild rash, otherwise need to
give vancomycin for more severe reactions
Lithium
Mechanism: inhibits synaptic transmission in CNS by inhibiting adenylate cyclase cAMP
100% renally cleared!
Potentiates duration succinylcholine & non-depolarizers (pancuronium). NOT
associated with sux & hyperkalemia
Li is exchanged for Na+ in proximal convoluted tubules if low Na+ => high Li+, risk
toxicity, especially in patient taking diurectics
Treatment Li induced polyuria: thiazide diuretics (metolazone, chlorthalidone,
indapamide)
Lasix reduces renal clearance of lithium retain Lithium
Side
effects:
o Nephrogenic DI o
Hypothyroidism due to Li blocking release of thyroid
hormones o Sedative effects = MAC
NSAIDS-Ketorolac
Thomboxane: (1)
vasoconstriction, (2)
platelet aggregation by inhibiting
adenylate cyclase cAMP
Prostacyclin: (1) vasodilation, (2)
platelet adhesiveness by
stimulating production of cAMP
PGF2: vasoconstriction
COX 1 constitutive enzymes
(present in
all cells)
COX 2 induced by inflammatory
response
ASA
Inhibits cyclooxygenase and prevents for the formation of thromboxane (a potent platelet
aggregator)
91
92
93
94
DIURETICS
Mannitol
Freely filtered at the glomerulus and not reabsorbed increased osmolality in the renal
tubules free water follows free water excreted in excess of Na+
Free radical scavenger
Vasodilation effect, dependent on dose and rate of administration
Given IV over 20 mins, takes 15 mins to work, lasting about 2 hours
Loop Diuretics = Furosemide (Lasix), bumetanide (Bumex), ethacrynic acid (Edecrin)
Inhibit Na+ and Cl- reabsorption in the medullary portion of the ASCENDING limb
Increases urinary Ca+ and Mg+ excretion
Uses: Na+ overload states, acute pulmonary edema, cardiac failure, HTN, hypercalcemia,
rapid correction of hyponatremia, alterations in BBB do not influence ability of Lasix to
decrease ICP
Side effects:
o Increased delivery of Na+ to the distal and collecting tubules increases K+ and
H+ secretion hypokalemia and metabolic alkalosis
o Marked Na+ losses will lead to hypovolemia and prerenal azotemia o
Hypercalciuria can result in stone formation o
Hypomagnesemia
o Deafness in high doses
Thiazide-Type Diuretics = Metolazone, Chlorthalidone, Indapamide
Reduce reabsorption of Na+ & Cl- in DISTAL convoluted tubule and part of cortical
ASCENDING loop of Henule
Competes for Cl- site at Na+-Cl- carrier protein Na+ excretion
Use: HTN, Na+ overload, hypercalciuria ( Ca+ excretion), nephrogenic DI
K+-Sparing Diuretics
(1) Spironolactone (Aldactone)
95
Inhibit Na+ reabsorption and K+ secretion by decreasing the number of open Na+
channels likely in the proximal tubule
Inhibit Na- & Cl- reabsorption in medullary portion ASCENDING loop of Henule
Treatment of acute pulmonary edema best choice for CHF b/c reduces pulmonary
wedge pressure before diuresis occurs. Decreases ICP, able to give with disrupted BBB
Mannitol
Freely filtered at the glomerulus, NOT reabsorbed increases osmolality in the renal tubules
reduced efficiency of Na+ reabsorption
Do not use if BBB is disrupted mannitol enters brain causing edema
Maximum effect in rx of ICP occurs within 1-2 hours, lasting 6 hours
Urea
Spironolactone
Aldosterone antagonist, in the absence of aldosterone, it has NO effect
Amiloride, Triamterene
Directly blocking the epithelial sodium channel thereby inhibiting Na+ reabsorption in the
distal convoluted tubules and collecting ducts in the kidneys. This promotes the loss of
sodium and water from the body, but without depleting potassium.
