M5 Anatomy 4/29/2016 7:09:00 PM

Airway innervations to know

Anterior 2/3 tongue: Trigeminal, mandibular division (CN V3)
o Forms lingual nerve
o General sensation
Posterior tongue: glossopharyngeal (IX)
o Taste/sensation posterior 2/3
Taste anterior 2/3: Facial nerve CN VII (branch forms chorda tympani)
Intrinsic muscles of tongue: Hypoglossal CNXII
Soft palate: glossopharyngeal (IX)
Oropharynx: glossopharyngeal (IX)
Hypopharynx (oropharynx below level of epiglottis): internal branch of
laryngeal nerve (X)
Vocal cords: both internal branch of SLN and Recurrent LN (CNX)
Larynx (below VC but above trachea): recurrent laryngeal nerve (X)
Trachea: recurrent laryngeal (X)

3 AIRWAY BLOCKS TO KNOW:

Anterior tonsillar pillar (base): blocks glossopharyngeal (tonsillar,
lingual and pharyngeal branches)
Inferior aspect of greater cornu of hyoid: blocks internal branch of
SLN (external branch)
Transtracheal: recurrent laryngeal

- Sensory innervation of airway: vallecula up is CN IX. Underside of epiglottis to cords is

internal branch of superior laryngeal nerve. Below cords is RLN.

External branch of SLN: motor innervation to cricothyroid muscle (elongates

VC) allowing HIGH pitch

Sensory:
X internal laryngeal nerve ABOVE vocal cords
X recurrent laryngeal nerve below vocal cords

Trigeminal: nasopharynx down to soft palate (maxillary division)

Glossopharyngeal: soft palate to epiglottis, pharyngeal nerves to pharyngeal
mucosa, tonsillar nerves to tonsils/soft palate, posterior 3rd of tongue
Vagus
Below epiglottis
SLN
o Crosses cornu of hyoid and divides into internal and external
branches
o Internal branch penetrates thyrohyoid membrane and innervates
mucosa from epiglottis to cords
o External branch to cricothyroid
Injury to RLN is more deleterious as it innervates all of the intrinsic muscles
of the laryngx, except for the cricothyroid muscle which is innervated by the
SLN.
Unilateral RLN injury produces abdocutor vocal cord paralysis affected
cord in paramedian position

(1) Abduct vocal cord: posterior cricoarytenoid (RLN)

(1) Tensor muscle: cricothyroid (innervated by external branch of SLN)
(3) Adductor muscles
Adduct VC: Lateral cricoarytenoid

Sniffing position:
Pharyngeal and laryngeal axis parallel
Oral axis at 30 degree relative to these 2

RUL bronchus: 2cm below carina

Type I pneumocytes: gas exchange

Type II pneumocytes: make surfactant, differentiate into type I, more
numerous

Sympathetic innervation of lungs: T1-T4

Mediate bronchodilation
Cardioaccelerators
o Travel up through stellate ganglion 1st
Subclavian Vein
Anterior to artery
SCV - Anterior to anterior scalene
SCA courses between middle and anterior scalene
Both then course over (superior) to the 1st rib

IJ Vein
Lies between 2 heads of SCM (superior to clavicle, lateral to carotid
artery)

Spinal Cord blood supply

1 anterior spinal artery
o originates from vertebral arteries
o supplied by posterior intercostal arteries
o at level of lumbar/sacral SC: supplied from artery of
adamkiewicz (arises from a single posterior intercostal artery)
2 paired posterior spinal arteries

Anterior Spinal Artery syndrome

Motor paralysis, loss of pain/temp
Preserved proprioception/vibratory sensastion (Posterior spinal artery
supplies these tracts)

Spinal cord ends at L1 in adults!

Neonates: L3

Inferior tip of scapula: T7

Most prominent cervical process: C7 (vertebra prominents)
Superior aspect of iliac crest: L4 (aka Tuffiers line)
Posterior superior iliac spine at the S2

Interlaminar foramen
Lumbar level: at the level of interspace
Thoracic: 1-3 cm cephalad to the interspace

Innervation of facet joint:

 Medial branch of posterior division of spinal nerves
Medial branch block

Stellate ganglion block

C6/C7
Results in vasodilation of ipsilateral arm
Unopposed parasympathetic effects and ipsilateral Horners syndrome,
increased pulses
Horners syndrome: nasal stuffiness, ptosis, enopthalmos, miosis,
anhydrosis

Celiac plexus: located at L1, anterior to aorta

Sympathetic innervation to midgut (stomach, SI, ascending/transverse
colon
Blocking nerve blocks sympathetic/pain
Results in unopposed parasympathetic
o Increased motility, diarrhea
Contains afferent/efferent fibers from T5-T12

** KNOW THE BRACHIAL PLEXUS

Musculocutaneous nerve:
Derived from lateral cord of brachial
plexus
Carries C5, C6, C7

Lumbar Plexus:
4 roots ventral rami of L1-L4
o L1 divides into superior and
inferior branches
Superior: ilioinguiinal/iliohypogastric
Inferior: joins L2 to form genitofemoral n
o L2-L3: branches to form lat. Fem. Cutaneous
o L2-L4: feoral + obturator
Innervation of lower extremity
Thigh
o Femoral nerve (primarily)
Saphenous is terminal branch
o Exception:
Medial thigh obturator innervation
Lateral thigh lateral femoral cutaneous
Lower Leg
o Sciatic nerve: L4-L5 + S1-S3 (lumbosacral trunk)
Sensation to posterior hip/knee
Motor to hamstrings/all LE distal to knee
Sensation distal to knee except anteromedial
(saphenous)
Terminal branches:
posterior tibial
sural
deep peroneal
superficial pernoeal
Exception
o Medial leg saphenous (terminal branch of femoral)
o Posterior lateral LE sural nerve (branch of tibial)
Remainder common or superficial peroneal nerve

5 Nerve blocks required for complete ankle block

Posterior Tibial nerve
Deep peroneal
Superficial peroneal sensation to all toes except
1st web space
Sural nerve continues from the tibial nerve,
sensation to LATERAL foot
Saphenous nerve (anteromedial)- anterior to
medial malleolus
Medial ankle: saphenous
Anterior lower leg: saphenous (L3-L4)/peroneal (L4-S1)
Popliteal fossa: femoral: L2-L3
Brachial plexus: C5-T1
3 Trunks:
SUPERIOR Trunk: C5-C6
(above subclavian artery)
o Suprascapular n.
Middle trunk: C7
Inferior trunk: C8-T1
o Intercostal n.

6 Divisions (trunks divide into ventral/dorsal divisions at level of 1st rib)

Dorsal division: extensors
Ventral divisions: flexors
Form cords entering axilla
3 Cords:
Lateral 3 branches
o 2 major: Musculocutaneous n. , Half of median n.
o 1 minor: Lateral pectoral n.
Posterior 5 extensor branches
o 2 major: radial and axillary nn
o 3 minor: thoracodorsal, 2 subscapular
Medial 5 branches
o 2 major: ulnar and medial
o 3 minor: medial pectoral, medial cutaneous of arm/forearm
Interscalene block
25% reduction in lung function (phrenic nerve)
spares ulnar nerve (C8-T1)

Innervation of the UE
Median nerve: C5-C7 (lateral cord) + C8-T1 (medial cord)
o Travels medial to brachial artery
o Sensation to palmar surface of thumb, index/middle fingers,
lateral of 4th finger, small distal portions of dorsal surface of
thumb/middle/index
o Motor to abductor pollicis brevis, opponens pollicis, 1-2 lumb
Local anesthetic toxicity by site:
Intercostal > caudal > epidural > brachial plexus > sciatic
M5 Cardiac Phys 4/29/2016 7:09:00 PM

Normal PAP values:

CO 5L/min
CI: 3L/min/m^2
SV: 70 cc
SVI: 40 cc/m^2
SVR: 1,000 dynes*sec/cm^5
PVR 200 dyn*sec/cm^5
PAP: 25/15

Innervation of the heart:

Parasympathetic
o Arise from dorsal vagal nucleus and nucleus ambiguous (carried
by vagus nerve)
o Muscarinic acetylcholine receptors are greatest at SA node then
AV node
Stimulation: chronotropy (HR), dromotropy
(conduction)
Sympathetic: T2, T3, T4
o Carried in stellate ganglion 1st then down to heart as cardiac
nerves
Heart Sounds:
S1 beginning of systole
o Before c wave on CVP
o After QRS complex
S2 end of systole
o Isovolumetric relaxation, aortic pressure greater than ventricular
pressureclosing aortic valve
o A2/P2
S3 rapid ventricular filling during early diastole
o Knocking sound after S2
o Noncompliant ventricle
o DDX: Heart failure
S4: due to atrial contraction against non-compliant LV
o Chronic hypertension and aortic stenosis
o Occurs AFTER p wave
A2 closes before P2, splitting is greater with inspiration due to increased
preload in the RV and decreased preload in LV
S2 heard after T wave..or during/just before the v on cvp
S1, BEGINNING OF SYSTOLE.JUST BEFORE C WAVE ON CVP AFTER qrs

Pathologic splitting:
due to increased RV volume
o R L ASD or pulm stenosis

CVP waveform
a wave:
o end diastole
o atrial contraction
c wave
o early systole
o isovolumic ventricular contraction, TV moving toward RA
x descent
o mid systole
o atrial relaxation
v wave
o late systole
o systolic filling of atrium
y descent
o early diastole
o early ventricular filling

LV perfusion pressure = aortic DP = LV EDP

Who gets echo?
Pt w/ intermediate or high risk elective surgery, < 4
METS

Coronary distribution
LCX: V5-V6, aVL (perpendicular to left lateral wall)
LAD: V1-V4, V5-V6
RCA (inferior MI)
o II, III, aVF
5 ways to Increase coronary perfusion
Increase aortic diastolic pressure
o Con: afterload, LV wall tension and O2 consumption
Decrease LVEDP
HR
Decreasing contractility
Dilating coronary arteries

Ryanodine receptor: calcium-induced calcium channel

Locked open in MH

Contraction of myocardial cells

Troponin/tropomysin normally prevent interaction of actin and myosin
Troponin has 3 subunits: I, C, T
Calcium causes conformational change and actin can interact with
myosin
ATP is required for release of myosin from actin

ANTI-ARRHYTHMICS:
Amiodarone: Class III antiarrhythmic K-blocking agent
Delay phase 3 repolarization
Also has some Class Ia, II and IV effects
AV nodal blocking agent
Large Vd (requires bolus + drip)
o 150 mg bolus (over 15 min)
o Drip: 1mg/min over 6 hours
Side Effects:
o Pulm fibrosis
Restrictive lung disease ( DLCO)
o Hypothyroidism
o Transaminitis and jaundice
o Peripheral neuropathies

Myocardial Wall tension: La Places Law

T = Pr/2h
Wall tension is largest component of cardiac O2 DEMAND
 WALL THICKNESS WITH THE SAME RADIUS / PRESSURE WILL
TENSION

POISEUILLES LAW: Laminar Flow

Q= (pi P r^4)/(8nl)
o The longer the tubing or higher viscosity.slower the flow

Boyles Law: P1V1 = P2V2

Pascals Law: pressure = density x gravity x height

Primary source of SVR = arterioles

Other sources of resistance
o Aortic impedance
o Arterial pressure wave reflection
o viscosity
o Negative intrathoracic pressure

SVR = [(MAP CVP) / CO] x 80

Preload decreases with HR

Preload = LVEDV (estimated by LVEDP)
o preload = Stroke volume

Cardiac index increases up to 120 then falls

Max for kids = 150
As HR , SV

CI is maximized at HR of 90
SV is greatest at HR 60

Distribution of CO: Liver > kidney > brain

High: Liver, muscle, heart/lungs, kidneys
Medium: brain, intestines
Low: skin, other organs

Von Bezold-Jarisch reflex

 Mechano/chemo receptors fire in the setting of low pressure
Vagal afferents lead to bradycardia/hypotension/coronary vasocilation
Can occur w/ sudden in preload or after MI w/ coronary reperfusion

Brainbridge atrial reflex

Paradoxical tachycardia in response to fluid bolus
MOA: vagal tone

Vasovagal reflex
Stimulus from mesenteric retraction or distention leading to vagal
afferents, sending signal to brainstem and then the brainstem (nucleus
tractus solitarii) sending out vagal efferents w/ resultant bradycardia,
hypotension, apnea

Baroreceptor reflex
blood pressure will lead to firing of action potentials from
barorecptors in carotid sinus
Afferent signal carried by: Hering nerve (glossopharyngeal)
Net effect: inhibition of sympathetic activity, parasympathetic
outflow, HR, contractility, vascular tone

Alpha-mediated vasoconstriction:
Alpha-1: Gq receptor phospholipase C activated
o PLC IP3 formation. IP3 allows calcium release from SR into
cytosol
Phenylephrine alpha-1 receptor PLC IP3 Ca release from SR
contraction

Beta-2 agonism: cAMP production, Ca reuptake into SR from cytosol and

contractions
Beta-2 R -- cAMP uptake of Ca back into SR contraction

Nitric Oxide: endothelium-derived relaxing factor

Produced by endothelial cells by nitric oxide synthase.diffuses to
smooth muscle cells, activates guanylate cyclaseproduced cGMP
o Controls regional blood flow
 contractility
Inhaled: improves VQ mismatch by interrupting hypoxic pulm.
Vasoconstriction
Ultra short acting: < 5 sec

Inhibitors of ADH release:

Hypervolemia ANP
Ethanol
ADH
Hypovolemia, plasma osmolality
Angiotensin II
Cholecystokinin
Pain
nicotine

Starling Equation
Q = kA * [(Pc Pi) + (i c)]
o Q = net filtration
o K = capillary coefficient of water
o = reflection coefficient (of albumin)
o Pc = capillary hydrostatic
o Pi = interstitial hydrostatic
o i = interstitial colloid osmotic pressure
o c = colloid osmotic pressure

Action Potential of cardiac cells

SA node: Phase 1, 3, 4
Myocardial
o Phase 0: activation of fast Na channels
o Phase 1: early rapid repolarization, fast
Na channel inactivation, K
permeability
o Phase 2: PLATEAU phase Ca2+
channels opening, prolonging AP
o Phase 3: Ca2+ channels and K permeability
 Automaticity of SA node is depressed by volatile agents
o MOA: indirectly release of calcium from sarcoplasmic retic
o Opioids AV nodal conductance.lesser affect on SA node