Inhibits reabsorption of HCO3 and prevents the secretion of H+ (dump HCO3) hypokalemic
metabolic acidosis
Haldoperidol = butyrophenone
Side effects:
o Anti-cholinergic effects rarely with Haldol
o Highly sedating
o -blockers orthostatic hypotension o
Lowered seizure threshold
o Cardiac toxicity in overdose prolong QT, torsades de pointe
Droperidol = butyrophenone
Mechanisms:
o Inhibits histamine-N-methyl-transferase ,which metabolizes
histamine o
Inhibits dopamine in chemoreceptor trigger zone
of medulla
96
Drugs that inhibit or prevent the action of dopamine in the basal ganglia o
= chlorpromazine, promazine o
Butyrophenones = droperidol
o Metoclopramide
o Viral
encephalitis o
Atherosclerosis
Phenothiazines
Chlorpromazine a phenothiazine
Effective anti-psychotic drug, blocks D2 receptors
Anti-emtic, sedative
Lowers seizure threshold
Blocks anti-HTN effects of guanethidine & guanadrel
Potentiates depressant effects of narcotics
-Methyl Dopa
Pre-synaptic central
2 receptor agonist
RARE rebound HTN (more common with clonidine or propranolol)
Trimethaphan
Nicotinic AChR antagonist at autonomic ganglia blocks sympathetic &
parasympathetic outflow
Side effects mydriasis, orthostatic hypotension, tachycardia, constipation
Causes LEAST CBV & ICP compared to other anti-hypertensive drugs
Fenoldopam
97
Sodium Nitroprusside
Side effects:
o CN- & thiocyanate toxicity o
Rebound HTN o
Intracranial HTN o
Blood coagulation abnormalities o
Inhibits hypoxic pulmonary vasoconstriction shunt
hypoxemia o
Hypothyroidism
Cyanide Toxicity
Toxic blood levels (= 100 mcg/dL) occur when 1 mg/kg sodium nitroprusside given over 2
hours; max rate 10 mcg/kg/min. Can see toxicity at really any level.
Si/Sx: metabolic acidosis, SvO2, acute tachyphylaxis, also see dysrhythmias, N/V,
confusion, muscle weakness
Thiocyanate Toxicity
Nitroglycerin
Mechanism: metabolized to nitric oxide (NO) in vascular SM wall cGMP SM relaxation
dilate veins > arteries myocardial O2 demand by preload & wall tension. See
subendocardial O2 delivery. Does not increase total coronary blood flow in angina
Indications: pulmonary HTN, MI, HTN
Side effects:
o Nitrate, a metabolite, can cause methemoglobinemia; Rx: IV methylene blue (1-2
mg/kg) o
Hypotension, reflex tachycardia
o Arrhythiamis
o MI
Relative contraindications: angina due to AS or IHSS, tachyarrhythmias
Guanethadine
98
REGIONAL
99
Side effects
Orthostatic hypotension (most common) correct
with fluid bolus LR
Intravascular injection into the vena cava is more
likely to produce a severe systemic rxn than intraaortic
seizure
SAB is the most serious complication
Retroperitoneal hematoma (rare)
Diarrhea unopposed parasympathetics
100
Anatomy the ganglion impar is the most cadual part of the sympathetic trunk located
midline, anterior to the coccyx
Technique: needle inserted at medial edge of SCM just below the level of the cricoid cartilage
at the level of the TP of C6 or C7.
Success interruption of sympathetic supply = Horners syndrome ipsilateral ptosis,
myosis, enophthalmos (sunken eye ball), unilateral nasal congestion, anhydrosis, flushing of
the conjunctiva & skin.
Complications: intravascular, SAB, hematoma, pneumothorax, epidural anesthesia, brachial
plexus block, hoarseness from recurrent laryngeal nerve (avoid bilateral blocks), osteitis or
mediastinitis following esophageal puncture
If block fails, using guanethidine or reserpine can be used with Bier block technique.
101
Anesthesia of the ipsilateral face, cornea, sclera, anterior tongue (posterior tongue by
CN IX) o
Trigeminal neuralgia: sharp facial pain in the maxillary br of V2 o
Definitive Rx: neurolytic block with glycerol or pulse radiofrequency ablation o
Pharmacologic Rx: carbamazepine
Anatomy: CN V roots join one another to form the gasserian ganglion in Meckels cave
(middle cranial fossa) which contains CSF risk total SAB
Brachial Plexus
Anterior primary divisions (ventral rami) of C5-T1
Roots, Trunks, Divsions, Cords, Branches (Robert Trunk Drinks Cold Beer)
Brachial plexus begins with 5 nerves and terminates with 5 nerves (ARM MU): Axillary,
Radial, Median, Musculocutaneous, Ulnar
In the axilla, 3 cords are formed, named by relationship to the axillary artery:
o Lateral cord (flexor surface): superior and
middle trunks
lateral head of the median nerve (C6-T1)
terminates as musculocutaneous nerve (C4-6) o
Medial cord (flexor surface):
inferior trunk
medial head of the median nerve (C5-T1)
terminates as ulnar nerve (C8, T1)
medial antebrachial nerve
medial brachial cutaneous nerve o
Posterior cord (extensor surface): posterior
division of all 3 trunks
axillary nerve (C5-6)
terminates as radial nerve (C6-T1)
Interscalene block
Progresses proximal to distal, interosseous muscles (abduct & adduct fingers) are most
distal & last blocked, innervated by ulnar nerve
If need to cover skin over the shoulder, must block superficial cervical plexus (C1-C4) at
posterior border SCM
Onset of block is faster than either supraclavicular or axillary
Supraclavicular block
Blocks trunks (superior, middle, inferior)
**Miss suprascapularis nerve which supplies supraspinatus, infraspinatus, shoulder
capsule** Axillary Nerve Block
Best for procedures distal to the elbow
Proximal spread of L.A. in axillary perivascular space is promoted by (1) increased volume of
agent, (2) digital pressure distal to injection site, (3) cephalad direction of needle, (4)
adduction of shoulder after injection
Misses
(1) Musculocutaneous nerve (C6 dermatome) - sensory to lateral forearm, motor to
coracobrachialis & biceps, must block with injection into the coracobrachialis.
(2) Intercostobrachial nerve (T2 dermatome) apex of axilla
(3) Median cutaneous nerve medial upper arm (part of T2 dermatome)
Radial Nerve
102
Radial nerve is motor to arm, forearm, wrist extension; innervates triceps; sensory to mid
forearm, wrist, extending onto (medial) dorsum hand and small bit of thenar (palmar surface)
At the wrist lateral to medial: N A / N / A N radial n. - radial a. - flexor carpi radialis
median n. - palmaris longus - ulnar a. - ulnar n.
At the elbow 4 fingers above the lateral epicondyle, b/t brachioradialis & biceps
tendon
Injury wrist drop
Ulnar Nerve
Motor to all hand muscles (interosseus), except 1st & 2nd lumbricals & thenar muscles (median
n.); sensory little finger & medial of ring finger (palmar & dorsal sides)
At the wrist
N A / N / A N medial to ulnar a.
At the elbow b/t olecranon & medical epicondyle
Injury interosseus atrophy = clawed hand
Median Nerve
Motor to thenar eminence & 1st & 2nd lumbricals, wrist & finger flexion, allows you to oppose
thumb and little finger
Sensation palmar aspect of thumb, palmar aspect lateral 2 fingers + finger tips dorsal
aspect
At the wrist N A / N / A N radial n. - radial a. - flexor carpi radialis median n. palmaris longus - ulnar a. - ulnar n.
At the elbow medial to the brachial artery b/t 2 heads of pronator teres
Injury thenar atrophy
Absorption rates of local anesthetics
IV > intra-tracheal > intercostal = intrapleural > caudal > epidural > brachial plexus >
sciatic Neurolytic Nerve Blocks
Not used directly on peripheral nerves b/c risk development of denervation dysesthesia
Used in epidural block bilateral block
Used in subarchnoid unilateral block
Ethanol 100% (hypobaric) cause more intense neural destruction and is more painful
Phenol 5-10% in glcerine (hyperbaric) gives a more predictable block, painless b/c dual
action as a local anesthetic & neurolytic. Initial block wears off in 24 hrs then neurolysis
begins
103
104
Psoas
Ankle Block
105
Sensory: dorsum (top) of the foot and all 5 toes, except b/t great & 2nd toes
4. Posterior tibial
Posterior to medial malleolus with posterior tibial artery, branching into lateral and
medial plantar nerves & medial calcaneal branches
Sensory: heel (medial calcaneal br), plantar surface of the foot (plantar n)
Motor: plantar flexion & inversion
5. Sural
Continuation of the tibial nerve & 1 br of common peroneal nerve
Between the Achilles tendon and posterior to lateral malleolus
Sensory: lateral foot, lower posterolateral leg, 5th toe
Deep peroneal, superficial peroneal, and saphenous nerves can all be blocked using a
single injection site
At ankle only sensory only nerves = sural, saphenous, superficial peroneal
Intercostal Block
Exits from the spine at the intervertebral foramen and travel along the underside of
the corresponding rib, with artery & vein; nerve is most inferior (VAN)
Technique: mid & posterior axillary line.