1 = atrial systole (in late diastole)

o a wave
2 = superior displacement of AV valve during ventricular systole
o isovolumic contraction
3 = inferior displacement of AV valve during late ventricular contraction
o x descent
4 = pressure buildup w/in atrium due to venous return
o v wave
5 = AV valve opening allowing
ventricle fill
o y descent

SVR= afterload
Arterial impedence to ejection of blood
Afterload = Vaso-elastic properites of aorta + arteriolar tone +
density/viscosity of blood + returning pulse waves in blood
SVR is only the arteriolar tone

Acidosis will most affect heart contractility

Diastolic dysfunction
Higher LVEDP
Pulm edema
a/w concentric hypertrophy (from high pressures)
E to A ratio < 0.8 (E less than A)
o Doppler pattern across mitral valve demonstrates characteristic
patterns of early diastolic flow (E) and peak atrial flow (A)
A wave larger than E wave only consistent w/
impaired relaxation
Acute MI 2/2 PDA occlusion, left-dominant coronary circ -- > Q waves in
lead III
Right ventricle is perfused in diastole/systole (b/c RV systolic pressures are
less than aortic diastolic pressure)
Endocardium is more likely to suffer ischemia
presenting w/ ST depressions

V-fib
Chest compressions
Defibrillation at 360 J monophasic or 200 biphasic
Unstable A-fib
Cardioversion with biphasic 120 J
SVT
6 mg adenosine then 12 mg (twice) then cardioversion

Mitral Regurgitation
Diagnosis via Echo:
o Regurgitant jet > 2/3 length of left atrium
o Regurgitant stroke volume > 65 cc
o Pulmonary vein flow reversal during systole
Results in eccentric hypertrophy due to volume overload
Goal of management:
o regurgitant SV, favor forward flow
o Afterload reduction!
o High HR (80-100) is goal
Low HR. diastolic timecan further distort annulus
Pressor Choice
o Neo: may worsen by SVR and HR
o Levophed: although modest in HR, primarily alpha-1
o Esmolol: HR regurtitant fraction

Flow through CPB circuit

Venous cannula in right heart to venous reservoir
Oxygenator
Heat exchanger
Main pump
Arterial filter
Aortic cannula back to pt
Hemodynamic changes with CARDIAC TAMPONADE
Clinical Signs:
o BECKS TRIAD
HYPOTENSION
JVD
Muffled Heart Sounds
o pulsus paradoxus: SBP of 10mmHg during inspiration
o Kussmauls sign: distension of jugular veins in inspiration
EKG signs:
o Low amplitude QRS, ST changes
o ELECTRICAL ALTERANS
Echo:
o Diastolic dysfunction w/ impaired right heart filling
o Equalization of diastolic pressures
o Pericardial effusion
o Low Cardiac output
Angiogram:
o Equalization of mean RA, RV diastolic, PAWP
CVP: Prominent x descent + Blunted or absent y descent
PA catheter: y descent
Emergency Management:
o Ensure adequate oxygenation and ventilation
o VOLUME expansion (hemodynamic compromise is 2/2 preload)
o Inotropic support
o Open chest if post heart surgery
o Subxiphoid pericardiocentises

CVP waveform in constrictive pericarditis

Steep y descent as rapid early filling of RV occurs
Prominent a wave

CARDIO-PULMONARY BYPASS
Benefits of Off-pump bypass:
Decreased pulm infections
incidence of A-fib
less inotrope use
 fewer blood transfusions

Bypass access: Aortic cannula > Venous > aortic clamp

Resistance to heparin when starting bypass

Likely AT3 deficiency
Heparin works by accelerating action of AT3 inhibition on thrombin and
factors 9/10
Tx: Transfuse FFP.will give AT3

Effect of cross clamping Aorta

MAP
segmental wall motion abnormalities
LV wall tension
EF, CO, RBF
CVP
CBF

Protamine side effects

Anaphylaxis in pts w/ prior exposure or using NPH insulin (not regular
insulin)---often not responsive to epi
Allergy to fish, prior vasectomy
Dose dependent effects on mast cell degranulation
Heparin-protamine complexes activate complementresults in
thromboxane release from macrophages

Digitalis Toxicity:
PVC (bigeminy MC), Salvador Dali mustache sign on ECG
AV nodal block
Anorexia/nausea
Exacerbated by:
o Hypokalemia
o Hypomag
o Hypoxia
o Hypercalcemia
BETA-BLOCKERS
1) Beta-1 Receptor: Myocardium
STIMULATION: HR, contractility, conduction velocity & CARDIAC
OUTPUT
2) Beta-2 Receptor: Skeletal/coronary arteries, bronchioles, uterus, kidneys,
liver
STIMLATION: Vasodilation, bronchodilation, uterine relaxation, renin
secretion, glycogenolysis, gluconeogenesis

Clinical effects of BETA BLOCKERS:

ANTIARRHYTHMIC: Sympathetic input
B2: bronchospasm
Antinociceptive properties, opioid doses
flycogenolysis and glucagon secretion (lower glucose levels)
aqueous humor secretion from ciliary epithelium (beta 2 agonism
increases production)
production of renin/aldosterone release
Beta 1 agonism in macula densa: renin productionangiotensin/ANG II
formation
peripheral conversion of T4 to T3

BB w/ ISA
Penbutolol
Pindolol
Acebutolol (beta-1)

Beta-1 Selective Beta-blockers:

Metoprolol
Atenolol
Acebutolol
Bisoprolol
Esmolol
NON-Cardioselective
Propranolol
Nadalol
Pindolol
 Timolol
Sotalol
Fenoldapam= selective dopamine-1 receptor agonist (vasodilator)
Can be used instead of sodium nitroprusside
o NO thiocyanate toxicity, rebound effect or coronary steal
o Does contain sodium bisulfite

PCWP > LVEDP: Mitral stenosis, atrial myxoma, PEEP

PCWP < LVEDP: Non-compliant LV, LVEDP > 25, AS leading to mitral closure

Pulmonary Hypertension Treatment

Prostacyclin
o Epoprostenol (PGI2)
o Treprostinil
o Iloprost
Endothelin receptor antagonists
o Sitraxsentan, bosentan
PDE-5 inhibitors
o Sildenafil, tadalafil
Alprostadil (PGE1)

Best to treat hypotension:
o NEO
o VASOPRESSIN
o NOREPI
o Maintain preload & contractility

Risk of post-op Afib in CT surgery ( sympathetic stimulation in the setting

cardiac inflammation & ischemia, electrolyte abnormalities)
Age > 60
Male
Preop tachy
Hx of Afib
post op CO
post op BNP
SVT:
Standard Tx: Adenosine
In pts w/ asthma or on dipyrdamole: verapamil, digoxin or BB are drug
of choice

WPW
Short PR int, wide QRS, delta wave
Accessory pathway (bundle of Kent)
AVNRT: most common tachydysrhythmia
o DOC: Procainamide or amio
Avoid drugs that slow conduction thorugh AV node
o CCB, BB, dig, adenosine

Antiplatelet drugs:
ASA: Cox inhibitor
Dipyridamole: adenosine reuptake inhibitor
Plavix: ADP receptor inhibitor
Ticlodipine: ADP receptor inhibitor
Abciximab: GIIb/IIIA inhibitor

Mitral regurg goals: ( CO by SVR & HR)

Preload:
Afterload:
Contractility:
Rate: -- Avoid bradycardia ( regurgitant volume)
Rhythm: controlled
Best tx for hypotension: dobutamine

Promote vasodilation & mild tachycardia. Allows reduction of afterload

& effective forward flow of blood from LV to aorta vs regurg.

Aortic Insufficiency goals:

Preload:
Afterload:
Rate:
Rhythm: controlled
Aortic Stenosis goals:
Preload: Full
Afterload: Maintain coronary perfusion
Contractility: Inotropic support if persistent hypotension
Rate: Avoid bradycardia (CO) & tacghycardia (ischemia)
Rhythm: Sinus

HOCM goals:
Preload: Full
Afterload:
Contractility: , avoid inotropes
Rate: Normal
Rhythm: sinus, atrial pacing if required

TEE: Best intra-op view for MI:

Transgastric mid-papillary left ventricular short-axis view Can
visualize LAD, CX & RCA

Mid-esophageal 4-chamber view: anterolateral LAD/CX & inferoseptal

(LAD or RCA) walls only
Long axis view: anterior septal (LAD) *& inferolateral (CX or RCA)
2-chamber view: anterior (LAD) and inferior (RCA) walls

In-hospital, witnessed cardiac arrest (assume V-fib)

One biphasic shock then 5 cycles CPR (30 compressions/1breath)
Out-of-hospital: 5 cycles CPR prior to checking EKG/shocking
PACEMAKERS:
DOO: simplest pacemaker setting
o R on T phenomenon exists if native HR exceeds programmed
rate or w/ frequent PVC, PACs
Pacemaker failure: 3 causes
o Generator failure
o Lead failure
Undersense, oversense, loss of capture
o Abrupt in pacing threshold
Myocardial ischemia, infarct
Acid-base disturbance
Electrolyte abnormalities
Antiarrhythmic drug levels
Amrinone & milrinone are both PDE3 inhibitors = cAMP
Milrinone has less THROMBOCYTOPENIA

ALPHA STAT VS PH STAT

Partial pressure of CO2 as temp
pH-stat: goal to maintain pH of blood at 7.4 regardless of temp
alpha-stat: goal to maintain electrochemical neutrality of the imidazole
buffering system
o temp of patient is not required
As temp , PaCO2 w/ ph stat vs alpha leads to CBFE

Common acid base disturbance after Cardiac arrest: Resp. acidosis +

metabolic acidosis
M5 Endocrine/Allergy 4/29/2016 7:09:00 PM

Effects of Insulin
protein synthesis
Glut-4 transporter (translocation to cell surface
Glycogenesis
glycogen destruction
gluconeogenesis
activity of Na/K/ATPasewhich decreases serum K

Insulin Receptor:
Tyrosine kinase receptor
o Adds phosphate to tyrosine residues of proteins
Downstream signaling
o Activation of protein kinase B
o PIP 2 PIP3
(no cAMP involved directlybut cAMP does insulin secretion)

What cAMP?
Beta agonism
Phosphodiesterase inhibitors inhibit cAMP breakdown

Insulin:
SQ:
o Onset: 15 min
o Peak: 1-2 hr
o Duration: 4-6 hrs
IV
o Onset: 1 min
o Duration: 1 hour
NPH:
o Onset: 2-4 hrs
o Peak 4-10 hrs
o Duration: 18 hr
Glargine:
o Onset: 2-4 hour
o Duration: 24 hrs
 1 unit of insulin should glucose 25 points (goal glucose < 180)

Hyperglycemic hyperosmolar State

More common in type 2 diabetes
Glucose > 600 g/dL
pH > 7.3, higher serum bicarb, osmolality > 320
no serum or urine ketones
Tx: hydration, insulin, replete K

Diabetic ketoacidosis
Due to deficiency in insulin and excess counterregulatory hormones
(such as glucagon, catecholamines, cortisol, growth hormone)
HyperK (but total body K LOW)
Lipolysis FFA
Tx:
o Fluid resuscitation
o Correct K
o Insulin (bolus 0.1-0.2 U/kg) then drip
o Add 5% dextrose to fluids when glucose normalizes

Hyperthyroidism
Avoid Ketamine, ephedrine, pancuronium
Esmolol gtt often used for hemodynamics
o Also helps conversion of T4 to T3
Goiter = awake FOB
Pre-op: Tx w/ K iodide & propranolol

Hypothyroid
Heart: CO, HR, SV
Lungs: pleural effusions -- restriction

Recurrent Laryngeal nerve innervates all but 1 muscle of VC (cricothyroid)

Unilateral damage: hoarseness
Bilateral damage: stridor/aphonia
Average time to complications after thyroid surgery:
RLN injury - essentially immediately after surgery
Hematoma - typically within first 24 hours
Thyrotoxic storm - 6-24 hrs
Hypocalcemia/hypoparathyroidism - average 24-72 hrs

Post-op hypoparathyroidism
calcium
presents 6-12 hrs post-op

Cushing Syndrome
Due to primary tumor in adrenal gland, ACTH secretion
Pituitary = DISEASE
Tumors = ectopic ACTH syndrome
Results in:
o Insulin resistance/hyperglycemia
o Hypertension 2/2 hypervolemia
o Osteoporosis
o Hypokalemic alkalosis
o sensitivity to muscle relaxants
o difficult intubation 2/2 obesity/swelling
o
Supplemental steroids:
Normal production: 300 mg cortisol/day when max stressed out (20mg
on normal day)

Pheochromocytoma
Most are solitary tumors on 1 adrenal glad (right side)
o 5% MEN IIA (medullary carcinoma of thyroid, parathyroid
hyperplasia) or IIB (medullary carcinoma of thyroid)
alpha-blocker: 10-14 days before surgery
o phenoxybenzamine: long-acting (24-48 hrs), noncompetitive
presynaptic (alpha 2) and postsynaptic (alpha 1) blocker
o Doxazosin-selective alpha1 blocker
Drugs to avoid
o Ephedrine/ketamine
 o Drugs w/ vagolytic activity
Pancuronium
o Histamine releasing drugs
Morphine, Meperidine, reglan, glucagon, naloxone
Ligation of adrenal vein hypotension as it removes the
catecholamines

Carcinoid Syndrome
Release vasoactive substances (serotonin, kallikrein, histamine) which
lead to hypotension/bronchospasm
S/Sx:
o Flushing/diarrhea
o Some have bronchospasm
o Tricuspid regurg
Chronic effects
o Fibrotic patches on right heart
o Tricuspid regurgitation/pulm stenosis
Anesthetic management
o Avoid catecholamine surges
o Avoid hypotension
o Avoid histamine releasing drugs
Morphine/meperiddine
o Octreotide gtt may release of carcinoid mediators
o
Anaphylactoid vs anaphylaxis
Both result in mast cell release of histamine, tryptase, proteoglycans
Anaphylaxis IgE mediated
Tx:
o Volume
o Epinephrine
o H1/H2 blockers
o Steroids
o Refractory to all medsadd glucagon if on beta blocker

Rheumatoid Arthritis
Atlanto-axial instability: 25%
 Pericarditis, endocarditis, valvulitis and LVH w/ diastolic dysfunction
Vasculitits, MI, conduction block, stroke

Diabetes Insipidus: Central vs Nephrogenic vs Neurogenic

Dilute urine, dehydration, hyperosmolality, hypernatremia
Tx: Fluids, Vasopressin, desmopressin

SIADH: Hyponatremia + concentrated urine

Tx: Free H20 restriction, diuretics

Primary Hyperaldosteronism (Conn):

Aldosterone excess = sodium absorption K or H excretion in renal
tubules
Hypertension
Low RENIN due to inhibition by high levels of aldosterone
High urine K excretion (>30 mEq/d)
Hypokalemic alkalosis
Inability to concentrate urine = hypokalemic nephropathy
weakness
Secondary Hyperaldosteronism
high renin
M5 Equipment/Physics 4/29/2016 7:09:00 PM

O2 cylinder:
625 L
2200 psi
Critical temp: -119C
US color: White
Nitrous oxide
1590 L
745 psi
Critical temp 36 (above RTbelow this temp exists as liquid)

Safety:
Pin index safety system (PISS): E&H cylinders
Wall connections: Diameter index system (DISS)
Color coding

What can cause rebreathing?

Channeling
Malfunction of inspiratory or expiratory valves

W/o CO2 absorbent, minimal gas flow to prevent rebreathing = 5L

CHARACTERISTICS OF COMPRESSED GASES STORED IN E SIZE

CYLINDERS
Gas Cylinder E- Cylinder Cylinder Pressure Form in Crit
color Cylinder weight weight (psi) cylinder temp*
Capacity empty full
(L) (kg)
O2 Green 625 5.9 6.76 2200 Gas -120
C***
Air Yellow 625 5.9 1800 Gas -140 C
N2O Blue 1590 5.9 8.8 745- Liquid & 36 C
750** gas
CO2 Gray 1590 5.9 8.9 845 Liquid 31 C

What prevents delivery of hypoxic mixture?

 DISS
Oxygen supply failure alarm
Fail safe mechanism prevents N20 from entering circuit if O2
PRESURE IS TOO LOW
O2 manifold downstream the other gas flowmeteres
Flowmeter proportioning system

OXYGEN ELECTRODES
Clark Electrode: polar-graphic electrode
Amount of current correlates to concentration of O2
Consumable parts
Needs frequently calibrated (electrode gels are consumed)
Anode: silver
Cathode: platinum or gold

Paramagnetic Device
no consumable parts
faster response time
self-calibrating
more expensive

Anode: Lead
Cathode: silver or gold

Mapleson Circuits low yield

http://www.frca.co.uk/SectionContents.aspx?sectionid=149

Capnography:
http://www.capnography.com/new/index.php?option=com_content&vie
w=article&id=99&Itemid=61/

Electrical Safety
Line Isolation Monitors (LIMS): measures the amount of current that
could flow if a second short circuit should develop and sounds the
alarm if current exceeds 2mA or 5mA
Microshock: 10-100 microampere

What is necessary for fire

Oxidizing Gas + fuel + ignition source

Vent Check

Overside blood pressure cuff:

Width > 40-50% the circumference
Width > 20% diameter
Normal bladder length should encircle 60% of the arm

Add 0.7mmHg for ever

Capnography:
Phase I:inspiration, expiration starts
Phase II: Expiration continues
Phase III: peak of expiration
Phase IV: beginning of inspiration

A: Prolonged Phase II, II, increased angle, and steeper phase III suggest
bronchospasm or airway obstruction.

B, Expiratory valve malfunction resulting in elevation of the baseline, and

the angle between the alveolar plateau and the downstroke of inspiration is
increased from 90. This is due to rebreathing of expiratory
gases from the expiratory limb during inspiration.

C, Inspiratory valve malfunction resulting in rebreathing of expired gases

from inspiratory limb during inspiration (reference 5 for details).

D, Capnogram with normal phase II but with increased slope of phase III.
This capnogram is observed in pregnant subjects under general anesthesia
(normal physiologic variant and details in reference 9).

E, Curare cleft: Patient effort. Or surgical movement.

F: Rebreathing EtCO2
G: Esophageal intubation
H: Spontaneously breathing
I: Dual capnogram after lung transplant. First peak from new lung, second
peak from native lung.
J: MH
K: Ripple effect during expiratory pause w/ cardiogenic oscillation
L: Sudden raise in baseline and ETCO2 due to contamination of sensor or
water vapor.
M: Intermittent mechanical ventiatlion w/ spontaneous breathing.
N: CPR
O: Rebreathing during inspiration. Normal in Mapleson D or Bain
(rebreathing circuits)

EEG findings:
Deep sleep: low frequency delta waves, increased amplitude

Osborne Waves--> HYPOTHERMIA

Spectra Edge = method of processing complex raw EEG data into simple
term, which is the frequency at which 95% of the power exists below.

SSEPs:
Peripheral nerve--> dorsal column--> sensory cortex
Meds w/ little effect: Opioids, ketamine, etomidate, droperidol
Look at Miller Table 38-9
Etomidate can latency and amplitude
Sensitivity to volatiles from least to most: BAEPs > SSEPSs> MEPS >
VEPS
Neuro 4/29/2016 7:09:00 PM

CBF in pt w/ iso: 10cc/100g/min

CBF w/ halothane: 18-20cc/100/min
CBF w/ enflurane: 15cc/100g/min

Nitrous:
CMRO2
CBF
cerebral vasodilation

Halo/Iso/Sevo/Des
CMRO2
CBF if > 1 MAC
Cerebral vasodilation

PaCO2 20-80:
CBF 1-1.5cc x 100g/brain wt/min for each 1 mmHg in PaCO2D
CBV 0.05 cc x 100g/brain wt/min for each 1 mmHg in PaCO2

Spinocerebellar Tract

Cerebral blood flow & CMRO2
Inhaled anesthetics: cause uncoupling & CBF
o Halothane the most
CBF: Propofol/etomidate/thiopental

EEG
Delta rhythm (03 Hz) Deep sleep, deep anesthesia, or pathologic
states (e.g., brain tumors, hypoxia, metabolic encephalopathy)
 Theta rhythm (47 Hz) Sleep and anesthesia in adults, hyperventilation
in awake children and young adults
Alpha rhythm (813 Hz) Resting, awake adult with eyes closed;
predominantly seen in occipital leads
Beta rhythm (>13 Hz) Mental activity, light anesthesia

Treating VAE:
Stop more air entrapment
o Flood field w/ fluid
o Bone wax etc
o Compress IJ vein
Aspirate
Turn off Nitrous
Cardia support

SSEP path
Dorsal column
Brain stem
Medial lemniscus
Internal capsule
Contralateral somatosensory cortex

Do NOT evaluate corticospinal OR Ventral/lateral spinothalamic tracts

PEDS 4/29/2016 7:09:00 PM

Normal VS:
Preterm: HR 160, SBP 50, DBP 30, RR 50
Term: HR 130, SBP 60, DBP 40, RR 50
1 YR: HR 120, SBP 80, DBP 60, RR 25
Toddler: HR 90, SBP 100, DBP 60, RR 20

Blood Volumes:
Newborn: 90 cc/kg
Infant: 75 cc/kg
Toddler: 70 cc/kg

ABG:
Birth: pH 7.2, paO2 50, paCO2 50
1 wk after birth: pH 7.4, paO2 70, paCO2 35
Toddler: pH 7.4, paO2 95, paCO2 40

Normal umbilical artery blood gas:

pH 7.3, paO2 20, paCO2 50

Normal umbilical VEIN blood gas:

7.35, paO2 30, paCO2 40

Fetal circulation: placenta --> vein --> heart --> arterial --> placenta

F-Hb (fetal hemoglobin) --> affinity for oxygen. Unable to bind 2,3 DPG
P50 = 19 (adult = 27)

Prior to birth: placental oxygenated blood is delievered via UMBILICAL VEIN

thorugh LIVER (& ductus venosus) to IVC and into RA.
Blood from IVC has HIGH O2 tensions, blood from SVC has LOW O2
tensions.
Blood from IVC--> foramen ovale--> LV --> AORTA --> Mixes w/
deoxyganed blood from ductus arteriosis.

Failure of PDA to close:

persistent pulm HTN
After birth, high oxygen tensions causes PVR to fall, blood will now flow
through pulm circulation and NOT ductus arteriosus.

Patent Ductus arteriosus:

machine-line continuous murmur at LUSB, bounding pulses, widened
pulse pressure
Usually left to right shunt
Before 60 weeks post-conceptual age, an infant should have a
minimum of 12 hours apneic free before discharge

Infants desaturate quickly due to VO2 as well as a lower FRC

Infants have a FASTER inhalation induction due to INCREASED MV/FRC ratio

Neonatal ratio: 5:1
o Why so high? b/c O2 consumption is higher w/ same/lower
FRC
Adults: 1.5:1

Neonatal diaphragm25% type 1 fibers (vs 55% in adults)

Type 1 fibers: fatigue resistant (twitch)endurance

Both hypoxic and hypercarbic drives are immature at birth

Neonates have chest wall compliance

FRC = point at which outward elastic recoil of chest matches inward recoil of
lung (at end-expiration)
Both decreased in neonates
FRC

Pediatric Upper Airway differences

Head is proportionately largersniffing position is harder
o Use shoulder roll
Glottis is at C4 instead of C6
Cricoid cartilage = narrowest portion

Normal neonatal glucose can be as low as 30

 After day 1 of life: Hypoglycemia = < 45

Spinal Anesthetic in Infant:

Spinal cord ends at L3
o After 1 year it ends at L1
Dural sac ends at S4 in neonates
o S2 for 1year-adult
Ropivicaine is less cardiotoxic than bupivacaine
Neonatal Ventilation
HFOV: High frequency oscillatory ventilation
SIMV or AC
ECMO
Bronchopulmonary dysplasia is a continuum of RDS

Lecithin-sphingomyelin (L/S): 2.0 = sufficient surfactant production

L/S 1.5

Propofol (lipophilic) redistributes faster in neonates due to blood volume

PRIS:
Inhibits proteins that allow transfer to FA into mitochondriamito are
starved of energy
Lactic acidosis..necrosis

Infants are more sensitive to opioids/benzos/barbiturates

Thiopental/propofol: sensitivitydue to BV

INFANTS REQUIRE DOSE OF SUX COMPARED W/ KIDS DUE TO Volume

of distribution and they dont have sensitivity to sux as they do other NMB

Masseter muscle spasm in MH: 30%

Put pulse ox on right hand in infants (PRE-DUCTAL)

Retinopathy of prematurity:
 Pathophysiology: retinal artery constrictionproliferation of abnormal
vesselts resulting in scar/hemorrhage and retinal detachment
Risk factors:
o O2
o Genetic: sex/Caucasian

Post-anesthetic apnea in newborn

Definition: apnea for 15+ sec or apnea of any duration resulting in
desat or bradycardia
Delay elective surgry until 44-60 weeks
Pulmonar surgery: 6 months
Risk of apnea w/ caffeine or aminophylline

Chemical pneumonitis
Pulm edema
Hypoxia
Pulmonary hypertension

ACLS FOR NEONATE:
Hypoxia w/o bradycardia--> supplemental O2
HR < 100 --> ppv
HR < 60--> Chest compressions at 120min but FIRSTmask ventilation
Chest compression:ventilation ratio = 90:30 (3:1)
o Adults = 3:2
Epinephrine:
o Tracheal epi: 10 x the IV dose 0.1mg/kg
o IV: 0.01-0.03 (ALWAYS USE 1:10,000 for IV)
APGAR
Appearance
Pulse
Grimace
Activity
Respiration

Omphalocele: midline, covered by sac

Necrotizing enterocolitis pressor of choice = DOPAMINE
Most common TEF: IIIB = proximal esophageal atresia, distal fistula
2nd Most common: Esophageal atresia
3rd most common: H-ype (fistula between trachea and intact
esophagus)
o Associated w/ VACTERL type V
Vertebral
Anal defects
Cardiac (VSD,ASD, TOF)
TEF
Esophageal atresia
Renal/radial atresia
Other limbs
Pyloric stenosis --> metabolic alkalosis
Hypochloremia, hypokalemia (early)
o Respiratory compensation: MV, retention of CO2
Late: acidotic

Tetralogy of Fallot
Most common CHD
4 features:
o VSD
o RVH
o Over-riding aorta
o Right ventricular outflow tract obstruction
ECG: RAD, RVH
CXR: pul vascular markings, rt aortic arch
Tet spell: hypercyanotic attack, peak 2-6 mo (feeing, crying,
defecating)
o SVR = hypoxemia
Tx: O2, chest-knee position, morphine
o Anesthetized pt: SVR = Lft to right shunt (Neo, BB, fluids)
Hemodynamic goals:
o preload
o Slow sinus rhythm
o contractility
o SVR
 o PVR
ANESTHESIA:
o No spinal! Early epidural is goodmay PVR

Down Syndrome:
CHD
ASD
Upper Airway Obstruction/Sleep Apnea
Hypothyroidism

NPO guidelines
Clears: 2 hrs
Breast milk: 4 hours
Infant formula: 6 hours
Solids/non-human milk: 6-8 hrs

Post-op Apnea in preterm infants

Risk varies inversely w/ age at birth & postconceptual age
Post-conceptual age is the single most important determinant of postop
apnea
Anemia (Hct < 30%)
Small for gestational-age infants have risk of post-op apnea

Neonates/normal lab values:

Glucose: 5-90 (tx at 40)
Hemoglobin: 15-20
Creat: <0.8
Platelets: normal 250

PULM of neonate vs adult:

compliance of chest
TLC: 160cc (63cc/kg) [ Adult 6,000 cc]
TV: 21 cc/kg (vs 575 cc/kg in adult)
O2 consumption: 6-8 cc/kg/min (vs 3-4 in adult)
FRC ~ 30cc/kg due to laryngeal breaking = termination of exhalation
prior to relaxation vol.
LEFT RIGHT shunt
ASD
VSD
PDA

RIGHTLEFT shunt
Tetrology
Truncus
Transposition
Total Anomalous
Tricuspid stenosis
HEME 4/29/2016 7:09:00 PM
o Coag Cascasde

o
Platelet Function:
Adhesion:
GP 1b: vWF bound to collagen in exposed endothelium binds to GP 1b
Activation
Plt changes shape, exposing GP IIb/IIIa and degranulation of plt
Granules release thromboxane A1 and platelet activating factor which leads to
aggregation and vasoconstriction
Aggregation
GP IIb/IIIa BINDS TO FIBRINOGEN

Intrinsic Pathway (PTT/ACT): 12--> 11 --> 9 --> 8 --> 10 --> 5--> 2-->1

Extrinsic Pathway (PT): 3--> 7 --> 10--> 5--> 21

Factor 3 = Tissue factor (released by damaged endothelium) binds soluble factor
7..and then activates the rest of the cascade