Complications: highest blood levels of L.A. per volume injected of any block in
the body
Common Nerve Injuries
Brachial plexus stretching by head of the humerus or compression b/t clavicle & 1 st
rib
Radial n. wrist drop (cant extend metocarpophalangeal jts), weakness thumb
abduction
Median n. inability to oppose thumb and little finger, loss sensation palmar
surface lateral 3 fingers
Ulnar n. due to compression of posterior aspect of medial epicondyle of humerus
inability to abduct little finger, loss sensation over both dorsal & palmar surfaces of
medial 1 fingers
Sciatic n. due to stretching in lithotomy position weakness below the knee and
loss sensation of all of the foot EXCEPT inner arch (saphaneous n.)
106
107
OSA
Fibrosis
Pregnancy
Hiker at altitude
pH
7.38
7.39
7.41
7.55
PCO2
58
41
34
24
PO2
56
59
81
57
108
Obesity
Supine position
Shunt Equation
Qs/Qt = CcO2 CaO2
CcO2 CvO2
Dead Space
Vd/Vt = PaCO2 PETCO2, normal < 0.3 (intubate if > 0.6)
PaCO2
Normal Vd = 150 ml or 2 ml/kg = weight in lbs.
Normal Vt = 450 ml or 6 ml/kg
Factors that increase physiologic (anatomic + alveolar) dead space (thus Vd/Vt)
Age
Anti-cholinergics
Bronchodilators
Upright position
Hypotension, hypothermia, hypovolemia
Smoking
PE, pulmonary hypoperfusion
Emphysema/COPD
Positive pressure ventilation
Neck extension
General anesthesia
ARDS maybe due to hypoxic vasoconstriction
Shock/low cardiac output
Factors that decrease dead space (thus Vd/Vt)
Supine
109
Neck flexion
Artificial airway
Increased cardiac output increases perfusion to apical zones (West zone 1) of the lung
CO
ml O2/g Hgb
Increase SvO2
permeanently wedged PA catheter
Cyanide toxicity due to (VO2)
Methemoglobinemia (VO2)
Sepsis (VO2)
Hypothermia (VO2)
High C.O. states burns, L R
shunts, AV fistula, excessive
inotropic drugs,
hepatitis, pancreatitis
Milrinone
Side effects of Bicarbonate
SpO2
HyperNa+
Hyperosmolarity
100%
L shift Hgb curve due to
95%
Intracerebral hemorrhage 90%
PvO2
Left shift Hgb Curve = Hgb
P50
mmHg
Decrease SvO2
Anemia
Low SaO2
Low C.O. MI, CHF, hypovolemia
High VO2
Right shift Hgb curve
PaO2
700 mmHg
100 mmHg
60 mmHg
40 mmHg
26 mmHg
Cyanide, nitric acid, ammonia all combine with Hgb at O 2 binding sites displace O2
Methemoglbinemia, carbon monoxide, sulfhemoglobin, fetal hgb
H+ = metabolic & respiratory alkalosis
temperature
2,3 DPG (occurs with blood txn)
Right shift Hgb Curve = Hgb affinity for O2, P50 > 26 mmHg
H+ = metabolic & respiratory acidosis
temperature
2,3 DPG
Pregnancy
Abnormal hemoglobins sickle cell (P50 = 31), thalassemia
Volatile anesthetics at 1 MAC
Bohr Effect
The effects of PaCO2 and pH on the position of the oxyhemoglobin dissociation curve
Attributed primarily to the action of CO2 and pH on erythrocyte 2,3 DPG metabolism
Methemoglobinemia
110
Hgb is oxidized to ferric (3+) unable to bind O2 & left shift Hgb curve, difficult to unload O2
Hallmark:
Adequate PaO2, but SpO2= 85%
Chocolate urine & blood
Cyanosis when methemoglobin > 1.5 gm/dl
2 types
(1) congenital
(2) acquired i.e. nitroglycerin, nitroprusside, EMLA cream, benzocaine, phenacetin, Prilocaine
due to metabolism to o-toluidine oxidizes Hgb
Treatment: methylene blue 1-2 mg/kg, if fail then require exchange transfusion
Carboxyhemoglobinemia
Non-smokers 1-3%, smokers 15%
Si/Sx: HA, dizzy, N/V, confusion, cherry red skin of COHb >40%
CO can result from interaction of desiccated absorbent, soda lime or baryalyme 30% level.