Plasmin: protease that degrades fibrinlysing clot.releasing D-dimers
Plasminogen is activated by tPA
Amicar/TXA/Aprotinin are plasmin inhibitors

Platelet function: Bleeding time

Haemophilia A
Factor 8 deficiency, X-linked coagulopathy
50% activity required for minor surgery
100% required for major
Factor 8 concentrate: 40 units per cc
 Cryo: 5-10 units/cc (100 u per bag)
DDAVP upregulates natural production of Factor 8 and vWF

vWD
Type I: quantitative defect in vWF. Responsive to DDAVP
Type IIB: DDAVP can cause paradoxical thrombosis/platelet consumption
Type III: DDAVP is ineffective
Tx: Cryo, Humate-P (factor 8/vWF), FFP
Monitoring: bleeding time

Irradiation prevent graft vs. host

Leukoreductionprevent alloimmunitation/febrle reactions

UNIVERSAL DONOR = TYPE O POSITIVE

UNIVERSAL RECIPIENT = TYPE AB positive

PRODUCTS
RBC:
RBC 35-42 days at 2-6deg.
Stored blood: looses ATP, 2-3DPG, increased K
FFP:
Contains ALL plasma proteins and clotting factors
Frozen to -18 tp -30, volume 250cc, stored up to 1 year
ABO identical or compatible required
Indications:
o Rapid reversal of warfarin
o Correct factor deficiencies (if factor concentrates not available)
o Correct antithrombin III deficiency
o Microvascular bleeding (if received a lot of PRBC)
Transfuse w/in 6 hours

Platelets
Store at room temp (20-24)
ABO compatibility not necessary but compatible have longer lifespan
Indications not clear but rarely for count > 100,000
CRYO
Cold insoluble portion of plasma, remains after FFP thawed.
Contains (3): Factor VIII (100 IU), vWF, factor XIII, fibrinogen
Indications:
 o Hemophilia - Used for emergency back up when factor concentrates are not
available.
o von Willebrands's disease - Not currently recommended unless last reserve.
dDAVP is first line, followed by factor concentrates.
o Hypofibrinogenemia (<100)
o Bleeding from excessive anticoagulation - FFP contains most of the
coagulation factors, and is a much better choice when anticoagulation has to
be quickly reversed.
o Massive bleed - RBCs and volume expanders are preferred therapies.
o DIC
Administered as a pool of 4-6units.
Dosing: 1 unit per 10kg body weight (LBW)
o 1 unit contains 250 mg fibrinogen
o Increases fibrinogen by 50-75 in 70kg adult
o 1unit cryo= 3 units FFP (900 cc)
Transfuse at Room temp, NOT through warmer w/in 4 hrs

COLLOID VOLUME EXPANDERS (3)

Dextrans not used often 2/2 risk of anticoagulant properties
o High risk of anaphylactoid reactions
Hetastartch (Hydroxyethyl starch)
o Mild anticoagulant properties (>20cc/kg/24h)
o Coagulation Effects of Hydroxyethyl starch
Dilution
Reduction in factor VIII and vWF levels
Reduction in glycoprotein IIb/IIIa availability
Direct movement into fibrin clots
o Hextend is another hydroxyethyl with smaller units, which may not affect
coagulation as much as as Hespan
Albumin
o More expensive but well tolerated, low rates of infection/allergic reactions
o Inc. mortality in TBI pts

DRUGS
Argatroban/Lepirudin = direct thrombin inhibitor
Prevent fibrinogen formation at the last step in the cascade

Fondaparinus -= accelerates activity of antithrombin III, inhibiting on ly Factors Xa

Lovenox = accelerates AT3, inhibiting Factor Xa and thrombin

Abciximab/Eptifibatide =platelet glycoprotein IIb/IIIa inhibitor

Plavix =platelet ADP receptor (activation phase)

Warfarin = inhibits synthesis of vitamin K dependent clotting factors

Heparin = accelerates AT3 activitywhich inhibits thrombin and factors 9/10

Protamine = binds ionically to heparin, used for reversal
1mg Protamine neutralizes 80-100 u heparin, check efficacy with ACT
AE: Noncardiogenic pulm edema, pulm vasoconstriction, right heart
decompensation, cardiovascular collapse
Derived from salmon sperm--> hypersensitivity

Megaloblastic anemia & nitrous:

Irreversibly inhibits Vit B12

GPIIb/IIIa inhibitors: Tirofiban (Aggrastat)/abciximab/Eptifibatide (Integrellin)

Chimeric, monoclonal Ab, peptide (eptifibatide) & non-peptide
GPIIb/IIIa is a receptor that bings fibrinogen & vWF

Transfusion Reactions:
Massive transfusion
> 10u PRBC in 24 hrs
Replacement of half a patients blood volume in 3-4 hours
> 4 units in 1 hour
Metabolic complications
o Hyperkalemia
o Citrate toxicity
Binds Ca & Mg
Hypocalcemia: Hypotension, narrow pulse pressure, prolonged QT
int, inc. intraventricular EDP
o Metabolic alkalosis: citrate in stored blood is metabolized to bicarbonate by
liver via Krebs
o Avoid LETHAL TRIAD: Hypothermia Acidosis coagulopathy
Clotting factor deficiency:
o Dilutional
o Factor V & VIII have short t1/2 in FFP & not present in PRBC or platelets
Acute
TRALI: Non-cardiogenic pulm edema, hypoxemia, hypotension, fever, cyanosis
Leading cause of blood related mortality: 13-21% (35-58% in critically ill)
2 possible mechanisms:
o Immune: Reaction b/w donor anti-HLA or antileukocyte Abs & recipient
leukocytes sequestration in microcirculation of lungs capillary endothelial
damage/leak.
o Non-immune: transfusion of non-leukocyte elements, biologically active
lipids, cause alveolar damage
Risk Factors:
o Plasma-containing products (Plat > FFP > RBC)
o transfusion from multiparous female ( HLA)
o sepsis, liver disease, EtOH abuse, mechanical vent
Diagnosis: ALI + recent transfusion
o ALI:
Timing: Acute
Hypoxemia: PaO2/FiO2 </= 300 or SpO2 < 90% on RA
CXR: Bilateral infiltrates
Edema (not hydrostatic): No evidence of elevated LAP

TACO: Pulm edema 2/2 limited cardiac reserve

Signs of volume overload
Risk factors: extreme age, CHF, CKD, low albumin, pos fluid balance
Acute Hemolytic transfusion reaction
Anxiety, fever, urticarial, hypotension, DIC, hemoglobinuria, ARF
Infection:
Hep B: 1: 205,000
Hep C: 1 in 1,935,000
HIV: 1 in 2,135,000
M5 GI 4/29/2016 7:09:00 PM

ABG changes
Acute diarrhea: non-anion gap metabolic acidosis with hypokalemia
RTA type IV (aldosterone deficiency): non-anion gap acidosis w/ K

Thoracic epidural (T10) has been shown to reduce ileus

Advantages of AoBP in cardiogenic shock:

Afterload reduction
Aortic Diastolic pressure

NPO guidelines
2 hrs for clears (adults/kids)
Breast mild: 4 hours
Non-human milk/formula: 6 hours
Light meal: 6 hours
Heave meal: 8 hours

strength of LES
Anti-cholinergics: Glyco/scopolamine
Opioids
Thiopental
volatiles

Reglan is the only med that has proven to reduce gastric vlumes
H2/PPI gastric pH & reduce volume

LMAs LES tone

Propranolol
Nonselective, beta-1 antagonist ( HR, CO), beta-2 anagonist
(peripheral vasoconstriction, bronchoconstriction)
Portal Hypertension
Gradient between IVC and portal vein > 5
> 12mmHg = symptomatic

Child-Pugh score (score C = high perioperative mortality)
 Plasma albumin
Bilirubin
PT or INR
Ascites/encephalopathy

Hepatopulmonary syndrome (shunt)

Minimal increase in PaO2 w/ supplemental O2

Portopulmonary Hypertension
PAH + portal HTN
Mean PAP > 25
PAOP < 15

Refeeding syndrome:
Phos
Mg
K
Hyperglycemia

K EY FACTS : INTE STINAL MOTI L IT Y

Inhibited by pre-ganglionic sympathetic fibers (T8-L3) via celiac,
superior and inferior mesenteric ganglia
o Adrenergic alpha 1 receptor stimulationSphincter relaxation
o Adrenergic beta 2 receptor stimulationSmooth muscle
inhibition
o NorepinephrinePostganglionic sympathetic neurotransmitter
Mediated by beta-2 receptors
o Cholinergic response Vagus-end organ ganglia
o Smooth muscle contractionPredominant
o AcetylcholineParasympathetic neurotransmitter

Respiratory complications during laparoscopic surgery:

Gas Embolism:
o Desat, hypotension, tachy, arrhythmia, CVP, Right sided heart
strain, mill-wheel murmur
PTX:
 o Same as embolism but also w/ inc. PAP
Endobronchial intubation
Insufflation of gas into subcutaneous space
o
M5 Induction Agents 4/29/2016 7:09:00 PM

Induction agents receptors

GABA-A
o Barbiturates (Thiopental)
o Benzos
o Propofol
NMDA
o Ketamine (receptor antag)

Hypotension on induction with propofol

SVR ( afterload)
LVEDV ( preload)
SV ( contractility)
Impairs baroreceptor reflex

Pretreatment with opioid decreases myoclonus with etomidate

Vd = dose / concentration
Hydrophillic drug = small peripheral volume of distrubtion

Zero order kinetics

Constant amount of drug is cleared per minute
o Eg. Ethanol
Graph: linear
First order kinetics
Constant proportion is cleared per minute
Graph: geometric but if on logarithmic scale will be linear

Propofol is completely metabolized by the liver on a single passand
concentration post liver will be zero

G-protein mediated
Opioids
Alpha and beta agonists
Serotonin
Prostaglandins
histamines

Gprotein + PKA:
Beta receptors
Gprotein mediated decrease in cAMP
Alpha-2 and opioids
Gprotein + IP3

GABA-A: ligand gated ion channel

GABA-B: G-protein coupled

Barbiturate injection into an artery

Spasm and Prolonged vasoconstriction, limb loss
Normal effects:
o Vasodilation (w/o baroreceptor blunting)
o Hypotension
o Apnea
o Dec brain CMRO2 and CBF/ICP
o Decrease pain tolerance
Tx: Stellate ganglion block
Pulmonary Physiology 4/29/2016 7:09:00 PM

DRUGS NOT TO USE WITH ACUTE INTERMITTENT PORPHYRIA

Etomidate
Ketamine
Barbiturates
Diazepam
Phenytoic
Steroids
Pentazocine

Myotonic Dystrophy
Autosomal dominant
Myotonia = persistent contracture after muscle contraction or electrical
stimulation, progressive weakness/wasting due to abnormal calcium
metabolism
Steinerts disease (MD1) most common, (1:8,000)
Clinical:
o Pulmonary: cranial muscle weakness, aspiration, hypoventilation
o Cardiac: conduction abnormalities (AV blocks, cardiomyopathy)
o Inc. sensitivity to opioids
o Normal response to NDNMB
o Prolonged contraction w/ Sux
o Etomidate/Prop/methohexital and neostigmine may provoke
myotonia
o Myotonia w/ hypothermia, shivering, meds, electrical/mechanical
stimuli
Tx:
o Muscle infiltration w/ local anesthetic
o Phenytoin
o Procainamide
o Quinine (300-600mg IV)

SSEP: useful for sensory cortex supplied by MCA

Posterior tibial, median, ulnar nerve

Volatiles that impair autoregulation: H> E> I>S>D

0.77 mmHg decrease in BP for each cm difference in ehight
Myasthenia Gravis
Post-synaptic anti-nAChr Ab results in acetylcholine receptors at NMJ
80% pts seropositive
Skeletal muscle weakness occurs in response to exercise, improves w/
rest
Diagnose: Tensilon test, antibody titer (definitive)
o Tensilon test also used to differentiate cholinergic from
myasthenic crisis
Resistance to SuxDOA may be prolonged due to plasmapheresis
and/or pyridostigmine

Eaton-Lambert Syndrome
Antibodies to PREsynaptic voltage-gated Calcium channels results in
Ach release
Exercise improves strength
Anticholinesterases dont help
Strong association w/ neoplasm
Sensitive to both depolarizing and ND NMB

For morbidly obese patients..use LBW for induction doses of propofol and
TBW for continuous infusion
Use LBW for infusion of remifentanil
TWB for Sux

Direct thrombin inhibitor: Dabigatran

Osler-Weber Rendou syndromeassociated w/ 20% AVM

Drugs that Lithium toxicity:

Toradol
Lithium SE:
- Most common is tremor. Also hypothyroidism, DOWNBEAT NYSTAGMUS,
nephrogenic DI, headache, dazed feeling.
Patients with paraplegia have increased TOF responses to peripheral nerve
stimulation in paretic extremities when compared with normal extremities.

A child is undergoing general anesthesia that includes nitrous oxide being

delivered at 2 L/min from an E cylinder. The tank pressure has just started
to decrease. Which of the following is the BEST estimate of the remaining
amount of time that nitrous oxide can continue to be delivered?

Answer: 3 hrs

Review the RCRI

Use of insulin is strong predictor
Age is not risk factor
risk only w/ intrathoracic, intraperitoneal and aortic surgeries

Transient Neurologic Symptoms:

Independent of drug concentrations ranging from 0.5-5
Independent of lido dose
Unchanged by baricity
Most affected by position

Look up: VVE-DDDRV

Familial periodic paralysis (PP) is divided into hyperkalemic and

hypokalemic types. In the hyperkalemic type, sodium channel mutations,
triggered by increased serum potassium, cause attacks of flaccid paralysis.
In the hypokalemic type, either abnormal calcium or sodium channels,
triggered by low serum potassium levels, cause attacks of paralysis. Both PP
types are autosomal dominant. Exercise elevates serum potassium and
triggers attacks in patients with hyperkalemic PP. Glucose-insulin infusions
lower serum potassium and trigger attacks of paralysis in patients with
hypokalemic PP. Succinylcholine administration can cause prolonged muscle
paralysis but does not trigger life-threatening hyperkalemia in these
patients.

SIADH
 Na < 130
Plasma osmolality < 270
Urine is hypertonic relative to plasma
UOP is low or normal

Cerebral Salt Wasting Syndrome

Hyponatremia, UOP
Urinary sodium

Preop drugs for Acute porphyria

1. Diagrammatic representation of neuromuscular transmission. (1) Action
potential arriving at nerve terminal triggers opening of voltage-gated
calcium channels (VGCCs) and entry of calcium.
(2) Rise in intracellular calcium triggers release of packets of acetylcholine
(ACh).
(3) Interaction of ACh with ACh receptors (AChR) depolarizes postsynaptic
membrane.
(4) Voltage-gated sodium channels (VGSCs) open, triggering muscle action
potential.
(5) ACh esterase (AChE) breaks ACh into acetyl and choline, which are taken
up by the nerve terminal to be reformed into ACh.
(6) Opening of voltage-gated potassium channels (VGKCs) repolarizes nerve
termina

Parkland Formula:
4 cc x pt wt (kg) x % body burned
o Ant. Upper trunk/lower trunk/each leg = 9 %
o Entire arm/head = 9%

Tourniquet Use
Release can cause PCWP
Release of metabolic waste: CO2, lactic acid, K arterial pressure
minute ventilation
Long times can cause neuro injury, loss of motor function and rhabdo,
compartment syndrome

Oculocardiac Reflex = Aschner phenomenon

Afferent: Signal carried through cilliary nerves to ciliary ganglion
(behind orbit)
From ciliary ganglionit travels along 1st division of trigeminal nerve to
the trigeminal ganglion (gasserian ganglion)
Signal reaches trigeminal nucleus and communicates w/ vasomotor
enter leading to efferent vagal pathway producing bradycardia
Distractors:
o Geniculate ganglion: carries facial nerve impulses
o Petrous: carries some glossopharyngeal nerve impulses
 o Jugular ganglion: carries vagal/accessory impulses
o
Eye stretch receptors Short and long ciliary nerves Ciliary ganglion
Ophthalmic division of trigeminal nerve Gasserian ganglion
(sensory nucleus of cranial nerve V in the fl oor of the fourth ventricle)
Motor nucleus of vagus nerve in the floor of the fourth ventricle
Parasympathetic outflow via vagus nerve Heart

Hyperesthesia: sensitivity to stimulation, excluding special senses

Hyperpathia: painful syndrome, abnormally painful reaction to a stimulus,
repetitive stimulus, threshold
Dysethesia: unpleasant abnormal sensation, spontaneous or evoked
Paresthesia: Abnormal sensation, spontaneous or evoked

Most potent mineralocorticoid: prednisone/methylprednisone

Adrenal insufficiency: HYPOGLYCEMIA + blood ketones

Autonomic hyper-reflexia:
Common w/ injuries above T6
Hypertension + vasoconstriction
Baroreceptor-mediated reflex bradycardia + vasodilation
Visceral & muscle spasm, sweating, piloerection, uncontrolled motor
activity
Unmodulated sympathetic NS can lead to cerebral hemorrhage, seizure
Incompetent Inspiratory valve:
CO2
linearly prolonged expiratory plateau phase (III)
Prolonged phase I and progressively EtCO2 at baseline

HR values
< 24 h: 120
1-7 days: 135
1 week-1month: 160
3-12 mo: 140

Cardiac output: 200-325 cc/kg/min

BP
Neonate: 55-75/35-45
0-3mo: 65-85/45-55
3-6mo: 70-90/50-65
6-12 mo: 80-100/55-56

Hyperkalemia:
ECG:
o P amplitude
o Peak T waves
o Widened QRS
o Sinusoidal
Tx:
o Calcium chloride
o Insulin + dextrose
o Na HCO3
o Hypervent
o Inhaled beta 2
o Loop diuretics
o Kayexalate
o HD

Post-op 3rd degree AVB: DDD

METHEMOGLOBINEMIA
NORMAL PAO2 on ABG
SpO2 85%
methemoglobin levels on cooximetry
cyanosis
chocolate-brown colored blood

Loop diuretic in sulfa allergic = ethacrynic acid

Glasgow Coma Scale

Eye Opening: 4\
o Spontaneous
o Verbal command
o Pain
o None
Best Verbal response
o Oriented
o Disoriented
o Inappropriate words
Best motor
o Obeys verbal commands
o Localize to pain

TBI based on GCS

> 13 = mild
9-12: moderate
< 8 = severe

BURN PT: Resistance to NDNMB (due to receptors)

Anticholinesterase Poisoning
Parasympathetic stimulation:
o Miosis
o Abodminal cramping
o Excess salivation
o Loss of bowel/bladder control
 o Bradycardia
o bronchoconstriction

Benzodiazepines
Lipid solubility: Midazolam > Diazepam > Lorazepam
High protein binding
Midazolam is 2x, LORAZEPAM 5-6x more potent than diazepam
Versed:
o Metabolized in liver: oxidative hydroxylation to active 1- and 4-
hydroxymidazolam
o Active metabolites build up in renal failure
o Substrate of CYP450
o Versed itself is a weak inhibitor of CYP3A4

Post-op shivering:
Clonidine
Precede
Propofol
Ketanserin
Tramadol
Magnesium
Narcotics
Physostigmine

Ischemic optic neuropathy:

venous outflow and O2 delivery to optic nerve

Metabolites of alfentanil, meperidine, tramadol are prolonged in LIVER
failure

Meperidine and morphine: prolonged in kidney failure

Accumulated morphine-3-glucuronide may compromise analgesia

Receptors involved in PONV

D2
5-HT3
HI
Muscarinic
NK2I

ASA Definition of sedation

Minimal (normal response to verbal stim)
Moderate = Conscious sedation (purposeful response to verbal or
tactile stim)
Deep sedation
General anesthesia

Abdominal compartment syndrome:

Normal IAP 5-7 mmHg
Intra-abdominal HTN: 5-8
Compartment syndrome: > 20

Hypothyroidism:
A/w other autoimmune disease: SLE, RA, DM, hypoparathyroidism,
Addisons, amyloidosis
Cardiac changes due to diminished function of beta-adrenergic
receptors ( inotropy & chronotropy)
o Resulting imbalance favors alpha receptor activity = SVR,
diastolic pressure, pulse pressure
o afterload = o2 consumption
o prolonged QT
 o associatedwith autoimmune adrenal insufficiency is termed
Schmidt's syndrome

Radial Artery occlusion risks

Longer periods
Non-Teflon
Female
Size of radial artery
Hematoma at puncture site
# of attempts
ratio between outer diameter & vessel diameter

thrombosis is most likely to occur w/ in 48 hrs of decannulation

ANGIODEMA
Causes:
o Hereditary: C1 esterase deficiency
o PCN/sulfa drugs
o ACE inhibitors
o NSAID ( prostaglandin)
Treatment:
o Airway involvement: Epi, Benadryl, steroids, intubation
o Epsilon-aminocaproic acid & danazol may prevent in hereditary
form

Doxorubicin: Cardiomyopathy

Bainbridge reflex: HR due to CVP

Mediated by stretch receptors in atria, afferent impulses through vagus
to spinal medulla
Example: Autotransfusion after delivery

Baroreceptor reflex: bradycardia in response to MAP

Afferent: stretch receptors in walls of arteries/carotid sinus/aortic
bodies
o Nerve of Hering & Vagus nerve to Medulla
 o Result: HR bp contractility
o Exmample: Neo/Valsalva

Bezold-Jarisch: bradycardia, peripheral vasodilation, hypotension

Mediated by chemo & mechano sensitive receptors in ventricles
Afferent: unmyelinated vagal nerves

Propofol infusion syndrome

Metabolic acidosis
HyperK
Rhabdo

Best place to monitor core temp:

Nasopharynx
Tympanic membrane
Distal esophagus
Pulm artery

Bladder temp UNDERestimates in rewarming from cardiac surgery (risk
of hyperthermia)

PCN allergy
Cross-reactivity w/ cephalosporin due to common beta-lactam ring
Alternative: Vanc/Clinda

Loop diuretics (Lasix, bumex, ethacrynic acid)

Na, HC03
K, Cl, Mg
No change in calcium
Tx HTN in pregnant pt: Labetalol, hydralazine, nifedipine
Hydralazine SE: hypotension
o Neonate: thrombocytopenia, SLE-like syndrome
Labetalol: IV bolus has peak effect in 20 min, duration ~ 6 hrs
o SE: dizziness, nausea, HA, fetal brady
Methyldopa: only used for chronic HTN treatment in pregnancy
ACE: renal tubular dysplasia, craniofacial abnormalities & pulmonary
hypoplasia

VTACH in pediatric
w/ pulse = synchronized cardioversion
IV amio 5mg/kg over 20-60 min or 15mg/kg IV procainamide

4 conditions required for reentrant arrhythmia

 unidirectional blockade
2 areas of myocardiam w/ different conductivityform closed electrical
loop
sufficient length of circuit or slowed conduction that allows recovery of
the initially blocked path
restimulation of the initially blocked path by a retrograde impulse

Witnessed cardiac arrest w/ vifib = defibrillation immediately

Seizure duration and ECT

by caffeine
hypercapnia & hypoxia duration
pre-tx w/ glycol is common due to the parasympathetic discharge w/
ECT

Autonomic hyperreflexia
Commonly caused by bladder/GI distension
Ascending reflex via spinothalamic tract (sympathetic response)
Baroreceptors detect Hypertensive response in carotid sinus
Vasodilate ABOVE level of lesion but below is still vasoconstricted
Reflex bradycardia

vWF type I: DDAVP

LITHIUM: prolonged response to Sux & NDNMB

Inhibits neuromuscular transmission by activating K channels
initial dose
a/w HypoK & hypercalcemia, also may block effect of ADH on renal
tubules

Methemoglobinemia:
Produced when iron in Hgb is oxidized from ferrous to ferric
NADH reductase reduces to Hgb

Prilocaine (EMLA cream)

 Benzocaine
Nitroglycerin
Sodium nitroprusside
Nitric oxide
Phenytoin
o Typical toxicity: nystagumus, slurred speech, ataxia, drowsiness
Dapsone
Sulfonamides
Lidocaine

Left shift OHDC

Hypothermia
Alkalosis
Fetal Hgb
Methemoglobin
Carboxyhemoglobin
23 DPG
Right shift
Hyperthermia
Acidosis
Pregnancy
23DPG
Halogenated volatiles
Sickle Hg

General anesthesia both VO2 and VCO2keeping RQ the same

Hemidiaphragmatic paralysis most indices of pulm funcdtion by 25%.

INterscalene nerve block--> phrenic nerve palsyk

Normal resting intrapulmonary pressure: -5cmH20
During inspiration, pleural pressures are more negative
At end inspiration, airflow ceases, alveolar pressure raises to 0,
intrapleural pressure remains -9cmH20
Alveolar pressure raises from 0 to +4
Factors that FRC:
Restrictive lung disease
Obesity
Pregnancy
Posture
Height
Gender (men have more than women)

Closing capacity = Residual volume + closing volume

Does not change w/ obesity but since the ERV (and FRC) TV shift
down towards RV.TV now exist at a volume less than CC
CC w/ age w/ GA

Airflow: V= IR (solve for flow, I = V/R)

Laminar flow distal airwayswhere velocity is highest near center
Turbulent flow larger airways, branching points, higher velocities

Dead space = ventilation w/o perfusion

w/ positive pressure ventilation
COPD
Pulmonary embolism
Extreme hypotension

Compliance in spontaneously breathing patient: highest at base

Increasing CO will reduce A-a GRADIENT

DLCO
COPD
Sarcoid
Asbestosis
TB
Heart failure
Anemia
DLCO
 Exercise
Asthma
Polycythemia
Left to right intracardiac shunting
Pulm. hemorrhage

PFTs w/ COPD:
FEV1, ratio FEV1/FVC, FRC, TLC
Pregnancy
FRC ~ 500 cc due to
o RV
o ERV

Transpulmonary pressure: Alveolar (plateau) pressure pleural

(esophageal )pressure
Measure pleural pressure via esophageal pressure

Plateau pressure --> static lung compliance (alveolar pressure)

Pressure required to overcome elastic resistance to ventilation w/ no
gas flow (End inspiration)
Static compliance = Volume/pressure = tidal volume/(plateau pressure
PEEP)

Peak inspiratory pressure--> dynamic compliance

PIP w/ no change in PP = airway resistance ( bronchospasm,
secretions) or inspiratory gas flow rate
Both PIP & PP = increase in TV or pulmonary compliance (pulm
edema, pleural effusion, tension pneumothorax, ascites)
** DIFFERENCE BETWEEN PEAK AND PLATEAU REPRESENTS THE
RESISTANCE FLOW.
Calculate physiologic dead space
Vd = (PaCO2 PECO2)VE/PaCO2

Sternal angle = level of the CARINA

Abdominal surgery FRC ---this lung compliance and shunting/hypoxia
FRC is due to 25% loss in ERV
RV by 10%, TV moderately, TLV

ECG findings w/ COPD

Signs of right heart straing:
o Poor R wave progression
o Enlarged P-waves
o R waves greater than S waves in V1
o RBBB
o RAD
LOW VOLTAGE
Multifocal atrial tachycardia (MAT)

Effects of anticholinergics: (Ach muscarinic receptor, G-protein, PLC, IP3)

Lungs
Atropine bronchomotor tone + thickens bronchial secretions
Anticholinergic
Blocks M3 receptors
Eyes
Mydriasis & cycloplegia, can IOP
Interferes w sweating = temperature

Cardiac: SA conduction, HR
Cutaneous: vasoconstriction, flushing
GI/GU: Constipation/urinary retention, gastric acid secretion, LES tone
CNS: agitation/confusion
Eye: OP
INDICATIONS FOR BI-PAP
Post-op thoracic/abdominal surgery
Pulm edema 2/2 decom heart failure
Acute exacerbation of COPD
Immunosuppression

CONTRAINDICATED for:
AMS
resp drive
aspiration risk
HD instability
PTX
Patient refusal/noncompliance

BiPaP settings: iPAP, ePAP, FiO2

Static compliance: reflects elastic properties

Plateau pressure
Cstat = VT/Pplat - PEEP

OXYGEN DELIVERY: DO2 = Qt (CO) X CaO2 x 10

CaO2 = (1.39 x Hb x SaO2/100) + (0.003 x PO2)

Normal conditions: O2 consumption = 25% of delivery

The five major types of abnormal flow:volume loops are:

1. Obstructive pattern the loop is left shifted (towards the TLC) due to
hyperinflation and air trapping (increased RV). Decreased
expiratory flows show up in the top half of the loop with a
typical "scooped out" appearance.