Predisposition to production of CO: o Degree of absorbent dryness o Use of Baralyme
o High concentration of volatile anesthetic (more CO at higher
concentrations) o High temperatures o Type of volatile used:
desflurane >> sevoflurane
Treatment: Oxygen!
o T CO 4-6 hrs while on room air, reduced to 1 hr on 100%
o If hyperbaric therapy fails, consider transfusion fo blood, sedation to alter O 2 demans,
diuretics, steroids
Gaussian distribution = data sets follow a normal distribution around a center point.
Derived from the assumption that there is a center, true value and that deviations from the
center are random and diminish in likelihood the farther the values get from the center
When data follow a normal distribution or any specific mathematical distribution, the methods
of parametric statistics can be used refers to the ability to describe the distribution when
a specific set of values
111
Frequently data does not follow a normal distribution non-parametric statistical methods
need to be used
The larger the SD, the wider the bell-shaped curve, and the smaller the SD, the
narrower the curve
REGRESSION ANALYSIS
1ST step is to choose the variables that will be used as independent variables
Univariate analysis only one variable is used for the data fit, and the data are plotted and
the computations performed by using that one variable to describe the data.
o i.e. the weights of a group of subjects may be compared with their heights
Multivariate analysis more than one variable can almost always be used to determine an
outcome o
i.e. the subjects weight might be analyzed by using heights, ages, and gender
HYPOTHESIS TESTING
Null hypothesis = there is no difference b/t 2 groups of data
Alternative hypothesis = there is a difference b/t 2 groups of data
A level of significance, termed the alpha () value, and declare that if P < alpha, the result
is statistically significant and accepted as true
If P > alpha we reject the hypothesis = accept the null hypothesis that there is no difference
b/t 2 groups of data
P value is the chance that the null hypothesis was true
Typically alpha = 0.5 (5%) and desire P < 0.5 if, in fact, there was no association in the
population b/t the independent and dependent variables, the observed association would be
expected to occur by chance less than 5 times in 100 samples.
Power
Beta error probability of falsely accepting the null hypothesis
Power = 1 = 1 probability of making type II error
Sample size sample size = power
As power increases, the chance of a type II error () decreases
Type I error ()
Rejecting null hypothesis incorrectly (should have been accepted)
Probability of observing difference between 2 groups when there is actually no difference
E.g. positive pregnancy test in a patient that is not pregnant
112
Type II error ()
Accepting null hypothesis incorrectly (should have been rejected)
Probability of observing no difference between 2 groups when there is actually a difference
E.g. negative pregnancy test, when in fact patient is pregnant
Confidence Intervals
A range of values may be given such that it is determined with some likelihood (often picked
at 95%) that the true values lie within that range
For expressing simple results, the CI is equivalent to providing a mean +/- SD
Observational study: if CI includes 1 findings are NOT statistically significant
Randomized control trial: if CI includes 0 findings are NOT statistically significant
BAYESIAN APPROACH TO PROBABILITY
(+)
test
(-)
test
disease
true positives
(TP)
false negatives
(FN)
no disease
false positives
(FP)
true negatives
(TN)
STATISTICAL ANALYSIS
Must first determine what kind of data is being collected --- categorical or
continuous
Categorical = male/female; blood type; sick/well; receive drug/dont receive drug. One
either has it or not, one receives a drug or not. There is NO average.
o Requires chi-square
Continuous = blood pressure; weight; height; reaction time. These are numbers and taking
an average makes sense. I.e., taking an average blood pressure makes sense, but taking an
average of maleness does not.
o Requires linear regression or student t-test
Students t-test
Most valid for comparing mean values of 2 groups!!