2. Restrictive pattern a small volume loop that is shifted

towards the right. Both volumes and, to a lesser extent, flow
are decreased.

3. Fixed Upper Airway Obstruction - both inspiratory and

expiratory flows are decreased. The FVC is nearly normal.

4. Variable Intrathoracic Obstruction Peak expiratory flow is

markedly decreased in the presence of a nearly normal FVC.
FEF50/FIF50 <1

5. Variable Extrathoracic Obstruction - Peak inspiratory flow is

markedly decreased in the presence of a nearly normal FVC
FEF50/FIF50 >1
M5 Renal 4/29/2016 7:09:00 PM

Anatomy
Glomerulus contains Bowmans capsule which filters blood
Quantity of filtrate is dependent on blood flow and pressure w/in
glomerulus
Afferent artiole constriction decreases pressure and decreases filtrate
o Caused by sympathetic activation, ANG II, mesangial
constriction and endothelin
o Afferent dilation: prostaglandins, NO, ANP, dopamine and
bradykinin
Efferent constriction increases pressure w/in capsule, increases
filtrate
Angiotensin II (vasoconstrictor) works on both afferent and efferent.
Efferent are more sensitive. Low levels of ATII efferent affected more
and GFR increases

Autoregulation
Occurs between arterial pressure 70-120
Maintains RBC 1.25L/min
Maintains GFR at 125cc/min

Renal diuretic action of dopamine

Reduce Na reabsorption in the proximal tubule
Proximal tubule: ultrafilrate absorbed isotonically

Furosemide
MOA: Inhibits Na-K-2Cl transporter in the thick ascending loop of henle
(excreted in tubular lumen)
Transporter normally allows reabsorption of Na, K and chloride ions
Decreases tonicity of medullary interstitium and Increases tonicity of
the ultrafiltrate
Decreases gradient and decreasing water reuptake in the kidney and
diluting the urine
Weakly inhibits carbonic anhydrase and weakly inhibits Na-Cl transport
system
Inhibits tubuloglomerular feedback
Causes renal vasodilation by affecting prostaglandin levels
 Oral bioavailability is 50%
Can cause deficiencies in Na, K, Mg and Calcium
Metabolic alkalosis due to hypochloremia
Ototoxicity
Can cause digoxin toxicity

Thiazides: MOA: inhibits Na-Cl transporter in CCT

Acetazolamide works at proximal tubule

Carbonic anhydrase inhibitor
Bicarbonate uptake is decreases and H+ excretion decreases
Creates a non-gap acisosis

Aldosterone:
Mineralocorticoid, controls sodium secretion
ANG II stimulates release from adrenal cortex w/ BP, RBF,
hypovolemia, hyponatremia, hyperkalemia, ACTH , surgical stimlus
enhances Na uptake and potassium release into the urine at the
collecting duct

Main effector peptide of RAAS: AngII

o BINDS 2 RECEPTORS: 1) AT1 vasoconstriction, Na
reabsorption, sympathetic stim, aldosterone secretion,
vasopressin, endothelin

Conn syndrome = Primary hyperaldosteronism

Different from secondary hyperaldo due to LOW RENIN
Hypertension
Persistent hypokalemia
High urine excretion of K ((>30)
Underlying ischemic heart disease

Renin is released in response to B1 sympathetic stimulation an ddecreased

blood flow in the JGA
RAAS is responsible for blood pressure and lfuid homeostatsis
 In response to low afferent flow or sympathetic stimulationrenin is
released
Renin converts angiotensinogen to angiotensin I
Ang I AngII by ACE in the lungs
Ang II causes mesangial cells in the JGA to contract and decreases
blood flowthus further stmulating renin release
Ang II also increases aldosterone release from adrenal cortex

D1 receptors: dopamine/fenoldapam causes dilation of afferent and efferent

FENA < 1% or BUN/Cr > 15-20 = pre-renal

Acute interstitial nephritis: Tx w/ steroids

Tx of Hyperkalemia
Calcium: decreases resting potential of myocardial cells and raises
threshold potential
Insulin: stimulates many intermediaries including protein kinase B
o Increases number of Na/K ATPase on cell surface and increases
intracellular uptake of K
Bicarbonate: increases pH, drives H+ out of the cell and Na
inintracellular Na then stimulates Na/K ATPase
Beta-2 agonists: increases Na/K ATPase activity (K shifted inside cells)

Goal of ACE/ARB in CHF: stop the pathological increases in Na retention
caused by the heart failure

Acute tubular necrosis:

MOA: low cardiac output epithelial cell death
Classic causes aminoglycoside Abx, contrast, immunosuppressant,
chemo, HIV drugs, sepsis w/ low CO
Pathognomonic Muddy brown casts
Tx: Reestablish RBF

Oliguria: < 0.5 cc/kg/hr
Know metabolic acidosis/alkalosis in the setting of diuretics

Diuretics
Proximal Tubule:
Acetazolamide
Mannitol
Thick ascending limb: NKCC2 (sodium potassium di chloride inhibitor)
inhibition
Lasix
Ethacrynic acid
DCT: Na/Cl cotransporter inhibited
HCTZ
Metolazone
Collecting duct
Amiloride (epithelial Na channel inhibition), spironolactone (aldosterone
inhibition)
Thiazide diuretics increase calcium reabsorption
Loop diuretics lead to hypocalcemia

Digoxin:
Cardiac glycoside used to control HR in Afib
Reversibly inhibits N/K/ATPase in cardiac myocyte
o Ion pump normally generates extracellular Na gradient that
drives the Na/Ca exchanger which normally removes Ca from the
cellw/o Na gradient, more Ca accumulates resulting in inc
contraction of heart muscle
o Also inhibits Na/K/ATPase in renal tubuli- reduced Na
reabsorption and increased diuresis
o Low doses: decreases renin, aldosterone and norepi levels
Toxicity
o Arrhythmias (ventricular)
o Malaise
o Vision changes
o Salvodor Dali ECG signs
o Medications that causes HYPOKALEMIA inc. risk of toxicity
CRRT vs HD
CRRT: pressure driven
o Fluid can be given back
o Less effective?
o 2 types: CVVH and CVVHDf
convection vs ountercurrent diffusion
HD: high volumes/flows

Normal plasma osmolality: 290 mOsm/kg H20

(2xNa) + (Glu/18) + (BUN /2.8)

Hyperglycemia --- Na is underestimated

For every increase of glucose of 100Na will fall by 1.6

Salt wasting nephropathy---kidney loses ability to concentrate the urine

Spot urine Na should be < 20

Decrease K:
Insulin
Raising serum pH
Hypothermia
Beta 2 sympathetic stim

Hypokalemia ECG changes:

1) Increases myocyte automaticity
2) Delayed repolarization (weakness)
U waves, prolonged PR, T wave flattening, ST depression

Hypercalcemia
ECG: short QT and ST segments
o Tx w/ crystalloid and Lasix
o
HYPOPHOSPHATEMIA: respiratory failure or prolonged muscle relaxant
Cardiomyopathy, dec. immune function, hepatic dysfunction, platelet
dysfunction and acidosis
HYPOMAGNESAEMIA:
ECG: lengthening of PR and QT
HYPERMAG:
Vasodilation
Muscle weakness
bradycardia

Strong Ion gap (SIG) measure of all cations (Na, , Ca, Mg) - anions (Cl,
HCO3, lactate) and conj bases (A-) of strong acids
Normal: 40 mEq/L = 40 of unmeasured anions
When Cl levels inc. SIG decreases
SIG: Metabolic alkalsis
SIG: Metabolic acidosis

Common peroneal nerve injury:

Inc risk in thin people
Loss of dorsiflexion (foot drop)

Obturator reflex: occurs when electrocautery is applied to lateral bladder

wall
Obturator nerve: L2-L4
Requires GA as saddle block will not work

Bladder innervation:
General visceral afferentsderived from hypogastric plexus (which
itself receives innervation from T10)

TURP syndrome:
S/S: restless, SOB, dizzy, seizure, coma, HTN, brady
Classic Triad: SBP, DBP, HR
Common:
o Hyperammonemia (glycine solutions)
o Hypernatremia
o Hyperglycemia (sorbitol and glycine)
o Transient blindness
Distilled H20--> Hemolysis
Sorbitol--> converted to fructose--> hyperglycemia --> acidosis
Glycine (inhibitory neurotransmitter): transit blindness--> ammonia-->
encephalopathy

Regional for cystoscopy: T6

T8 needs to be blocked for loss of sensation
2 dermatomes higher for cold distrimination

Level of spinal for TURP: T10

Higher levels prevent recognition of bladder perforation

TURP
Regional Anesthesia:
o Sensory: T9-10
Bladder perforation:
o Bradycardia
o Hypotension
o Diaphoresis
o Nausea
o Pain suprapubic, inguinal
o Shoulder pain
o Hiccups
o dyspnea
NMB 4/29/2016 7:09:00 PM

Succinylcholine:
Only depolarizing muscle relaxant
Partial agonist at AChR, binds alpha subunit
Bind both nicotinic and muscarinic
ED95 = 0.3 0.6 mg/kg
o RSI = 2x ED95
o Intubation dose: 1-1.5 mg/kg
o Single dose = Phase 1 block
o Phase II block when doses > 3-5 mg/kg w/ volatile or >8mg/kg
w/ TIVA
Does not bind pre-synaptic receptors (unlike NDNMB)
Metabolized by plasma cholinesterase (PChE) to Suxmonochline
(active)
Adverse effects (4 large categories)
o 1) Ant-muscarinic Action
Muscarinic receptors are found in brain, heart, PNS
Can cause bradycardia, idioventricular rhythm
risk with high vagal tone (kids, manipulation of
cervix)
Atropine only prevents bradyarrhythmias, not
ventricular
o 2)Potassium release: 0.5 mmol/L
o 3) Allergic reaction: IgE mediated
o 4) Nonspecific
Fasciculations/myalgia
ocular pressure
IP
Pseudocholinesterase = Butyrlcholinesterase
Serine hydrolase, alpha-2 receptor globulin
Metabolizes Ach, Sux, mivacurium, trimethaphan, ester-local
anesthetics

Dibucaine number
Dibucaine inhibits plasma cholinesterase
Heterozygote atypical: inhibits 40-60%
Homozygote atypical: 20% --- 4-8 hr blocked
 Metabolized by different esterase compared w/ esmolol
o Esmolol is metabolized by RBC esterase (t1/2 10-20 min)
Homozygous typical:
o Di #: 70-80
o Response to Sux/Miva: normal
Heterozygous, atypical
o Di#: 50-60
o Response to Sux/Miva: Lengthened by 50-100%
o Occurs in 1/480
Homozygous atypical:
o Di#: 23-30
o Effects prolonged 4-8 hrs

UPregulation of nicotinic Ach-R outside NMJ following umn INJURY = EXTRA-

JUNCTIONAL ACH-R
Avoid Sux 24 hrs afrter burn occurs

Myasthenia gravis
Autoimmune, auto-Ab to acetylcholine R
Decreased number of functional Ach receptors
response to depolarizing NMB
o ED50 = 2x, ED95 = 2.6 x normal
o More likely to have phase II block
o Patients take anti-cholinesterases for treatment = prolonged
activity
Sensitivity to NDNMB
Physostigmine inhibits pseudocholinesterase to a lesser extent than
neostigmine
Edrophonium does not effect pseudocholinesterase
Tensilon test: Edrophonium
o Used to differentialte myasthenia gravis and cholinergic crisis
and Eaton-Lambert syndrome
o MG: improve strength
o Cholinergic crisis will become worse

Lambert-Eaton Myasthenic Syndrome (LEMS)

 Associated w/ oat cell carcinoma of the bronchus
Antibody-mediated destruction or presynaptic voltage-gated calcium
channels
o release of Ach at NMJ = weakness
Exercise improves weakness
Not improved with AChE inhibitors

Irreversible Acetylcholine esterase inhibitor: organophosphate, insectisides,

nerve gases

Physostigmine: AChE inhibitor: hydrolyzed in hours

Drugs used to treat Alzheimers: Rivastigmine, donepezil, galantamine
Pyridostigmine: used to great MG

Cerebral palsy: sensitivity to NDNMB, normal Sux

SLE: Sensitivity to all NMB

Cisatracurium
Metabolized by organ-independent Hoffman elimination in plasma
o Slowed by hypothermia
Laudanosine is a byproduct, metabolized by liver, excreted in kidney
o levels can cause seizure
not associated w/ histamine release

NM metabolized by pseudocholinestersase
Mivacurium ad sux

Extubation Criteria
Tetanus > 5 sec, sustained head lift
TV > 5 cc/kg
VC > 10 cc/kg
NIF more neg than -20
PaCO2 < 50
RR < 30
RSBI < 105 (RR/TV)
MUSCARINIC STIMULATION BY ACH
Myosis
Salivary secretion
Bradycardia
Bronchospasm
Insulin secretion
Bowel motility
Bladder sphincter relaxation
Cerebral excitation (only tertiary/pass BBB physostigmine)

MONITORING NMJ

* NMJ Transmission
voltage-gated ion channel
influx of calcium
Ach vesicles fuse w/ membrane and ach released
Bind to nicotinic receptors on motor end plate
Opens ion channels and epolarizes

Sustained head lift = at least 70% of function returned

Ulnar nerveadductor pollicis
Facial nerveplace elctrodes on mandlible and maxilla
Posterior tibial

Modes of stimulation:
Single twitch: supramaximal stimuli, 0.1-1Hz
TOF: 4 supramaximal stimuli at 2Hz, may be repeated at min every 10
sec
o 4th response lost = 75-80 blocked
o 3rd response lost= 85%
o 2nd lost = 90% blocked
o T4/T1 = 0.9 --- GOLD STANDARD
TETANUS

Electrolyte disturbances that enhance NMB:

 Hypokalemia
Hypercalemia
Hypermagnesemia
Hypernatremia

NMB & histamine release:

Sux, Mivacuriu, atracurium cause histamine release
Aminosteroid NMB do not

Burns and NMB

4 days 18 months = risk period
Higher induction doses of NMB required, duration of action increases

Patients w/ muscular dystrophy/MG have sensitivity

Critical Illness Myopathy

Normal nerve conduction studies
Absent compound musle action potentials on EMG
Myosin filament loss w/ preservation of actin on muscle biopsy

Risk:
o female
o APACHE score
o SIRS/sepsis
o MODS
o Prolonged mv
Regional 4/29/2016 7:09:00 PM

Topographical Anatomy and Landmarks

Order of structures for spinal needle:

Supraspinous
Interspinous
LIgamentum flavum
Dura
Arachnoid

Posterior nerve root: somatic visceral sensation (pain)

Anterior: motor and sympathetic outflow

Differential blockade:
Large myelinated neurons are more resistant to LA (A-alphja, motor)
o A-delta (pain, temp)thin, myelinated
o C (pain, temp)small, unmyelinated

Sympathetic chain: T1-L2

Cardioaccelerators: T1-T4
Spinal anesthesia blocks preload and afterload

Transient Neurogolic symptoms: radicular irritation after spinal anesthesia

Lidocaine is the most common offender

Lipid soluble LA: Bupivicaine & Ropivicaine

Bupivicaine toxicity is ACLS-resistant

Plain tetracaine/bupivacaine/ropivacaine: 1.5-2hr block
Adding epi has minimal effects on ropiv/Bupiv
Epi+ tetracaine: extends 1 hour

Chloroprocaine: short acting agent (also procaine)
Lidocaine: intermediate
Lido + Epi: surgical block 90 min
ASRA guidelines and spinal/epidural
D/C Plavix 7 days prior
INR < 1.5 = ok
PTT > 40 = not ok
PPX Lovenox: 12 h after last dosethen restart low cdose 6 hours later
BID Lovenox (therapeutic)-place block 24 h after last dose, restart 24
hours later

Adding fentanyl results in faster onset of surgical anesthesia

Liphophilic

Intrathecal morphine:
Hydrophilic
Crosses dura slowerlonger lifespan w/in CSF
Greater rostral spread
Lumbar intrathecal injection will produce analgesia into HIGH
THORACIC levels
2 peaks of respiratory depression:
o 2nd peak: 6 hrs after injection
 o Peak analgesis effects are at 6-12 hours..lasts 24 hours

Meperidine
Atropine like effects
Cardiac depressant effects
Euphoria
Local anesthetic properties
Post-op shivering

Side effects of intrathecal morphine:

Pruritus (worse than IV opioids)
o MOA: central (not histamine release)
o Tx: Zofran, propofol, naloxone Nalbuphine is best
Urinary retension (Fentanyl > Morphine)

Chlorprocaine for epidural:

Very fast onset but SHORT DURATION
Dose: 3% for epidural
Metabolized by pseudocholinesterase
Interferes w/ opioid mediated analgesia

Sacral Sparing: patchy epidural or less dense in L5-S2 due to large size of
nerve roots
Remedy: bolus in reverse trendelenburg
KNOW THESE:
Abciximab: 2 days
Argatroban/Bivaliriudin/Lepirudin: PTT < 40
Alteplase: 10 days
 Plavix: 7 days
Dabigatran: 3 days
Dalteparin (ppx)/full dose: 12/24 hrs
Fondaparinux (PPX/full): 48/72 hrs
Ticlopidine: 14 days
Tirofiban/Eptifibatide: 8 hrs

Interscalene block
Primary use: shoulder surgery (ALSO arm/elbow)
Target: nerves of upper brachial plexus: C4-C7
o Distal roots or proximal trunks
o Blocks suprascapular nerve (C4)top of shoulder
LANDMARKS: Anterior/ middle scalene muscles, Subclavian artery
o Pleura lies anteromedial to inferior trunk
o Posterior border of clavicular head of SCM
o Thyroid cartilage
o EJ (anterior)
Ulnar nerve sparing (C8, T1) (4th/5th fingers)
Side Effects:
o Phrenic nerve paralysis (100%)
o Horners syndrome (stellage ganglion)
Myosis, ptosis, anhydrosis, nasal stuffiness
o Recurrent laryngeal nerve block: hoarse voice
o Vertebral artery injection: too deep/directed more caudad
o Carotid artery injection: too anterior
o Epidural/subdural/intrathecal injection: too caudad
o Pneumothorax
o Bezold-Jarisch reflex: hypotension, bradycardia, coronary
vasodilation

Supraclavicular:
Purpose: Elbow, wrist, hand surgery
Target: Distal trunks/divisions
Side effects:
o Phrenic nerve paralysis (but as often as interscalne)
 o PTX
Landmarks:
o bundle of grapes, lateral & superficial to Subclavian artery
o posterior/lateral to Subclavian artery

Infraclavicular:
Purpose: same as supraclavicular block (wrist/hand)
o Spares C5-C6
Performed at level of CORDS: medial/lat/post
o Nerves located around axillary artery
o Lateral cord: SUPERIOR
o Posterior cord: POSTERIOR
o Medial cord: POSTERIOR/MEDIAL
Complications comparable to axillary
Contraindicated w/ coagulopathy
Advantages:
o Pt does not have to abduct arm
o Bilateral blocks can be done--> phrenic nerve not involved
o Continuous catheter can be placed
o Musculocutaneous does not have to be supplemented

Axillary Block:
Nerves: Median, ulnar, radial (misses musculocutaneous &
coracobrachialis)
Target: 3 terminal branches
Must supplement musculocutaneous
 Clockwise around axillary artery under ultrasound: MUR
o Median (supero-LATERAL, crosses at elbow then medial)
o Ulnar: Superior-Medial
o Radial: posterior
Problems: Neuropathy
Uses: Hand/wrist surgery

NERVE INJURY
Radial nerve
Axilla injury: unable to extend forearm (triceps)
Spiral groove: wrist drop

Musculocutaneous nerve injury:

weakness of elbow flexion (biceps) & supination of forearm
Median nerve injury: wrist flexion
paralysis of thenar muscles, loss of sensation over thumb, adjacent 2
fingers, and radial 2/3 of palm
weal wrist flexion

Ulnar nerve injury: claw hand/pinch

Sensation over 4th/5th fingers

Prominent Landmarks:
Prominent cervical thoracic process: C7
Inferior tip of scapula: T7
Superior iliac: L4
Posterior superior iliac spine: S2

In supine position: hyperbaric local anesthetic will not move above T5-T7

What CSF volume? And thus result in HIGHER BLOCK:

Pregnancy
Ascites
Advanced age
Kyphoscoliosis
Basic vertebral anatomy
7 cervical
12 thoracic
5 lumbar
5 sacral (fused)
Each vertebra is composed of:
Anterior: Vertebral body
Anterolateral: Bilateral pedicles
Posterolateral: bilateral transverse processes, bilaterall lamina
Posterior: spinous process

Surface Anatomy
C2 1st palpable spinous process
C7 most prominent
T7 inferior tip of scapula
L4 or L4/L5 interspace: superior point of iliac crests
S2: posterior-superior iliac spine

Dermatomes
C8 - 4th/5th digits of hand
T4- Nipple
o Required for upper abdominal surgery
o T6 is required for lower intestinal, uro/gyn
T7-xiphoid
T10-umbilicus
o Required for labor/vaginal delivery/hip surgery
S2-S5 saddle block for anl surgeries

Caudal space
Continuous w/ lumbar epidural space
Located on sacrum
5 fused spinal processesbut the 5th one is only fused
anteriorly..leaving the SACRAL hiatus posteriorly
Sacral hiatus is covered by the sacrococcygeal ligamentextension of
ligamentum flavum
How to locate:
 o Find coccyx and travel superiorlyabove gluteal cleft, until
palpate 2 sacral cornua

Epidural space: between ligamentum flavum and dura

Upper limit: foramen magnum
Lower limit: tip of sacrum
Act on spinal nerve roots traversing epidural space, also cross dura to
CSF
Slower onset compared to subarach
Block is less dense, less reliable than spinal
Sacral sparing is common
Adding vasoconstrictors prolongs duration and increases density of
block

Subdural space: between dura and arachnoid

Side effects of neuroaxial opioids

N/V
Pruritus
Shivering
Respiratory depression
o Faster for lipid soluble: fentanyl/sufentanil
o Bimodal for morphine

o
5 nerves of ankle to block
Posterior tibial (heel, plantar foot, toes)
o Motor: Flexors of foot, Sensory: Sole of foot
o Located posterior to medial malleolus
Sural lateral foot (S1-S2)
o Motor: none; Sensory: lateral foot
o Located posterior to lateral malleolus
o Sensory to posterolateral leg, lateral foot, 5th toe
Superficial peroneal: L4-S1
o Motor: extensors, sensory: dorsum of foot (except webspace of
big toe)
Deep peroneal: L4-L5 (web space of big toe)
o Motor: extensors of foot; Sensory: 1st web space
o Located lateral to dorsalis pedis artery & extensor hallicus
longusinnervates flexors to toes, sensation between great and
2nd toe
Saphenous (L3-L4): only nerve from femoral
o Motor: none; Sensory: medial leg & foot
o Located anterior to medial malleolus
o Sensoty to anteromedial leg/medial foot

Blocks associated with greatest risk of systemic uptake of LA:

Intercostal > caudal > epidural > brachial plexus > sciatic-femoral >
SQ
I Cant Even Believe she Found Sally

Local anesthetic potency is directly correlated w/ lipid solubility

in non-ionized state
Drugs are cleared from subarachnoid space by vascular absorption in
epidural and subarachnoid space

Pneumatic tourniquet:
Must be inflated to excess 100mmHg
Pain: due to unmyelinated, slow-conducito C fibersresistant to local
anesthetic
 Can cause DVT
Cuff deflation: CVP, MAP , PaCO2, ETCO2 ,Lactate and K

TENs Unit
Produces tingling or vibratory sensation
MOA: produces analgesia by releasing endogenous endorphinsthese
activate inhibitor neurons
Increasing dose of LA will hasten onset and duration of epidural

Neuorolytic Nerve blocks

USED FOR INTRACTABE PAIN, often at end of life
Lidocaine:
o Painful, lasts 3-6 months
Phenol:
o Not painful, biphasic action, lasts 2-3 mothns
o
Post-dural Puncture headache
Risk: young adults, women, pregnant, larger needle, shape of tip
(Quincke)
Symptoms
o Ocular: Diplopia due to CN VI palsy
o Auditory: tinnitus/hypacusis (CN VIII)

Bupivacaine Toxicity:
Mechanism
o -Dose-dependent blockade of sodium channels. Of note,
o 1) bupivacaine binds more strongly to resting/inactivated Na
channels as compared to lidocaine, and
o 2) bupivacaine dissociates from Na channels during diastole
more slowly than lidocaine.
Diagnosis of LA Systemic Toxicity
o -CNS signs: Circumoral numbness, Slurred speech, Muscle
twitching, restlessness, agitation drowsiness seizures
o -Cardiovascular signs: Bradycardia, dysrhythmias, Hypotension,
Heart block arrest
Treatment
 o Supportive
o -Seizures: treat with GABA agonists.
o -Convulsions: treat with paralytics and airway management
o -Hypotension: vasopressors may be indicated, although at
decreased doses
o -CV collapse: CPR + 20% Intralipid [1.5- 4mL/kg, then 0.25-0.5
mL/kg/min infusion for 10-60 min]

Stellate ganglion block

Anatomy: Fusion of inferior cervical and T1 sympathetic ganglia,
located anterior to transverse process of C7;
o block is at C6 (Chassignacs tubercle) however to decrease
risk of pneumothorax
Relations of stellate ganglion
o Anterior: SCM muscle, carotid sheath. Dome of lung is anterior
and inferior.
o Medial: prevertebral fascia, C7 vertebral body, esophagus,
thoracic duct
o Posterior: longus colli muscle, anterior scalene muscle, vertebral
artery, brachial plexus sheath, 1st rib
Indications: CRPS, angina, phantom lib pain, herpes, Menieres disease,
hyperhidrosis, Raynauds
Complications
o Horners sign should occur EVERY time you do this block
o RLN injury (hoarseness)
o Hemidiaphragm
o Hematoma
o Brachial plexus injury
o PTX
o Esophageal perf
o Intrathecal/epidural/intravascular

Topical anesthesia
Lidocaine
Tetracaine
Cocaine
 Dibucaine
Benzocaine
Lido + Prilo = EMLA cream
IV regional/Bier Blocks
Esters are NOT used
Bupivacaine can cause cardiac problems
Use Lidocaine or Prilocaine

Short duration of action

Procaine & 2-chloroprocaine

Intermediate:
Lidocaine
Mepivacaine
Prilocaine
Long Duration:
Bupivacaine
Tetracaine
Ropivacaine

Criteria for intravascular epi+LA:

T wave amp by 25%
HR by 10
SBP 15

A-alpha:
efferent to skeletal muscle
A-beta:
Afferent from skin/joints
Touch, proprioception
A-gamma: Efferent to muscle spindles for tone
3-6 um, CV 15-35 m/sec
A-delta: Afferent
Myelinated
Sharp/localized pain/temp/touch
1-4um, CV 5-25
B fibers
Myelinated, preganglionic sympathetic
<3um, medium CV 3-15
autonomic nervous system control
C fibers:
Unmyelinated, post-ganglionic sympathetic, free nerve endings
Slow CV, 0.1-2 m/sec
Diameter = 1-4 nm
Afferent sensory
Nonlocalized pain, temp, touch

Spinal anesthetic in kids: requires larger volume and does not last as long

S1-2: ankle
L3-4: knee
C5-6: biceps, supinator
C7-8: triceps

Perivascular femoral (3 in 1 block) to lumbar plexus blocks = Femoral nerve

block
Femoral, Lateral fem cutaneous, Obturator
Only fem reliably blocked
Obturator is least likely to be blocked (L2-L4)

Distal Humerus surgery in pt w/ COPD

Interscalene will get all of the nerves but risk of phrenic nerve
paralysis = NO
Supraclav: all the nerves, lower risk of phrenic nerve BUT risk of PTX
= NO
Infraclav
Axillary block: minmal risk of PTX or phrenic nerve block
o Does NOT block musculocutaneous
Clopidogrel: 7 days
Ticlopidine: 10-14 days
Abciximab (ReoPro) - 48 hours
Ebtifibatide (Integrilin) - 8 hours
Tirofiban (Aggrastat) - 8 hours

Dabigatran (DTI (factor IIa) contraindicated for neuroaxial

Rivaroxaban (Xa inhib) contraindicated
Nerve Blocks to Know 4/29/2016 7:09:00 PM

Supraorbital and Supratrochlear nerve block

Ophthalmic division of trigeminal nerve (V1): sensory to anterior scalp

Infraorbital Block:
Used for analgesia after cleft lip repair
Terminal branch of maxillary division of trigeminal V1

Superficial Cervical Plexus Block

Ventral rami of C2-C4

TAP block: between transversuss abdominis and internal oblique

Triangle of Petit
Blocks T9-L1
o Subcostal (T12)
o Ilioinguinal (L1)
o Iliohypogastric (L1)
Bilateral block required
Visceral pain NOT reduced

Adductor canal block

US: Femoral artery & saphenous nerve is at 9pm
Advantage over femoral block
o Less motor block = earlier mobilization
Why? Saphenous nerve is purely sensory\
Difficulty:Saphenous nerve is LATERAL PROXIMAL, but crosses
MEDIAL (distal)

Femoral nerve block: sensory & motor

 o A = fascia lata
o B= fascia iliaca
3 structures that are essential to visualize:
o Femoral artery
o Fascia lata
o Fascia iliaca

Interscalene Block: The interscalene block is performed predominantly for

shoulder surgery. Interscalene blocks generally do not provide adequate
coverage of the arm due to only partially blocking the median nerve and
essentially not blocking the ulnar nerve.