Considered a robust test, especially when small sample size < 30
Used to test the null hypothesis that there is no difference b/t 2 means, 3 circumstances:
o To test if a sample mean differs significantly from a given population mean
o To test if the population means estimated by 2 independent samples differ
significantly
= unpaired t-test o
To test if the population means estimated by 2
dependent samples different significantly = paired t-test
Paired t-test used if the means for the 1st category come from the same people as the
means in the 2nd category. Occurs when you can test the same people under 2
conditions or circumstances
Analysis of variance
Must use when 3 or more means are present
Identical to the t-test when more than 2 means are being compared
113
Chi-Square Test
Most appropriate test to determine statistical significance
When the exposure (independent variable) and the result (observed data) are both
categories
The only method used to evaluate whether categorical data is associated with categorical
data
Case-control study = groups of subjects are compared, usually in regard to the effects
of some intervention. However, the factor separating the groups is determined AFTER
the intervention
Comparison groups defined by outcome (disease) and look
historically for exposure.
Persons are followed over time to determine the frequency of disease occurrence.
Cases are compared to controls.
Can be done prospectively or retrospectively
Cohort study = groups of subjects are compared, usually in regard to the effects of
some intervention, followed over time
Study group is monitored BEFORE the intervention
Relative risk used to measure of strength of association between exposure and
disease
EXPERIMENTAL studies:
o Randomized controlled trial (RTC)
reason to randomize: equally distribute confounding factors
between groups
assessment: single blind vs. double
blind
Strengths of RCT design
Selection bias occurs when we are comparing groups with respect to some
variable, but do not realize that the groups are different in other ways o
114
Measurement bias occurs if the methods used for making measurements when
comparing different groups have different scales or sensitivities o
i.e.
consider attempting to get a h/o chest pain in groups of patients with and w/o
known CAD. Patients who know they have heart disease might be imagined to
remember brief pain more thoroughly than healthy patient do
o Minimized in blinded studies
**Odds ratio
A
odds ratio (OR) =
B
*D
*C
THORACIC
TLC
FEV1/FVC
VC (> 60 ml/kg)
RV
RV/TLC
FRC (= wt in lbs.)
Spirometry, Flow-Volume Loops
Obstructive
Increased
Decreased
Normal or
decreased
Increased
Increased
Increased
Restrictive
Decreased
Normal or
increased
Decreased
115
116
PFTs
Best test for assessment of small, peripheral airways is FEF25-75 and MMEF
CANNOT measure FRC & RV by spirometry
DLCO determined by:
Area & thickness of alveolar membrane
Glood/gas solubility & MW of gas
Transmembrane partial pressure difference of the gas
Pulmonary blood volume
Hgb concentration
DLCO => anemia, emphysemia, dehydration, pulmonary HTN
DLCO = Asthma (unknown mech.)
Chronic Bronchitis
Emphysema
Loss of elastic recoil premature collapse during exhalation patients purse their lips to
delay closure of small airways pink puffers
Clinically DYSPNEA
Destruction of pulmonary capillaries in alveolar septa DLCO pulmonary hypertension
(vasoconstriction)
Normal PaCO2 & overinflation on CXR
117
Factors that decrease blood flow to the ventilated (dependent) lung counter act
the effect of
HPV by indirectly increasing blood flow to the collapsed lung o
High mean peak airway pressures in the ventilated lung o
Low FiO2 HPV in the ventilated lung o
Vasoconstrictors that may have greater effect on
normoxic vessels o
Intrinsic PEEP that develops due to
inadequate expiratory times
CO2 elimination is not affected by one-lung ventilation provided minute
ventilation is unchanged arterial CO2 tension is usually not appreciably altered
118
250 mmHg
High FiO2 can cause absorption atelectasis, oxygen toxicity, bleomycin-induced
injury o
Ventilate dependent lung with VT = 10-15 ml/kg; > 15 mg/kg
PVR, shunt blood to the non-ventilated lung
Maintain PaCO2 = 40 mmHg. Hypocarbia vasodilates lung vasculature &
inhibits HPV o
CPAP to the non-dependent lung is the most effective way to
PaCO2 elminiation. CPAP
= 5-10 cm H2O maintains patency of nondependent alveoli allowing gas
exchange o
PEEP to the dependent lung FRC & improves gas exchange.