Supraclavicular and Infraclavicular Blocks: Performed at the level of the

cords of the brachial plexus, these blocks are excellent for surgeries distal to
the mid-humeral level.

Axillary Block: The axillary block is frequently performed for surgeries distal
to the elbow.

Supraclavicular Nerve block

Brachial plexus, superior to clavicle, coursing next to subclavian artery
Side effects:
o Phrenic nerve blockade
o Horner syndrome
o PTX

BRACHIAL PLEXUS:
The brachial plexus is composed of the 5 nerve roots (C5-T1) that combine
to form the superior, middle, and inferior trunks. These trunks further divide
to form the lateral, medial, and posterior cords, which then branch off into
the peripheral nerves of the upper extremity (Table 1).

Nerve Motor Sensation

Musculocutaneous Arm flexion Lateral forearm
Elbow flexion
Median Lateral deviation of Medial aspect of palm
wrist and grip of thumb, including thumb, index,
index, and middle and middle fingers
fingers
Flexion of wrist
Flexion of 2nd, 3rd digigs
Pronation of forearm
Opposition of thumb
Ulnar Medial deviation of wrist Medial forearm and
and grip of 4th and 5th lateral aspect of hand
fingers including 4th and 5th
Flexion at wrist, fingers
adduction of thumb
Radial Arm and wrist extension Extensor surfaces of
Extension of all digits, arm and hand
wrist and elbow
Supination of forearm
Dermatome Block LEvels
Surgical Procedure Block Height
Upper abdominal surgery T4-5
Cesarean section

Appendectomy T6-8
Inguinal Herniorhaphy
Pelvic procedures

Transurethral resection of prostate T10

Obstetric vaginal delivery
Hip procedures

Lower extremity (below the knee) L2-3

Surgical perineal procedures S1-2

Blocks for labor

1st stage: T10-L1
 2nd stage: S1-3
Cesarean: dermatomal coverage up to T4

Knee flexion: tibial

Knee extension: femoral
Plantar flexion (tibial part) & dorsiflexion (peroneal) Sciatic nerve

All nerves of the foot (except saphenous) are derived from sciatic nerve

sciatic nerve branches to the tibial and common peroneal.

Saphenous is a branch of femoral
M5 Volatiles 4/29/2016 7:09:00 PM

Normal VS:
Preterm: HR 160, SBP 50, DBP 30, RR 50
Term: HR 130, SBP 60, DBP 40, RR 50
1 YR: HR 120, SBP 80, DBP 60, RR 25
Toddler: HR 90, SBP 100, DBP 60, RR 20

Blood Volumes:
Newborn: 90 cc/kg
Infant: 75 cc/kg
Toddler: 70 cc/kg

ABG:
Birth: pH 7.2, paO2 50, paCO2 50
1 wk after birth: pH 7.4, paO2 70, paCO2 35
Toddler: pH 7.4, paO2 95, paCO2 40

Normal umbilical artery blood gas:

pH 7.3, paO2 20, paCO2 50

Normal umbilical VEIN blood gas:

7.35, paO2 30, paCO2 40

Fetal circulation: placenta --> vein --> heart --> arterial --> placenta

F-Hb (fetal hemoglobin) --> affinity for oxygen. Unable to bind 2,3 DPG
P50 = 19 (adult = 27)

Prior to birth: placental oxygenated blood is delievered via UMBILICAL VEIN

thorugh LIVER (& ductus venosus) to IVC and into RA.
Blood from IVC has HIGH O2 tensions, blood from SVC has LOW O2
tensions.
Blood from IVC--> foramen ovale--> LV --> AORTA --> Mixes w/
deoxyganed blood from ductus arteriosis.

Failure of PDA to close:

persistent pulm HTN
After birth, high oxygen tensions causes PVR to fall, blood will now flow
through pulm circulation and NOT ductus arteriosus.

Patent Ductus arteriosus:

machine-line continuous murmur at LUSB, bounding pulses, widened
pulse pressure
Usually left to right shunt
Before 60 weeks post-conceptual age, an infant should have a
minimum of 12 hours apneic free before discharge

Infants desaturate quickly due to VO2 as well as a lower FRC

Infants have a FASTER inhalation induction due to INCREASED MV/FRC ratio

Neonatal ratio: 5:1
o Why so high? b/c O2 consumption is higher w/ same/lower FRC
Adults: 1.5:1

Neonatal diaphragm25% type 1 fibers (vs 55% in adults)

Type 1 fibers: fatigue resistant (twitch)endurance

Both hypoxic and hypercarbic drives are immature at birth

Neonates have chest wall compliance

FRC = point at which outward elastic recoil of chest matches inward recoil of
lung (at end-expiration)
Both decreased in neonates
FRC

Pediatric Upper Airway differences

Head is proportionately largersniffing position is harder
o Use shoulder roll
Glottis is at C4 instead of C6
Cricoid cartilage = narrowest portion

Normal neonatal glucose can be as low as 30

 After day 1 of life: Hypoglycemia = < 45

Spinal Anesthetic in Infant:

Spinal cord ends at L3
o After 1 year it ends at L1
Dural sac ends at S4 in neonates
o S2 for 1year-adult
Ropivicaine is less cardiotoxic than bupivacaine
Neonatal Ventilation
HFOV: High frequency oscillatory ventilation
SIMV or AC
ECMO
Bronchopulmonary dysplasia is a continuum of RDS

Lecithin-sphingomyelin (L/S): 2.0 = sufficient surfactant production

L/S 1.5

Propofol (lipophilic) redistributes faster in neonates due to blood volume

PRIS:
Inhibits proteins that allow transfer fo FA into mitochondriamito are
starved of energy
Lactic acidosis..necrosis

Infants are more sensitive to opioids/benzos/barbiturates

Thiopental/propofol: sensitivitydue to BV

INFANTS REQUIRE DOSE OF SUX COMPARED W/ KIDS DUE TO Volume

of distribution and they dont have sensitivity to sux as they do other NMB

Masseter muscle spasm in MH: 30%

Put pulse ox on right hand in infants (PRE-DUCTAL)

Retinopathy of prematurity:
 Pathophysiology: retinal artery constrictionproliferation of abnormal
vesselts resulting in scar/hemorrhage and retinal detachment
Risk factors:
o O2
o Genetic: sex/Caucasian

Post-anesthetic apnea in newborn

Definition: apnea for 15+ sec or apnea of any duration resulting in
desat or bradycardia
Delay elective surgry until 44-60 weeks
Pulmonar surgery: 6 months
Risk of apnea w/ caffeine or aminophylline

Chemical pneumonitis
Pulm edema
Hypoxia
Pulmonary hypertension

Acls FOR NEONATE:
Hypoxia w/o bradycardia--> supplemental O2
HR < 100 --> ppv
HR < 60--> Chest compressions at 120min but FIRSTmask ventilation
Chest compression:ventilation ratio = 90:30 (3:1)
o Adults = 3:2
Epinephrine:
o Tracheal epi: 10 x the IV dose 0.1mg/kg
o IV: 0.01-0.03 (ALWAYS USE 1:10,000 for IV)

APGAR
Appearance
Pulse
Grimace
Activity
Respiration

Omphalocele: midline, covered by sac

Necrotizing enterocolitis pressor of choice = DOPAMINE

Most common TEF: IIIB = proximal esophageal atresia, distal fistula

2nd Most common: Esophageal atresia
3rd most common: H-ype (fistula between trachea and intact
esophagus)
o Associated w/ VACTERL type V
Vertebral
Anal defects
Cardiac (VSD,ASD, TOF)
TEF
Esophageal atresia
Renal/radial atresia
Other limbs
Pyloric stenosis --> metabolic alkalosis
Hypochloremia, hypokalemia (early)
o Respiratory compensation: MV, retention of CO2
Late: acidotic

Tetrology of Fallot
Most common CHD
RIGHT LEFT shunt, pulm blood flow, hypoxemia
o SVR or spasm of unfundibular cardiac muscle causes pulm
blood flow & r to left shunt
4 features:
o VSD
o RVH
o Over-riding aorta
o Right ventricular outflow tract obstruction
ECG: RAD, RVH
CXR: pul vascular markings, rt aortic arch
Tet spell: hypercyanotic attack, peak 2-6 mo (feeing, crying,
defecating)
o SVR = hypoxemia
Tx: O2, chest-knee position, morphine
o Anesthetized pt: SVR = Lft to right shunt (Neo, BB, fluids)
 Hemodynamic goals:
o preload (squatting, Neo, fluid bolus)
o Slow sinus rhythm (beta blockers)
o contractility (volatile?)
o SVR (Neo)
o PVR (Hi FiO2, hyperventilate)
ANESTHESIA:
o No spinal! Early epidural is goodmay PVR
o AVOID: Atropine, nitrous, iso ( HR), Epi, dop

Down Syndrome:
CHD
ASD
Upper Airway Obstruction/Sleep Apnea
Hypothyroidism

NPO guidelines
Clears: 2 hrs
Breast milk: 4 hours
Infant formula: 6 hours
Solids/non-human milk: 6-8 hrs

Post-op Apnea in preterm infants

Risk varies inversely w/ age at birth & postconceptual age
Post-conceptual age is the single most important determinant of postop
apnea
Anemia (Hct < 30%)
Small for gestational-age infants have risk of post-op apnea

Neonates/normal lab values:

Glucose: 5-90 (tx at 40)
Hemoglobin: 15-20
Creat: <0.8
Platelets: normal 250

PULM of neonate vs adult:

 compliance of chest
TLC: 160cc (63cc/kg) [ Adult 6,000 cc]
TV: 21 cc/kg (vs 575 cc/kg in adult)
O2 consumption: 6-8 cc/kg/min (vs 3-4 in adult)
FRC ~ 30cc/kg due to laryngeal breaking = termination of exhalation
prior to relaxation vol.

Anesthetic Uptake (volatile reaching alveolus and being taken up by mixed

venous blood)
Depends on
o Solubility of the agent
Partition coefficient
o Difference in partial pressures between alveolus and venous
blood
Lower partial pressure of agent in blood and highter in
alveolus results in greatest pressure difference
o Pulmonary blood flow
CO will speed of induction

Induction : FA/FI
Solubility: less soluble = faster induction
Cardiac output: decreased = faster induction
o CO ----FA lags behind FI
o Increasing ventilation
FA increases and FI does not change
Ratio increases
Shunt (right to left)
o Blood bypasses lungs, dilutes mixed venous blood returning from
pulm circulation causing increased gradient between alveoli and
arterial blood slows induction
Concentration effect = at igh concentrations, speed of induction
increases as FA approximates FI


Right mainstem intubation:
Shunt increases
Dec. concentration of gas in mixed venous blood
Greater concentration difference from alveoli to venous blood
More anesthetic will be pulled from alveoli into blood BUT less blood is
being exposed to lungs
Altogether, FA continues to approximate FI yet the arterial partial
pressure of volatile is decreased
Soluble agents are less affected

Left to right shunt will NOT SLOW induction time

Blood gas partition co-efficient

Des: 0.42 = blood will have 42% as much des when compared to
alveolar gas. (insoluble)
Iso = 1.4
Inc. Ventilation speeds induction by replacing agent in alveoli after it is
taken up (FA remains close to FI)
o Less agent removed by blood w/ insoluble agent (Des)
Right to left cardiac shunt will SLOW induction of DES more than iso
Meyer-Overton Rule= inhalation agents potency correlates with lipid
solubility
Solubility = blood/gas coefficients
Induction

1.3 MAC = ED95

5% of patients will move to surgical stimulation

6% decrease in MAC per decade of life after age 40

What metabolic disturbance INCREASES MAC?

Hypernatremia
Hypercarbia
Hyperthyroidism?
Chronic drug use

Respiratory changes @ 1MAC

bronchodilation
TV and MV, RR, dead space
o TV are not fully compensated by RR
blunted hypoxic pulm vasoconstriction
High levels: flaccid muscle tone, respiratory arrest, cardiovascular
collapse, pupils fixed/dilated

Nitrous
Preserved minute ventilation, no rise in apneic threshold
at 50-70%, stimulate sympathetic nervous system
small increase or no change in HR, MAP, CO
Mild myocardial depressing effects, outweighed by sympathetic
stimulation
PVR increases.can exacerbate pulm HTN
Preserved minute ventilation, no rise in apneic threshold
Inhibits enzymes
o Methionine synthetase myelin formation
o Thymidylate synthetase DNA synthesis
 Peripheral neuropathies, pernicious anemia, megaloblastic anemia,
depressed bone marrow
35x MORE SOLULB THAN NITROGEN IN BLOOD

Special properties of Desflurane:

Very high vapor pressure: 669mmHg
In traditional vaporizer: it would vaporize several more volumes
Boils just above room temp
High MAC
HIGH LOWER AMBIENT BAROMETRIC PRESSURES: partial pressure of
Des is
Isoflurane dilates coronary arteries the most
Burst suppression on EEG
1.5 MAC ISO

Rapid increases of des or Iso can lead to tachycardia/HTN

Metabolism of Volatiles
Sevoflurane ismetabolized the most @ 5%
Iso: 0.2%
Nitrous <0.2%
Halothane: 20%

Rapid increase in concentration of Des or iso can lead to transient

tachycardia and BP

levels of carboxyhemoglobin after use of desflurane: desiccated CO2

absorbent (classicaly barium hydroxide lime)

CO has more effect on the rate of change of FA/Fi for POORLY SOLUBLE
AGENTS (ISOFLURANE)(

Iso: 1.46
SEvo: 0.65
Des: 0.42
Nitrous
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