PEEP may compress small interalveolar vessels increasing shunt to the nondependent lung ultimately PaO2
119
Lambert-Eaton syndrome o
Seen with bronchial carcinomas
o Antibody-mediated destruction of pre-synaptic voltage gated Ca2+
channels deficient release of ACh at NMJ muscle weakness o
Proximal myopathy, muscle strength increases with repeated
effort/exercise
o Autonomic disturbance hypo- or hypertension, sinus tachycardia, diaphoresis
o
No improvement with administration of anticholinesterases o
Marked
sensitivity to both depolarizers & non-depolarizers; risk of sux induced hyperK+
o
Required A-line for BP monitoring given dysautonomia
o Treatment - plasmapheresis or IV immunoglobulins and supportive care;
Guanidine hydrochloride and 3,4 diaminopyridine (DAP) increase level of
ACh and improve symptoms
o Death may occur if severe pulmonary complications & dysautonomia are
present.
Non-small cell = 80% squamous cell, adenocarcinomas, large cell; peripheral lesions
involving the pleura adenocarcinoma occurs in non-smokers
Clinical Manifestations
Involvement of mediastinal structures:
o Hoarseness from compression of the recurrent laryngeal nerve o Horners syndrome o
Elevated hemidiaphragm from phrenic n. compression
o Dysphagia from compression of the esophagus
o SVC syndrome
Pancoast syndrome = extension of apical tumors to involve C7-T2 nerve roots of the
brachial plexus shoulder or arm pain
Metastases liver, bone, brain, adrenal glands
Treatment
Surgical resection for non-small cell in the absence of advanced LN involvement Small
cell is infrequently operated on!!
Lobectomy via posterior thoracotomy, 5th or 6th intercostal space is the procedure of choice o
Mortality = 2-3%
Pneumonectomy is necessary for curative treatment of lesions involving the L or R main
bronchus or when tumor extends to the hilum o Mortality = 5-7%, Right sided >> Left sided
b/c of greater loss of lung tissue o Pre-op FEV1 < 1 L = 40% mortality o
Most post-op
deaths are due to cardiac cause
120
High-Risk Patients
PaCO2 > 45 mmHg (on room air)
PaO2 < 50 mmHg
<2L
800 ml or < 40% of predicted
< 50% predicted
< 50% predicted
< 10 mL/kg/min
> 50%
< 2 L (normal = 60 ml/kg = 4.2
L)
The most commonly used criteria for operability is predicted post-op FEV 1 > 800 ml
% contribution of each lung to total FEV1 is assumed to be proportionate to % of total
pulmonary blood flow it receives, determined by radioisotopic scanning (133 Ke or 99 Tc)
Oxide
Vasodilator, acetylcholine stimulates its release from endothelial cells
In the lungs, NO synthetase combines oxygen with L-arginine to produce NO and L-citrulline
NO stimulates c-GMP decrease intracellular Ca2+ relaxation & vasodilation of vascular
SM decrease PA pressures and V/Q mismatching
A selective pulmonary vasodilator with NO systemic hemodynamic effects!
< 2 ppm is acceptable exposure, NO > 100 ppm and high FiO2 results in production of
NO2, a potent oxidant
>150 ppm for short duration is fetal
Tracheal Resection
121
PFTs are required by all patients undergoing elective tracheal resection b/c severe lung
disease necessitating post-op ventilation is a relative contraindication b/c PPV may cause
wound dehiscence.
VOLATILE ANESTHETICS
Agents
Halothane
Isoflurane
Enflurane
Sevoflurane
Desflurane
Nitrous oxide
MAC (%)
0.77
1.15
1.70
2.05
6.0
104
Vapor
Pressure
(mmHg,
20C)
243
239
175
157
664
39,000
Blood:Gas
partition
coefficient
2.3
1.4
1.8
0.69
0.42
0.47
MAC ( potency)
-Hyperthermia (>42C)
-Drugs that CNS
catecholamine levels: MAOI, TCA, ephedrine - Acute
cocaine, amphetamines
- Chronic EtOH abuse
-Infants at age 1 yr
-HyperNa+
MAC
- age (elderly)
-Hypothermia
-Hypercapnia (PaCO2 > 90)
-Hypoxia (PaO2 < 40)
-Hypotension (MAP < 40
mmHg) -CNS depressant:
sympatholytics, ketamine,
pancuronium -Acute EtOH
-Chronic amphetamines
-Lithium, Reserpine, methyldopa
-Cholinesterase inhibitors
-Pregnancy
- 2 agonists = Clonidine
-Neonates (0-30 days)
-Anemia (Hct < 10%)
-HyperCa2+
-HypoNa+
-Cardiopulmonary bypass
122
Studies have not shown an association b/t trace concentrations of waste gases found in
scavenged location and adverse health effect in health personnel
OSHA recommendations (not requirements!) o
N2O alone < 25 ppm o
N2O +
volatile anesthetics, with N2O < 0.5 ppm o Halogenated anesthetics < 2 ppm
Children have greater perfusion of VRG, FA/FI rises more rapidly o VRG
receives 75% of cardiac output
Intracardiac Shunts o
Impact of the shunt is greater with the less soluble
agents, most dependent on blood flow o
Right-to-Left Shunt portion of Q
bypasses the lung slows induction o
Left-to-Right Shunt no
significant change in the speed of induction
3. Alveolar to Venous partial pressure difference (PA-PV)
The uptake of anesthetic by blood perfusing the lung will increase (rate of rise of F A/FI will
decrease) as the gradient between the partial pressure of anesthetic between the alveoli &
blood increases. This gradient is large early in the course of anesthetic administration
o The factors that determine the fraction of anesthetic removed from blood traversing
a given tissue include: (1) tissue solubility, (2) tissue blood flow, (3) arterial to tissue
anesthetic partial pressure difference
4. Altitude & Barometric pressure
Altitude lowers barometric pressure uptake = FA/FI = slower induction
Vaporizers are NOT compensated for changes in barometric pressure.
123
124
125
Effects on CV system
Halothane
Enflurane
Isoflurane,
Desflurane,
Sevoflurane
Contractili
ty
___
SVR
---
SBP
(MAP)
SVR
126
MAP
MAP in a dose dependent manner = Enflurane >>
Desflurane, Isoflurane > Halothane (least)
Halothane
Isoflurane
Desflurane
Sevofluran
e
HR
--
CO/myocardial contractility/CI
CO = Halothane, Enflurane
Maintain CO = Isoflurane, Sevoflurane,
Desflurane
(profoundly SVR, with compensatory
HR)
HR
HR is unaffected by Halothane, due to altering carotid
baroreflex
HR = Desflurane > Isoflurane > Sevoflurane
SVR
---
CI
--
SUMMARY OF CV EFFECTS
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Risks: multiple short intervals (within 4 weeks) , middle age obese women (higher rate
defluorination), familial predisposition
Biotransformation/Metabolism of Volatile
Anesthetics o Methoxyflurane:
40%
o Halothane: 20% (oxidative
metabolism) o Sevoflurane: 3% o
Enflurane: 2% o
Isoflurane:
0.2% o
Desflurane: < 0.02%
Metabolism dependent on P450 enzymes in the endoplasmic reticulum of hepatocytes o
Cirrhosis & CHF may decrease overall metabolism o
Morbid obesity =>
increased defluorination of VA o
Inducing enzyme systems of the liver ARE NOT
associated with increased metabolism!!
Compound A
Sevloflurane is degraded in temperature-dependent fashion in soda & baralyme
nephrotoxin at proximal renal tubules
Increased concentrations seen with:
o Baralyme (instead of soda lime) o High
absorbent temperatures o
Higher
concentrations o
Closed circuit or low-flow
anesthesia o
Desiccated Baralyme (vs.
desiccated soda compound)
Combining MACs
Isoflurane 1% + N20 70% 1%/1.15% + 70%/104% = 0.86 + 0.7 => 1.5 MAC
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